psych case study & stat hw assignment due 12/1/12 by 4:30pm

psych case study & stat hw assignment

PSYC 430

Case Study: Schizophrenia Answer Sheet

Student Name:

Diagnosing Randy:

1. Go to the DSM-IV checklist for schizophrenia and list each of Randy’s behaviors that satisfy the symptom criteria for schizophrenia. Which of Randy’s symptoms meet any of the criteria? (Be sure to match specific symptoms with specific criteria.)

2. How long has Randy been experiencing symptoms that meet the criteria for schizophrenia?

3. What type of schizophrenia does Randy display?

4. What phase of schizophrenia was Randy in during the days before the diner incident?

5. What phase was he in at the time of the diner incident that led to his arrest?

Explaining Randy’s Schizophrenia:

1. What genetic factors may have played a part in Randy’s schizophrenia?

2. What biochemical abnormalities might account for Randy’s symptoms?

3. What might have been the role of family stress in Randy’s disorder?

4. What sociocultural factors may have played a role in Randy’s schizophrenia?

Treating Randy:

1. Assume that instead of being jailed for his offenses, Randy is referred to a community health center for treatment planning. You are assigned to be his caseworker. What kind of assessments will you need to do before you begin Randy’s treatment planning?

2. What type of medication might you recommend for Randy?

3. What mental health treatment modalities would be helpful to Randy in addition to medication?

4. What services other than mental health treatment might be beneficial for Randy?

·

You will complete a total of three (3) Case Study assignments.  For each assignment, read through the case study and complete the provided answer sheet of questions, utilizing information from the Comer textbook to formulate appropriate answers.  Submit the completed document as an attachment via the assignment submission link.
Grading will be based on the accuracy and quality of answers, the demonstration of higher-level critical thinking skills, and appropriate quantity/content of the answers.  Your answers should do the following:

· Be in complete sentences.

· Demonstrate focus and clarity of thought.

· Display grammar, spelling, and sentence structure appropriate for college-level work.

Access the case study above, navigating through it using the tabs at the top of the page and using the Previous/Next buttons on the bottom.  (The animations on this page require the Flash plug-in, version 6.0 or later.  This page works best in the Internet Explorer browser.)  Thoroughly read the case study, making sure to read the Presenting Complaint and Social/Family History tabs.  See also the DSM criteria regarding Schizophrenia in the Diagnosis tab.  Use the information from the case study and your textbook to answer the 13 questions on your Case Study: Schizophrenia Answer Sheet.  Do not use the question and answer blocks provided in the case study.  Answer all the questions in the document and submit your finished document for grading through the assignment submission link below

Page 1 of 7

Eating Disorders 283
4,1
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\\\nUir31( nU12 ,/, ‘
1. What are the symptoms and main
features of anorexia nervosa?
pp. 258-260
2. What are the symptoms and
main features of bulimia nervosa?
pp. 260-264
3. How are people with anorexia ner-
vosa similar to those with bulimia
nervosa? How are they different?
pp. 264-265
4. Theorists usually apply a multi-
dimensional risk perspective to
explain the eating disorders. What
does this mean? p. 265
5. According to Hilde Bruch, how
might parents’ failure to attend
appropriately to their baby’s internal
needs and emotions contribute to
the later development of an eating
disorder? pp. 265-266
6. How might a person’s hypothala-
mus and weight set point contribute
to the development of an eating
disorder? pp. 267-270
7. What evidence suggests that socio-
cultural pressures and factors may
set the stage for eating disorders?
pp. 270-275
8. When clinicians treat people with
anorexia nervosa, what are their
short-term and long-term goals?
What approaches do they use to
accomplish them? pp. 275-278
9. How well do people with anorexia
nervosa recover from their disor-
der? What factors affect a person’s
recovery? What risks and prob-
lems may linger after recovery?
pp. 278-279
10. What are the key goals and
approaches used in the treatment
of bulimia nervosa? How success-
ful are they? What factors affect
a person’s recovery? What risks
and problems may linger after
recovery? pp. 279-281
Search the Fundamentals of Abnormal Psychology Video Tool Kit
www.worthpublishers.com/apvtk
A Chapter 9 Video Cases
Imprisoned by an Eating Disorder
Anorexia Nervosa: Not for Women Only
Weight Gain: A Surprise Factor
A Video case discussions, study guides, and questions
Log on to the Corner Web Page
www.worthpublishers.com/comer
A Chapter 9 outline, learning objectives, research exercises, study tools,
and practice test questions
A Additional Chapter 9 case studies, Web links, and FAQs

SUBSTANCE-RELATED
DISORDERS CHAPTER

66 am Duncan. l am an alcoholic.” The audience settled deeper into their chairs at these
familiar words. Another chronicle of death and rebirth would shortly begin [at] Alcoholics
Anonymous. .
. . . “I must have been just past my 15th birthday when 1 had that first drink that everybody
to ks about. And like so many of them . . . it was like a miracle. With a little beer in my gut,
the world was transformed. l wasn’t a weakling anymore, 1 could lick almost anybody on the
block. And girls? Well, you can imagine how a couple of beers made me feel like l could have
any girl I wanted.
“Though it’s obvious to me now that my drinking even then, in high school, and after I got to
college, was a problem, l didn’t think so at the time. After oil, everybody was drinking and get-
ting drunk and acting stupid, and I didn’t really think l was different. . . . 1 guess the fact that
hadn’t really had any blackouts and that I could go for days without having to drink reassured
me that things hadn’t gotten out of control. And that’s the way it went, until 1 found myself
drinking even more—and mare often—and suffering more from my drinking, along about my
third year of college.
… “My roommate, a friend from high school, started bugging me about my drinking. It wasn’t
even that I’d have to sleep it off the whale next day and miss class, it was that he had begun
to hear other friends talking about me, about the fool I’d made of myself at parties. He sow
how shaky 1 was the morning after, and he saw how different I was when I’d been drinking
a lot—almost out of my head was the way he put it. And he could count the bottles that
I’d leave around the room, and he knew what the drinking and carousing was doing to my
grades. . . . [P]ortly because l really cared about my roommate and didn’t want to lose him
as a friend, i did cut down on my drinking by half or more. I only drank on weekends—and
then only at night. . . And that got me through the rest of college and, actually, through law
school as well. .
“Shortly after getting my law degree, l married my first wife, and … for the first time since
I started, my drinking was no problem at all. I would go for weeks at a time without touching
a drop. . . .
“My marriage started to go bad after our second son, our third child, was born. I was very
much career-and-success oriented, and I had little time to spend at home with my family. . . .
My traveling had increased a lot, there were stimulating people on those trips, and, let’s face
it, there were some pretty exciting women available, too. So home got to be little else but a
nagging, boring wife and children I wasn’t very interested in. My drinking had gotten bad again,
too, with being on the road so much, having to do a lot of entertaining at lunch when I wasn’t
away, and trying to soften the hassles at home. I guess I was putting down close to a gallon of
very good scotch a week, with one thing or another.
‘And as that went on, the drinking began to affect both my marriage and my career. With
enough booze in me and under the pressures of guilt over my failure to carry out my responsibili-
ties to my wife and children, I sometimes got kind of rough physically with them. I would break
furniture, throw things around, then rush out and drive off in the car. 1 had a couple of wrecks,
lost my license for two years because of one of them. Worst of all was when 1 tried to stop. By
then I was totally hooked, so every time / tried to stop drinking, I’d experience withdrawal in
all its horrors … with the vomiting and the ‘shakes’ and being unable to sit still or to fie down.
And that would go on for days at a time. . . .
TOPIC OVERVIEW
Depressants
Alcohol
Sedative-Hypnotic Drugs
Opioids
Stimulants
Cocaine
Amphetamines
Hallucinogens
Cannabis
Combinations of Substances
What Causes Substance-Related
Disorders?
Sociocultural Views
Psychodynamic Views
Cognitive-Behavioral Views
Biological Views
How Are Substance-Related
Disorders Treated?
Psychodynamic Therapies
Behavioral Therapies
Cognitive-Behavioral Therapies
Biological Treatments
Sociocultural Therapies
Putting It Together: New Wrinkles
to a Familiar Story

292 ://CHAPTER 10
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Alcohol and Auto Fatalities:
A Special Relationship .
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2008). The rate may increase to as many as 29 of every 1,000 babies of women who
are problem drinkers. In addition, heavy drinking early in pregnancy often leads to a
miscarriage. According to surveys, around 11 percent of pregnant American women
have drunk alcohol during the past month and 4.5 percent of pregnant women have
had binge-drinking episodes (NSDUH, 2008).
Sedative-Hypnotic Drugs
Sedative-hypnotic drugs, also called anxiolytic drugs, produce feelings of relaxation
and drowsiness. At low dosages, the drugs have a calming or sedative effect. At higher
dosages, they are sleep inducers, or hypnotics. The sedative-hypnotic drugs include bar-
biturates and benzadiazepines.
Barbiturates First discovered in Germany more than 100 years ago, barbiturates
were widely prescribed in the first half of the twentieth century to fight anxiety and to
help people sleep. Although still prescribed by some physicians, these drugs have been
largely replaced by benzodiazepines, which are generally safer drugs. Barbiturates can
cause many problems, not the least of which are abuse and dependence. Several thousand
deaths a year are caused by accidental or suicidal overdoses.
Barbiturates are usually taken in pill or capsule form. In low doses they reduce a per-
son’s level of excitement in the same way that alcohol does, by attaching to receptors on
the neurons that receive the inhibitory neurotransmitter GABA and by helping GABA
operate at those neurons (Ksir et al., 2008; Grilly, 2006). People can get intoxicated from
large doses of barbiturates, just as they do from excessive alcohol.At too high a dose, the
drugs can halt breathing, lower blood pressure, and lead to coma and death.
Repeated use of barbiturates can quickly result in a pattern of abuse (Dupont &
Dupont, 2005). Users may spend much of the day intoxicated, irritable, and unable to
do their work. Dependence can also result. The users organize their lives around the
drug and need increasing amounts of it to calm down or fall asleep. A great danger of
barbiturate dependence is that the lethal dose of the drug remains the same even while
the body is building up a tolerance for its sedating effects. Once the prescribed dose
stops reducing anxiety or inducing sleep, the user is all too likely to increase it without
medical supervision and eventually may ingest a dose that proves fatal. Those caught in
a pattern of barbiturate dependence may also experience withdrawal symptoms such
as nausea, anxiety, and sleep problems. Barbiturate withdrawal is particularly dangerous
because it can cause convulsions.
Risks and Consequences of Drug Misuse
Opioids
———
Sedative-hypnotics
Barbiturates
Benzodiazepines
. ———–
Risk of Risk of Risk of Severe
Organ Severe Social or Long-Lasting
Intoxication Dependency Damage or Economic Mental and
Potential Potential or Death Consequences Behavioral Change
High High Low High Low to moderate
Moderate

Moderate to high Moderate to high Moderate to high Low
Moderate

Moderate Low Low Low
Stimulants (cocaine,
amphetamines) High High Moderate Low to moderate Moderate to high
i Alcohol High Moderate High High High
Cannabis High Low to moderate Low Low to moderate Low
r Mixed drugs High High High High High
Source: Ksir et al., 2008; APA, 2000; Gold, 1986, p. 28.

Substance-Related Disorders :1/ 293
Benzodiazepines Chapter 4 described benzodiazepines, the antianxiety drugs
developed in the 1950s, as the most popular sedative-hypnotic drugs available. Xanax,
Ativan, and Valium are just three of the dozens of these drugs in clinical use. Altogether,
about 100 million prescriptions are written each year for this group of drugs (Bisaga,
2008). Like alcohol and barbiturates, they calm people by binding to receptors on the
neurons that receive GABA and by increasing GABA’s activity at those neurons (Ksir
et al., 2008). These drugs, however, relieve anxiety without making people as drowsy as
other kinds of sedative-hypnotics.They are also less likely to slow a person’s breathing, so
they are less likely to cause death in the event of an overdose (Nishino et al., 1995).
When benzodiazepines were first discovered, they seemed so safe and effective
that physicians prescribed them generously, and their use spread. Eventually it became
clear that in high enough doses the drugs can cause intoxication and lead to abuse or
dependence (Bisaga, 2008).As many as 1 percent of the adults in North America abuse
or become physically dependent on these antianxiety drugs at some point in their lives
(Sareen et al., 2004; Goodwin et al, 2002) and thus become subject to some of the same
dangers that researchers have identified in barbiturate misuse.
Opioids
Opioids include opium—taken from the sap of the opium poppy—and the drugs de-
rived from it such as heroin, morphine, and codeine. Opium itself has been in use for
thousands of years. In the past it was used widely in the treatment of medical disorders
because of its ability to reduce both physical and emotional pain. Eventually, however,
physicians discovered that the drug was physically addictive.
In 1804 a new substance, morphine, was derived from opium. Named after Mor-
pheus, the Greek god of sleep, this drug relieved pain even better than opium did and
initially was considered safe. However, wide use of the drug eventually revealed that it,
too, could lead to addiction. So many wounded soldiers in the United States received
morphine injections during the Civil War that morphine dependence became known
as “soldiers’ disease.”
In 1898 morphine was converted into yet another new pain reliever, heroin. For
several years heroin was viewed as a wonder drug and was used as a cough medicine
and for other medical purposes. Eventually, however, physicians learned that heroin is
even more addictive than the other opioids. By 1917 the U.S. Congress had concluded
that all drugs derived from opium were addictive (see Table 10-3), and it passed a law
making opioids illegal except for medical purposes.
Still other drugs have been derived from opium, and synthetic (laboratory-blended)
opioids such as methadone have also been developed.All these opioid drugs—natural and
synthetic—are known collectively as narcotics. Each drug has a different strength, speed
of action, and tolerance level. Morphine and codeine are medical nar-
cotics usually prescribed to relieve pain. Heroin is illegal in the United
States in all circumstances.
Narcotics are smoked, inhaled, snorted, injected by needle just
beneath the skin (“skin popped”), or injected directly into the blood-
stream (“mainlined”). Injection seems to be the most common method
of narcotic use, although the other techniques have been used increas-
ingly in recent years (NSDUH, 2008). An injection quickly brings on
a rush—a spasm of warmth and ecstasy that is sometimes compared
with orgasm. The brief spasm is followed by several hours of a pleasant
feeling called a high or nod. During a high, the drug user feels relaxed,
happy, and unconcerned about food, sex, or other bodily needs.
Opioids create these effects by depressing the central nervous
system, particularly the centers that help control emotion. The drugs
attach to brain receptor sites that ordinarily receive endorphins—
neurotransmitters that help relieve pain and reduce emotional tension
(Kreek, 2008; Ksir et al., 2008). When neurons at these receptor sites
*sedative – hypnotic drugeA drug used
in low doses to reduce anxiety and in
higher doses fo help people sleep. Also
called anxiolytic drug.
obarbiturateseAddictive sedative-
hypnotic drugs that reduce anxiety and
help produce sleep.
obenzadiazepineseThe most com-
mon group of antianxiety drugs, which
includes Valium and Xanax.
QopioidoOpium or any of the drugs
derived from opium, including morphine,
heroin, and codeine.
eopiumoA highly addictive substance
made from the sap of the opium poppy.
0morphine0A highly addictive sub-
stance derived from opium that is
particularly effective in relieving pain.
oheroinoOne of the most addictive
substances derived from opium.
oendorphinseNeurotransmitters that
help relieve pain and reduce emotional
tension. They are sometimes referred fo
as the body s own opioids.

•• •• • • . •• • • • • •
!PIO. .•
Substance Misuse and Depressants
The misuse of substances (or drugs) may lead to temporary changes such as intoxi-
cation. Long-term and high use can lead to substance abuse or substance depen-
dence. People who become dependent on a drug may develop a tolerance for it,
experience unpleasant withdrawal symptoms when they abstain from it, or both.
’00
294 :A/CHAPTER I0
1.t! -Zik
1%.
Nonmedical:;llse: of Pain Relievers.:
it IP I
11 I •
receive opioids, they produce pleasurable and calming feelings just as they
would do if they were receiving endorphins. In addition to reducing pain
and tension, opioids cause nausea, narrowing of the pupils (“pinpoint pu-
pils”), and constipation.
Heroin Abuse and Dependence Heroin use exemplifies the kinds
of problems posed by opioids. After taking heroin repeatedly for just a few
weeks, users may become caught in a pattern of abuse:The drug interferes
significantly with their social and occupational functioning. In most cases,
heroin abuse leads to a pattern of dependence as well, and users soon cen-
ter their lives on the substance, build a tolerance for it, and experience a
withdrawal reaction when they stop taking it (Kreek, 2008). At first the
withdrawal symptoms are anxiety, restlessness, sweating, and rapid breath-
ing; later they include severe twitching, aches, fever, vomiting, diarrhea, loss
of appetite, high blood pressure, and weight loss of up to 15 pounds (due to
loss of bodily fluids).These symptoms usually peak by the third day, gradually subside, and
disappear by the eighth day. A person in withdrawal can either wait out the symptoms or
end withdrawal by taking heroin again.
People who are dependent on heroin soon need the drug just to avoid going into
withdrawal, and they must continually increase their doses in order to achieve even that
relief.The temporary high becomes less intense and less important.The individuals may
spend much of their time planning their next dose, in many cases turning to criminal
activities, such as theft and prostitution, to support the expensive “habit” (Allen, 2005).
Surveys suggest that close to 1 percent of adults in the United States become addicted
to heroin or other opioids at some time in their lives (APA, 2000). The rate of such de-
pendence dropped considerably during the 1980s, rose in the early 1990s, fell in the late
1990s, and now seems to be relatively high once again (NSDUH, 2008). The number
of persons currently addicted to these drugs is estimated to be as much as 323,000. The
actual number may be even higher, however, given the reluctance of many people to
admit an illegal activity.
What Are the Dangers of Heroin Abuse? The most immediate danger of
heroin use is an overdose, which closes down the respiratory center in the brain, almost
paralyzing breathing and in many cases causing death. Death is particularly likely dur-
ing sleep, when a person is unable to fight this effect by consciously working to breathe.
People who resume heroin use after having avoided it for some time often make the fatal
mistake of taking the same dose they had built up to before. Because their bodies have
been without heroin for some time, however, they can no longer tolerate this high level.
Each year approximately 2 percent of persons dependent on heroin and other opioids
die under the drug’s influence, usually from an overdose (Theodorou & Haber, 2005;
APA, 2000).
Users run other risks as well. Often the heroin they purchase has been mixed with
a cheaper drug or even a deadly substance such as cyanide or battery acid. In addition,
dirty needles and other unsterilized equipment spread infections such as AIDS, hepatitis
C, and skin abscesses (Batki & Nathan, 2008). In some areas of the United States the
HIV infection rate among persons dependent on heroin is reported to be as high as 60
percent (APA, 2000).

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Substance-Related Disorders :11 295

ecocaineoAn addictive stimulant
obtained from the coca plant. It is the
most powerful natural stimulant known.
Depressants are substances that slow the activity of the central nervous system.
Long-term and excessive use of these substances can lead to a pattern of abuse or
dependence.
Alcoholic beverages contain ethyl alcohol, which is carried by the blood to
the central nervous system, depressing its function. Intoxication occurs when the
concentration of alcohol in the bloodstream reaches 0.09 percent. Among other
actions, alcohol increases the activity of the neurotransmitter GABA at key sites in
the brain. The sedative-hypnotic drugs, which produce feelings of relaxation and
drowsiness, include barbiturates and benzodiazepines. These drugs also increase
the activity of GABA.
Opioids include opium and drugs derived from it, such as morphine and heroin,
as well as laboratory-made opioids. They all reduce tension and pain and cause
other reactions. Opioids operate by binding to neurons that ordinarily receive
endorphins.
*Stimulants
Stimulants are substances that increase the activity of the central nervous system, result-
ing in increased blood pressure and heart rate, greater alertness, and sped-up behavior
and thinking. Among the most troublesome stimulants are cocaine and amphetamines,
whose effects on people are very similar. When users report different effects, it is often
because they have ingested different amounts of the drugs. Two other widely used and
legal stimulants are caffeine and nicotine.
Cocaine
Cocaine —the central active ingredient of the coca plant, found in South America—is
the most powerful natural stimulant now known. The drug was first separated from the
plant in 1865. Native people of South America, however, have chewed the leaves of the
plant since prehistoric times for the energy and alertness the drug offers. Processed cocaine
is an odorless, white, fluffy powder. For recreational use, it is most often snorted so that
it is absorbed through the mucous membrane of the nose. Some users prefer the more
powerful effects of injecting cocaine intravenously or smoking it in a pipe or cigarette.
For years people believed that cocaine posed few problems aside from intoxication
and, on occasion, temporary psychosis. Only later did researchers come to appreciate
its many dangers.Their insights came after society witnessed a dramatic
increase in the drug’s popularity and in problems related to its use. In the
early 1960s an estimated 10,000 persons in the United States had tried
cocaine. Today 28 million people have tried it, and 2.4 million—most of
them teenagers or young adults—are using it currently (NSDUH, 2008).
In fact, 2 percent of all high school seniors have used cocaine within the
past month ( Johnston et al., 2007).
Cocaine brings on a euphoric rush of well-being and confidence.
Given a high enough dose, this rush can be almost orgasmic, like the one
produced by heroin. At first cocaine stimulates the higher centers of the
central nervous system, making users feel excited, energetic, talkative, and
even euphoric. As more is taken, it stimulates other centers of the central
nervous system, producing a faster pulse, higher blood pressure, faster and
deeper breathing, and further arousal and wakefulness.
Cocaine apparently produces these effects largely by increasing sup-
plies of the neurotransmitter dopamine at key neurons throughout the
brain (Haney, 2008; Kosten et al., 2008) (see Figure 10-2). Excessive
amounts of dopamine travel to receiving neurons throughout the central

efree-baseoA technique for ingesting
cocaine in which the pure cocaine basic
alkaloid is chemically separated from
processed cocaine, vaporized by heat
from a flame, and inhaled with a pipe.
ocrackGA powerful form of ready-to-
smoke free-base cocaine.
nervous system and overstimulate them. In addition, cocaine appears to increase the
activity of the neurotransmitters norepinephrine and serotonin in some areas of the brain
(Haney, 2008; Ksir et al., 2008).
High doses of the drug produce cocaine intoxication, whose symptoms are poor
muscle coordination, grandiosity, bad judgment, anger, aggression, compulsive behavior,
anxiety, and confusion. Some people experience hallucinations, delusions, or both, a
condition known as cocaine-induced psychotic disorder (APA, 2000).
A young man described how, after free-basing, he went to his closet to get his clothes, but
his suit asked him, “What do you want?” Afraid, he walked toward the door, which told
him, “Get back!” Retreating, he then heard the sofa say, “If you sit on me, kick your
ass.” With a sense of impending doom, intense anxiety, and momentary panic, the young
man ran to the hospital where he received help.
(Allen, 1985, pp. 19-20)
As the stimulant effects of cocaine subside, the user experiences a depression-like let-
down, popularly called crashing, a pattern that may also include headaches, dizziness, and
fainting (Doweiko, 2006). For occasional users, the aftereffects usually disappear within
24 hours, but they may last longer for people who have taken a particularly high dose.
These individuals may sink into a stupor, deep sleep, or, in some cases, coma.
Cocaine Abuse and Dependence Regular use of cocaine may lead to a pat-
tern of abuse in which the person remains under its effects much of each day and func-
tions poorly in social relationships and at work. Regular use may also cause problems in
short-term memory or attention (Kubler et al., 2005). Dependence may also develop, so
that cocaine dominates the person’s life, higher doses are needed to gain the desired ef-
fects, and stopping it results in depression, fatigue, sleep problems, irritability, and anxiety
(Barry et al., 2009).These withdrawal symptoms may last for weeks or even months after
drug use has ended.
In the past, cocaine use and impact were limited by the drug’s high cost. Moreover,
cocaine was usually snorted, a form of ingestion that has less powerful effects than either
smoking or injection. Since 1984, however, the availability of newer, more powerful,
and sometimes cheaper forms of cocaine has produced an enormous increase in abuse
and dependence. Currently, close to 1 percent of all people over the age of 11 in the
United States display cocaine abuse or dependence in a given year (NSDUH, 2008).
Many people now ingest cocaine by free -basing, a technique in which the pure co-
caine basic alkaloid is chemically separated, or “freed,” from processed
cocaine, vaporized by heat from a flame, and inhaled through a pipe.
Millions more use crack, a powerful form of free-base cocaine that has
been boiled down into crystalline balls. It is smoked with a special pipe
and makes a crackling sound as it is inhaled (hence the name). Crack is
sold in small quantities at a fairly low cost, a practice that has resulted in
crack epidemics among people who previously could not have afforded
cocaine, primarily those in poor urban areas (Acosta et al., 2005).Almost
2 percent of high school seniors report having used crack within the
past year ( Johnston et al., 2007).
What Are the Dangers of Cocaine? Aside from cocaine’s
harmful effects on behavior, the drug poses serious physical dangers
(Kosten et al., 2008). Its growing use in powerful forms has caused the
annual number of cocaine-related emergency room incidents in the
United States to multiply by more than 100 times since 1982, from
around 4,000 cases to 450,000 (SAMHSA, 2007). In addition, cocaine
296 ://CHAPTER 10

A CI °SEP iflOK •
Tobacco, Nicotine, and Addiction
‘most 30 percent of all Americans
over the age of 11 regularly smoke
tobacco (NSDUH, 2008). Surveys also
suggest that 22 percent of all high school
seniors have smoked in the past month
(Johnston et al., 2007). At the same time,
440,000 persons in the United States die
each year as a result of smoking. Smok-
ing is directly tied to high blood pressure,
coronary heart disease, lung disease,
cancer, strokes, and other deadly medical
problems (George & Weinberger, 2008;
Hymowitz, 2005). Nonsmokers who inhale
cigarette smoke from their environment
have a higher risk of lung cancer and
other diseases. And the 16.4 percent of
all pregnant women who smoke are more
likely than nonsmokers to deliver premature
and underweight babies (Ksir et al., 2008;
NSDUH, 2008).
So why do people continue to smoke?
Because nicotine, the active substance
in tobacco and a stimulant of the central
nervous system, is as addictive as heroin,
perhaps even more so (Ksir et al., 2008;
Report of the Surgeon General, 1988).
Indeed, the World Health Organization
estimates that 1.1 billion people worldwide
are addicted to nicotine (Hasman & Holm,
2004). Regular smokers develop a toler-
ance for nicotine and must smoke more and
more in order to achieve the same results.
When they try to stop smoking, they experi-
ence withdrawal symptoms—irritability, in-
creased appetite, sleep disturbances, slower
metabolism, cognitive difficulties, and crav-
ings to smoke (Brandon et al., 2009; APA,
2000). As a stimulant, nicotine acts on the
same neurotransmitters and reword center
in the brain as amphetamines and cocaine
(George & Weinberger, 2008).
The declining acceptability of smoking
in our society has created a market for
products and techniques to help people
kick the habit. A fairly helpful behavioral
treatment for nicotine addiction is aversion
therapy. In one version of this approach,
known as rapid smoking, the smoker sits in
a closed room and puffs quickly on a ciga-
rette, as often as once every six seconds,
until he or she begins to feel ill and cannot
take another puff. The feelings of illness
become associated with smoking, and the
smoker develops an aversion to cigarettes
(George & Weinberger, 2008).
Several biological treatments have also
been developed. A common one is the
use of nicotine gum, an over-the-counter
product that contains a high level of nico-
tine that is released as the smoker chews.
Theoretically, people who obtain nicotine
by chewing will no longer feel a need to
smoke. A similar approach is the nico-
tine patch, which is attached to the skin
like a Band-Aid. Its nicotine is absorbed
through the skin throughout the day, sup-
posedly easing withdrawal and reducing
the smoker’s need for nicotine. Studies find
that both nicotine gum and the nicotine
patch help people to abstain from smok-
ing (George & Weinberger, 2008; Grilly,
2006). Still other popular biological prod.
ucts are nicotine lozenges, nicotine
nasal spray, and the antidepressant
drug bupropion (brand names Zyban
and Wellbutrin).
The more one smokes, the harder
it is to quit. On the positive side,
however, former smokers’ risk of
disease and death decreases steadily
the longer they continue to avoid
smoking. This assurance may be a
powerful motivator for many smokers,
and, in fact, around 46 percent of
regular smokers want to stop and are even-
tually able to stop permanently (NSDUH,
2008). In the meantime, more than 1,000
people die of smoking-related diseases
each day.
0- =■ ,*..,
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Substance-Related Disorders :fi 297
use has been linked to as many as 20 percent of all suicides by men under 61 years of age
(Garlow, 2002).
The greatest danger of cocaine use is an overdose. Excessive doses have a strong ef-
fect on the respiratory center of the brain, at first stimulating it and then depressing it,
to the point where breathing may stop. Cocaine can also create major, even fatal, heart
irregularities or brain seizures that bring breathing or heart functioning to a sudden
stop (Ksir et al., 2008). In addition, pregnant women who use cocaine run the risk of

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having a miscarriage and of having children with abnormalities in immune functioning,
attention and learning, thyroid size, and dopamine and serotonin activity in the brain
(Kosten et al., 2008).
Amphetamines
The amphetamines are stimulant drugs that are manufactured in the laboratory. Sonic
common examples are amphetamine (Benzedrine), dextroamphetamine (Dexedrine),
and methamphetamine (Methedrine). First produced in the 1930s to help treat asthma,
amphetamines soon became popular among people trying to lose weight; athletes seek-
ing an extra burst of energy; soldiers, truck drivers, and pilots trying to stay awake; and
students studying for exams through the night. Physicians now know the drugs are far
too dangerous to be used so casually, and they prescribe them much less freely.
Amphetamines are most often taken in pill or capsule form, although some people
inject the drugs intravenously or smoke them for a quicker, more powerful effect. Like
cocaine, amphetamines increase energy and alertness and reduce appetite when taken
in small doses; produce a rush, intoxication, and psychosis in high doses; and cause an
emotional letdown as they leave the body. Also like cocaine, amphetamines stimulate the
central nervous system by increasing the release of the neurotransmitters dopamine, nor-
epinephrine, and serotonin throughout the brain, although the actions of amphetamines
differ somewhat from those of cocaine (Haney, 2008; Rawson & Ling, 2008).
Tolerance to amphetamines builds very quickly, so users are at great risk of becom-
ing dependent (Acosta et al., 2005). People who start using the drug to reduce their
appetite and weight, for example, may soon find they are as hungry as ever and increase
their dose in response. Athletes who use amphetamines to increase their energy may
also find before long that larger and larger amounts of the drug are needed. So-called
speed freaks, who pop pills all day for days at a time, have built a tolerance so high
that they now take as much as 200 times their initial amphetamine dose.When people
who depend on the drug stop taking it, they may plunge into a deep depression and
extended sleep identical to the withdrawal from cocaine. Around 0.4 percent of adults
display amphetamine abuse or dependence each year (NSDUH,2008).As many
as 2 percent become dependent on amphetamines at some point in their lives
(APA, 2000; Anthony et al., 1995).
One kind of amphetamine, methamphetamine (nicknamed crank), has
had a major surge in popularity in recent years and so warrants special discus-
sion. Almost 6 percent of all persons over the age of 11 in the United States have
used this stimulant at least once.Around 0.3 percent use it currently (NSDUH,
2008). It is available in the form of crystals, also known by the street names ice
and crystal meth, which are smoked by users.
Most of the nonmedical methamphetamine in the United States is made in
small “stovetop laboratories,” which typically operate for a few days in a remote
area and then move on to a safer location (Ksir et al., 2008). Such laboratories
have increased eightfold over the past decade. A major health concern is that
they expel dangerous fumes and residue (Burgess, 2001).
Since 1989, when the media first began reporting about the dangers of
smoking methamphetamine crystals, the rise in usage has been dramatic.At this
point, 15 million Americans have tried this stimulant at least once (NSDUH,
2008). Until recently, use of the drug was much more prevalent in western
parts of the United States, but its use has now spread east as well (NSDUH,
2007). Similarly, methamphetamine-linked emergency room visits are rising in
hospitals throughout all parts of the country (DAWN, 2008).
Methamphetamine is about as likely to be used by women as men. Around
40 percent of current users are women. The drug is particularly popular today
among biker gangs, rural Americans, and urban gay communities and has gained
wide use as a “club drug,” the term for those drugs that regularly find their way
to all-night dance parties, or “raves” (Fchevarry & Nettles, 2009).
DON’T LET DRUG DEALERS CHANGE
THE FACE OF YOUR NEIGHBOURHOOD.
Call CrIrnestoppers anonymously on 0800 555111.

Stimulan
Stimulants are substances that increase the activity of the central nervous system.
They may lead to intoxication, abuse, and dependence, including a withdrawal
pattern marked by depression, fatigue, and irritability. Cocaine and amphetamines
produce their effects by increasing the activity of dopamine, norepinephrine, and
serotonin in the brain.
Substance-Related Disorders :11 299
Like other kinds of amphetamines, methamphetamine increases activity of the neu-
rotransmitters dopamine, serotonin, and norepinephrine, producing increased arousal,
attention, and related effects (Rawson & Ling, 2008). It can have serious negative effects
on a user’s physical, mental, and social life (NSDUH, 2007). Of particular concern is
that it damages nerve endings (Rawson & Ling, 2008). But users focus more on meth-
amphetamine’s immediate positive impact, including perceptions by many that it makes
them feel hypersexual and uninhibited ( Jefferson, 2005). Such perceived effects have
contributed to several societal problems. For example, one-third of all men who tested
positive for HIV in Los Angeles in 2004 reported having used this drug. In the area of
law enforcement, one survey of police agencies had 58 percent of them reporting that
methamphetamine is the leading drug they battle today.
oarnphetaminegA stimulant drug that is
manufactured in the laboratory.
omethomplietamine.A powerful
amphetamine drug whose surge in popu-
larity in recent years has posed major
health and law enforcement problems.
ehallucinogenGA substance that causes
powerful changes primarily in sensor),
perception, including stronger percep-
tions, illusions, and hallucinations. Also
called psychedelic drug.
eLSD (lysergic add diethylarnide)GA
hallucinogenic drug derived from ergot
alkaloids.
*Hallucinogens, Cannabis,
and Combinations of Substances
Other kinds of substances may also cause problems for their users and for society. Hallu-
cinogens produce delusions, hallucinations, and other sensory changes. Cannabis substances
produce sensory changes, but they also have depressant and stimulant effects, and so they
are considered apart from hallucinogens in DSM-IV-TR. And many individuals take
combinations of substances.
Hallucinogens
Hallucinogens are substances that cause powerful changes in sensory perception, from
strengthening a person’s normal perceptions to inducing illusions and hallucinations.
They produce sensations so out of the ordinary that they are sometimes called
“trips.” The trips may be exciting or frightening, depending on how a person’s
mind interacts with the drugs. Also called psychedelic drugs, the hallucinogens
include LSD, mescaline, and MDMA (Ecstasy). Many of these substances come
from plants or animals; others are laboratory-produced.
LSD (lysergic acid diethylamide), one of the most famous and most
powerful hallucinogens, was derived by Swiss chemist Albert Hoffman in 1938
from a group of naturally occurring drugs called ergot alkaloids. During the 1960s,
a decade of social rebellion and experimentation, millions of persons turned to
the drug as a way of expanding their experience. Within two hours of being
swallowed, LSD brings on a state of hallucinogen intoxication, sometimes called
hallucinosis, marked by a general strengthening of perceptions, particularly visual
perceptions, along with psychological changes and physical symptoms. People
may focus on small details—the pores of the skin, for example, or individual
blades of grass. Colors may seem enhanced or take on a shade of purple. Illu-
sions may be experienced in which objects seem distorted and may appear to
move, breathe, or change shape. A person under the influence of LSD may also
hallucinate—seeing people, objects, or forms that are not actually present.
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300 ://CHAPTER 10
What Are the Dangers
of Using Ecstasy?
As MDMA has gained wider and wider
use, the drug has received increasing
research scrutiny. As it turns out, the mood
and energy lift produced by MDMA comes
at a high price (Ksir et al., 2008; Weaver
& Schnoll, 2008; Wiegand et al., 2008).
The problems that the drug may cause in-
clude the following:
Immediate psychological problems
such as confusion, depression, sleep
difficulties, severe anxiety, and para-
noid thinking. These symptoms may
also continue for weeks after ingestion
of MDMA.
Significant impairment of memory and
other cognitive skills.
Physical symptoms such as muscle ten-
sion, nausea, blurred vision, faintness,
and chills or sweating. MDMA also
causes many people to clench and
grind their teeth for hours at a time.
Increases in heart rate and blood pres-
sure, which place people with heart
disease at special risk.
Reduced sweat production. At a hot,
crowded dance party, taking Ecstasy
can even cause heat stroke, or hyper-
thermia. Users generally try to fix this
problem by drinking lots of water, but
since the body cannot sweat under
the drug’s influence, the excess fluid
intake can result in an equally danger-
ous condition known as hyponafremia,
or “water intoxication.”
Potential liver damage. This may
happen when users take MDMA in
combination with other drugs that are
broken down by the same liver en-
zyme, such as the cheaper compound
DXM, which is commonly mixed in
with Ecstasy by dealers.
How Does MDMA Operate
in the Brain?
MDMA works by causing the neurotransmit-
ters serotonin and (to a lesser extent) dopa-
mine to be released all at once throughout
the brain, at first increasing and then de-
pleting a person’s overall supply of the neu-
rotransmitters (Ksir et al., 2008; Malberg &
Bonson, 2001). MDMA also interferes with
the body’s ability to produce new supplies
of serotonin. With repeated use, the brain
eventually produces less and less serotonin
(Baggot & Mendelson, 2001).
Ecstasy’s impact on these neurotransmit-
ters accounts for its various psychological
effects—and associated problems. High
levels of serotonin, such as those produced
after one first ingests MDMA, produce feel-
ings of well-being, sociability, and even
euphoria. Conversely, abnormally low sero-
tonin levels are associated with depression
and anxiety. This is why “coming down”
off a dose of Ecstasy often produces those
psychological symptoms (Malberg & Bon-
son, 2001). Moreover, because repeated
use of Ecstasy leads to long-term serotonin
deficits, the depression and anxiety may
be long-lasting. Finally, serotonin is linked
to our ability to concentrate; thus the re-
peated use of Ecstasy may produce prob-
lems in memory and learning (Zakzanis et
al., 2007).
End of the Honeymoon?
The dangers of MDMA do not yet seem
to outweigh its pleasures in the minds of
many individuals. In fact, use of the drug
is still expanding to many social settings
beyond raves, dance clubs, and college
scenes (Weaver & Schnoll, 2008). Clearly,
despite the research indications listed here,
the honeymoon for this drug is not yet over.
Chi’) Jrtk-js: tilicIrks the (Wrong) Spot
DU probably know of the drug MDMA
L’j 3,4-methylenedioxymethamphetamine)
by its common street name, Ecstasy. It is
also known as X, Adam, hug, beans, and
love drug. This laboratory-produced drug
is technically a stimulant, similar to amphet-
amines, but it also produces hallucinogenic
effects and so is often considered a hal-
lucinogenic drug. MDMA was developed
as far back as 1910, but only in the past
two decades has it gained life as a “club
drug”—one of the drugs that are extremely
popular at all-night techno-dance parties
known as “raves.” Today, in the United
States alone, consumers collectively take
hundreds of thousands of doses of MDMA
weekly despite the drug’s illegal status
(Weaver & Schnoll, 2008; McDowell,
2005). Altogether, 12 million Americans
over the age of 11 have tried MDMA at
least once in their lifetimes, 2 million in
the past year (NSDUH, 2008). Around
6.5 percent of all high school seniors
have used it within the past year (Johnston
et al., 2007).
What is Ecstasy’s allure? As a stimulant
and hallucinogen, it helps to raise the
mood of many partygoers and provides
them with an energy boost that enables
them to keep dancing and partying. How-
ever, it also turns out to be a dangerous
drug, particularly when taken repeatedly.

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Substance-Related Disorders :fi 301
Hallucinosis may also cause one to hear sounds more clearly, feel tingling or numb-
ness in the limbs, or confuse the sensations of hot and cold. Some people have been
badly burned after touching flames that felt cool to them under the influence of LSD.
The drug may also cause different senses to cross, an effect called synesthesia, Colors, for
example, may be “heard” or “felt.”
LSD can also induce strong emotions, from joy to anxiety or depression.The percep-
tion of time may slow dramatically. Long-forgotten thoughts and feelings may resurface.
Physical symptoms can include sweating, palpitations, blurred vision, tremors, and poor
coordination. All of these effects take place while the user is fully awake and alert, and
they wear off in about six hours.
It seems that LSD produces these symptoms primarily by binding to some of the
neurons that normally receive the neurotransmitter serotonin, changing the neurotrans-
mitter’s activity at those sites (Julien, 2008; Ksir et al., 2008). These neurons ordinarily
help the brain send visual information and control emotions (as you saw in Chapter 7);
thus LSD’s activity there produces various visual and emotional symptoms.
More than 14 percent of all persons in the United States have used LSD or another
hallucinogen at some point in their lives. Around 0.4 percent are currently using it
(NSDUH, 2008). Although people do not usually develop tolerance to LSD or have
withdrawal symptoms when they stop taking it, the drug poses dangers for both one-
time and long-term users. It is so powerful that any dose, no matter how small, is likely
to produce enormous perceptual, emotional, and behavioral reactions. Sometimes the
reactions are extremely unpleasant—an experience called a “bad trip.” Reports of LSD
users who injure themselves or others usually involve a reaction of this kind:
A 2 I-year-old woman was admitted to the hospital along with her lover. He had had a
number of /..SD experiences and had convinced her to take it to make her less constrained
sexually. About half an hour after ingestion of approximately 200 microgm., she noticed
that the bricks in the wall began to go in and out and that light affected her strangely. She
became frightened when she realized that she was unable to distinguish her body from the
chair she was sitting on or from her lover’s body. Her fear became more marked after she
thought that she would not get back into herself At the time of admission she was hyper-
active and laughed inappropriately. Her stream of talk was illogical and affect labile. Two
days later, this reaction had ceased.
(Frosch, Robbins, & Stern, 1965)
Another danger is the long-term effect that LSD may have (Weaver & Schnoll,
2008). Some users eventually develop psychosis or a mood or anxiety disorder. And
some have flashbacks—a recurrence of the sensory and emotional changes after the LSD
has left the body (Halpern, 2003). Flashbacks may occur days or even months after the
last LSD experience.
Cannabis
Cannabis sativa, the hemp plant, grows in warm climates throughout the world. The
drugs produced from varieties of hemp are, as a group, called cannabis. The most
powerful of them is hashish; the weaker ones include the best-known form of cannabis,
marijuana, a mixture derived from the buds, crushed leaves, and flowering tops of
hemp plants_ Of the several hundred active chemicals in cannabis, tetrahydrocannabi-
nol (THC) appears to be the one most responsible for its effects.The greater the THC
content, the more powerful the cannabis.
When smoked, cannabis produces a mixture of hallucinogenic, depressant, and stimu-
lant effects.At low doses, the smoker typically has feelings of joy and relaxation and may
become either quiet or talkative. Some smokers, however, become anxious, suspicious,
*cannabis drugseDrugs produced from
the varieties of the hemp plant Cannabis
sativa. They cause a mixture of hallucino-
genic, depressant, and stimulant effects.
• morijuanocOne of the cannabis
druas, derived from buds, leaves,
and floweringtops of the hemp plant
Cannabis sativa.
oteirahydracannabinol (THC GI – he
main active ingredient of cannabis
substances.

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302 ://CHAPTER 10
or irritated, especially if they have been in a bad mood or are
smoking in an upsetting environment. Many smokers report
sharpened perceptions and fascination with the intensified
sounds and sights around them. Time seems to slow down, and
distances and sizes seem greater than they actually are. This
overall “high” is technically called cannabis intoxication. Physical
changes include reddening of the eyes, fast heartbeat, increases
in blood pressure and appetite, dryness in the mouth, and dizzi-
ness. Some people become drowsy and may fall asleep.
In high doses, cannabis produces odd visual experiences,
changes in body image, and hallucinations. Smokers may be-
come confused or impulsive. Some worry that other people
are trying to hurt them. Most of the effects of cannabis last
two to six hours. The changes in mood, however, may con-
tinue longer.
Marihuana Abuse and Dependence Until the early
1970s, the use of marijuana, the weak form of cannabis, rarely
led to a pattern of abuse or dependence.Today, however, many
people, including large numbers of high school students, are
caught in a pattern of marijuana abuse, getting high on mari-
juana regularly and finding their social and occupational or
academic lives greatly affected (see Figure 10-3). Many regular
users also become physically dependent on marijuana. They
develop a tolerance for it and may experience finlike symp-
toms, restlessness, and irritability when they stop smoking
Marijuana
LSD
MOMA (Ecstasy)
Cocaine/Crack
Heroin a
17)
Amphetamines tn
Barbiturates
Alcohol
Cigarettes
Percentage of Teenagers Who Say Substance
Is Easy to Get
(Chen et al., 2005).Around 1.7 percent of all persons in the United States have displayed
marijuana abuse or dependence in the past year; as many as 5 percent fall into one of
these patterns at some point in their lives (NSDUH, 2008).
Why have patterns of marijuana abuse and dependence increased in the last three
decades? Mainly because the drug has changed. The marijuana widely available in the
United States today is at least four times more powerful than that used in the early
1970s. The THC content of today’s marijuana is, on average, 8 percent, compared to 2
percent in the late 1960s (APA, 2000). Marijuana is now grown in places with a hot,
dry climate, which increases the THC content.
is Ma ri Pia na Dangerous? As the strength and use of marijuana have increased, re-
searchers have discovered that smoking it may pose certain dangers. It occasionally causes
panic reactions similar to the ones caused by hallucinogens, and some smokers may fear
they are losing their minds (Doweiko, 2006).Typically such reactions end in three to six
hours, along with marijuana’s other effects.
Because marijuana can interfere with the performance of complex sensorimotor tasks
and with cognitive functioning, it has caused many automobile accidents (Ramaekers
et al., 2006). Furthermore, people on a marijuana high often fail to remember informa-
tion, especially anything that has been recently learned, no matter how hard they try
to concentrate; thus heavy marijuana smokers are at a serious disadvantage at school or
work (Lundqvist, 2005).
One study compared blood flow in the brain arteries of chronic marijuana users and
nonusers (Herning et al., 2005). After one month of abstinence from smoking mari-
juana, chronic users continued to display higher blood flow than nonusers.Though still
higher than normal, the blood flow of light marijuana users (fewer than 16 smokes per
week) and of moderate users (fewer than 70 smokes per week) had improved somewhat
over the course of the abstinence month. The blood flow of heavy users, however, had
shown no improvement.This lingering effect may help explain the memory and think-
ing problems of long-term heavy users of marijuana.
There are indications that regular marijuana smoking may also lead to long-term
health problems (Deplanque, 2005). It may, for example, contribute to lung disease.

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Studies show that marijuana smoking reduces the ability to expel air from the lungs
even more than tobacco smoking does (Tashkin, 2001). In addition, marijuana smoke
contains more tar and benzopyrene than tobacco smoke (Ksir et al., 2008). Both of
these substances have been linked to cancer. Another concern is the effect of regular
marijuana smoking on human reproduction. Studies since the late 1970s have discov-
ered lower sperm counts in men who are chronic smokers of marijuana, and abnormal
ovulation has been found in female smokers (Schuel et al., 2002).
Efforts to educate the public about the growing dangers of repeated marijuana use
appeared to have a major impact throughout the 1980s.The percentage of high school
seniors who smoked the substance on a daily basis decreased from 11 percent in 1978
to 2 percent in 1992 ( Johnston et al., 1993). Today, however, 5 percent of high school
seniors smoke marijuana daily, and 45 percent do not believe that regular use can be
harmful (Johnston et al., 2007).
Cannabis and Society: A Redly Relationship For centuries cannabis played
a respected role in medicine. It was recommended as a surgical anesthetic by Chinese
physicians 2,000 years ago and was used in other lands to treat cholera, malaria, coughs,
insomnia, and rheumatism.When cannabis entered the United States in the early twen-
tieth century, mainly in the form of marijuana, it was likewise used for various medical
purposes. Soon, however, more effective medicines replaced it, and the favorable view of
cannabis began to change. Marijuana began to be used as a recreational drug, and its il-
legal distribution became a law enforcement problem.Authorities assumed it was highly
dangerous and outlawed the “killer weed.”
In the 1980s researchers developed precise techniques for measuring THC and for
extracting pure THC from cannabis; they also developed laboratory forms of THC.
These inventions opened the door to new medical applications for cannabis (Mack &
Joy, 2001), such as its use in treating glaucoma, a severe eye disease. Cannabis was also
found to help patients with chronic pain or asthma, to reduce the nausea and vomiting
of cancer patients in chemotherapy, and to improve the appetites of AIDS patients and
so combat weight loss in people with that disorder.
In light of these findings, several interest groups campaigned during the late 1980s
for the medical legalization of marijuana, which operates on the brain and body more
quickly than the THC capsules developed in the laboratory. Government agencies re-
sisted this movement, saying that prescriptions for pure THC serve all needed medical
functions. But the battle between advocates and opponents of the legalization of mari-
juana for medical purposes was just beginning, and, in fact, that battle has continued to
the present day.
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304 ://CHAPTER 10
In 2005, the U.S. Supreme Court ruled 6 to 3 that medically ill marijuana smokers
and those who help them grow or obtain marijuana can be prosecuted, even if their
physicians prescribe it and even if they live in one of the 14 states where medical mari-
juana use has been declared legal. Although this ruling was initially considered a blow
to the medical marijuana cause, proponents fought on, and in 2009 the U.S. Attorney
General directed federal prosecutors to not pursue cases against medical marijuana users
or their caregivers who are complying with state laws.
In the meantime, the Canadian government has taken a different tack. Based on re-
search and trial programs, Health Canada, the country’s health care regulator, now legally
permits the medical use of marijuana by individuals who are suffering from severe and
debilitating illnesses, and it allows the sale of medical marijuana in select pharmacies,
making Canada the second country in the world, after the Netherlands, to do so.
Combinations of Substances
Because people often take more than one drug at a time, a pattern called polysubstance
use, researchers have studied the ways in which drugs interact with one another. When
different drugs are in the body at the same time, they may multiply, or potentiate, each
other’s effects. The combined impact, called a synergistic effect, is often greater than
the sum of the effects of each drug taken alone:A small dose of one drug mixed with a
small dose of another can produce an enormous change in body chemistry.
One kind of synergistic effect occurs when two or more drugs have similar actions.
For instance, alcohol, benzodiazepines, barbiturates, and opioids—all depressants—may
severely depress the central nervous system when mixed (Ksir et al., 2008). Combin-
ing them, even in small doses, can lead to extreme intoxication, coma, and even death.
A young man may have just a few alcoholic drinks at a party, for example, and shortly
afterward take a moderate dose of barbiturates to help him fall asleep. He believes he
has acted with restraint and good judgment—yet he may never wake up.
A different kind of synergistic effect results when drugs have opposite, or antagonistic,
actions, Stimulant drugs, for example, interfere with the liver’s usual disposal of barbitu-
rates and alcohol. Thus people who combine barbiturates or alcohol with cocaine or
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Hallucinogens, Cannabis, and Combinations of Substances
Hallucinogens, such as LSD, are substances that cause powerful changes primarily
in sensory perception. Perceptions are intensified and illusions and hallucinations
can occur. LSD apparently causes such effects by disturbing the release of the neu-
rotransmitter serotonin.
The main ingredient of Cannabis sativa, a hemp plant, is tetrahydrocannabinol
(THC). Marijuana, the most popular form of cannabis, is more powerful today than
it was in years past. It can cause intoxication, and regular and excessive use con
lead to abuse and dependence.
Many people take more than one drug at a time, and the drugs interact. The
use of Iwo or more drugs at the same time—polysubstance use—has become in-
creasingly common. Similarly, polysubstance-related disorders have also become a
major problem.
Substance-Related Disorders :fi 305
amphetamines may build up toxic, even lethal, levels of the depressant drugs in their
systems. Students who take amphetamines to help them study late into the night and
then take barbiturates to help them fall asleep are unknowingly placing themselves in
serious danger.
Each year tens of thousands of people are admitted to hospitals with a multiple-
drug emergency, and several thousand of them die (SAMHSA, 2007). Sometimes the
cause is carelessness or ignorance. Often, however, people use multiple drugs precisely
because they enjoy the synergistic effects. In fact, polysubstance -related disorders
are becoming as common as individual substance-related disorders in the United States,
Canada, and Europe (Rosenthal & Levounis, 2005). As many as 90 percent of persons
who use one illegal drug are also using another to some extent.
Fans still mourn the deaths of many celebrities who have been the victims of poly-
substance use. Elvis Presley’s balancing act of stimulants and depressants eventually killed
him. Janis Joplin’s mixtures of wine and heroin were ultimately fatal.And John Belushi’s
and Chris Farley’s liking for the combined effect of cocaine and opioids (“speedballs”)
also ended in tragedy.
*What Causes Substance-Related Disorders?
Clinical theorists have developed sociocultural, psychological, and biological explana-
tions for why people abuse or become dependent on various substances. No single
explanation, however, has gained broad support. Like so many other disorders, exces-
sive and long-term drug use is increasingly viewed as the result of a combination of
these factors.
Sociocuitural Views
A number of sociocultural theorists propose that people are most likely to develop pat-
terns of substance abuse or dependence when they live under stressful socioeconomic
conditions. In fact, studies have found that regions with higher levels of unemployment
have higher rates of alcoholism. Similarly, lower socioeconomic classes have substance-
abuse rates that are higher than those of the other classes (Franklin & Markarian, 2005;
Khan et al., 2002). In a related vein, more than 18 percent of unemployed adults cur-
rently use an illegal drug, compared to around 9 percent of full-time and part-time
employed workers (NSDUH, 2008).
Other sociocultural theorists propose that substance abuse and dependence are more
likely to appear in families and social environments where substance use is valued, or at
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306 ://CHAPTER 10
least accepted. Researchers have, in fact, found that problem drinking is more common
among teenagers whose parents and peers drink, as well as among teenagers whose
family environments are stressful and unsupportive (Ksir et al., 2008; Lieb et al., 2002).
Moreover, lower rates of alcohol abuse are found among Jews and Protestants, groups
in which drinking is typically acceptable only as long as it remains within clear limits,
whereas alcoholism rates are higher among the Irish and Eastern Europeans, who do
not, on average, draw as clear a line (Ksir et al., 2008; Ledoux et al., 2002).
Psychodynarnic Views
Psychodynamic theorists believe that people who abuse substances have powerful
dependency needs that can be traced to their early years (Lightdale et al., 2008; Stetter,
2000). They claim that when parents fail to satisfy a young child’s need for nurturance,
the child is likely to grow up depending excessively on others for help and comfort,
trying to find the nurturance that was lacking during the early years. If this search for
outside support includes experimentation with a drug, the person may well develop a
dependent relationship with the substance.
Some psychodynamic theorists also believe that certain people respond to their
early deprivations by developing a substance- abuse personality that leaves them particularly
prone to drug abuse. Personality inventories and patient interviews have in fact indi-
cated that people who abuse or depend on drugs tend to be more dependent, antisocial,
impulsive, novelty-seeking, and depressive than other people (Ksir et al., 2008; Coffey
et al., 2003). These findings are correlational, however, and do not clarify whether such
personality traits lead to drug use or whether drug use causes people to be dependent,
impulsive, and the like.
In an effort to establish clearer causation, one longitudinal study measured the per-
sonality traits of a large group of nonalcoholic young men and then kept track of each
man’s development ( Jones, 1971, 1968).Years later, the traits of the men who developed
alcohol problems in middle age were compared with the traits of those who did not.
The men who developed alcohol problems had been more impulsive as teenagers and
continued to be so in middle age, a finding suggesting that impulsive men are indeed
more prone to develop alcohol problems. Similarly, in one laboratory investigation,
“impulsive” rats—those that generally had trouble delaying their rewards—were found
to drink more alcohol when offered it than other rats (Poulos, Le, & Parker, 1995).
A major weakness of this line of argument is the wide range of personality traits
that have been tied to substance abuse and dependence. In fact, different studies point
to different “key” traits. Inasmuch as some people with a drug addiction appear to be
dependent, others impulsive, and still others antisocial, researchers cannot presently
conclude that any one personality trait or group of traits stands out in substance-related
disorders (Chassin et al., 2001).
Cognitive-Behavioral Views
According to behaviorists, operant conditioning may play a key role in substance abuse
(Bradizza & Stasiewkz, 2009; Higgins et al., 2004).They argue that the temporary reduc-
tion of tension or raising of spirits produced by a drug has a rewarding effect, thus in-
creasing the likelihood that the user will seek this reaction again. Similarly, the rewarding
effects of a substance may eventually lead users to try higher dosages or more powerful
methods of ingestion. In addition, cognitive theorists argue that such rewards eventu-
ally produce an expectancy that substances will be rewarding, and this expectation helps
motivate individuals to increase drug use at times of tension (Chassin et al., 2001).
In support of these behavioral and cognitive views, studies have found that many
people do in fact drink more alcohol or seek heroin when they feel tense (Ham et al.,
2002). In one study, as participants worked on a difficult anagram task, a confederate
planted by the researchers unfairly criticized and belittled them (Marlatt et al., 1975).
The participants were then asked to participate in an “alcohol taste task,” supposedly

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Substance-Related Disorders :1/ 307
to compare and rate alcoholic beverages. The individuals who had been harassed drank
more alcohol during the taste task than did the control participants who had not been
criticized.
In a manner of speaking, the cognitive-behavioral theorists are arguing that many
people take drugs to “medicate” themselves when they feel tense. If so, one would ex-
pect higher rates of drug abuse among people who suffer from anxiety, depression, and
other such problems. And, in fact, more than 22 percent of all adults who suffer from
psychological disorders have been dependent on or abused alcohol or other substances
within the past year (NSDUH, 2008).
A number of behaviorists have proposed that classical conditioning may also play a role
in substance abuse and dependence (Haney, 2008). Objects present in the environment at
the time drugs are taken may act as classically conditioned stimuli and come to produce
some of the same pleasure brought on by the drugs themselves. just the sight of a hypo-
dermic needle, drug buddy, or regular supplier, for example, has been known to comfort
people who abuse heroin or amphetamines and to relieve their withdrawal symptoms.
In a similar manner, objects that are present during withdrawal distress may produce
withdrawal-like symptoms. One man who had formerly been dependent on heroin
experienced nausea and other withdrawal symptoms when he returned to the neighbor-
hood where he had gone through withdrawal in the past—a reaction that led him to start
taking heroin again (O’Brien et al., 1975). Although classical conditioning certainly ap-
pears to be at work in particular cases or aspects of drug abuse and dependence, research
has not found it to be the key factor in such patterns probes et al., 2001).
Biological Views
In recent years researchers have come to suspect that drug misuse may have biological
causes. Studies on genetic predisposition and specific biochemical processes have pro-
vided some support for these suspicions.
Genetic Predisposition For years breeding experiments have been conducted to
see whether certain animals are genetically predisposed to become dependent on drugs
(Kreek, 2008; Li, 2000). In several studies, for example, investigators have first identi-
fied animals that prefer alcohol to other beverages and then mated them to one another.
Generally, the offspring of these animals have been found also to display an unusual pref-
erence for alcohol (Melo et al., 1996).

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• < 308 ://CHAPTER 10 Similarly, some research with human twins has suggested that people may inherit a predis- position to abuse substances (Ray & Hutchi- son, 2009). One classic study found that if one identical twin abused alcohol, the other twin also abused alcohol in 54 percent of the cases, whereas among fraternal twins, the rate was only 28 percent (Kaij, 1960). Other stud- ies have found similar twin patterns (Tsuang et al., 2001). As you have read, however, such findings do not rule out other interpretations. For one thing, the parenting received by two identical twins may be more similar than that received by two fraternal twins. A clearer indication that genetics may play a role in substance abuse and dependence comes from studies of alcoholism rates in people adopted shortly after birth (Walters, 2002; Cadoret et al., 1995; Goldstein, 1994). These studies have compared adoptees whose biological parents are dependent on alcohol with adoptees whose biological parents are not. By adulthood, the individuals whose biological parents are dependent on alcohol typically show higher rates of alcohol abuse than those with nonalcoholic biological parents. Genetic linkage strategies and molecular biology techniques provide more direct evi- dence in support of a genetic explanation (Gelernter & Kransler, 2008). One line of investigation has found an abnormal form of the so-called dopamine-2 (D2) receptor gene in a majority of research participants with alcohol, nicotine, or cocaine dependence but in less than 20 percent of nondependent participants (Preuss et al., 2007; Blum et al., 1996, 1990). Other studies have tied still other genes to substance-related disorders (Gelernter & Kranzler, 2008; Kreek, 2008). Biochemical Factors Over the past few decades, researchers have pieced together several biological explanations of drug tolerance and withdrawal symptoms (Kleber & Galanter, 2008; Koob, 2009, 2008). According to one of the leading explanations, when a particular drug is ingested, it increases the activity of certain neurotransmitters whose normal purpose is to calm, reduce pain, lift mood, or increase alertness. When a person keeps on taking the drug, the brain apparently makes an adjustment and reduces its own production of the neurotransmitters. Because the drug is increasing neurotransmit- ter activity, release of the neurotransmitter by the brain is less necessary. As drug in- take increases, the body's production of the neurotransmitters continues to decrease, leaving the person in need of more and more of the drug to achieve its effects. In this way, drug takers build tolerance for a drug, becoming more and more reliant on it rather than on their own biological processes to feel comfortable or alert. If they suddenly stop taking the drug, their natural supply of neurotransmitters will be low for a time, producing the symptoms of withdrawal.Withdrawal continues until the brain resumes its normal production of the neurotransmitters. Which neurotransmitters are affected depends on the drug used. Repeated and excessive use of alcohol or benzodiazepines may lower the brain's production of the 2C 46 H a ri 11 1,4 tu n C ar ko pt cA xc er i .. ,4 What Causes Substance-Related Disorders? Several explanations for substance abuse and dependence have been put forward. Together they are beginning to shed light on the disorders. According to the sociocultural view, the people most likely to abuse drugs are those living in stressful socioeconomic conditions or whose families value or accept drug use. In the psychodynamic view, people who turn to substance abuse have Substoraelated Disorders :1/ 309 °reward centereA dopamine-rich path- way in the brain that produces feelings of pleasure when activated. oreward - deficiency syndromeeA condition, suspected to be present in some individuals, in which the brain's reward center is not readily activated by the usual events in their lives. "Say when." neurotransmitter GABA, regular use of opioids may reduce the brain's production of endorphins, and regular use of cocaine or amphetamines may lower the brain's produc- tion of dopamine (Haney, 2008;Volkow et al., 2004, 1999). In addition, researchers have identified a neurotransmitter called anandamide that operates much like THC; excessive use of marijuana may reduce the production of this neurotransmitter (Hitti, 2004; Johns, 2001). This theory helps explain why people who regularly take substances experience tolerance and withdrawal reactions. But why are drugs so rewarding, and why do certain people turn to them in the first place? A number of brain-imaging studies suggest that many, perhaps all, drugs eventually activate a reward center, or "pleasure pathway," in the brain (de Wit & Phan, 2010; Haney, 2008).A key neurotransmitter in this pleasure pathway app ears to be dopamine (Koob, 2009; Volkow et al., 2004). When dopamine is activated along the pleasure pathway, a person experiences pleasure. Music may activate dopamine in the reward center. So may a hug or a word of praise. And so do drugs. Some researchers believe that other neurotransmitters may also play important roles in the reward center. Certain drugs apparently stimulate the reward center directly. Remember that cocaine and amphetamines directly increase dopamine activity. Other drugs seem to stimulate it in roundabout ways.The biochemical reactions triggered by alcohol, opioids, and marijuana probably set in motion a series of chemical events that eventually lead to increased dopamine activity in the reward center. A number of theorists suspect that people who abuse drugs suffer from a reward-deficiency syndrome: Their reward center is not readily activated by the usual events in their lives, so they turn to drugs to stimulate this pleasure pathway (Blum et al., 2000). 31 0 ://CHAPTER 10 excessive dependency needs traceable to the early stages of life. Some psychody- namic theorists also believe that certain people have a substance-abuse personality that makes them prone to drug use. The leading behavioral view proposes that drug use is reinforced initially because it reduces tensions and raises spirits, and the lead- ing cognitive view holds that such reductions of tension then lead to an expectancy that drugs will be comforting and helpful. The biological explanations are supported by twin, adoptee, genetic linkage, and molecular biology studies, suggesting that people may inherit a predisposition to substance dependence. Researchers have also learned that drug tolerance and withdrawal symptoms may be caused by cutbacks in the brain's production of par- ticular neurotransmitters during excessive and repeated drug use. Finally, biologi- cal studies suggest that many, perhaps all, drugs may ultimately lead to increased dopamine activity in the brain's reward center. 1\1.-1.,R - 1-..r.-r-M, ,,. tl, ifil9. T;X.J..11.1... --f. p .L1-. ci !FP''' ! l'ilit';1 ■ firti'f7-07.'igi'll 1 I i-iitii 1 t., ,r=9_ 1--t., lit, : ,,-:4 -1 lio f-iti-i-d tdiirl7,. '0,D ,:i1),:il -Jitifft,i,,Ifi,) ,?zb;,,it'il t=',F f.--JltCt 1 ,1911 1 -.1 .}71 - 7.j..F.iiiii2. aie 'il., *How Are Substance-Related Disorders Treated? Many approaches have been used to treat substance-related disorders, including psycho- dynamic, behavioral, cognitive-behavioral, and biological approaches, along with several sociocultural therapies. Although these treatments sometimes meet with great success, more often they are only moderately helpful (Myrick & Wright, 2008).Today the treat- ments are typically used on either an outpatient or inpatient basis or a combination of the two (Carroll, 2008, 2005; Weiss et al., 2008) (see Figure 10-4). Psychodynamic Therapies Psychodynamic therapists first guide clients to uncover and work through the underly- ing needs and conflicts that they believe have led to the disorder.The therapists then try to help the individuals change their substance-related styles of living (Lightdale et al., 2008). Although often applied, this approach has not been found to be particularly effective in cases of substance-related disorders (Cornish et al., 1995). It may be that drug abuse or dependence, regardless of its causes, eventually becomes a stubborn in- dependent problem that must be the direct target of treatment if people are to become drug-free. Psychodynamic therapy tends to be of greater help when it is combined with other approaches in a multidimensional treatment program (Lightdale et al., 2008). Behavioral Therapies A widely used behavioral treatment for substance-related disorders is aversion therapy, an approach based on the principles of classical conditioning. Individuals are repeatedly presented with an unpleasant stimulus (for example, an elec- tric shock) at the very moment that they are taking a drug. After repeated pairings, they are expected to react negatively to the substance itself and to lose their craving for it. Aversion therapy has been applied to alcohol abuse and dependence more than to other substance-related disorders. In one version of this therapy, drinking behavior is paired with drug-induced nausea and vomiting (Owen-Howard, 2001; Welsh & Liberto, 2001). The pairing of nausea with alcohol is expected to produce negative responses to alcohol itself. Another version of aversion therapy requires people Self-help group I 2.2 million Outpatient rehabiliation I 1.6 million outpatient mental health center 1.1 million 934,000 816,000 Inpatient rehabilitation Hospital inpatient 610,000 Private doctor's office Prison or jail • 420, 000 Emergency room 397,000 Number of Patients T re a tm e n t L o ca ti o n jp. 0Fo o, Tr1-* 1).; Substance-Related Disorders :11 311 with alcoholism to imagine extremely upsetting, repulsive, or frightening scenes while they are drinking (Cautela, 2000; Kassel et al., 1999). Here the pairing of the imagined scenes with liquor is expected to produce negative responses to liquor. Here are the kinds of scenes therapists may guide a client to imagine: I'd like you to vividly imagine that you are tasting the (beer, whiskey, etc.). See yourself tasting it, capture the exact taste, color and consistency. Use all of your senses. After you've tasted the drink you notice that there is something small and white floating in the glass—it stands out. You bend closer to examine it more carefully, your nose is right over the glass now and the smell fills your nostrils as you remember exactly what the drink tastes like. Now you can see what's in the glass. There are several maggots floating on the surface. As you watch, revolted, one manages to get a grip on the glass and, undulating, creeps up the glass. There are even more of the repulsive creatures in the glass than you first thought. You realise that you have swallowed some of them and you're very aware of the taste in your mouth. You feel very sick and wish you'd never reached for the glass and had the drink at all. (Clarke & Saunders, 1988, pp. 143-144) A behavioral approach that has been effective in the short-term treatment of people who abuse cocaine and some other drugs is contingency management, which makes in- centives (such as cash, vouchers, prizes, or privileges) contingent on the submission of drug-free urine specimens (Barry et al., 2009; Kosten et al., 2008). In one pioneering study, 68 percent of cocaine abusers who completed a six-month contingency training program achieved at least eight weeks of continuous abstinence (Higgins et al., 1993). Behavioral interventions for substance abuse and dependence have usually had only limited success when they are the sole form of treatment (Carroll, 2008).A major problem is that the approaches can be effective only when individuals are motivated to continue with them despite their unpleasantness or demands (DiClemente et al., 2008). Generally, behavioral treatments work best in combination with either biological or cognitive approaches (Higgins & Silverman, 2008). °aversion therapyoA treatment in which clients are repeatedly presented with unpleasant stimuli while performing undesirable behaviors such as taking a drug. 312 :If/CHAPTER l0 arc de mficatio Absti o is not alwa medically- super or voluntary, This sufferer of co begins to experience sy Ithdrawal soon:: after bein d for public] *behavioral self-control training (BSCT)®A cognitive-behavioral approach to treating alcohol abuse and depen- dence in which clients are taught to keep track of their drinking behavior and to apply coping strategies in situations that typically trigger excessive drinking. orelapse-prevention training°An approach to treating alcohol abuse that is similar to BSCT and also has clients plan ahead for risky situations and reactions. odetoxificationeSystematic and medi- cally supervised withdrawal from a drug. *antagonist drugs*Drugs that block or change the effects of an addictive drug. Cognitive-Behavioral Therapies Two popular approaches combine cognitive and be- havioral techniques to help people gain control over their substance-related behaviors (Carroll, 2008). In one, behavioral self-control training (BSCT), applied to alcoholism in particular, therapists first have clients keep track of their own drinking behavior (Bishop, 2008; Miller et al., 1992; Miller, 1983). Writing down the times, locations, emotions, bodily changes, and other cir- cumstances of their drinking, they become more aware of the situations that place them at risk for excessive drinking. They are then taught coping strategies to use when such situations arise. They learn, for example, to set limits on their drinking, to recognize when the limits are being approached, to control their rate of drinking (perhaps by spacing their drinks or by sipping them rather than gulping), and to practice relaxation tech- niques, assertiveness skills, and other coping behaviors in situations in which they would otherwise be drinking. Approximately 70 percent of the people who complete this training apparently show some improvement, particularly younger drinkers who are not physically dependent on alcohol (Deas et al., 2008; Ksir et al., 2008). In a related cognitive-behavioral approach, relapse-prevention training, heavy drinkers are assigned many of the same tasks as clients in BSCT (Blume et al., 2009; Witkiewitz & Marlatt, 2007, 2004). They are also taught to plan ahead of time how many drinks are appropriate, what to drink, and under what circumstances. The ap- proach often lowers the frequency of intoxication, although the majority of clients achieve success only after repeated relapse-prevention treatments. The approach has also been used, with some success, in the treatment of marijuana and cocaine abuse as well as with other kinds of disorders such as sexual paraphilias (see Chapter 11). Biological Treatments Biological approaches may be used to help people withdraw from substances, abstain from them, or simply maintain their level of use without further increases. As with the other forms of treatment, biological approaches alone rarely bring long-term improve- ment, but they can be helpful when combined with other approaches. •• • Detoxi f ication Detoxification is systematic and medically supervised withdrawal from a drug. Some detoxification programs are offered on an outpatient basis. Others are located in hospitals and clinics and may also offer individual and group therapy, a "full- service" institutional approach that has become popular. One detoxification approach is to have clients withdraw gradually from the substance, taking smaller and smaller doses until they are off the drug completely (Wright & Thompson, 2002). A second—often medically preferred—detoxification strategy is to give clients other drugs that reduce the symptoms of withdrawal (Caldeiro et al., 2009; Ksir et al., 2008). Antianxiety drugs, for example, are sometimes used to reduce severe alcohol withdrawal reactions such as delirium tremens and seizures. Detoxification programs seem to help motivated people withdraw from drugs (DiClemente et al., 2008). However, relapse rates tend to be high for those who fail to receive a follow-up form of treatment—psychological, biological, or sociocultural—after successful detoxification (Polydorou & Kleber, 2008). Antagonist Drugs After successfully stopping a drug, people must avoid falling back into a pattern of abuse or dependence. As an aid to resisting temptation, some people with substance-related disorders are given antagonist drugs, which block or change the effects of the addictive drug (O'Brien & Kampman, 2008). Disulfiratn (Antabuse), Medial HOME SEND EXPLORE Substanceakted Disorders :1/ 313 In Real Time, Amy Winehouse's Deeper Descent BY JON PARES, NEW YORK TIMES, JANUARY 24, 2008 I. was witty ... when Amy Winehouse sang, "They tried to make me go to rehab/I said no, no, no" on her album "Back to Black." . . . But there was nothing amusing, and barely any surprise, in Ms. Winehouse's recent, notorious and possibly inadvertent public appearance: on a video released by an Eng- lish tabloid, The Sun. The homemade clip . . . shows Ms. Winehouse, with her recent blond hairdo, in her London apartment, using a glass pipe to smoke what The Sun says is crack. . . . Performers thrive on attention, and sometimes admit that it's an addiction; now, the Internet enables that addiction all too easily. The unintended consequence is that we can now watch stars self-destruct in real time. Images of Ms. Winehouse looking intoxicated, disheveled, half-dressed and wild-eyed are all over the tabloids and the Internet. She has appeared to be drunk onstage, barely able to get through a song.. . . Ms. Winehouse, who writes her own lyrics, . . has often sung about harmful appetites, not just in "Rehab" but in "Addicted" (about a freeloading pot smoker) and in "Back to Black," in which she sings, "You love blow and I love puff/And life is like a pipe." .. . Addiction might start with experiments by performers so young they feel invulnerable; it might seem to be, at first, a way to ease the stress of a peculiar lob. It might be a way to act out the old Romantic image of the artist as daredevil. And there's no shortage of temptation in a musician's work environment of bars, clubs, late nights and party people. Rock stars weren't the first musicians to drink or drug themselves to death. What's different, in the 21st century, is that we can watch the breakdowns almost as they happen. One day there's a grainy video of Ms. Winehouse spreading across the Internet. . In the '60s and '70s there were occasional photos of Janis Joplin hoisting a bottle of Southern Comfort, and word-of-mouth about many bands' backstage excesses or drunken exploits, but those were occasional glimpses and dispatches. Rockers dosed themselves, mostly, behind closed doors. Now digital video and photography, coupled with the Inter- net, can odd up to near-constant surveillance.. . . There's an en- tire industry in celebrity scandal, much of it remarkably callous. In their times the deaths of Jim Morrison and Kurt Cobain were sudden and shocking, leaving them a legacy as handsome rock martyrs. . .. But they were pre-Internet stars. Now, there's a sleazy symbiosis that connects instantaneous worldwide Hy, publicity, marketing and narcissism. Attention addicts can get their fix with a few mouse clicks. Why, for instance, was Ms. Winehouse letting someone shoot video, in a private setting, of her puffing that pipe in the first place? Maybe it's some version of "keepin' it real," . . . Maybe it's obliviousness, ... Maybe she mistakenly trusted that whoever made the video would resist another temptation: the potential profit to be made providing it to a tabloid. Perhaps Ms. Winehouse misunderstood what should be clear in the age of the Internet: Everything recorded can be dupli- cated and distributed. And possibly the video was, in its own bleary way, a kind of performance. She is keeping her audience informed if not exactly entertained. Mostly, however, she's just supplying material for the sphere of celebrity interaction that only wants to see idols torn down. Her fans—those of us who believe she has more superb songs yet to write—would prefer she grow less visible and consider- ably more boring.... [S]he would do well to disappear for a while, into rehab or private recovery, and then to hole up in a recording studio and work up some new songs. (She definitely has enough ups and downs to write about, realistically or not.) In the era of total exposure Ms. Winehouse would serve herself and her listeners best by working behind closed doors. Copyright © 2008. Reprinted by permission of PARS International Corp. on behalf of The New Ybrk Times. [Note: Two weeks after this article was printed, Amy Winehouse won five Grammy Awards, including ones for best new artist, song of the year ("Rehab"), and best pop vocal album ("Back to Black").] one sa el. th a e i.s itse -a narc lf - 0 / e a dangerous as other opioi of taken ender -safe -medical su ere a couple pratest_aga iinst ethadone treatment tacl . . iii 1 • Pq.114?" 31 4 ://CHAPTER 10 "methadone maintenance program"An approach to treating heroin dependence in which clients are given legally and medically supervised doses of a substitute drug, methadone. "Alcoholics Anonymous (AA)°A self- help organization that provides support and guidance for persons with alcohol abuse or dependence. "residential treatment center®A place where people formerly dependent on drugs live, work, and socialize in a drug-free environment while undergo- ing treatment. Also called a therapeutic community. for example, is often given to people who are trying to stay away from alcohol. By itself a low dose of this drug seems to have few negative effects, but a person who drinks al- cohol while taking disulfiram will experience intense nausea, vomiting, blushing, faster heart rate, dizziness, and perhaps fainting. People taking disulfiram are less likely to drink alcohol because they know the terrible reaction that awaits them should they have even one drink. Disulfiram has proved helpful, but again only with people who are motivated to take it as prescribed (DiClemente et al., 2008). In addition to disulfiram, several other alcohol antagonist drugs are now being tested (De Sousa et al., 2008). In the realm of opioid dependence, several narcotic antagonists, such as naloxone and naltrexone, are used to treat people who are addicted to drugs of that kind (Caldeiro et al., 2009). These antagonists attach to endorphin receptor sites throughout the brain and make it impossible for the opioids to have their usual effect. Without the rush or high, con- tinued drug use becomes pointless. Although narcotic antagonists have been helpful— particularly in emergencies, to rescue people from an overdose of opioids—they can in fact be a dangerous form of treatment for opioid dependence. These antagonists must be given very carefully because of their ability to throw a person with an addiction into severe withdrawal. Recent studies indicate that narcotic antagonists may also be useful in the treatment of alcohol and cocaine dependence (Bishop, 2008; Oslin, 2006). Drug Maintenance Therapy A drug-related lifestyle may be a greater problem than the drug's direct effects. Much of the damage caused by heroin addiction, for ex- ample, comes from overdoses, unsterilized needles, and an accompanying life of crime. Thus clinicians were very enthusiastic when methadone maintenance programs were developed in the 1960s to treat heroin addiction (Dole & Nyswander, 1967, 1965). In these programs, people with an addiction are given the laboratory opioid methadone as a substitute for heroin.Although they then become dependent on methadone, their new addiction is maintained under safe medical supervision. Unlike heroin, methadone can be taken by mouth, thus eliminating the dangers of needles, and needs to be taken only once a day. At first, methadone programs seemed very effective, and many of them were set up throughout the United States, Canada, and England. These programs became less popular during the 1980s, however, because of the dangers of methadone itself. Many clinicians came to believe that substituting one addiction for another is not an accept- able "solution" for substance dependence, and many persons with an addiction com- plained that methadone addiction was creating an additional drug problem that simply complicated their original one (McCance-Katz & Kosten, 2005). In fact, methadone is sometimes harder to withdraw from than heroin because the withdrawal symptoms can last longer (Ksir et al., 2008). Moreover, pregnant women maintained on methadone have the added concern of the drug's effect on their fetus. Despite such concerns, maintenance treatment with methadone—or with buprenor- phine, another widely used substitute drug—has again sparked interest among clinicians in recent years, partly because of new research support (Strain & Lofwall, 2008) and partly because of the rapid spread of the HIV virus and the hepatitis C virus among intravenous drug abusers and their sex partners and children (Galanter & Kleber, 2008; Schottenfeld, 2008). Not only is methadone treatment safer than street opioid use, but many methadone programs now include AIDS education and other health instructions in their services (Sorensen & Copeland, 2000). Research suggests that methadone main- tenance programs are most effective when they are combined with education, psycho- therapy, family therapy, and employment counseling (Schottenfeld, 2008; O'Brien & McKay, 2002). Today thousands of clinics provide methadone treatment across the United States (MTC, 2008). Sociocultural Therapies As you have read, sociocultural theorists—both family-social and multicultural theorists— believe that psychological problems emerge in a social setting and are best treated in a social context. Three sociocultural approaches have been applied to substance-related ii yaj .= • . . • • • • • • r•:.(:) i • •• III! li11111.1.01111 — .111111r1011111:,111111:1:1111111!,i111111:,:oi1111 , 4 ■ I•• • . . in Ptrihoris at 90 ientionsi :in obhTeu:s LI( a . taal Froaedrarumg meditate re a des psyc aci d me h bilitation p apa lchol nro• rameralioe inc u ad. 31u .r .c3 bstance a I Substance-Related Disorders :11 315 disorders: (1) self-help programs, (2) culture- and gender-sensitive programs, and (3) community prevention programs (Ritvo & Causey, 2008). Self-Help and Residential Treatment Programs Many people who abuse drugs have organized among themselves to help one another recover without profes- sional assistance.The drug self-help movement dates back to 1935, when two Ohio men suffering from alcoholism met and wound up discussing alternative treatment possibili- ties.The first discussion led to others and to the eventual formation of a self-help group whose members discussed alcohol-related problems, traded ideas, and provided support. The organization became known as Alcoholics Anonymous (AA). Today AA has more than 2 million members in 113,000 groups across the United States and 1S0 other countries (AA World Services, 2008). It offers peer support along with moral and spiritual guidelines to help people overcome alcoholism. Different members apparently find different aspects of AA helpful (Tonigan & Connors, 2008). For some it is the peer support; for others it is the spiritual dimension. Meetings take place regularly, and members are available to help each other 24 hours a day. By offering guidelines for living, the organization helps members abstain "one day at a time," urging them to accept as "fact" the idea that they are powerless over alcohol and that they must stop drinking entirely and permanently if they are to live normal lives (Nace, 2008). Related self-help organizations, Al-Anon and Alateen, offer support for people who live with and care about persons with alcoholism (Galanter, 2008). Self- help programs such as Narcotics Anonymous and Cocaine Anonymous have been developed for other substance-related disorders. Many self-help programs have expanded into residential treatment centers, or therapeutic communities —such as Daytop Village and Phoenix House—where people formerly dependent on drugs live, work, and socialize in a drug-free environment while undergoing individual, group, and family therapies and making a transition back to community life (Brook, 2008; De Leon, 2008). The evidence that keeps self-help and residential treatment programs going comes largely in the form of individual testimonials. Many tens of thousands of persons have revealed that they are members of these programs and credit them with turning their lives around. Studies of the programs have also had favorable findings, but their numbers have been limited (De Leon, 2008; Moos & Timko, 2008; Tonigan & Connors, 2008). lkia—ocZ wy; • gt4"i -F1 Ivo-stilted -in.p.fatO1 to 8241' (4y Suc h 1a V ° r t PF theistliOcN - 1,1I . 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Culture- and Gender-Sensitive Programs Many persons who abuse sub-
stances live in a poor and perhaps violent setting.A growing number of today’s treatment
programs try to be sensitive to the special sociocultural pressures faced by drug abusers
who are poor, homeless, or members of minority groups (Cabaj, 2008; Westermeyer
& Dickerson, 2008). Therapists who are sensitive to their clients’ life challenges can do
more to address the stresses that often lead to relapse.
Similarly, therapists have become more aware that women often require treatment
methods different from those designed for men (Brady & Back, 2008). Women and
men often have different physical and psychological reactions to drugs, for example.
In addition, treatment of women who abuse substances may be complicated by the
impact of sexual abuse, the possibility that they may be or may become pregnant while
taking drugs, the stresses of raising children, and the fear of criminal prosecution for
abusing drugs during pregnancy (Finnegan & Kandall, 2008).Thus many women with
such disorders feel more comfortable seeking help at gender-sensitive clinics or resi-
dential programs; some such programs also allow children to live with their recovering
mothers.
Community Prevention Programs Perhaps the most effective approach to
substance-related disorders is to prevent them (Sloboda, 2009; Clayton et al., 2008; Ksir
et al., 2008).The first drug-prevention efforts were conducted in schools.Today preven-
tion programs are also offered in workplaces, activity centers, and other community
settings, and even through the media (NSDUH, 2008). Over 11 percent of adolescents
report that they have participated in substance use prevention programs outside school
within the past year. Around 80 percent have seen or heard a substance use prevention
message. And almost 60 percent have talked to their parents in the past year about the
dangers of alcohol and other drugs.
Prevention programs may focus on the individual (for example, by providing educa-
tion about unpleasant drug effects), the family (by teaching parenting skills), the peer group
(by teaching resistance to peer pressure), the school (by setting up firm enforcement of
drug policies), or the community at large (by public service announcements such as the
“Just say no” campaign of the 1980s and 1990s). The most effective prevention efforts
focus on several of these areas to provide a consistent message about drug abuse in all
areas of individuals’ lives (Clayton et al., 2008; Ksir et al., 2008). Some prevention pro-
grams have even been developed for preschool children.

F1.1 r\Y,11 :1=1 10,11;:: Li
Substance-Related Disorders :1/ 317
•
How Are Substance-Related Disorders Treated?
Treatments for substance abuse and dependence vary widely. Usually several ap-
proaches are combined. Psychodynamic therapies try to help clients become aware
of and correct the underlying needs and conflicts that may have led to their use of
drugs. A common behavioral technique is aversion therapy, in which an unpleasant
stimulus is paired with the drug that the person is abusing. Cognitive and behavioral
techniques have been combined in such forms as behavioral self-control training
(BSCT) and relapse-prevention training. Biological treatments include detoxification,
antagonist drugs, and drug maintenance therapy. Sociocultural treatments approach
substance-related disorders in a social context by means of self-help groups (for
example, Alcoholics Anonymous), culture- and gender-sensitive treatments, and
community prevention programs.
PUTTING IT… together
New Wrinkles to a Familiar Story
In some respects the story of the misuse of drugs is the same today as in the past. Sub-
stance use is still rampant, often creating damaging psychological disorders. New drugs
keep emerging, and the public goes through periods of believing, naively, that they are
“safe.” Only gradually do people learn that these drugs, too, pose dangers. And treat-
ments for substance-related disorders continue to have only limited effect.
Yet there are important new wrinkles in this familiar story. Researchers have begun
to develop a clearer understanding of how drugs act on the brain and body. In treatment,
self-help groups and rehabilitation programs are flourishing. And preventive education
to make people aware of the dangers of drug misuse is also expanding and seems to be
having an effect. One reason for these improvements is that investigators and clinicians
have stopped working in isolation and are instead looking for intersections between
their own work and work from other models. The same kind of integrated efforts that
have helped with other psychological disorders are bringing new promise and hope to
the study and treatment of substance-related disorders.
Perhaps the most important insight to be gained from these integrated efforts is
that several of the models were already on the right track. Social pressures, personality
characteristics, rewards, and genetic predispositions all seem to play roles in substance-
related disorders, and in fact to operate together. For example, some people may inherit
a malfunction of the biological reward center and so may need special doses of external
stimulation—say, intense relationships, an abundance of certain foods, or drugs—to
stimulate their reward center. Their pursuit of external rewards may take on the char-
acter of an addictive personality (Ebstein & Kotler, 2002). Such individuals may be es-
pecially prone to experimenting with drugs, particularly when their social group makes
the drugs available or when they are faced with intense social and personal stress.
Just as each model has identified important factors in the development of substance-
related disorders, each has made important contributions to treatment. As you have
seen, the various forms of treatment seem to work best when they are combined with
approaches from the other models, making integrated treatment the most productive
approach.
These recent developments are encouraging. At the same time, however, enormous
and increasing levels of drug use continue. New drugs and drug combinations are dis-
covered almost daily, and with them come new problems and the need for new research
and new treatments. Perhaps the most valuable lesson is an old one: There is no free
lunch. The pleasures derived from these substances come with high psychological and
biological costs, some not yet even known.
I
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318 :IICHAPTER 1 0
\\■ f3RITINI, ‘THOUr.;NTS///
• …A A.
g
1. Various kinds of club drugs (e.g.,
Ecstasy and crystal meth), drugs
.0.1;
used at all-night dance parties called
” raves,” seem to fall in and out of
favor rather quickly. Why might
Os
young people readily move from one
such drug to another? pp. 298-299,
300
lif: 2. What effects might the use of drugs
70–;
54
by some rock, rap, and other musical
young adults? performers hav Who has the greater
e on teenagers and
42,-;
.ey•
impact on the drug behaviors of
teenagers and young adults: perform-
\\\KEy TEP/S///
intoxication, p. 286
f hallucinosis, p. 286
0: substance abuse, p. 286
substance dependence, p. 286
0 tolerance, p. 286
withdrawal, p. 286
alcohol, p. 287
.?:
O.: delirium tremens (DTs), p. 289 cirrhosis, p. 291
Korsakoff’s syndrome, p. 291
fetal alcohol syndrome, p. 291
sedative-hypnotic drug, p. 292
opioid, p. 293
gi endorphins, p. 293
cocaine, p. 295
417:
‘)U12/” :
ers who speak out against drugs or
performers who praise the virtues of
drugs? pp. 304-305, 313, 317
3 What different kinds of issues might
be confronted by drug abusers from
different ethnic groups or genders,
and how might such issues influence
their efforts at recovery? pp. 305-
306, 316
4. Popular talk show host Oprah
Winfrey has revealed, with great
emotion, that she was physically
dependent on cocaine in the
free-basing, p. 296
crack, p. 296
amphetamine, p. 298
hallucinogen, p. 299
lysergic acid diethylamide (LSD), p. 299
cannabis drugs, p. 301
marijuana, p. 301
tetrahydrocannabinol (MC), p. 301
synergistic effect, p. 304
polysubstance-related disorder, p. 305
substance-abuse personality, p. 306
dopamine-2 (D2) receptor gene, p. 308
reward center, p. 309
aversion therapy, p. 310
contingency management, p. 311
-• • AA. ..*•,A1-.
mid-1970s. What impact might
admissions like Winfrey’s have on
people’s willingness to seek treatment
for substance abuse? pp. 310-316
5. Since the major dangers of heroin
come from overdose, unsterilized
needles, and a criminal lifestyle,
society has periodically tried legal,
medically supervised use of heroin {in
Great Britain) or a heroin substitute
(in the United States) to combat this
drug problem. In many cases, such
approaches have had limited effec-
tiveness. Why? p. 314
behavioral self-control training (BSCT),
p. 312
relapse-prevention training, p. 312
detoxification, p. 312
antagonist drug, p. 312
disulfiram (Antabuse), p. 312
narcotic antagonist, p. 314
methadone maintenance program,
p.314
self-help program, p. 315
Alcoholics Anonymous (AA), p. 315
residential treatment center, p. 315
culture- and gender-sensitive program,
p. 316
community prevention program, p. 316
1. How does alcohol act on the brain
and body? What are the problems
and dangers of alcohol misuse?
pp. 287-292
2. Describe the features and problems
of the misuse of barbiturates and
benzodiazepines. pp. 292-293
3. Compare the various opioids
(opium, heroin, morphine). What
problems may result from their use?
pp. 293-294
4. List and compare two kinds of stimu-
lant drugs. Describe their biological
actions and the problems caused by
each of them. pp. 295-299
5. Why has cocaine use become a
major problem in recent years?
pp. 295-298
6. What are the effects of hallucino-
gens, particularly LSD? pp. 299-301
t A 4A.1*2_A_.6*.f. A A.•

Substance-Related Disorders :// 319
What are the effects of marijuana
and other cannabis substances?
Why is marijuana a greater danger
today than it was 30 years ago?
pp. 301-304
,40,1
,ot • •.•,•,• %•.0.
8. What special problems does polysub-
stance use pose? pp. 304-305
9. Describe the leading explanations for
substance-related disorders. Row well
supported are these explanations?
pp. 305-309
10. What are the leading treatments for
substance-related disorders? How
effective are they? pp. 310-316
4
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SEXUAL DISORDERS
AND GENDER IDENTITY
DISORDER

obert, a 57-year-old man, came to sex therapy with his wife because of his inability to
get erections. He had not had a problem with erections until six months earlier, when
they attempted to have sex after an evening out during which he had had several drinks.
UThey attributed his failure to get an erection to his being “a little drunk,” but he found
himself worrying over the next few days that he was perhaps becoming impotent. When they
next attempted intercourse, he found himself unable to get involved in what they were doing
because he was so intent on watching himself to see if he would get an erection. Once again
he did not, and they were both very upset. His failure to get an erection continued over the
next few months. Robert’s wife was very upset and . . . frustrated, accusing him of having an
affair, or of no longer finding her attractive. Robert wondered if he was getting too old, or if
his medication for high blood pressure, which he had been taking for about o year, might be
interfering with erection. . . . When they came for sex therapy, they had not attempted any
sexual activity for over two months.
LoPiccolo, 1992, p. 492
Sexual behavior is a major focus of both our private thoughts and public discus-
sions. Sexual feelings are a crucial part of our development and daily functioning,
sexual activity is tied to the satisfaction of our basic needs, and sexual performance
is linked to our self-esteem. Most people are fascinated by the abnormal sexual
behavior of others and worry about the normality of their own sexuality.
Experts recognize two general categories of sexual disorders: sexual dysfunc-
tions and paraphilias. People with sexual dysfunctions experience problems with
their sexual responses. Robert, for example, had a dysfunction known as erectile
disorder, a repeated failure to attain or maintain an erection during sexual activ-
ity. People with paraphilias have repeated and intense sexual urges or fantasies in
response to objects or situations that society deems inappropriate, and they may
behave inappropriately as well. They may be aroused by the thought of sexual
activity with a child, for example, or of exposing their genitals to strangers, and
they may act on those urges. In addition to the sexual disorders, DSM-IV-TR
includes a diagnosis called gender identity disorder, a sex-related pattern in which
people persistently feel that they have been born to the wrong sex and in fact
identify with the other gender.
As you will see throughout this chapter, except for gender differences, little
is known about racial and other cultural differences in sexuality. This is true for
normal sexual patterns, sexual dysfunctions, and paraphilias alike. Although dif-
ferent cultural groups have for years been labeled hypersexual, “hot blooded,”
exotic, passionate, submissive, and the like, such incorrect stereotypes have grown
strictly from ignorance or prejudice, not from objective observations or research
(McGoldrick et al., 2007). In fact, sex therapists and sex researchers have only
recently begun to attend systematically to the importance of culture and race.
TOPIC OVERVIEW
Sexual Dysfunctions
Disorders of Desire
Disorders of Excitement
Disorders of Orgasm
Disorders of Sexual Pain
Treatments for Sexual Dysfunctions
What Are the General Features
of Sex Therapy?
What Techniques Are Applied
to Particular Dysfunctions?
What Are the Current Trends
in Sex Therapy?
Paraphilias
Fetishism
Transvestic Fetishism
Exhibitionism
Voyeurism
Frotteurism
Pedophilia
Sexual Masochism
Sexual Sadism
A Word of Caution
Gender Identity Disorder
Explanations of Gender Identity
Disorder
Treatments for Gender Identity
Disorder
Putting It Together: A Private Topic
Draws Public Attention

iAlgt Ll la 0
Favorite Part of the Sexual Cycle
I ,
“di 1 .0
11!
to
I •
°sexual dysfunctioneA disorder
marked by a persistent inability to func-
tion normally in some area of the human
sexual response cycle.
°desire phaseeThe phase of the sexual
response cycle consisting of an urge to
have sex, sexual fantasies, and sexual
attraction to others.
°hypoactive sexual desire
disordereA disorder marked by a lack
of interest in sex and hence a low level
of sexual activity.
°sexual aversion disordereA disorder
characterized by an aversion to and
avoidance of genital sexual interplay.
1’y Sexual Dysfunctions
Sexual dysfunctions, disorders in which people cannot respond normally in key
areas of sexual functioning, make it difficult or impossible to enjoy sexual intercourse. A
large study suggests that as many as 31 percent of men and 43 percent of women in the
United States suffer from such a dysfunction during their lives (Laumann et al., 2005,
1999; Heiman, 2002). Sexual dysfunctions are typically very distressing, and they often
lead to sexual frustration, guilt, loss of self-esteem, and interpersonal problems (Basson,
2007). Often these dysfunctions are interrelated; many patients with one dysfunction
experience another as well. Sexual dysfunctioning will be described here for hetero-
sexual couples, the majority of couples seen in therapy. Homosexual couples have the
same dysfunctions, however, and therapists use the same basic techniques to treat them
(LoPiccolo, 2004, 1995).
The human sexual response can be described as a cycle with four phases: desire, excite-
ment, orgasm, and resolution (see Figure 11-1). Sexual dysfunctions affect one or more
of the first three phases. Resolution consists simply of the relaxation and reduction in
arousal that follow orgasm. Some people struggle with a sexual dysfunction their whole
lives; in other cases, normal sexual functioning preceded the dysfunction. In some cases
the dysfunction is present during all sexual situations; in others it is tied to particular
situations (APA, 2000).
Disorders of Desire
The desire phase of the sexual response cycle consists of an urge to have sex, sexual
fantasies, and sexual attraction to others. Two dysfunctions—hypoactive sexual desire dis-
order and sexual aversion disorder—affect the desire phase.A client named Clara Bryarton
experiences both of these disorders:
[Randall and Clara Bryarton] have been married for 14 years and have three children,
ages 8 through 12. They [complain that Clara] has never enjoyed [sex] since they have
been married.
Before their marriage, although they had intercourse only twice, [Clara] had been
highly aroused by kissing and petting and felt she used her attractiveness to “seduce”
her husband into marriage. She did, however, feel intense guilt about their two episodes
of premarital intercourse; during their honeymoon, she began to think of sex as a chore
that could not be pleasing. Although she periodically passively complied with intercourse,
she had almost no spontaneous desire for sex. She never masturbated, had never reached
orgasm, thought of all variations such as oral sex as completely repulsive, and was preoc-
cupied with a fantasy of how disapproving her family would be if she ever engaged in any
of these activities.
[Clara feels] certain that no woman she respects in any older generation has [truly]
enjoyed sex, and that despite the “new vogue” of sexuality, only sleazy, crude women
let themselves act like “animals.” These beliefs have led to a pattern of regular, but in-
frequent, sex that at best is accommodating and gives little or no pleasure to her or her
husband. Whenever [Clara] comes close to having a feeling of sexual arousal, numerous
negative thoughts come into her mind, such as “What am I, a tramp?” “If 1 like this,
he’ll just want it more often.” Or “How could l look myself in the mirror after something
like this?” These thoughts almost inevitably are accompanied by a cold feeling and an
insensitivity to sensual pleasure. As a result, sex is invariably on unhappy experience. Al-
most any excuse, such as fatigue or being busy, is sufficient for her to rationalize avoiding
intercourse.
Yet, intellectually [Clara] wonders, “Is something wrong with me?”
(Spitzer et al., 1994, p. 251)
322 ://CHAPTER 1 1

Male

Female
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Low – Low
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Sexual Disorders and Gender Identity Disorder :// 323
People with hypoactive sexual desire disorder lack interest in sex and, in turn,
display little sexual activity (see Table 11-1). Nevertheless, when these individuals do
have sex, their physical responses may be normal and they may enjoy the experience.
While our culture portrays men as wanting all the sex they can get, hypoactive sexual
desire may be found in as many as 16 percent of men, and the number seeking therapy
has increased during the past decade (Maurice, 2007; Laumann et al., 2005, 1999). It may
also be found in 33 percent of women. A number of people experience normal sexual
interest and arousal but choose, as a matter of lifestyle, not to engage in sexual relations.
These individuals are not diagnosed as having hypoactive sexual desire disorder.
DSM-IV-TR_ defines hypoactive sexual desire as “deficient or absent sexual fanta-
sies and desire for sexual activity,” but it does not specify what a “deficient” level is. In
fact, this criterion is difficult to define (Maurice, 2007; LoPiccolo, 2004, 1995). Age,
number of years married, education, social class, and other factors may all influence the
frequency of sex. In one survey, 93 happily married couples were asked to report how
often they desire sexual encounters. Almost all of them said that they desire sex at least
once every two weeks, and around 85 percent reported a desire rate of several times a
week or more. On the basis of this survey, sexual desire would be considered hypoactive
only when a person desires sex less frequently than once every two weeks.
People with sexual aversion disorder find sex distinctly unpleasant or repulsive.
Sexual advances may sicken, disgust, or frighten them. Some people are repelled by a
particular aspect of sex, such as penetration of the vagina; others experience a general
aversion to all sexual stimuli, including kissing or touching. Aversion to sex seems to be
quite rare in men and somewhat more common in women (Wincze, Bach, & Barlow,
2008; Heiman, 2002).
A person’s sex drive is determined by a combination of biological, psychological,
and sociocultural factors, and any of them may reduce sexual desire. Most cases of low
sexual desire or sexual aversion are caused primarily by sociocultural and psychological
factors, but biological conditions can also lower sex drive significantly.
Biologica Causes A number of hormones interact toproduce sexual desire and
behavior, and abnormalities in their activity can lower the sex drive (Ashton, 2007;
Hyde, 2005). In both men and women, a high level of the hormone prolactin, a low
level of the male sex hormone testosterone, and either a high or low level of the female
sex hormone estrogen can lead to low sex drive. Low sex drive has been linked to the
high levels of estrogen contained in some birth control pills, for example. Conversely, it
has also been tied to the low level of estrogen found in many postmenopausal women

324 ://CHAPTER 1 1

or women who have recently given birth. Long-term physical illness can also lower
the sex drive (Basson, 2007; Stevenson & Elliott, 2007).The low drive may be a direct
result of the illness or an indirect result because of stress, pain, or depression brought on
by the illness.

e )caterns or Sexual Behavior
1 -,11,exual dysfunctions are, by definition,
klifferent from the usual patterns of
sexual functioning. But in the sexual realm,
what is “the usual”? Studies conducted
over the past Iwo decades have provided a
wealth of useful, sometimes eye-opening in-
formation about sexual patterns in the “nor-
mal” populations of North America (CDC,
2007; Lindau et al., 2007; McAnulty &
Burnette, 2006; Smith, 2006; Kelly, 2005;
Laumann et cd., 2005, 1999, 1994; Brown
& Ceniceros, 2001; Seidman & Rieder,
1995; Janus &Janus, 1993).
Teenagers
More than 90 percent of boys masturbate
by the end of adolescence, compared to
50 percent of girls. For the vast majority
of them, masturbation began by age 14.
Males report masturbating an average of
one to two times a week, females once a
month.
Around 20 percent of teenagers have
heterosexual intercourse by the age of 15,
and 80 percent by age 19. Today’s teen-
agers are having intercourse younger than
those of past generations. Most teens who
are sexually experienced engage in only
one sexual relationship at a time. Over the
course of their teen years, however, most
have at least two sex partners.
Extended periods without sex are still
common, even for teenagers in a relation-
ship. Half of sexually experienced adoles-
cent girls have intercourse once a month or
less. Sexually experienced teenage boys
spend an average of six months of the
year without intercourse.
Condom use by teenagers has in-
creased somewhat during the past decade,
partly because of warnings about AIDS.
However, at most half of teenagers report
having used a condom the last time they
had sex. Less than a third of teenagers use
condoms consistently and appropriately.
Early Adulthood (Ages 18-24)
More than 80 percent of unmarried young
adults have intercourse in a given year. Of
those who are sexually active, around a
third have intercourse two or three times a
month and another third engage in it two
or three times a week. Masturbation re-
mains common in young adulthood: Close
to 60 percent of men masturbate, a third of
them at least once a week, and 36 percent
of women masturbate, a tenth of them at
least once a week.
Mid-Adulthood (Ages 25-59)
From the ages of 25 to 59, sexual relation-
ships last longer and are more monoga-
mous. More than 90 percent of people in
this age range have sexual intercourse in a
given year. Half of the unmarried men have
two or more partners in a given year, com-
pared to a quarter of the unmarried women.
Among sexually active adults, close to
60 percent of men hove intercourse up to
three times a week and around 60 percent
of women once or twice a week. Middle-
aged adults are still masturbating. Half of
all middle-aged men masturbate at least
monthly. Half of all women between 25 and
50 masturbate at least monthly, but only a
third of those between 51 and 64 do so.
Old Age (Over Age 60)
More and more people stop having inter-
course as the years go by—a total of 10
percent in their 40s, 15 percent in their 50s,
30 percent in their 60s, and 45 percent in
their 70s. The decline in men’s sexual activ-
ity usually comes gradually as they advance
in age and their health fails. Sexual activity
is more likely to drop off sharply for elderly
women, commonly because of the death
or illness of a partner. Elderly women also
seem to lose interest in sex before elderly
men do. Half of the women in their 60s
report limited sexual interest, compared to
fewer than 10 percent of the men.
Among elderly persons who remain
sexually active, those in their 60s have
intercourse an average of four times a
month, those in their 70s two or three times
a month. Around 70 percent of elderly
men and 50 percent of elderly women con-
tinue to have sexual fantasies. Around half
of men and a fourth of women continue to
masturbate into their 90s.
• lb

Sex drive can be lowered by some pain medications, certain psychotropic
drugs, and a number of illegal drugs such as cocaine, marijuana, amphet-
amines, and heroin (Stevenson & Elliott, 2007). Low levels of alcohol may
raise the sex drive by lowering a person’s inhibitions, yet high levels may
reduce it (Ksir et al., 2008).
Psychological Causes A general increase in anxiety, depression, or anger
may reduce sexual desire in both men and women (Basson, 2007). Frequently,
as cognitive theorists have noted, people with hypoactive sexual desire and
sexual aversion have particular attitudes, fears, or memories that contribute to
their dysfunction, such as a belief that sex is immoral or dangerous (Wincze
et al., 2008; LoPiccolo, 2004, 1995). Other people are so afraid of losing con-
trol over their sexual urges that they try to resist them completely. And still
others fear pregnancy.
Certain psychological disorders may also contribute to hypoactive sexual
desire and sexual aversion. Even a mild level of depression can interfere with
sexual desire,. and some people with obsessive-compulsive symptoms find
contact with another person’s body fluids and odors to be highly unpleasant (Maurice,
2007; LoPiccolo, 2004, 1995).
Sociocultu r’ol Causes The attitudes, fears, and psychological disorders that contrib-
ute to hypoactive sexual desire and sexual aversion occur within a social context, and so
certain sociocultural factors have also been linked to these dysfunctions. Many suffer-
ers are feeling situational pressures—divorce, a death in the family, job stress, infertility
difficulties, having a baby (Basson, 2007; Lau mann et al., 2005). Others may be having
problems in their relationships (Wincze et al., 2008). People who are in an unhappy re-
lationship, have lost affection for their partner, or feel powerless and dominated by their
partner can lose interest in sex (Maurice, 2007). Even in basically happy relationships, if
one partner is a very unskilled, unenthusiastic lover, the other can begin to lose interest
in sex. And sometimes partners differ in their needs for closeness. The one who needs
more personal space may develop hypoactive sexual desire as a way of keeping distance
(LoPiccolo, 2004, 1995).
Cultural standards can also set the stage for hypoactive sexual desire and sexual aver-
sion. Some men adopt our culture’s double standard and thus cannot feel sexual desire
for a woman they love and respect (Maurice, 2007). More generally, because our society
equates sexual attractiveness with youthfulness, many middle-aged and older men and
women lose interest in sex as their self-image or their attraction to their partner dimin-
ishes with age (LoPiccolo, 2004, 1995).
The trauma of sexual molestation or assault is especially likely to produce the fears,
attitudes, and memories found in these sexual dysfunctions. Sexual aversion is very
common in victims of sexual abuse and may persist for years, even decades (Hall, 2007;
Heiman & Heard-Davison, 2004). In some cases, individuals may experience vivid
flashbacks of the assault during adult sexual activity.
Disorders of Excitement
The excitement phase of the sexual response cycle is marked by changes in the pelvic
region, general physical arousal, and increases in heart rate, muscle tension, blood pres-
sure, and rate of breathing. In men, blood pools in the pelvis and leads to erection of the
penis; in women, this phase produces swelling of the clitoris and labia (the folds of skin
on each side of the vagina), as well as lubrication of the vagina (see Figure 11-2 on the
next page). Dysfunctions affecting the excitement phase are female sexual arousal disorder
(once referred to as “frigidity”) and wale erectile disorder (once called “impotence”).
Female Sexual Arousal Disorder Women with a female sexual arousal dis-
order are persistently unable to attain or maintain proper lubrication or genital swelling
during sexual activity (see Table 11-2, also on the next page). Understandably, many of
Sexual Disorders and Gender Identity Disorder :1/ 325
41.
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‘, excitement phaseeThe phase of
the sexual response cycle marked by
changes in the pelvic region, general
physical arousal, and increases in heart
rate, muscle tension, blood pressure, and
rate of breathing.
female sexual arousal disorderoA
female dysfunction marked by a persis-
tent inability to attain sexual excitement,
including adequate lubrication or genital
swelling, during sexual activity.

Labia
swell
Rectal
sphincter
contracts
Rhythmic
contractions in
orgasmic platform
Excitement

Orgasm
IL
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1.1111•1 c■ 1 _
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326 :A/CHAPTER 1 1
them also experience an orgasmic disorder or other sexual dysfunction. In fact, this disor-
der is rarely diagnosed alone (Heiman, 2007). Studies vary widely in their estimates of its
prevalence, but most agree that more than 10 percent of women experience it (Laumann
et al., 2005, 1999,1994; Bancroft et al., 2003). Because lack of sexual arousal in women is
so often tied to an orgasmic disorder, researchers usually study and explain the two prob-
lems together. Correspondingly, this chapter will consider the causes of these problems
together in the section on orgasmic disorder.
Ma ke Erectile Disorder Men with male erectile disorder persistently fail to attain
or maintain an adequate erection during sexual activity.This problem occurs in about 10
percent of the general male population, including Robert, the man whose difficulties
opened this chapter (Laumann et al., 2005, 1999; Heiman, 2002). Carlos Domera also has
erectile disorder:
Carlos Domera is a 30-year-old dress manufacturer who came to the United States from
Argentina at age 22. He is married to … Phyllis, also age 30. They have no children. Mr.
Domera’s problem was that he had been unable to have sexual intercourse for over a year
due to his inability to achieve or maintain an erection. He had avoided all sexual contact
with his wife for the prior five months, except for two brief attempts at lovemaking which
ended when he failed to maintain his erection.
The couple separated a month ago by mutual agreement due to the tension that sur-
rounded their sexual problem and their inability to feel comfortable with each other. Both
professed love and concern for the other, but had serious doubts regarding their ability to
resolve the sexual problem. . . .
[Carlos.] conformed to the stereotype of the “macho Latin lover,” believing that he
“should always have erections easily and be able to make love at any time.” Since he
couldn’t “perform” sexually, he felt humiliated and inadequate, and he dealt with this by
avoiding not only sex, but any expression of affection for his wife.
[Phyllis] felt “he is not trying; perhaps he doesn’t love me, and I can’t live with no sex,
no affection, and his bad moods.” She had requested the separation temporarily, and he
readily agreed. However, they had recently been seeing each other twice a week. . . .
During the evaluation he reported that the onset of his erectile difficulties was concur-
rent with a tense period in his business. After several “failures” to complete intercourse, he

Sexual Disorders and Gender Identity Disorder :1/ 327
concluded he was “useless as a husband” and therefore a “total failure.” The anxiety of
attempting lovemaking was too much for him to deal with.
He reluctantly admitted that he was occasionally able to masturbate alone to a full,
firm erection and reach a satisfying orgasm. However, he felt ashamed and guilty about
this, from both childhood masturbatory guilt and a feeling that he was “cheating” his wife.
It was also noted that he had occasional firm erections upon awakening in the morning.
Other than the antidepressant, the patient was taking no drugs, and he was not using
much alcohol. There was no evidence of physical illness.
(Spitzer et al., 1983, pp. 105-106)
°male erectile disorder0A dysfunction
in which a man repeatedly fails to attain
or maintain an erection during sexual
activity.
°nocturnal penile tumescence (NPT)0
Erection during sleep.
Unlike Carlos, most men with an erectile disorder are over the age of 50, largely
because so many cases are associated with ailments or diseases of older adults (Cameron
et al., 2005). The disorder is experienced by 7 percent of men who are under 30 years
old and increases to 50 percent of men over 60 (Rosen, 2007). Moreover, according to
surveys, half of all adult men experience erectile difficulty during intercourse at least
some of the time.
Most cases of erectile disorder result from an interaction of biological, psychological,
and sociocultural processes (Rosen, 2007). One study found that only 10 of 63 cases of
this disorder were caused by purely psychosocial factors, and only 5 were the result of
physical impairment alone (LoPiccolo, 1991).
BIOLOGICAL CAUSES The same hormonal imbalances that can cause hypoactive sexual de-
sire can also produce erectile disorder (Hyde, 2005). More commonly, however, vascular
problems—problems with the body’s blood vessels—are involved (Wincze et al., 2008;
Rosen, 2007) .An erection occurs when the chambers in the penis fill with blood, so any
condition that reduces blood flow into the penis, such as heart disease or clogging of the
arteries, may lead to the disorder. It can also be caused by damage to the nervous system
as a result of diabetes, spinal cord injuries, multiple sclerosis, kidney failure, or treatment
by dialysis (Wincze et al., 2008; Stevenson & Elliott, 2007). In addition, as
is the case with hypoactive sexual desire, the use of certain medications and
various forms of substance abuse, from alcohol abuse to cigarette smoking,
may interfere with erections.
Medical procedures, including ultrasound recordings and blood tests,
have been developed for diagnosing biological causes of erectile disorder.
Measuring nocturnal penile tumescence (NPT), or erections during
sleep, is particularly useful in assessing whether physical factors are respon-
sible. Men typically have erections during rapid eye movement (REM) sleep,
the phase of sleep in which dreaming takes place.A healthy man is likely to
have two to five REM periods each night, and perhaps two to three hours
of penile erections. Abnormal or absent nightly erections usually (but not
always) indicate some physical basis for erectile failure.As a rough screening
device, a patient may be instructed to fasten a simple “snap gauge” band
around his penis before going to sleep and then check it the next morning. A broken
band indicates that erection has occurred during the night. An unbroken band indicates
a lack of nigh_ttime erections and suggests that the person’s general erectile problem may
have a physical basis. A newer version of this device further attaches the band to a com-
puter, which provides precise measurements of erections throughout the night (Wincze
et al., 2008). Such devices are less likely to be used in clinical practice today than in past
years. As you’ 11 see later in the chapter,Viagra and other drugs for erectile disorder are
typically given to patients without much evaluation of their problem (Rosen, 2007).
PSYCHOLOGICAL CAUSES Any of the psychological causes of hypoactive sexual desire can
also interfere with arousal and lead to erectile disorder (Rosen, 2007). As many as 90
percent of all men with severe depression, for example, experience some degree of
erectile dysfunction (Stevenson & Elliott, 2007).
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“Everybody’s a critic.”
328 ://CHAPTER 11
verformance anxietyeThe fear of
performing inadequately and a related
tension experienced during sex.
()spectator roleoA state of mind that
some people experience during sex,
focusing on their sexual performance to
such an extent that their performance
and their enjoyment are reduced.
°orgasm phaseeThe phase of the
sexual response cycle during which an
individual s sexual pleasure peaks and
sexual tension is released as muscles in
the pelvic region contract rhythmically.
orapid ejaculationoA dysfunction
in which a man reaches orgasm and
ejaculates before, on, or shortly after
penetration and before he wishes to.
Also known as premature ejaculation.
()male orgasmic disordereA male
dysfunction characterized by repeated
inability to reach orgasm or long delays
in reaching orgasm after normal sexual
excitement.
One well-supported psychological explanation for erectile disorder
is the cognitive-behavioral theory developed by William Masters and
Virginia Johnson (1970). The explanation emphasizes performance
anxiety and the spectator role. Once a man begins to experience
erectile problems, for whatever reason, he becomes fearful about failing
to have an erection and worries during each sexual encounter. Instead
of relaxing and enjoying the sensations of sexual pleasure, he remains
distanced from the activity, watching himself and focusing on the goal of
reaching erection. Instead of being an aroused participant, he becomes a
judge and spectator. Whatever the initial reason for the erectile dysfunc-
tion, the resulting spectator role becomes the reason for the ongoing
problem. In this vicious cycle, the original cause of the erectile failure
becomes less important than fear of failure.
SOCIOCULTURAL CAUSES Each of the sociocultural factors that contribute
to hypoactive sexual desire has also been tied to erectile disorder. Men
who have lost their jobs and are under financial stress, for example, are
more likely to develop erectile difficulties than other men (Morokoff & Gillilland,
1993). Marital stress, too, has been tied to this dysfunction (Wincze et al., 2008). Two
relationship patterns in particular may contribute to it (Rosen, 2007; LoPiccolo, 2004,
1991). In one, the wife provides too little physical stimulation for her aging husband,
who, because of normal aging changes, now requires more intense, direct, and lengthy
physical stimulation of the penis for erection to occur. In the second relationship pattern,
a couple believes that only intercourse can give the wife an orgasm. This idea increases
the pressure on the man to have an erection and makes him more vulnerable to erectile
dysfunction. If the wife reaches orgasm manually or orally during their sexual encounter,
his pressure to perform is reduced.
Disorders of Orgasm
During the orgasm phase of the sexual response cycle, an individual’s sexual pleasure
peaks and sexual tension is released as the muscles in the pelvic region contract, or draw
together, rhythmically (see Figure 11-3).The man’s semen is ejaculated, and the outer third
of the woman’s vaginal wall contracts. Dysfunctions of this phase of the sexual response
cycle are rapid, or premature, ejaculation; male orgasmic disorder; and female orgasmic disorder
Rapid, or Premi4ure, Ejaculation Eddie is typical of many men in his experience
of rapid ejaculation:
Eddie, a 20-year-old student, sought treatment after his girlfriend ended their relation-
ship because his premature ejaculation left her sexually frustrated. Eddie had had only
one previous sexual relationship, during his senior year in high school. With two friends he
would drive to a neighboring town and find a certain prostitute. After picking her up, they
would drive to a deserted area and take turns having sex with her, while the others waited
outside the car. Both the prostitute and his friends urged him to hurry up because they
feared discovery by the police, and besides, in the winter it was cold. When Eddie began
his sexual relationship with his girlfriend, his entire sexual history consisted of this rapid
intercourse, with virtually no foreplay. He found caressing his girlfriend’s breasts and geni-
tals and her touching of his penis to be so arousing that he sometimes ejaculated before
complete entry of the penis, or after at most only a minute or so of intercourse.
(LoPiccolo, 1995, p. 495)
A man suffering from rapid, or premature, ejaculation persistently reaches orgasm
and ejaculates with very little sexual stimulation before, on, or shortly after penetration,

Excitement Orgasm
Partially
stimulated
state
Unstimulated
state
Partial elevation
of testes
Full
erection
Internal sphincter
of bladder doses
Urethral
contractions
Seminal
vesicles
contract
Contractions force
the seminal fluid
through the urethra
Prostate gland
contracts
Rectal sphincter
contracts
Penile
contractions
ti
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DSM Checklisi
Sexual Disorders and Gender Identity Disorder :1/ 329
and before he wishes to (see Table 11-3). As many as 30 percent of men in the United
States experience rapid ejaculation at some time ( jannini & Lenzi, 2005; Laumann et al.,
2005, 1999, 1994). The typical duration of intercourse in our society has increased over
the past several decades, in turn increasing the distress of men who suffer from rapid
ejaculation. Although the dysfunction is certainly experienced by many young men,
research suggests that men of any age may in fact suffer from it (Althof, 2007; Laumann
et al., 2005, 1999).
Psycholo gical, particularly behavioral, explanations of rapid ejaculation have received
more research support than other kinds of explanations. The dysfunction is common,
for example, among young, sexually inexperienced men such as Eddie, who simply have
not learned Co slow down, control their arousal, and extend the pleasurable process of
making love (Althof, 2007). In fact, rapid ejaculation often occurs when a young man
has his first sexual encounter.With continued sexual experience, most men gain greater
control over their sexual responses. Men of any age who have sex only occasionally are
also prone to ejaculate rapidly.
Clinicians have also suggested that rapid ejaculation may be related to anxiety, hur-
ried masturbation experiences during adolescence (in fear of being caught” by parents),
or poor reco gnition of one’s own sexual arousal (Althof, 2007;Westheimer & Lopater,
2005). However, these theories have only sometimes received clear research support.
There is a growing belief among some clinical theorists that biological factors may
also play a key role in many cases of rapid ejaculation. Research is at the earliest of stages,
but three biological theories have emerged (Althof, 2007; Mirone et al., 2001;Waldinger
et al., 1998). One theory states that some men are born with a genetic predisposition to
develop this dysfunction.A second argues that the brains of men with rapid ejaculation
contain certain serotonin receptors that are overactive and others that are underactive.
A third explanation holds that men with this dysfunction experience greater sensitivity
or nerve conduction in the area of their penis, a notion that has received inconsistent
research support thus far.
Male Orgasmic Disorder A man with male orgasmic disorder is repeatedly
unable to reach orgasm or is very delayed in reaching orgasm after normal sexual excite-
ment (see Table 11-4 on the next page). The disorder occurs in 8 percent of the male
population (Hartmann & Waldinger, 2007; Laumann et al., 2005, 1999) and is typically a
source of great frustration and upset, as in the case ofJohn:

lightly Visits
I I 41,2, ,11:!i
.
6″: ”
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John, a 38-year-old sales representative, had been married for 9 years. At the insistence of
his 32-year-old wife, the couple sought counseling for their sexual problem—his inability to
ejaculate during intercourse. During the early years of the marriage, his wife had experi-
enced difficulty reaching orgasm until he learned to delay his ejaculation for a long period
of time. To do this, he used mental distraction techniques and regularly smoked marijuana
before making love. Initially, John felt very satisfied that he could make love for longer and
longer periods of time without ejaculation and regarded his ability as a sign of masculinity.
About 3 years prior to seeking counseling, after the birth of their only child, John found
that he was losing his erection before he was able to ejaculate. His wife suggested differ-
ent intercourse positions, but the harder he tried, the more difficulty he hod in reaching
orgasm. Because of his frustration, the couple began to ovoid sex altogether. John expe-
rienced increasing performance anxiety with each successive failure, and an increasing
sense of helplessness in the face of his problem.
(Rosen & Rosen, 1981, pp. 317-318)
A low testosterone level, certain neurological diseases, and some head or spinal cord
injuries can interfere with ejaculation (Stevenson & Elliott, 2007; McKenna, 2005). Drugs
that slow down the sympathetic nervous system (such as alcohol, some medications for
high blood pressure, and certain psychotropic medications) can also affect ejaculation. For
example, certain serotonin-enhancing antidepressant drugs appear to interfere with ejacu-
lation in at least 30 percent of men who take them (Ashton, 2007; Clayton et al., 2002).
A leading psychological cause of male orgasmic disorder appears to be performance
anxiety and the spectator role, the cognitive-behavioral factors also involved in male
erectile disorder. Once a man begins to focus on reaching orgasm, he may stop being
an aroused participant in his sexual activity and instead become an unaroused, self-
critical, and fearful observer (Hartmann &Waldinger, 2007;Wiederman, 2001). Another
psychological cause of male orgasmic disorder may be past masturbation habits. If, for
example, a man has masturbated all his life by rubbing his penis against sheets, pillows, or
other such objects, he may have difficulty reaching orgasm in the absence of the sensa-
tions and mechanics tied to those objects (Wincze et al., 2008). Finally, male orgasmic
disorder may develop out of hypoactive sexual desire (Apfelbaum, 2000). A man who
engages in sex largely because of pressure from his partner, without any real desire for
it, simply may not get aroused enough to reach orgasm.
Female Orgasmic Disorder Stephanie and Bill, married for three years, came for
sex therapy because of her lack of orgasm.
Stephanie had never had an orgasm in any way, but because of Bill’s concern, she had
been faking orgasm during intercourse until recently. Finally she told him the truth, and
they sought therapy together. Stephanie had been raised by a strictly religious family. She
could not recall ever seeing her parents kiss or show physical affection for each other. She
was severely punished on one occasion when her mother found her looking at her own
genitals, at about age 7. Stephanie received no sex education from her parents, and when
she began to menstruate, her mother told her only that this meant that she could become
pregnant, so she mustn’t ever kiss a boy or let a boy touch her. Her mother restricted
her dating severely, with repeated warnings that “boys only want one thing.” While her
parents were rather critical and demanding of her (asking her why she got one B among
otherwise straight A’s on her report card, for example), they were loving parents and their
approval was very important to her.
(LoPircolo, 1995, p. 496)
330 ://CHAPTER 11

.female orgasmic disordereA dys-
function in which a woman rarely has an
orgasm or repeatedly experiences a very
delayed one.

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Sexual Disorders and Gender !deadly Disorder :fi 331
Women with female orgasmic disorder rarely reach orgasm or generally experi-
ence a very delayed one (see again Table 11-4).Around 24 percent of women apparently
have this problem to some degree—including more than a third of postmenopausal
women (Heiman, 2007, 2002; Laumann et al., 2005, 1999, 1994). Studies indicate that
10 percent or more of women have never had an orgasm, either alone or during inter-
course, and at least another 9 percent rarely have orgasms (Bancroft et al., 2003).At the
same time, half of all women experience orgasm in intercourse at least fairly regularly
(LoPiccolo & Stock, 1987). Women who are more sexually assertive (Hurlbert, 1991)
and more comfortable with masturbation (Kelly et al., 1990) tend to have orgasms more
regularly. Female orgasmic disorder appears to be more common among single women
than among women who are married or living with someone (Laumann et al., 2005,
1999, 1994)
Most clinicians agree that orgasm during intercourse is not mandatory for normal
sexual functioning (Wincze et al., 2008). Many women instead reach orgasm with their
partners by direct stimulation of the clitoris (LoPiccolo, 2002, 1995). Although early
psychoanalytic theory considered a lack of orgasm during intercourse to be pathologi-
cal, evidence suggests that women who rely on stimulation of the clitoris for orgasm
are entirely normal and healthy (Heiman, 2007).
As you saw earlier, female orgasmic disorder typically is linked to female sexual
arousal disorder, and the two tend to be studied, explained, and treated together. Once
again, biological, psychological, and sociocultural factors may combine to produce these
disorders (Heiman, 2007).
BIOLOGICAL CAUSES A variety of physiological conditions can affect a woman’s arousal and
orgasm (Wincze et al., 2008; Heiman, 2007). Diabetes can damage the nervous system
in ways that interfere with arousal, lubrication of the vagina, and orgasm. Lack of orgasm
has sometimes been linked to multiple sclerosis and other neurological diseases, to the
same drugs and medications that may interfere with ejaculation in men, and to changes,
often postmenopausal, in skin sensitivity and structure of the clitoris, vaginal walls, or
the labia.
PSYCHOLOGICAL CAUSES The psychological causes of hypoactive sexual desire and sexual
aversion, including depression, may also lead to the female arousal and orgasmic disorders
(Heiman, 2007; Heard-Davison et al., 2004). In addition, as psychodynatnic theorists
might predict, memories of childhood traumas and relationships have sometimes been
associated with these disorders. In one large study, memories of an unhappy childhood
or loss of a parent during childhood were tied to lack of orgasm in adulthood (Raboch
& Raboch, 1992). In other studies, childhood memories of a dependable father, a posi-
tive relationship with one’s mother, affection between the parents, the mother’s positive
personality, and the mother’s expression of positive emotions were all predictors of
orgasm (Heiman, 2007; Heiman et al., 1986).
SOCIOCULTURAL CAUSES For years many clinicians have believed that fe-
male arousal and orgasmic disorders may result from society’s recurrent
message to women that they should repress and deny their sexuality,
a message that has often led to “less permissive” sexual attitudes and
behavior among women than among men (see Figure 11-4). In fact,
many wome n with female arousal and orgasmic disorders report that
they had an overly strict religious upbringing, were punished for child-
hood masturbation, received no preparation for the onset of menstrua-
tion, were restricted in their dating as teenagers, and were told that
“nice girls don’t” (LoPiccolo & van Male, 2000; LoPiccolo, 1997).
A sexually restrictive history, however, is just as common among
women who function well in sexual encounters (LoPiccolo, 2002,
1997; LoPiccolo & Stock, 1987). In addition, cultural messages about
female sexuality have been more positive in recent years, while the rate
of female arousal and orgasmic disorders remains the same. Why, then,
do some women and not others develop sexual arousal and orgasmic
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ovaginisniuseA condition marked by
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edyspareunia®A disorder in which a
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dysfunctions? Researchers suggest that unusually stressful events or relationships may
help produce the fears, memories, and attitudes that often accompany these dysfunctions
(Westheimer & Lopater, 2005). For example, many women molested as children or raped
as adults have arousal and orgasm dysfunctions (Hall, 2007; Heiman, 2007).
Research has also related orgasmic behavior to certain qualities in a woman’s inti-
mate relationships (Heiman, 2007; Metz & Epstein, 2002; Heiman et al., 1986). Studies
have found, for example, that the likelihood of reaching orgasm may be tied to how
much emotional involvement a woman had during her first experience of intercourse
and how long that relationship lasted, the pleasure the woman obtained during the
experience, her current attraction to her partner’s body, and her marital happiness. Inter-
estingly, the same studies have found that erotic fantasies during sex with their current
partner are more common in orgasmic than in nonorgasmic women.
Disorders of Sexual Pain
Two sexual dysfunctions do not fit neatly into a specific phase of the sexual response
cycle. These are the sexual pain disorders, vaginismus and dyspareunia, each marked by
enormous physical discomfort when sexual activity is attempted.
VaginiSMUS In vaginismus, involuntary contractions of the muscles around the
outer third of the vagina prevent entry of the penis (see Table 11-5). Severe cases can
prevent a couple from ever having intercourse. Estimates are that perhaps 20 percent of
women occasionally experience pain during intercourse and that vaginismus occurs in
less than 1 percent of all women (LoPiccolo & van Male, 2000; LoPiccolo, 1995).
Most clinicians agree with the cognitive-behavioral position that vaginismus is usu-
ally a learned fear response, set off by a woman’s expectation that intercourse will be
painful and damaging. A variety of factors apparently can set the stage for this fear, in-
cluding anxiety and ignorance about intercourse, exaggerated stories about how painful
and bloody the first occasion of intercourse is for women, trauma caused by an unskilled
lover who forces his penis into the vagina before the woman is aroused and lubricated,
and the trauma of childhood sexual abuse or adult rape (Binik et al., 2007; Hall, 2007;
Heiman & Heard-Davison, 2004).
Some women experience painful intercourse because of an infection of the vagina
or urinary tract, a gynecological disease such as herpes simplex, or the physical effects of
menopause. In such cases vaginismus can be overcome only if the women receive medi-
cal treatment for these conditions (LoPiccolo, 2002, 1995). Many women who have
vaginismus also have other sexual dysfunctions (Heard-Davison et al., 2004; Reissing
et al., 2003). Some, however, enjoy sex greatly, have a strong sex drive, and reach orgasm
with stimulation of the clitoris. They just fear penetration of the vagina.
Dyspareunia A person with dyspareunia (from Latin words meaning “painful
mating”) experiences severe pain in the genitals during sexual activity. Surveys suggest
that as many as 14 percent of women and 3 percent of men suffer from this problem to
some degree (Heiman, 2007, 2002; Laumann et al., 2005, 1999).As many as 8 percent of
women experience painful intercourse on all or most occasions (Wincze et al., 2008).
Sufferers typically enjoy sex and get aroused but find their sex lives very limited by the
pain that accompanies what used to be a positive event.
Dyspareunia in women usually has a physical cause (Binik et al., 2007; Bergeron et
al., 2002). Among the most common is an injury (for example, to the vagina or pelvic
ligaments) during childbirth. Similarly, the scar left by an episiotomy (a cut often made
to enlarge the vaginal entrance and ease delivery) can cause pain. Dyspareunia has also
been tied to collision of the penis with remaining parts of the hymen, infections of the
vagina, wiry pubic hair that rubs against the labia during intercourse, pelvic diseases,
tumors, cysts, and allergic reactions to either the chemicals in vaginal douches and con-
traceptive creams, the rubber in condoms or diaphragms, or the protein in semen.
Although psychological factors (for instance, heightened anxiety or overattentive-
ness to one’s body) or relationship problems may contribute to this disorder, psycho-
332 ://CHAPTER

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Sexual Disorders and Gender Identity Disorder 333
social factors alone are rarely responsible for it (Binik et al., 2007, 2002). In cases that
are truly psychogenic, the woman is in fact likely to be suffering from hypoactive sexual
desire (Steege & Ling, 1993).That is, penetration into an unaroused, unlubricated vagina
is painful.
Sexual Dysfunctions
Sexual dysfunctions make it difficult or impossible for a person to have or enjoy
sexual intercourse. DSM-IV-TR lists two disorders of the desire phase of the sexual
response cycle: hypoactive sexual desire disorder and sexual aversion disorder. Bio-
logical causes for these disorders include abnormal hormone levels, certain drugs,
and some medical illnesses. Psychological and sociocultural causes include specific
fears, situational pressures, relationship problems, and the trauma of having been
sexually molested or assaulted.
Disorders of the excitement phase are female sexual arousal disorder and
male erectile disorder. Biological causes of male erectile disorder include abnormal
hormone levels, vascular problems, medical conditions, and certain medications.
Psychological and sociocultural causes include the combination of performance
anxiety and the spectator role, situational pressures such as job loss, and relation-
ship problems.
Rapid, or premature, ejaculation, a disorder of the orgasm phase of the sexual
response cycle, has been related most often to behavioral causes, such as inappro-
priate early learning and inexperience. Male orgasmic disorder, another orgasm
disorder, can have biological causes, such as low testosterone levels, neurologi-
cal diseases, and certain drugs, and psychological causes, such as performance
anxiety and the spectator role. The dysfunction may also develop from hypoactive
sexual desire.
Female orgasmic disorder has, along with female sexual arousal disorder, been
tied to biological causes such as medical diseases and changes that occur after
menopause, psychological causes such as memories of childhood traumas, and
sociocultural causes such as relationship problems.
In vaginismus, one of the sexual pain disorders, involuntary contractions of
the muscles around the outer third of the vagina prevent entry of the penis. In dys-
pareunia, the person experiences severe pain in the genitals during sexual activity.
Dyspareunia usually occurs in women and typically has a physical cause, such as
injury resulting from childbirth.
*Treatments for Sexual Dysfunctions
The last 35 years have brought major changes in the treatment of sexual dysfunctions.
For the first half of the twentieth century, the leading approach was long-term psycho-
dynamic therapy. Clinicians assumed that sexual dysfunctioning was caused by failure
to progress properly through the psychosexual stages of development, and they used
techniques of free association and therapist interpretations to help clients gain insight
about themselves and their problems. Although it was expected that broad personality
changes would lead to improvement in sexual functioning, psychodynamic therapy was
typically unsuccessful (Bergler, 1951).
In the 1 950s and 1960s, behavioral therapists offered new treatments for sexual
dysfunctions. Usually they tried to reduce the fears that they believed were causing
the dysfunctions by applying such procedures as relaxation training and systematic
desensitization (Lazarus, 1965; Wolpe, 1958). These approaches had some success, but
they failed to work in cases where the key problems included misinformation, negative
attitudes, and lack of effective sexual technique (LoPiccolo, 2002, 1995).

334 ://CHAPTER
A revolution in the treatment of sexual dysfunctions occurred with
the publication of William Masters and Virginia Johnson’s landmark book
Human Sexual Inadequacy in 1970.The sex therapy program they introduced
has evolved into a complex approach, which now includes interventions
from the various models, particularly cognitive-behavioral, couple, and
family systems therapies, along with a number of sex-specific techniques
(Leiblum, 2007; Bach et al., 2001). In recent years, biological interventions,
particularly drug therapies, have been added to the treatment arsenal.
What Are the General Features of Sex Therapy?
Modern sex therapy is short-term and instructive, typically lasting 15 to
20 sessions. It centers on specific sexual problems rather than on broad
personality issues (Wincze et al., 2008; LoPiccolo, 2002, 1995). Carlos
Domera, the Argentine man with an erectile disorder whom you met
earlier, responded successfully to the multiple techniques of modern sex
therapy:
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At the end of the evaluation session the psychiatrist reassured the couple that
Mr. Domera had a “reversible psychological” sexual problem that was due to
several factors, including his depression, but also more currently his anxiety
and embarrassment, his high standards, and some cultural and relationship
difficulties that made communication awkward and relaxation nearly impos-
sible. The couple was advised that a brief trial of therapy, focused directly on
the sexual problem, would very likely produce significant improvement within
ten to fourteen sessions. They were assured that the problem was almost
certainly not physical in origin, but rather psychogenic, and that therefore the
prognosis was excellent.
Mr. Domera was shocked and skeptical, but the couple agreed to commence the ther-
apy on a weekly basis, and they were given a typical first “assignment” to do at home: a
caressing massage exercise to try together with specific instructions not to attempt genital
stimulation or intercourse at all, even if on erection might occur.
Not surprisingly, during the second session Mr. Domera reported with a cautious smile
that they had “cheated” and had had intercourse “against the rules.” This was their first
successful intercourse in more than a year. Their success and happiness were acknowl-
edged by the therapist, but they were cautioned strongly that rapid initial improvement
often occurs, only to be followed by increased performance anxiety in subsequent weeks
and a return of the initial problem. They were humorously chastised and encouraged to
try again to have sexual contact involving caressing and non-demand light genital stimula-
tion, without an expectation of erection or orgasm, and to avoid intercourse.
During the second and fourth weeks [Carlos] did not achieve erections during the love
play, and the therapy sessions dealt with helping him to accept himself with or without
erections and to learn to enjoy sensual contact without intercourse. His wife helped him
to believe genuinely that he could please her with manual or oral stimulation and that,
although she enjoyed intercourse, she enjoyed these other stimulations as much, as long as
he was relaxed.
[Carlos] struggled with his cultural image of what a “man” does, but he had to admit
that his wife seemed pleased and that he, too, was enjoying the nonintercourse caressing
techniques. He was encouraged to view his new lovemaking skills as a “success” and to
recognize that in many ways he was becoming a better lover than many husbands, be-
cause he was listening to his wife and responding to her requests.
By the fifth week the patient was attempting intercourse successfully with relaxed con-
fidence, and by the ninth session he was responding regularly with erections. if they both

Sexual Disorders and Gender identity Disorder :// 335
agreed, they would either have intercourse or choose another sexual technique to achieve
orgasm. Treatment was terminated after ten sessions.
(Spitzer et al., 1983, pp. 106-107)
As Carlos Domera’s treatment indicates, modern sex therapy includes a variety of
principles and techniques. The following ones are applied in almost all cases, regardless
of the dysfunction:
1. Assessment and conceptualization of the problem. Patients are initially given
a medical examination and are interviewed concerning their “sex history.”
The therapist’s focus during the interview is on gathering information about
past life events and, in particular, current factors that are contributing to the
dysfunction (Heiman, 2007; Leiblum, 2007). Sometimes proper assessment
requires a team of specialists, perhaps including a psychologist, urologist, and
neurologist.
2. Mutual responsibility. Therapists stress the principle of mutual responsibility.
Both partners in the relationship share the sexual problem, regardless of who
has the actual dysfunction, and treatment will be more successful when both
are in therapy (Hall, 2007; Bach et al., 2001).
3. Education about sexuality. Many patients who suffer from sexual dysfunctions
know very little about the physiology and techniques of sexual activity
(Wincze et al., 2008; Rosen, 2007).Thus sex therapists may discuss these
topics and offer educational materials, including instructional books, videos,
and Internet sites.
4. Attitude change. Following a key principle of cognitive therapy, sex therapists
help patients examine and change any beliefs about sexuality that are pre-
venting sexual arousal and pleasure (Wincze et al., 2008; Heiman, 2007).
Some of these mistaken beliefs are widely shared in our society and can
result from past traumatic events, family attitudes, or cultural ideas.
5. Elimination of performance anxiety and the spectator role. Therapists often
teach couples sensate focus, or nondemand pleasuring, a series of sensual tasks,
sometimes called “petting” exercises, in which the partners focus on the
sexual pleasure that can be achieved by exploring and caressing each other’s
body at home, without demands to have intercourse or reach orgasm—
demands that may be interfering with arousal. Couples are told at first to
refrain from intercourse at home and to limit their sexual activity to
kissing, hugging, and sensual massage of various parts of the body,
but not of the breasts or genitals. Over time, they learn how to give
and receive greater sexual pleasure and they build back up to the
activity of sexual intercourse.
6. Increasing sexual and general communication skills. Couples are taught
to use their sensate-focus skills and apply new sexual techniques
and positions at home. They may, for example, try sexual positions
in which the person being caressed can guide the other’s hands and
control the speed, pressure, and location of sexual contact (Heiman,
2007) _ Couples are also taught to give instructions to each other in a
nonthreatening, informative manner (“It feels better over here, with
a little less pressure”), rather than a threatening uninformative man-
ner (“The way you’re touching me doesn’t turn me on”). Moreover,
couples are often given broader training in how best to communi-
cate with each other (Wincze et al., 2008; Bach et al., 2001).
7. Changing destructive lifestyles and marital interactions. A therapist
may encourage a couple to change their lifestyle or take other steps
to improve a situation that is having a destructive effect on their
cALLARAN
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relationship—to distance themselves from interfering in-laws, for example, or
to change a job that is too demanding. Similarly, if the couple’s general rela-
tionship is marked by conflict, the therapist will try to help them improve it
(Rosen, 2007; Metz & Epstein, 2002).
8. Addressing physical and medical factors. When sexual dysfunctions are caused
by a medical problem, such as disease, injury, medication, or substance abuse,
therapists try to address that problem (Ashton, 2007; Basson, 2007). If anti-
depressant medications are causing a man’s erectile disorder, for example, the
clinician may lower the dosage of the medication, change the time of day
when the drug is taken, or consider prescribing a different antidepressant.
What Techniques Are Applied to Particular Dysfunctions?
In addition to the general components of sex therapy, specific techniques can help in
each of the sexual dysfunctions.
Hypoactive Sexual Desire and Sexual Aversion Hypoactive sexual desire
and sexual aversion are among the most difficult dysfunctions to treat because of the
many issues that may feed into them (Maurice, 2007; LoPiccolo, 2004, 2002).Thus thera-
pists typically apply a combination of techniques. In a technique called affectual awareness,
patients visualize sexual scenes in order to discover any feelings of anxiety, vulnerability,
and other negative emotions they may have concerning sex. In another technique, pa-
tients receive cognitive self- instruction training to help them change their negative reac-
tions to sex. That is, they learn to replace negative statements during sex with “coping
statements,” such as “I can allow myself to enjoy sex; it doesn’t mean I’ll lose control.”
Therapists may also use behavioral approaches to help heighten a patient’s sex drive.
They may instruct clients to keep a “desire diary” in which they record sexual thoughts
and feelings, to read books and view films with erotic content, and to fantasize about
sex. Pleasurable shared activities such as dancing and walking together are also encour-
aged (LoPiccolo, 2002, 1997).
For sexual aversion that has resulted from sexual assault or childhood molestation,
additional techniques may be needed (Hall, 2007). A patient may be encouraged to
remember, talk about, and think about the assault until the memories no longer arouse
fear or tension. Or the individual may be instructed to have a mock dialogue with the
molester in order to express lingering feelings of rage and powerlessness (LoPiccolo,
2002, 1995).
These and related psychological approaches apparently help many women and men
with hypoactive sexual desire and aversion disorders eventually to have intercourse
more than once a week (Heard-Davison et al., 2004; Hurlbert, 1993). However, only
a few controlled studies have been conducted. Finally, biological interventions, such as
hormone treatments, have been used, particularly for women whose problems arose after
removal of their ovaries or later in life. The interventions have received some prelimi-
nary research support (Ashton, 2007; Davis, 2000, 1998).
Erectile Disorder Treatments for erectile disorder focus on reducing a man’s perfor-
mance anxiety, increasing his stimulation, or both, using a range of behavioral, cognitive,
and relationship interventions (Rosen, 2007; Segraves & Althof, 2002). In one technique,
the couple may be instructed to try the tease technique during sensate-focus exercises:The
partner keeps caressing the man, but if the man gets an erection, the partner stops caress-
ing him until he loses it.This exercise reduces pressure on the man to perform and at the
same time teaches the couple that erections occur naturally in response to stimulation,
as long as the partners do not keep focusing on performance. In another technique, the
couple may be instructed to use manual or oral sex to try to achieve the woman’s orgasm,
again reducing pressure on the man to perform (LoPiccolo, 2004, 2002, 1995).
Biological approaches gained great momentum with the development in 1998 of
sildengfil (trade name Viagra). This drug increases blood flow to the penis within one
336 ://CHAPTER 11

Sexual Disorders and Gender identity Disorder :1/ 337
hour of ingestion; the increased blood flow enables the user to attain an erection dur-
ing sexual activity. Sildenafil appears to be relatively safe except for men with certain
coronary heart diseases and cardiovascular diseases, particularly those who are taking
nitroglycerin and other heart medications (Stevenson & Elliott, 2007). Over the past
decade, two other erectile dysfunction drugs have been approved—tadaiafit (Cialis) and
vardenafil (Levitra)—and are now actively competing withViagra for a share of the lucra-
tive marketplace. Collectively, the three drugs are the most common form of treatment
for erectile disorder (Rosen, 2007). They effectively restore erections in 75 percent of
men who use them.
Prior to the development of Viagra, Cialis, and Levitra, a range of other medical
procedures -were developed for erectile disorder. These procedures are now viewed as
“second-line” treatments that are applied primarily when the medications are unsuc-
cessful or too risky for individuals (Rosen, 2007; Frohman, 2002). Such procedures
include gel suppositories, injections of drugs into the penis, and a vacuum erection device
(VED), a hollow cylinder that is placed over the penis. Here a man uses a hand pump to
pump air out of the cylinder, drawing blood into his penis and producing an erection.
Male Orgasmic Disorder Like the treatments for male erectile disorder, thera-
pies for male orgasmic disorder include techniques to reduce performance anxiety and
increase stimulation (Hartmann & Waldinger, 2007; LoPiccolo, 2004). In one of many
such techniques, a man may be instructed to masturbate to orgasm in the presence of his
partner or to masturbate just short of orgasm before inserting his penis for intercourse
(Marshall, 1997). This increases the likelihood that he will ejaculate during intercourse.
He then is instructed to insert his penis at ever earlier stages of masturbation.
When male orgasmic disorder is caused by physical factors such as neurological
damage or injury, treatment may include a drug to increase arousal of the sympathetic
nervous system (Stevenson & Elliott, 2007). However, few studies have systematically
tested the effectiveness of such treatments (Hartmann &Waldinger, 2007).
Rapid Eiaculation Rapid, or premature, ejaculation has been treated successfully
for years by behavioral procedures (Althof, 2007; Masters & Johnson, 1970). In one such
approach, the stop-start, or pause, procedure, the penis is manually stimulated until the
man is highly aroused. The couple then pauses until his arousal subsides, after which the
stimulation is resumed.This sequence is repeated several times before stimulation is car-
ried through to ejaculation, so the man ultimately experiences much more total time of
stimulation than he has ever experienced before (LoPiccolo, 2004, 1995). Eventually the
couple progresses to putting the penis in the vagina, making sure to withdraw it and to
pause whenever the man becomes too highly aroused.According to clinical reports, after
two or three months many couples can enjoy prolonged intercourse without any need
for pauses (Althof, 2007; LoPiccolo, 2004, 2002).
Some clinicians treat rapid ejaculation with SSRIs, the serotonin-enhancing antide-
pressant drugs. Because these drugs often reduce sexual arousal or orgasm, the reasoning
goes, they may be helpful to men who experience rapid ejaculation. Many studies report
positive results with this approach (Althof, 2007, 1995; Ashton, 2007). The effect of this
approach is consistent with the biological theory, mentioned earlier, that serotonin re-
ceptors in the brains of men with rapid ejaculation may function abnormally.
Female Arousal and Orgasmic Disorders Specific treatments for female
arousal and orgasmic dysfunctions include cognitive-behavioral techniques, self-
exploration, enhancement of body awareness, and directed masturbation training
(Heiman, 2007, 2002, 2000; LoPiccolo, 2002, 1997) .These procedures are especially use-
ful for women who have never had an orgasm under any circumstances. Biological treat-
ments, including hormone therapy, have also been tried, but research has not found such
interventions to be consistently helpful (Heiman, 2007).
In directed masturbation training, a woman is taught step by step how to
masturbate effectively and eventually to reach orgasm during sexual interactions. The
training includes use of diagrams and reading material, private self-stimulation, erotic

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338 ://CHAPTER 1 1
material and fantasies, “orgasm triggers” such as holding her breath or thrusting her
pelvis, sensate focus with her partner, and sexual positioning that produces stimulation
of the clitoris during intercourse. This training program appears to be highly effective:
Over 90 percent of women learn to have an orgasm during masturbation, about 80
percent during caressing by their partners, and about 30 percent during intercourse
(Heiman, 2007; LoPiccolo, 2002, 1997).
As you read earlier, a lack of orgasm during intercourse is not necessarily a sexual
dysfunction, provided the woman enjoys intercourse and can reach orgasm through
caressing, either by her partner or by herself. For this reason some therapists believe that
the wisest course is simply to educate women whose only concern is lack of orgasm
during intercourse, informing them that they are quite normal.
V
. .
aginismus Specific treatment for vaginismus, involuntary contractions of the muscles
around the vagina, typically takes two approaches (Kabakci & Batur, 2003). First, a woman
may practice tightening and relaxing her vaginal muscles until she gains more voluntary
control over them. Second, she may receive gradual behavioral exposure treatment to
help her overcome her fear of penetration, beginning, for example, by inserting increas-
ingly large dilators in her vagina at home and at her own pace and eventually ending
with the insertion of her partner’s penis (Binik et al., 2007; Rosenbaum, 2007). Most
women treated for vaginismus with such procedures eventually have pain-free intercourse
(ter Kuile et al., 2009; Heiman, 2002). In recent years, some medical interventions have
also been applied. For example, several clinical investigators have injected the problematic
vaginal muscles with Bo tox to help reduce spasms in those muscles (Ghazizadeh & Nikzad,
2004; Romito et al., 2004). However, studies of this approach have been unsystematic.
Dyspareunia As you saw earlier, the most common cause of dyspareunia, genital
pain during intercourse, is physical, such as pain-causing scars, lesions, or infection after-
effects.When the cause is known, pain management procedures (see pages 333-334) and
sex therapy techniques may be tried, including helping a couple to learn intercourse
positions that avoid putting pressure on the injured area. Medical interventions—from
topical creams to surgery—may also be tried, but they must still be combined with
other sex therapy techniques to overcome the years of sexual anxiety and lack of arousal
(Binik et al., 2007; Heard-Davison et al., 2004). Many experts believe that most cases of
dyspareunia (and for that matter, vaginismus) are best assessed and treated by a team of
professionals, including a gynecologist, physical therapist, and sex therapist or other men-
tal health professional (Rosenbaum, 2007).
What Are the Current Trends in Sex Therapy?
Sex therapists have now moved well beyond the approach first developed by Masters
and Johnson. For example, today’s sex therapists regularly treat partners who are living
together but not married. They also treat sexual dysfunctions that arise from psychologi-
cal disorders such as depression, mania, schizophrenia, and certain personality disorders
(Leiblum, 2007; Bach et al., 2001). In addition, sex therapists no longer screen out clients
with severe marital discord, the elderly, the medically ill, the physically handicapped, gay
clients, or individuals who have no long-term sex partner (Nichols & Shernoff, 2007;
Stevenson & Elliott, 2007). Sex therapists are also paying more attention to excessive
sexuality, sometimes called hypersexuality or sexual addiction (Kafka, 2007, 2000).
Many sex therapists have expressed concern about the sharp increase in the use of
drugs and other medical interventions for sexual dysfunctions, particularly for hypo-
active sexual desire and male erectile disorder. Their concern is that therapists will
increasingly choose the biological interventions rather than integrating biological,
psychological, and sociocultural interventions. In fact, a narrow approach of any kind
probably cannot fully address the complex factors that cause most sexual problems
(Leiblum, 2007; Rosen, 2007). It took sex therapists years to recognize the considerable
advantages of an integrated approach to sexual dysfunctions. The development of new
medical interventions should not lead to its abandonment.

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JOSEPH E. LEVINE MIKE NICHOLS-LAWRENCE TLIFIMANI
THE GRADUATE.
ANNE BANCROFT.. DUSTIN HOFFMAN KATHARINE ROSS
FALO’ER WILLINGHAM BUCK HENRY PAUL SIMON NM — GARFUNKEL
LAWRENCE TURMAN MIKE NICHOLS TECHNICOLOR’ RANAASION’ Ir°(4-1″1″T

Sexual Disorders end Gender Identity Disorder :1/ 339

oparaphiliasuDisorders characterized
by recurrent and intense sexual urges,
fantasies, or behaviors involving nonhu-
man objects, children, nonconsenting
adults, or experiences of suffering or
humiliation.
Treatments Sexud Dysfunctions
In the 1970s the work of William Masters and Virginia Johnson led to the develop-
ment of sex therapy. Today sex therapy combines a variety of cognitive, behavioral,
couple, and family systems therapies. It generally includes features such as care-
ful assessment, education, acceptance of mutual responsibility, attitude changes,
sensate-focus exercises, improvements in communication, and couple therapy. In
addition, specific techniques have been developed for each of the sexual dysfunc-
tions, The use of biological treatments for sexual dysfunctions is also increasing.
oParaphilias
ParaphiIias are disorders in which individuals repeatedly have intense sexual urges
or fantasies or display sexual behaviors that involve nonhuman objects, children, non-
consenting adults, or the experience of suffering or humiliation. Many people with a
paraphilia can become aroused only when a paraphilic stimulus is present, fantasized
about, or acted out. Others need the stimulus only during times of stress or under other
special circumstances.
According to DSM-IV-TR, a diagnosis of paraphilia should be applied only when
the urges, fantasies, or behaviors last at least six months (see Table 11-6 on the next page).
For most paraphilias, the urges, fantasies, or behaviors must also cause great distress or
interfere with one’s social life or job performance in order for a diagnosis to be applied
(APA, 2000). For certain paraphilias, however, DSM-IV-TR clarifies that performance
of the sexual behavior indicates a disorder even if the individual experiences no distress
or impairment (APA, 2000). People who initiate sexual contact with children, for ex-
ample, warrant a diagnosis of pedophilia regardless of how troubled the individuals may
or may not be over their behavior.
Some people with one kind of paraphilia display others as well (Marshall et al.,
2008). Relatively few people receive a formal diagnosis of paraphilia, but the large Inter-
net and consumer market in paraphilic pornography leads clinicians to suspect that the
patterns may be quite common (APA, 2000). People whose paraphilias involve children
or nonconsenting adults often come to the attention of clinicians when they get into
legal trouble (Maletzky & Steinhauser, 2004).

340 ://CHAPTER 1 1

Although theorists have proposed various explanations for paraphilias, there is little
formal evidence to support them (Abramowitz, 2008). Moreover, none of the many
treatments applied to paraphilias have received much research or proved clearly effective
(Roche & Quayle, 2007; McConaghy, 2005). Psychological and sociocultural treatments
for paraphilias have been available the longest, but today’s professionals are also using
biological interventions. Some practitioners administer drugs called a fitiandrogens that
lower the production of testosterone, the male sex hormone, and reduce the sex drive
(Marshall et al., 2008). Although antiandrogens do indeed reduce paraphilic patterns,
several of them disrupt normal sexual feelings and behavior as well.Thus the drugs tend
to be applied primarily when the paraphilias are of danger either to the individuals
themselves or to other people. Clinicians are also increasingly administering SSRIs, the
serotonin-enhancing antidepressant medications, to treat persons with paraphilias, hop-
ing that the drugs will reduce these compulsion-like sexual behaviors just as they help
reduce other kinds of compulsions (Wright & Hatcher, 2006). In addition, of course, a
common effect of the SSRIs is to lower sexual arousal.
Fetishism
Key features of fetishism are recurrent intense sexual urges, sexually arousing fantasies,
or behaviors that involve the use of a nonliving object, often to the exclusion of all other
stimuli. Usually the disorder, which is far more common in men than in women, begins
in adolescence. Almost anything can be a fetish; women’s underwear, shoes, and boots
are particularly common (APA, 2000). Some people with fetishism commit thievery in
order to collect as many of the desired objects as possible. The objects may be touched,
smelled, worn, or used in some other way while the person masturbates, or the indi-
vidual may ask a partner to wear the object when they have sex (Marshall et al., 2008).
Several of these features are seen in the following case:

ofetishismeA paraphilia consisting of
recurrent and intense sexual urges, fanta-
sies, or behaviors that involve the use of
a nonliving object, often to the exclusion
of all other stimuli,
°masturbatory satiation0A behav-
ioral treatment in which a client
masturbates for a very long period of
time while fantasizing in detail about
a paraphilic object. The procedure is
expected to produce a feeling of bore-
dom that in turn becomes linked to the
object.
°orgasmic reorientation0A proce-
dure for treating certain paraphilias
by teaching clients to respond to new,
more appropriate sources of sexual
stimulation.
otransvestic fetishismoA paraphilia
consisting of repeated and intense
sexual urges, fantasies, or behaviors that
involve dressing in clothes of the oppo-
site sex. Also known as transvestism or
cross-dressing.
A 32-year-old, single male . related that although he was somewhat sexually attracted
by women, he was far more attracted by “their panties.”
To the best of the patient’s memory, sexual excitement began at about age 7, when
he came upon a pornographic magazine and felt stimulated by pictures of partially nude
women wearing “panties.” His first ejaculation occurred at 13 via masturbation to fan-
tasies of women wearing panties. He masturbated into his older sister’s panties, which
he had stolen without her knowledge. Subsequently he stole panties from her friends and
from other women he met socially. He found pretexts to “wander” into the bedrooms of
women during social occasions, and would quickly rummage through their possessions
until he found a pair of panties to his satisfaction. He later used these to masturbate into,
and then “saved them” in a “private cache.” The pattern of masturbating into women’s
under-wear had been his preferred method of achieving sexual excitement and orgasm
from adolescence until the present consultation.
(Spitzer et al., 1994, p. 247)

Researchers have not been able to pinpoint the causes of fetishism. Behaviorists
propose that fetishes are acquired through classical conditioning (Roche & Quayle,
2007; Akins, 2004). In a pioneering behavioral study, male participants were shown a
series of slides of nude women along with slides of boots (Rachman, 1966). After many
trials, the participants became aroused by the boot photos alone. If early sexual experi-
ences similarly occur in the presence of particular objects, perhaps the stage is set for
development of fetishes.
Behaviorists have sometimes treated fetishism with aversion therapy Wright & Hatcher,
2006; Krueger & Kaplan, 2002). In one study, an electric shock was administered to the
arms or legs of participants with fetishes while they imagined their objects of desire

Sexual Disorders and Gender Identify Disorder :1/ 341
(Marks & Gelder, 1967).After two weeks of therapy all men in the study showed at least
some improvement. In another aversion technique, people with fetishism are guided to
imagine the pleasurable object and repeatedly to pair this image with an imagined aversive
stimulus until the object of sexual pleasure is no longer desired.
Another behavioral treatment for fetishism is masturbatory satiation (Wright
& Hatcher, 2006). In this method, the client masturbates to orgasm while fantasizing
about a sexually appropriate object, then switches to fantasizing in detail about fetishistic
objects while masturbating again and continues the fetishistic fantasy for an hour. The
procedure is meant to produce a feeling of boredom, which in turn becomes linked to
the fetishistic object.
Yet another behavioral approach to fetishism, also used for other paraphilias, is
orgasmic reorientation, which teaches individuals to respond to more appropriate
sources of sexual stimulation (Wright & Hatcher, 2006). People are shown conventional
stimuli while they are responding to unconventional objects.A person with a shoe fetish,
for example, may be instructed to obtain an erection from pictures of shoes and then
to begin masturbating to a picture of a nude woman. If he starts to lose the erection,
he must return to the pictures of shoes until he is masturbating effectively, then change
back to the picture of the nude woman. When orgasm approaches, he must direct all
attention to the conventional stimulus.
Transvestic Fetishism
Transvestic fetishism, also known as transvestism or cross-dressing, is a recurrent
need or desire to dress in clothes of the opposite sex in order to achieve sexual arousal.
In the following passage, a 42-year-old married father describes his pattern:
1 have been told that when I dress in drag, at times I look like Whistler’s Mother [laughs],
especially when I haven’t shaved closely. I usually am good at detail, and I make sure
when I dress as a woman that 1 have my nails done just so, and that my colors match.
Honestly, it’s hard to pin o date on when I began cross dressing. . . . If pressed, I would
have to say it began when I was about 10 years of age, fooling around with and putting
on my mom’s clothes.. . . / was always careful to put everything back in its exact place,
and in 18 years of doing this in her home, my mother never, 1 mean never, suspected, or
questioned me about putting on her clothes. I belong to a transvestite support group . . . ,
a group for men who cross dress. Some of the group are homosexuals, but most are not.
A true transvestite—and 1 am one, so 1 know—is not homosexual. We don’t discriminate
against them in the group at all; hey, we have enough trouble getting acceptance as nor-
mal people and not just a bunch of weirdos ourselves. They are a bunch of nice guys . . . ,
really. Most of them are like me.
Most of [the men in the group] have told their families about their dressing inclina-
tions, but those that are married are a mixed lot; some wives know and some don’t, they
just suspect. I believe in honesty, and told my wife about this before we were married.
We’re separated now, but I don’t think it’s because of my cross dressing. . . . Some of
my friends, when I was growing up, suggested psychotherapy, but I don’t regard this as a
problem. If it bothers someone else, then they have the problem. . . I function perfectly
well sexually with my wife, though it took her some time to be comfortable with me wear-
ing feminine underwear; yes, sometimes I wear it while making love, it just makes it more
exciting.
(Janus &Jamts, 1993, p. 121)
Like this man, the typical person with transvestism, almost always a heterosexual male
(Marshall et al., 2008), begins cross-dressing in childhood or adolescence (Langstrom
& Zucker, 2005; Doctor & Neff; 2001). He is the picture of characteristic masculinity

342 :1/CHAPTER 1 1
in everyday life and is usually alone when he cross-dresses. A small
percentage of such men cross-dress to visit bars or social clubs.
Some wear a single item of women’s clothing, such as underwear
or hosiery, under their masculine clothes. Others wear makeup and
dress fully as women. Some married men with transvestism involve
their wives in their cross-dressing behavior (Kolodny et al., 1979).
The disorder is often confused with gender identity disorder, but, as
you will see, they are two separate patterns that overlap only in some
individuals.
The development of transvestic fetishism sometimes seems to
follow the behavioral principles of operant conditioning. In such
cases, parents or other adults may openly encourage the individuals
to cross-dress as children or even reward them for this behavior. In
one case, a woman was delighted to discover that her young nephew
enjoyed dressing in girls’ clothes. She had always wanted a niece,
and she proceeded to buy him dresses and jewelry and sometimes
dressed him as a girl and took him out shopping.
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°exhibitionism®A paraphilia in which
persons have repeated sexually arousing
urges or fantasies about exposing their
genitals to another person, and may act
upon those urges.
ovoyeurismeA paraphilia in which a
person has repeated and intense sexual
desires to observe unsuspecting people
in secret as they undress or to spy on
couples having intercourse and may act
upon these desires.
afrotteurismoA parophilia consisting of
repeated and intense sexual urges, fan-
tasies, or behaviors that involve touching
and rubbing against a nonconsenting
person.
opedophiliaeA paraphilia in which a
person has repeated and intense sexual
urges or fantasies about watching, touch-
ing, or engaging in sexual acts with
prepubescent children and may carry out
these urges or fantasies.
Exhibitionism
A person with exhibitionism has recurrent urges to expose his genitals to another per-
son, almost always a member of the opposite sex, or has sexually arousing fantasies of doing
so. He may also carry out those urges but rarely attempts to initiate sexual activity with
the person to whom he exposes himself (Maletzky, 2002, 2000; APA, 2000). More often,
he wants to provoke shock or surprise. Sometimes an exhibitionist will expose himself in
a particular neighborhood at particular hours. In a survey of 2,800 men, 4.3 percent of
them reported that they perform exhibitionistic behavior (Langstrom & Seto, 2006).Yet
between one-third and one-half of all women report having seen or had direct contact
with an exhibitionist, or so-called flasher (Marshall et al., 2008).The urge to exhibit typi-
cally becomes stronger when the person has free time or is under significant stress.
Generally the disorder begins before age 18 and is most common in males (APA,
2000). Some studies suggest that persons with exhibitionism are typically immature in
their dealings with the opposite sex and have difficulty in interpersonal relationships
(Marshall et al., 2008; Murphy & Page, 2006). Around 30 percent of them are married
and another 30 percent divorced or separated; their sexual relations with their wives are
not usually satisfactory (Doctor & Neff, 2001). Many have doubts or fears about their
masculinity, and some seem to have a strong bond to a possessive mother. As with other
paraphilias, treatment generally includes aversion therapy and masturbatory satiation, pos-
sibly combined with orgasmic reorientation, social skills training, or cognitive-behavioral
therapy (Marshall et al., 2008; Murphy & Page, 2006).
Voyeurism
A person who engages in voyeurism has recurrent and intense urges to secretly observe
unsuspecting people as they undress or to spy on couples having intercourse.The person
may also masturbate during the act of observing or when thinking about it afterward
but does not generally seek to have sex with the person being spied on. This disorder
usually begins before the age of 15 and tends to persist (APA, 2000).
The vulnerability of the people being observed and the probability that they would
feel humiliated if they knew they were under observation are often part of the individu-
al’s enjoyment. In addition, the risk of being discovered often adds to the excitement.
Voyeurism, like exhibitionism, is often a source of sexual excitement in fantasy;
it can also play a role in normal sexual interactions, but in such cases it is engaged in
with the consent or understanding of the partner. The clinical disorder of voyeurism is
marked by the repeated invasion of other people’s privacy. Some people with voyeur-
ism are unable to have normal sexual relations; others, however, have a normal sex life
apart from their voyeurism.

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Sexual Disorders and Gender Identity Disorder :11 343
Many psychodynamic clinicians propose that people with voyeurism are seeking
by their actions to gain power over others, possibly because they feel inadequate or are
sexually or socially shy (Metzl, 2004). Behaviorists explain the disorder as a learned be-
havior that can be traced to a chance and secret observation of a sexually arousing scene.
If such observations are repeated on several occasions while the onlooker masturbates,
a voyeuristic pattern may develop.
Froiteurism
A person who develops frotteurism has repeated and intense sexual urges to touch and
rub against a nonconsenting person or has sexually arousing fantasies of doing so. The
person may also act on the urges. Frottage (from French frotto; “to rub”) is usually com-
mitted in a crowded place, such as a subway or a busy sidewalk (Horley, 2001; Krueger
& Kaplan, 2000). The person, almost always a male, may rub his genitals against the
victim’s thighs or buttocks or fondle her genital area or breasts with his hands. Typically
he fantasizes during the act that he is having a caring relationship with the victim.This
paraphilia usually begins in the teenage years or earlier, often after the person observes
others committing an act of frottage. After the person reaches the age of about 25, the
acts gradually decrease and often disappear (APA, 2000).
Pedophilia
A person with pedophilia gains sexual gratification by watching, touching, or engaging
in sexual acts with prepubescent children, usually 13 years old or younger. Some people
with this disorder are satisfied by child pornography (Linz & lmrich, 2001) or seemingly
innocent material such as children’s underwear ads; others are driven to actually watch,
fondle, or engage in sexual intercourse with children (Durkin & Hundersmarck, 2008).
Some people with pedophilia are attracted only to children; others are attracted to adults
as well (Roche & Quayle, 2007; APA, 2000). Both boys and girls can be pedophilia
victims, but there is evidence suggesting that two-thirds of them are girls (Doctor &
Neff, 2001; Ross & Heslet, 1992).
People with pedophilia usually develop their disorder during adolescence. Some
were themselves sexually abused as children, and many were neglected, excessively pun-
ished, or deprived of genuinely close relationships during their childhood (McAnulty,
2006; Berlin, 2000). It is not unusual for them to be married and to have sexual dif-
ficulties or other frustrations in life that lead them to seek an area in which they can
be masters. Often these individuals are immature: Their social and sexual skills may be
underdeveloped, and thoughts of normal sexual relationships fill them with anxiety
(McAnulty, 2006).
Some people with pedophilia also exhibit distorted think-
ing, such as, “It’s all right to have sex with children as long as
they agree” (Roche & Quayle, 2007; Abel et al., 2001, 1984).
Similarly, it is not uncommon for pedophiles to blame the chil-
dren for adult-child sexual contacts or to assert that the children
benefited from the experience (Durkin & Hundersmarck, 2008;
Lanning, 2001).
While many people with pedophilia believe that their feel-
ings are indeed wrong and abnormal, others consider adult
sexual activity with children to be acceptable and normal.
Some even have joined pedophile organizations that advocate
abolishing the age of consent laws.The Internet has opened the
channels of communication among such individuals. Indeed,
there is now a range of websites, newsgroups, chat rooms, and
discussion forums centered on pedophilia and adult-child sex
(Durkin & I-lundersmarck, 2008).
Studies have found that most men with pedophilia also
display at least one additional psychological disorder (McAnulty,
cvfigiM 1,0
eg..arid intethet
••• ‘.t> — • • • • f;
^’ ‘le
THERAPY: VIE POSSIBILITY
OF CHANCING . BEIVAVIOR

would more carefully weigh the potential conse-
quences of research publications.
344 ://CHAPTER 11
Serving fine Public Good
i 4s clinical practitioners and re-
searchers conduct their work,
should they consider the potential
impact of their decisions on society?
Many people, including a large
number of clinicians, believe that the
answer to this question is a resound-
ing yes. A decade ago two important
clashes between the clinical field and
the public interest—each centering on
the disorder of pedophilia—brought
this issue to life.
In 1994, the then-newly published
DSM-IV ruled that people should re-
ceive a diagnosis of pedophilia only
if their recurrent fantasies, urges, or
behaviors involving sexual activity
with children cause them significant
distress or impairment in social, occu-
pational, or other spheres of function-
ing. Critics worried that this criterion
seemed to suggest that pedophilic
behavior is acceptable, even normal,
as long as it causes no distress or
impairment. Even the U.S. Congress
condemned the DSM-IV definition.
In response to these criticisms,
the American Psychiatric Association
clarified its position in 1997, stating,
“An adult who engages in sexual
activity with a child is performing
a criminal and immoral act which
never can be considered moral or
socially acceptable behavior.” In
2000 the Association went further
R … • • .•
still and changed the criteria for
pedophilia in its newly published
DSM-IV-TR; the disorder is now diag-
nosed if persons act on their sexual
urges, regardless of whether they
experience distress or impairment
(APA, 2000). Similarly, acting on
one’s recurrent sexual urges or fanta-
sies warrants a diagnosis in cases of
exhibitionism, voyeurism, frotteurism,
and sexual sadism.
Another clash between the clinical
field and public sensibilities occurred
in 1998 when a review article in
the prestigious journal Psychological
Bulletin concluded that the effects of
child sexual abuse are not as long-
lasting as usually believed. The study
set off a firestorm, with critics arguing
that the conclusion runs counter to
evidence from a number of studies.
Furthermore, many people worried
that the article’s conclusions could be
used to legitimize pedophilia. After a
groundswell of criticism, the American
Psychological Association, publisher
of the journal, acknowledged that
it should have given more thought
to how the study would be received
and should have either presented the
article with an introduction outlining
the Association’s stance against child
sexual abuse or paired it with articles
offering different viewpoints. The As-
sociation also said that in the future it
2006). In recent years, some theorists have proposed that pedophilia may be related to a
biochemical or brain structure abnormality (Cantor et al., 2004; Maes et al., 2001), but
clear biological factors have yet to emerge in research.
Most pedophilic offenders are imprisoned or forced into treatment if they are caught
(Stone et al., 2000). After all, they are committing child sexual abuse when they take
any steps toward sexual contact with a child. Moreover, there are now many residential
registration and community notification laws across the United States that help law
enforcement agencies and the public account for and control where convicted child sex
offenders live and work (Sandler et al., 2009).
Treatments for pedophilia include those already mentioned for other paraphilias,
such as aversion therapy, masturbatory satiation, orgasmic reorientation, cognitive-
behavioral therapy, and antiandrogen drugs (Krueger & Kaplan, 2002; LoPiccolo,

Sexual Disorders and Gender Identify Disorder :// 345
1992). One widely applied cognitive-behavioral treatment for pedophilia, relapse-
prevention training, is modeled after the relapse-prevention programs used in the treat-
ment of sub-stance dependence (Wright & Hatcher, 2006; Marques et al., 2005) (see
page 312). In this approach, clients identify the kinds of situations that typically trigger
their pedophilic fantasies and actions (such as depressed mood or distorted thinking).
They then learn strategies for avoiding the situations or coping with them more ef-
fectively. Relapse-prevention training has sometimes, but not consistently, been of help
in pedophilia and in certain other paraphilias (Marshall et al., 2008).
Sexual Masochism
A person with sexual masochism is intensely sexually aroused by the act or thought
of being humiliated, beaten, bound, or otherwise made to suffer. Many people have
fantasies of being forced into sexual acts against their will, but only those who are very
distressed or impaired by the fantasies receive this diagnosis. Some people with the disor-
der act on the masochistic urges by themselves, perhaps tying, sticking pins into, or even
cutting themselves. Others have their sexual partners restrain, tie up, blindfold, spank,
paddle, whip, beat, electrically shock, “pin and pierce,” or humiliate them (APA, 2000).
An industry of products and services has arisen to meet the desires of people with
sexual masochism. Here a 34–year-old woman describes her work as the operator of a
sadomasochism house:
•
I get people here who have been all over looking for the right kind of pain they feel they
deserve. Don’t ask me why they want pain, I’m not a psychologist; but when they have
found us, they usually don’t go elsewhere. It may take some of the other girls an hour or
even two hours to make these guys feel like they’ve had their treatment—-I can achieve
that in about 20 minutes. . . . Remember, these are businessmen, and they are not only
buying my time, but they have to get back to work, so time is important.
Among the things I do, that work really quickly and well, are: I put clothespins on their
nipples, or pins in their (testicles]. Some of them need to see their own blood to be able
to get off . . .
. All the time that a torture scene is going on, there is constant dialogue. . . . I
scream at the guy, and tell him what a no-good rotten bastard he is, how this is even too
good for hire, that he knows he deserves worse, and I begin to list his sins. It works every
time. Hey, I’m not nuts, I know what I’m doing. I act very tough and hard, but I’m really a
very sensitive woman. But you have to watch out for a guy’s health … you must not kill
him, or have him get a heart attack. . . . I know of other places that have had guys die
there. I’ve never lost a customer to death, though they may have wished for it during my
“treatment.” Remember, these are repeat customers. I have a clientele and a reputation
that 1 value.
(Jarvis &Janus, 1993, p. 115)
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In one form of sexual masochism, hypoxyphilia, people strangle or smother them-
selves (or ask their partner to strangle them) in order to enhance their sexual pleasure.
There have, in fact, been a disturbing number of clinical reports of autoerotic asphyxia,
in which individuals, usually males and as young as 10 years old, may accidentally
induce a fatal lack of oxygen by hanging, suffocating, or strangling themselves while
masturbating. There is some debate as to whether the practice should be characterized
as sexual masochism, but it is at least sometimes accompanied by other acts of bondage
(Blanchard & Hucker, 1991).
Most masochistic sexual fantasies begin in childhood. However, the person does not
act out the urges until later, usually by early adulthood.The disorder typically continues
°sexual masochism®A poraphilia
characterized by repeated and intense
sexual urges, fantasies, or behaviors that
involve being humiliated, beaten, bound,
or otherwise made to suffer.

346 ://C HAPTER H
osexuai sadismeA paraphilia chorea,.
terized by repeated and intense sexual
urges, fantasies, or behaviors that
involve inflicting suffering on others.
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for many years. Some people practice more and more dangerous acts over time or dur-
ing times of particular stress (Santtila et al., 2006, 2002; APA, 2000).
In many cases sexual masochism seems to have developed through the behavioral
process of classical conditioning (Akins, 2004).A classic case study tells of a teenage boy
with a broken arm who was caressed and held close by an attractive nurse as the physi-
cian set his fracture, a procedure done in the past without anesthesia (Gebhard, 1965).
The powerful combination of pain and sexual arousal the boy felt then may have been
the cause of his later masochistic urges and acts.
Sexual Sadism
A person with sexual sadism, usually male, is intensely sexually aroused by the
thought or act of inflicting suffering on others by dominating, restraining, blindfolding,
cutting, strangling, mutilating, or even killing the victim (Marshall & Kennedy, 2003).
The label is derived from the name of the famous Marquis de Sade (1740-1814), who
tortured others in order to satisfy his sexual desires. People who fantasize about sadism
typically imagine that they have total control over a sexual victim who is terrified by
the sadistic act. Many carry out sadistic acts with a consenting partner, often a person
with sexual masochism. Some, however, act out their urges on nonconsenting victims
(Marshall et al., 2008; Marshall & Hucker, 2006).A number of rapists and sexual mur-
derers, for example, exhibit sexual sadism. In all cases, the real or fantasized victim’s
suffering is the key to arousal.
Fantasies of sexual sadism, like those of sexual masochism, may first appear in child-
hood ( Johnson & Becker, 1997); the sadistic acts, when they occur, develop by early
adulthood (APA, 2000). The pattern is long-term. Sadistic acts sometimes stay at the
same level of cruelty, but often they become more and more severe over the years
(Santtila et al., 2006, 2002). Obviously, people with severe forms of the disorder may be
highly dangerous to others.
Some behaviorists believe that classical conditioning is at work in sexual sadism
(Akins, 2004). While inflicting pain, perhaps unintentionally, on an animal or person,
a teenager may feel intense emotions and sexual arousal. The association between in-
flicting pain and being aroused sexually sets the stage for a pattern of sexual sadism.
Behaviorists also propose that the disorder may result from modeling, when adolescents
observe others achieving sexual satisfaction by inflicting pain. The many Internet sex
sites, sexual magazines, books, and videos in our society make such models readily avail-
able (Seto et al., 2001).
Both psychodynamic and cognitive theorists suggest that people with sexual sadism
inflict pain in order to achieve a sense of power or control, necessitated perhaps by
underlying feelings of sexual inadequacy. The sense of
power in turn increases their sexual arousal (Doctor,
2003; Rathbone, 2001). Alternatively, certain biologi-
cal studies have found signs of possible abnormalities in
the endocrine systems of persons with sadism (Langevin
et al., 1988). None of these explanations, however, has
been thoroughly investigated.
Sexual sadism has been treated by aversion therapy.
The public’s view of and distaste for this procedure have
been influenced by Anthony Burgess’s novel (later a
movie) A Clockwork Orange, which describes simultane-
ous presentations of sadistic images and drug-induced
stomach spasms to a sadistic young man until he is
conditioned to feel nausea at the sight of such images.
It is not clear that aversion therapy is helpful in cases
of sexual sadism. However, relapse-prevention training,
used in some criminal cases, may be of value (Wright &
Hatcher, 2006; Maletzky, 2003, 2002).

• Se):. c 11.
r
is
r
Sexual Disorders and Gender Identity Disorder :ll 347
A Word ®f Caution
The definitions of the paraphilias, like those of sexual dysfunctions, are strongly in-
fluenced by the norms of the particular society in which they occur. Some clinicians
argue that except when people are hurt by them, many paraphilic behaviors should not
be considered disorders at all. At the very least, we need to be extremely careful about
applying these labels to others or to ourselves. Keep in mind that for years clinicians
considered homosexuality a paraphilia, and their judgment was used to justify laws and
even police actions against gay individuals (Kirby, 2000). Only when the gay rights
movement helped change society’s understanding of and attitudes toward homosexual-
ity did clinicians stop considering it a disorder. In the meantime, the clinical field had
unintentionally contributed to the persecution, anxiety, and humiliation of millions of
people because of personal sexual behavior that differed from the conventional norms.
omosexuality is not new; it has al-
ways existed in all cultures, as has
the controversy that surrounds it. While
most cultures do not openly advocate
homosexuality, over the course of history
few have condemned it more fiercely than
Western culture has (Kauth, 2006). Never-
theless, research shows that a society’s ac-
ceptance or rejection of gay people does
not affect the rate of homosexuality.
Before 1973, the DSM listed homosexu-
ality as a sexual disorder. Protests by gay
activist groups and many psychotherapists
eventually led to its elimination from the
diagnostic manual as a sexual disorder
(Robertson, 2004). Most clinicians in the
Western world now view homosexuality as
a variant of normal sexual behavior, not a
disorder (Crary, 2007).
Psychologists do continue to debate one
issue: whether homosexuality is the result
of psychological factors (for example, cog-
nitive and emotional factors) or biological
factors (for example, genetic predisposi-
tions or events that occur in the uterus). The
debate has been fueled by a range of find-
ings that both support and contradict these
various factors (Kauth, 2006; Hyde, 2005;
Savic et al., 2005). Given such mixed
results, several interactionist theories have
also been proposed, but these have yet
to be tested systematically (Kauth, 2006,
2000; Diamond, 2003).
Gay people are found in every socio-
economic group, every race, and every
profession. It is impossible to identify a
characteristic that consistently separates
them from the rest of the population other
than their sexual orientation. The gay com-
munity argues that since sexual orienta-
tion is the only variable that consistently
separates homosexual from heterosexual
couples, gay couples should have the same
rights as heterosexual ones. In certain
states, marriages are now performed for
same-sex couples. Furthermore, gay cou-
ples are increasingly asserting their rights
in areas such as spousal health insurance
coverage, housing opportunities, tax and
inheritance laws, and social security ben-
efits; recent court decisions have endorsed
a number of these rights.
A consistent 4 to 7 percent of all Ameri-
cans continue to identify themselves as
gay. Now that most psychologists agree
that homosexuality is not a disorder, a key
issue remains: How will society react to
a significant proportion of its population
that typically differs from the rest in but
one way—their sexual orientation? So far,
Western society cannot claim to have dealt
very effectively or fairly with this question,
but at least a trend toward understand-
ing and equality seems to be unfolding.
Research suggests that through continued
education and exposure, people of differ-
ent sexual orientations can often learn to
accept and work with one another (Guth
et al., 2004).

3.48 :if/CHAPTER 1
YAV-A P4 \ I
Sex and the Law, Take 2
, I .1 :;:ff
•
Paraphilias
Paraphilias are disorders marked by recurrent and intense sexual urges, fantasies,
or behaviors involving either nonhuman objects, children, nonconsenting adults,
or experiences of suffering or humiliation. The disorders are found primarily in
men. The paraphilias include fetishism, transvestic fetishism (transvestism), exhibi-
tionism, voyeurism, frotteurism, pedophilia, sexual masochism, and sexual sadism.
Although various explanations have been proposed for these disorders, research
has revealed little about their causes. A range of treatments have been tried,
including aversion therapy, masturbatory satiation, orgasmic reorientation, and
relapse-prevention training.
*Gender Identity Disorder
As children and adults, most people feel like and identify themselves as males or
females—an identity that is consistent with the gender to which they are born. But
society has come to appreciate that many people do not experience such gender clar-
ity. Instead, they have transgender experiences— a sense that their actual gender identity is
different from the gender category to which they were born physically or that it lies
outside the usual male versus female categories (Carroll, 2007). Many people with such
transgender experiences come to terms with their gender inconsistencies, but others
experience gender dysphoria— unhappiness with their given gender—and often seek
treatment for their problem. DSM-IV-TR categorizes these latter individuals as having
gender identity disorder, a disorder in which people persistently feel that a vast mis-
take has been made and they have been born to the wrong sex (see Table 11-7).
The DSM-IV-TR categorization of gender identity disorder has become contro-
versial in recent years. Many people believe that transgender experiences reflect alter-
native—not pathological—ways of experiencing one’s gender identity. Moreover, they
argue, even transgender experiences that bring unhappiness, such as those called gender
dysphoria, should not be considered a disorder. At the other end of the spectrum, many
argue that gender identity disorder is in fact a medical problem that often produces per-
sonal unhappiness.They hold that gender identity disorder should not be categorized as
a psychological disorder, just as kidney disease and cancer, medical conditions that may
also produce unhappiness, are not categorized as psychological disorders. Although one
of these views may eventually prove to be an appropriate perspective, this chapter largely
will follow DSM-IV-TR’s current position that gender identity disorder represents
more than a variant lifestyle and is also far from a clearly defined medical problem, and
it will examine what clinical theorists believe they know about the pattern.
People with gender identity disorder would like to get rid of their primary and
secondary sex characteristics—many of them find their own genitals repugnant—and
acquire the characteristics of the other sex (APA, 2000). Men with gender identity dis-
order outnumber women by around 2 to 1. People with the problem often experience
anxiety or depression and may have thoughts of suicide (Hepp et al., 2005; Bradley,
1995). Such reactions may be related to the confusion and pain brought on by the dis-
order itself, or they may also be tied to the prejudice typically experienced by individuals
who display this pattern (Sanchez &Vilain, 2009). Studies also suggest that some people
with gender identity disorder further manifest a personality disorder (Hepp et al., 2005).
For most of today’s clinicians, the term “gender identity disorder” has replaced the old
term transsexualism, although the label “transsexual” is still commonly applied to those
individuals who desire and seek full gender change.
Sometimes gender identity disorder emerges in children (Carroll, 2007; Zucker, 2005).
Like adults with this disorder, the children feel uncomfortable about their assigned sex

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Sexual Disorders and Gender Identity Disorder :1/ 349
and yearn to be members of the opposite sex. This childhood pattern usually disappears
by adolescence or adulthood, but in some cases it develops into adult gender identity dis-
order (Cohen-Kettenis, 2001).Thus adults with this disorder may have had a childhood
gender identity disorder, but most children with the disorder do not become adults with
the disorder. Surveys of mothers indicate that about 1.5 percent of young boys wish to
be girls, and 3.5 percent of young girls wish to be boys (Carroll, 2007; Zucker & Bradley,
1995).Yet, considerably less than 1 percent of adults manifest gender identity disorder.
This age shift in the prevalence of gender identity disorder is, in part, why today’s leading
experts on the disorder strongly recommend against any form of physical treatment for
this pattern until individuals are at least 16 years of age (HBIGDA, 2001).
Explanations of Gender Identity Disorder
Various theories have been proposed to explain gender identity disorder (Carroll, 2007;
Gehring & Knudson, 2005), but research to test these views has been limited and gener-
ally weak. Many clinicians suspect that biological—perhaps genetic or prenatal—factors
play a key role in the disorder (Henningsson et al., 2005).
Consistent with a genetic explanation is evidence that the disorder sometimes runs
in families (Green, 2000). In addition, one biological study has received considerable at-
tention (Zhou et al., 1997, 1995). Dutch investigators autopsied the brains of six people
who had changed their sex from male to female. They found that a cluster of cells in the
hypothalamus called the bed nucleus of stria terniinalis (BSI) was only half as large in these
people as it was in a control group of “normal” men. Usually, a woman’s BST is much
smaller than a man’s, so in effect the men with gender identity disorder were found
to have a female-sized BST. Recent studies tell a similar story (Swaab, 2005). Scientists
do not know for certain what the BST does in humans, but they know that it helps
regulate sexual behavior in male rats. Thus, it may be that men who develop gender
identity disorder have a key biological difference that leaves them very uncomfortable
with their assigned sex characteristics.
Treatmen h for Gender Identity Disorder
In order to more effectively assess and treat those with gender identity disorder, clini-
cal theorists have tried to distinguish the most common patterns of gender dysphoria
encountered in clinical practice.
°gender identity disorder®A disor-
der in which a person persistently feels
extremely uncomfortable about his or her
assigned sex and strongly wishes to be a
member of the opposite sex.

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350 :A/CHAPTER 1 1
Types of Gender Dysphoria Clients Richard Carroll (2007), a leading theorist
on gender dysphoria, has described the three patterns of gender identity disorder for
which individuals most commonly seek treatment: (1) female-to-male gender dysphoria,
(2) male-to-female gender dysphoria: androphilic type, and (3) male-to-female gender dysphoria:
antogynephilic type.
FEMALE-TO-MALE GENDER DYSPHORIA People with a female-to-male gender dysphoria pat-
tern are born female but appear or behave in a stereotypically masculine manner from
early on—often as young as 3 years of age or younger. As children they always play
rough games or sports, prefer the company of boys, hate “girlish” clothes, and state their
wish to be male. As adolescents, they become disgusted by their physical changes of
puberty and are sexually attracted to females. However, lesbian relationships do not feel
like a satisfactory solution to them because they want other women to be attracted to
them as males, not as females.
MALE-TO-FEMALE GENDER DYSPHORIA: ANDROPHILIC TYPE People with an androphilic type
of male-to-female gender dysphoria are born male but appear or behave in a stereo-
typically female manner from birth. As children, they are viewed as effeminate, pretty,
and gentle; avoid rough games; and hate to dress in boys’ clothing. As adolescents, they
become sexually attracted to males, and they often come out as gay and develop gay
relationships (the term “androphilic” means attracted to males). But by adulthood, it be-
comes clear to them that gay relationships do not address their gender dysphoric feelings
because they want to be with heterosexual men who are attracted to them as women.
MALE-TO-FEMALE GENDER DYSPHORIA: AUTOGYNEPHILIC TYPE People with an autogynephilic
type of male-to-female gender dysphoria are not sexually attracted to males within their
pattern of gender dysphoria; rather, they are attracted to the fantasy of themselves being
females (the term “autogynephilic” means attracted to oneself as a female). Like males with
the paraphilia transvestic fetishism (see pages 341-342), persons with this form of gender
dysphoria behave in a stereotypically masculine manner as children, start to enjoy dress-
ing in female clothing during childhood, and, after puberty, become sexually aroused
when they cross-dress. Also, like males with transvestic fetishism, they are attracted to
females during and beyond adolescence. However, unlike individuals with transvestic
fetishism, these persons have fantasies of becoming female which become stronger and
stronger during adulthood. Eventually, they are consumed with the need to be female.
In short, cross-dressing is characteristic of both men with the paraphilia transvestic
fetishism and men with this type of male-to-female gender dysphoria. But the former

Sexual Disorders and Gender Identity Disorder :ll 351
HOME }—°. SEND )•••-• EXPLORE ”””’ •”” ” ” — “”” ” ‘”””‘”‘””” °”””
Battling a Culture of Shame
BY MARTIN ABBUGAO, AGENCE FRANCE-PRESSE, SEPTEMBER 10, 2007
he loves children and her lifelong dream is to be a wife
and a mother, but the raspy voice and masculine frame be-
tray the fact that Leona Lo was born a man.
Unlike many other transsexuals in Asia who prefer to live
privately because of the social stigma of sex change, the British-
educated,. Singaporean transsexual woman has chosen to live
a normal life, but in public. Smart, confident and articulate, the
communications specialist who heads her own public relations
company has embarked on a mission to help turn around the
“culture of shame” surrounding transsexuals in Singapore and
the region. “Somewhere out there, not just
in Singapore but throughout Asia, there
are lots of young people who are suffering
the way I suffered years ago,” Leona, 32,
[says] in an interview.
In her former life as a man, she was
called Leonard. These days, she draws on
her experiences of gender identity crisis,
rejection and discrimination to challenge
social mores on behalf of the so-called
silent community. . . . While a few trans-
sexuals are gaining prominence in Asia
most continue to live in silence….
Slim and taller than the average local
woman, Leona packs charm and gets
animated when talking about children.
But her lipsticked mouth creases into a
pensive smile when she says: “I can’t bear
children. I have to be on hormones for life
and I have this body structure of a guy.”
The hormone treatment has “feminised” the
former man. While traces of masculinity
are evident, Leona says she has already
come to terms with being a woman—
although a transsexual one. “I can’t deny
that biologically I’m different,” says Leona,
wearing a blue dress, the muscles on her shoulders and arms
clearly visible.
Discrimination is the biggest challenge faced by transsexuals,
she says, recalling repeated rejection by prospective employers
in Singapore despite her academic credentials. “Singapore may
be a cosrnospolitan city but many things are still swept under
the carpet,” Leona says. .. . “It’s because a lot of transsexual
women face discrimination at work and experience failure of re-
lationships that a lot end up in suicide, depression. They end up
on the streets as prostitutes,” she says.
This is why she has taken time away from her thriving public
relations consultancy promoting beauty products to wage her
campaign. After much persuasion, one local university allowed
her to speak to an audience of students but she is finding it hard
to pry open a window to share her thoughts in the corporate
world. . . . On September 14 she is to launch her autobiogra-
phy, “From Leonard to Leona—A Singapore Transsexual’s Jour-
ney to Womanhood.”.
As early as 10, Leonard had already started developing feel-
ings for boys. But he was forced to remain silent because of a
dearth of information about transsexual-
ism and for fear his traditional Chinese
family would be scandalized. “I did not
think I was gay, I just felt that I was a
woman trapped in a man’s body,” says
Leona, who has a younger sister. At age
15, Leonard discovered a book about
transsexualism. . . . “I discovered that
book in the library and I said ‘Oh my
God! There are actually people like me!”
she reminisces. “That changed my life and
I discovered that I could go for the sex
change operation.” . .
After military service, Leonard in 1996
went to study in Britain, where a more
tolerant university environment allowed
him to cross-dress for a year as part of
his preparation for sex-change surgery.
In 1 997, Leonard flew with his tuition
money from Britain to Bangkok, where he
walked into a clinic for the life-altering
operation. “I was afraid. I could go in
and I could die. But I knew at that point
that I was going to change my life for-
ever,” she recalls. “1 had carried that bur-
den within me for so long and I couldn’t
live anymore without doing it.” Leona endured a lot of pain dur-
ing the procedure . . . but the feeling of having a new identity
was “wonderful, euphoric!” ..
What is her dream now? “To be a wife and a mother,” she
says. “I look forward to a fulfilling relationship with a loving
man, getting married and adopting three children. . . . I’m
[also] more self-assured and finally able to lay to rest the painful
aspects of my past and move confidently as a woman.”
Copyright 0 2007 Agence France-Presse. Reprinted by permission.

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*sex-change surgeryeA surgical
procedure that changes a person’s sex
organs, features, and, in turn, sexual
identity. Also known as sexual reassign-
ment surgery.
individuals cross-dress strictly to become sexually amused, whereas the latter develop
much deeper reasons for cross-dressing, reasons of gender identity.
Types of Treatment for Gender Identify Disorder Many people with gender
identity disorder receive psychotherapy (Affatati et al., 2004), but a large number of them
further seek to address their concerns through biological interventions. For example,
many adults with this disorder change their sexual characteristics by means of hormone
treatments (Andreasen & Black, 2006). Physicians prescribe the female sex hormone estro-
gen for male patients, causing breast development, loss of body and facial hair, and change
in body fat distribution. Similar treatments with the male sex hormone testosterone are
given to women with gender identity disorder.
Hormone therapy and psychotherapy enable many persons with this disorder to
lead a satisfactory existence in the gender role that they believe represents their true
identity. For others, however, this is not enough, and they seek out one of the most
controversial practices in medicine: sex-change, or sexual reassignment, surgery
(Andreasen & Black, 2006).This surgery, which is preceded by one to two years of hor-
mone therapy, involves, for men, amputation of the penis, creation of an artificial vagina,
and face-changing plastic surgery. For women, surgery may include bilateral mastectomy
and hysterectomy. The procedure for creating a functioning penis, called phalloplaso; is
performed in some cases, but it is not yet perfected (Doctor & Neff, 2001). Doctors
have, however, developed a silicone prosthesis that gives the patient the appearance of
having male genitals. Studies in Europe suggest that 1 of every 30,000 men and 1 of
every 100,000 women seek sex-change surgery (Carroll, 2007; Bakker et al., 1993). In
the United States, more than 6,000 persons are estimated to have undergone this surgi-
cal procedure (Doctor & Neff, 2001).
Clinicians have debated heatedly whether sexual reassignment is an appropriate
treatment for gender identity disorder. Some consider it a humane solution, perhaps the
most satisfying one to people with the pattern. Others argue that sexual reassignment is
a “drastic nonsolution” for a complex disorder. Either way, sexual reassignment surgery
appears to be on the increase (Olsson & Moller, 2003).
Research into the outcomes of gender reassignment surgery points in favorable di-
rections, although most such studies have key methodological flaws (Carroll, 2007). In
the studies, the majority of patients—both female and male—state satisfaction with the
outcome of the surgery and report improvements in self – satisfaction and interpersonal
interactions (Michel et al., 2002). Improvements in sexual functioning after surgery,
however, are often lacking (Schroder & Carroll, 1999).
352 :IICHAPTER 1 1

Landmark Case
The rate of “poor” sexual reassignment outcomes appears to be at least 8 percent
(Carroll, 200 7;Abramowitz, 1986). Female-to-male patients consistently show the most
favorable psychosocial outcomes. Those who display the autogynephilic type of gender
dysphoria (that is, those whose problems seem to begin as transvestic fetishism) are more
likely than those with the other types of gender dysphoria to later regret sexual reas-
signment surgery and to have poor outcomes. Finally, patients with serious pretreatment
psychological disturbances (for example, a personality disorder) are particularly likely
to regret the surgery and are more likely than others to later attempt suicide. All of
this argues for very careful screening prior to surgical interventions and, of course, for
continued research to better understand both the patterns themselves and the long-term
impact of the surgical procedures.
r,–71 •
Gender k]enli;y Disorder
People with gender identity disorder persistently feel that they have been assigned to
the wrong sex. In recent years, a number of theorists have criticized the categoriza-
tion of such gender identity patterns as clinical disorders. Men with gender identity
disorder apparently outnumber females by around 2 to 1. Its causes are not well
understood. Hormone treatments and psychotherapy have been used to help some
people adopt the gender role they believe to be right for them. Sex-change opera-
tions have also been performed, but the appropriateness of surgery as a form of
“treatment” has been debated heatedly.
PUTTING IL. together
A Private Topic Draws Public Attention
For all the public interest in sexual disorders, clinical theorists and practitioners have
only recently begun to understand their nature and how to treat them. As a result of
research done over the past few decades, people with sexual dysfunctions are no longer
doomed to a lifetime of sexual frustration. At the same time, however, insights into the
causes and treatment of other kinds of sexual disorders—paraphilias and gender identity
disorder—remain limited.
Studies o f sexual dysfunctions have pointed to many psychological, sociocultural,
and biological causes. Often the various causes may interact to produce a particular dys-
function, as in erectile disorder and female orgasmic disorder. For some dysfunctions,
however, one cause alone is dominant, and integrated explanations may be inaccurate
and unproductive. Dyspareunia, for example, usually has a physical cause.
Recent work has also yielded important progress in the treatment of sexual dysfunc-
tions, and people with such problems are now often helped greatly by therapy. Sex therapy
today is usually a complex program tailored to the particular problems of an individual
or couple. Techniques from the various models may be combined, although in some in-
stances the particular problem calls primarily for one approach (Bach et al., 2001).
One of the most important insights to emerge from all of this work is that educa-
tion about sexual dysfunctions can be as important as therapy. Sexual myths are still
taken so seriously that they often lead to feelings of shame, self-hatred, isolation, and
hopelessness—feelings that themselves contribute to sexual difficulty. Even a modest
amount of education can help persons who are in treatment.
In fact, most people can benefit from a more accurate understanding of sexual
functioning. Public education about sexual functioning—through appropriate websites,
books, television and radio, school programs, group presentations, and the like—has be-
come a major clinical focus. It is important that these efforts continue and even increase
in the coming years.
Sexual Disorders and Gender Identity Disorder :1/ 353
i’VA 4.6., Eat,
Sexual Census
• • •:: • •• ::••• ••:

354 :I/CHAPTER 11
• •
\\\ GRITIPJAL TH001-11 1-5///i
7A 1. Why do you think the clinical field
has been so slow to investigate pos-
7: sible cultural and racial differences
in sexual behaviors, sexual dysfunc-
.??’ tions, and paraphilias across the 3
United States? p. 321

2. Prevalence rates for sexual behavior
71: are typically based on surveys of the
VA,:
7A
general population. However, many
people feel that sex is private and
47: refuse to participate in such surveys,
.512. and those who do respond tend 4
to be more liberal, sexually expe-
rienced, and unconventional than
the norm. What problems might this
cause for sex researchers? pp. 324,
322-333
Some theorists cite performance
anxiety and the spectator role as
contributing factors in certain sexual
dysfunctions. Are there other areas
of dysfunction in life that might also
be explained by performance anxiety
and the spectator role? pp. 328, 330
A key technique in sex therapy is to
have a couple explore and caress
each other’s body (sensate focus)
while resisting orgasm or intercourse.
Why might people become more
aroused during sexual caressing if
they are prohibited from reaching
orgasm or having intercourse? p. 335
5. Sex is one of the topics most com-
monly searched on the Internet. Why
might it be such a popular search
topic? Is the availability of sex chat
groups and other sexual material on
the Internet psychologically healthy or
damaging? pp. 343, 321-346

.1/
• \\\ KEY l’EPMS///
4,04. le: sexual dysfunction, p. 322
desire phase, p. 322
.5) hypoactive sexual desire, p. 323
sexual aversion disorder, p. 323
/re,: excitement phase, p. 325
female sexual arousal disorder, p. 325
male erectile disorder, p. 326
d,e7jj
nocturnal penile tumescence (NPT),
p. 327
#.,..?” performance anxiety, p. 328
spectator role, p. 328
orgasm phase, p. 328
rapid, or premature, ejaculation, p. 328
male orgasmic disorder, p. 329
female orgasmic disorder, p. 331
vaginismus, p. 332
dyspareunia, p. 332
sex therapy, p. 334
sensate focus, p. 335
sildenafil (Viagra), p. 336
directed masturbation training, p. 337
paraphilia, p. 339
fetishism, p. 340
aversion therapy, p. 340
masturbatory satiation, p. 341
orgasmic reorientation, p. 341
transvestic fetishism, p. 341
exhibitionism, p. 342
voyeurism, p. 342
frotteurism, p. 343
pedophilia, p. 343
relapse-prevention training, p. 345
sexual masochism, p. 345
sexual sadism, p. 346
transgender experiences, p. 248
gender dysphoria, p. 248
gender identity disorder, p. 248
androphilic type, p. 350
autogynephilic type, p. 350
hormone treatments, p. 352
sex-change surgery, p. 352
• •• PPPPPPP • • S ,•.•••• 1 1 ‘ •• T 7:
…7′. 1. What sexual dysfunctions are i’
associated with the desire phase
of the sexual response cycle? How
common are they, and what causes
4 ,71 them? pp. 322-325
/..7) 2. What are the symptoms and preva-
lence of female sexual arousal
ii:„…#’: disorder and male erectile disor-
W-()„,.. – -• •.:4-;:,’e.-,::,.• e ee…,..e.,..z.
• ……. ••
der? To which phase of the sexual
response cycle are they related?
pp. 325-328
3. What are the possible causes of male
erectile disorder? pp. 326-328
4. Which sexual dysfunctions seem to
involve performance anxiety and
the spectator role? pp. 328, 330
5. What are the symptoms, rates, and
leading causes of rapid ejaculation,
male orgasmic disorder, and female
orgasmic disorder? To which phase
of the sexual response cycle are
they related? pp. 328-332
6. Identify, describe, and explain the
sexual pain disorders. p. 332

Sexual Disorders and Gender Identity Disorder :1/ 355

7. What are the general features of
dmodern sex therapy? What particu-
lar techniques are further used to
treat specific sexual dysfunctions?
pp. 334-338
8. List, describe, and explain the lead-
/ ing paraphilias. pp. 339-346
” a: …. .. Zae2,:gY 4./.:’,.4″.0
9. Describe the treatment techniques
of aversion therapy, masturbatory
satiation, orgasmic reorientation,
and relapse-prevention training.
Which paraphilias have they been
used to treat, and how successful
are they? pp. 340-346
10. Distinguish transvestic fetishism
from gender identity disorder.
What are the various types of gen-
der identity disorder, and what are
today’s treatments for this disorder?
pp. 341-342, 348-353

„ … . . , .. …„ ♦4., •
……. .. 2″””
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SCHIZOPHRENIA CHAPTER

That … does schizophrenia mean to me? ft means fatigue and confusion, it means
I trying to separate every experience into the real and the unreal and sometimes not
being aware of where the edges overlap. It means trying to think straight when there
is a maze of experiences getting in the way, and when thoughts are continually being
sucked out of your head so that you become embarrassed to speak at meetings. It means feel-
ing sometimes that you are inside your head and visualizing yourself walking over your brain, or
watching another girl wearing your clothes and carrying out actions as you think them. it means
knowing that you are continually “watched,” that you con never succeed in life because the laws
ore all against you and knowing that your ultimate destruction is never far away.
Rollin, 1980, p. 162
Does it surprise you to see such a coherent firsthand description of how it feels
to suffer from schizophrenia? People who have this disorder, though they previ-
ously functioned well or at least acceptably, deteriorate into an isolated wilderness
of unusual perceptions, odd thoughts, disturbed emotions, and motor abnormalities.
They experience psychosis, a loss of contact with reality.Their ability to perceive
and respond to the environment becomes so disturbed that they may not be able to
function at home, with friends, in school, or at work.They may have hallucinations
(false sensory perceptions) or delusions (false beliefs), or they may withdraw into
a private world. As you saw in Chapter 10, taking LSD or abusing amphetamines
or cocaine may produce psychosis. So may injuries or diseases of the brain. Most
commonly, however, psychosis appears in the form of schizophrenia.
Approximately 1 of every 100 people in the world suffers from schizophrenia
during his or her lifetime (APA, 2000).An estimated 24 million people worldwide
are afflicted with this disorder, 2.5 million in the United States (Lambert & Kinsley,
2005). Its financial cost is enormous, and the emotional cost is even greater. In
addition, sufferers have an increased risk of suicide and of physical—often fatal—
illness (Casey & Hansen, 2009). As you read in Chapter 8, it is estimated that at
least 15 percent of people with the disorder attempt suicide (Heisel, 2008).
Although schizophrenia appears in all socioeconomic groups, it is found more
frequently in the lower levels (see Figure 12-1 on the next page), leading some
theorists to believe that the stress of poverty is itself a cause of the disorder. However,
it could be that schizophrenia causes its victims to fall from a higher to a lower so-
cioeconomic level or to remain poor because they are unable to function effectively
(Priebe & Fakhoury, 2008). This is sometimes called the downward drift theory.
Equal numbers of men and women receive a diagnosis of schizophrenia
(Seeman, 2008). The average age of onset for men is 21 years, compared to 27
years for women (Folsom et al., 2006). Almost 3 percent of all those who are
divorced or separated suffer from schizophrenia sometime during their lives,
compared to 1 percent of married people and 2 percent of people who remain
single. Again, however, it is not clear whether marital problems are a cause or a
result (Softer et al., 2004; Keith et al., 1991).
People today, like those of the past, show great interest in schizophrenia,
flocking to plays and movies that feature the disorder.Yet, as you will read, all too
many people with schizophrenia are neglected in our country, their needs almost
TOPIC OVERVIEW
The Clinical Picture
of Schizophrenia
What Are the Symptoms
of Schizophrenia?
What Is the Course
of Schizophrenia?
Diagnosing Schizophrenia
How Do Theorists Explain
Schizophrenia?
Biological Views
Psychological Views
Sociocultural Views
How Are Schizophrenia
and Other Severe Mental
Disorders Treated?
Institutional Care in the Past
Institutional Care Takes a Turn
for the Better
Antipsychotic Drugs
Psychotherapy
The Community Approach
Putting It Together:
An Important Lesson

Annual Prevalence of Schizophrenia
c
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Lower
Lower-
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16,1- 01
In Their Words
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358 ://CHAPTER 12
oschizophreniaoA psychotic disorder
in which personal, social, and occupa-
tional functioning deteriorate as a result
of strange perceptions, unusual emotions,
and motor abnormalities.
opsychosisoA state in which a person
loses contact with reality in key ways.
+,1•-.7i171rs,:
r. r ft:
entirely ignored. Although effective treatments have been developed, most sufferers live
without adequate care and without nearly fulfilling their potential as human beings
(Ritsner & Gibel, 2007).
3.-The Clinical Picture of Schizophrenia
The symptoms of schizophrenia vary greatly, and so do its triggers, course, and respon-
siveness to treatment (APA, 2000). In fact, a number of clinicians believe that schizo-
phrenia is actually a group of separate disorders that happen to have some features in
common (Tamminga et al., 2008). To see the variety of forms schizophrenia may take,
consider two people who were diagnosed as suffering from it.The cases are taken from
the files of Silvano Arieti (1974), a famous theorist on the disorder.
Laura, 40 years old: Laura’s desire was to become independent and leave home fin
Austria] as soon as possible. . . . She became a professional dancer at the age of 20 . .
and was booked for . . . theaters in many European countries. . .
It was during one of her tours in Germany that Laura met her husband. . . They were
married and went to live in a small provincial town in France where the husband’s business
was. . . She spent a year in that town and was very unhappy. . . [Finally] Laura and her
husband decided to emigrate to the United States… .
They had no children, and Laura . . . showed interest in pets. She had a dog to whom
she was very devoted. The dog became sick and partially paralyzed, and veterinarians felt
that there was no hope of recovery. .. . Finally [her husband] broached the problem to his
wife, asking her “Should the dog be destroyed or not?” From that time on Laura became
restless, agitated, and depressed…
. . . Later Laura started to complain about the neighbors. A woman who lived on the
floor beneath them was knocking on the wall to irritate her. According to the husband, this
woman had really knocked on the wall a few times; he had heard the noises. However,
Laura became more and more concerned about it. She would wake up in the middle of
the night under the impression that she was hearing noises from the apartment down-
stairs. She would become upset and angry at the neighbors. . . . Later she became more
disturbed. She started to feel that the neighbors were now recording everything she said;
maybe they had hidden wires in the apartment. She started to feel “funny” sensations.
There were many strange things happening, which she did not know how to explain;
people were looking at her in a funny way in the street; in the butcher shop, the butcher
had purposely served her last, although she was in the middle of the line. During the next
few days she felt that people were planning to harm either her or her husband. . . In the

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Schizophrenia :1/ 359
evening when she looked at television, it became obvious to her that the programs referred
to her life. Often the people on the programs were just repeating what she had thought.
They were stealing her ideas. She wanted to go to the police and report them.
(pp. 165-168)
Richard, 23 years old: In high school, Richard was an average student. After graduation
from high school, he [entered] the army. . . . Richard remembered [the] period … after
his discharge from the army … as one of the worst in his life. . . . Any, even remote,
anticipation of disappointment was able to provoke attacks of anxiety in him. . . .
Approximately two years after his return to civilian life, Richard left his job because he
became overwhelmed by these feelings of lack of confidence in himself and he refused
to go look for another one. He stayed home most of the day. His mother would nag him
that he was too lazy and unwilling to do anything. He became slower and slower in dress-
ing and undressing and taking care of himself When he went out of the house, he felt
compelled “to give interpretations” to everything he looked at. He did not know what
to do outside the house, where to go, where to turn. If he saw a red light at a crossing,
he would interpret it as a message that he should not go in that direction. If he saw an
arrow, he would follow the arrow interpreting it as a sign sent by God that he should go
in that direction. Feeling lost and horrified, he would go home and stay there, afraid to go
out because going out meant making decisions or choices that he felt unable to make. He
reached the point where he stayed home most of the time. But even at home, he was tor-
tured by his symptoms. He could not act; any motion that he felt like making seemed to
him an insurmountable obstacle, because he did not know whether he should make it or
not. He was increasingly afraid of doing the wrong thing. Such fears prevented him from
dressing, undressing, eating, and so forth. He felt paralyzed and lay motionless in bed. He
gradually became worse, was completely motionless, and had to be hospitalized. . .
Being undecided, he felt blocked, and often would remain mute and motionless, like a
statue, even for days.
(pp. 153-155)

fk° I !
itri)1+ IP [i
trAti{ie
*positive symptomsoSymptoms of
schizophrenia that seem to be excesses
of or bizarre additions to normal
thoughts, emotions, or behaviors.
edelusionoA strange false belief firmly
held despite evidence to the contrary.
*formal thought disorderoA disturb-
ance in the production and organization
of thought.
*loose associations0A common
thinking disturbance in schizophrenia,
characterized by rapid shifts from one
topic of conversation to another. Also
known as derailment.
*hallucination*The experiencing of
sights, sounds, or other perceptions in
the absence of external stimuli.
What Are the Symptoms of Schizophrenia?
Laura and Richard both deteriorated from a normal level of functioning to become
ineffective in dealing with the world. Each experienced some of the symptoms found
in schizophrenia.The symptoms can be grouped into three categories:positive symptoms
(excesses of thought, emotion, and behavior), negative symptoms (deficits of thought,
emotion, and behavior), and psychomotor symptoms (unusual movements or gestures).
Some people with schizophrenia are more dominated by positive symptoms and oth-
ers by negative ones, although both kinds of symptoms are typically present (Vahia &
Cohen, 2008). In addition, around half of people with schizophrenia display significant
difficulties with memory and other kinds of cognitive functioning ( Leavitt & Gold-
berg, 2009; Julien, 2008).
Positive Symptoms Positive symptoms are “pathological excesses,” or bizarre addi-
tions, to a person’s behavior. Delusions, disorganized thinking and speech, heightened perceptions
and hallucinations, and inappropriate affect are the ones most often found in schizophrenia.
DELUSIONS Many people with schizophrenia develop delusions, ideas that they believe
wholeheartedly but have no basis in fact. Some people hold a single delusion that domi-
nates their lives and behavior, whereas others have many delusions. Delusions of persecution
are the most common in schizophrenia (APA, 2000). People with such delusions believe
they are being plotted or discriminated against, spied on, slandered, threatened, attacked,
or deliberately victimized. Laura believed that her neighbors were trying to irritate her
and that other people were trying to harm her and her husband.
People with schizophrenia may also experience delusions of reference: They attach
special and personal meaning to the actions of others or to various objects or events.
Richard, for example, interpreted arrows on street signs as indicators of the direction
he should take. People who experience delusions of grandeur believe themselves to be
great inventors, religious saviors, or other specially empowered persons. And those with
delusions of control believe their feelings, thoughts, and actions are being controlled by
other people.
DISORGANIZED THINKING AND SPEECH People with schizophrenia may not be able to think
logically and may speak in peculiar ways. These formal thought disorders can cause
the sufferer great confusion and make communication extremely difficult. Often they
take the form of positive symptoms (pathological excesses), as in loose associations, neo-
logisms, perseveration, and clang.
People who have loose associations, or derailment, the most common formal
thought disorder, rapidly shift from one topic to another, believing that their incoher-
ent statements make sense. One man with schizophrenia, asked about his itchy arms,
responded:
The problem is insects. My brother used to collect insects. He’s now a man 5 foot
10 inches. You know, 10 is my favorite number. l also like to dance, draw, and watch
television.
Some people with schizophrenia use neologisms, made-up words that typically have
meaning only to the person using them. One individual stated, for example,”I am here
from a foreign university … and you have to have a plausity’ of all acts of amendment
to go through for the children’s code . . . it is an amorition’ law … the children have
to have this accentuative’ law …” (Vetter, 1969, p. 189). Others may display the formal
thought disorder of perseveration, in which they repeat their words and statements again
and again. Finally, some use clang, or rhyme, to think or express themselves.When asked
how he was feeling, one man replied, “Well, hell, it’s well to tell.” Another described
the weather as “So hot, you know it runs on a cot.” Research suggests that some dis-
360 ://CHAPTER 12

•
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Schizophrenia :// 361
organized speech or thinking may appear long before a full pattern of schizophrenia
unfolds (Covington et al., 2005; Metsanen et al., 2005).
HEIGHTENED PERCEPTIONS AND HALLUCINATIONS The perceptions and attention of some
people with schizophrenia seem to intensify. The persons may feel that their senses are
being flooded by all the sights and sounds that surround them. This makes it almost
impossible for them to attend to anything important:
Everything seems to grip my attention. . . I am speaking to you just now, but I can hear
noises going on next door and in the corridor. I find it difficult to shut these out, and it
makes it more difficult for me to concentrate on what I am saying to you.
(McGhie and Chapman, 1961)
Laboratory studies repeatedly have found problems of perception and attention
among people with schizophrenia (Savla et A, 2008; Rogers et al., 2007). Such problems
may develop years before the onset of the actual disorder (Cornblatt & Keilp, 1994). It
is also possible that these difficulties further contribute to the memory impairments that
are experienced by many individuals with the disorder (Fuller et al., 2009).
Another kind of perceptual problem in schizophrenia consists of hallucinations,
perceptions that occur in the absence of external stimuli. People who have auditory hal-
lucinations, by far the most common kind in schizophrenia, hear sounds and voices that
seem to come from outside their heads (Waters, Badcock, & Maybery, 2007).The voices
may talk directly to the hallucinator, perhaps giving commands or warning of dangers,
or they may be experienced as overheard:
The voices . .. were mostly heard in my head, though I often heard them in the air, or in
different parts of the room. Every voice was different, and each beautiful, and generally,
speaking or singing in a different tone and measure, and resembling those of relations or
friends. There appeared to be many in my head, I should say upwards of fourteen. I divide
them, as they styled themselves, or one another, into voices of contrition and voices of joy
and honour_
(“Perceval’s Narrative,” in Batesoit, 1974)
Research suggests that people with auditory hallucinations actually produce the
nerve signals of sound in their brains, “hear” them, and then believe that external sources
are responsible (Woodruff, 2004). One line of research measured blood flow in
Broca’s area, the region of the brain that helps people produce speech (Waters
et al., 2007; McGuire et al., 1996).The investigators found more blood flow in
Broca’s area while patients were experiencing auditory hallucinations.A related
study instructed six men with schizophrenia to press a button whenever they
experienced an auditory hallucination (Silbersweig et al., 1995). PET scans re-
vealed increased activity near the surfaces of their brains, in the brain’s hearing
center, when they pressed the button.
Hallucinations and delusional ideas often occur together (Bach, 2007). A
woman who hears voices issuing commands, for example, may have the delu-
sion that the commands are being placed in her head by someone else.A man
with delusions of persecution may hallucinate the smell of poison in his bed-
room or the taste of poison in his coffee. Might one symptom cause the other?
Whatever the cause and whichever comes first, the hallucination and delusion
eventually feed into each other:
1;1 rIYA ,/1 11
ealogisms NO Mote.::

)LY1 f.1i;t601 ‘,17,f) ,, -? r•to
0.1f • Jr -S ,
einappropriate affecteDisplay of emo
tions that are unsuited to the situation; a
symptom of schizophrenia.
enegative symptomseSymptoms of
schizophrenia that seem to be deficits in
normal thought, emotions, or behaviors.
oaioyl aeA decrease in speech or
speech content; a symptom of schizo-
phrenia. Also known as poverty of
speech.
°flat affectoA marked lack of
expressed emotions; a symptom of
schizophrenia.
ocataiania0A pattern of extreme psy-
chomotor symptoms found in some forms
of schizophrenia, which may include
catatonic stupor, rigidity, or posturing.
I thought the voices I heard were being transmitted through the walls of my apartment
and through the washer and dryer and that these machines were talking and telling me
things. / felt that the government agencies had planted transmitters and receivers in my
apartment so that I could hear what they were saying and they could hear what I was
saying.
(Anonymous, 1996, p. 183)
INAPPROPRIATE AFFECT Many people with schizophrenia display inappropriate affect,
emotions that are unsuited to the situation. They may smile when making a somber
statement or upon being told terrible news, or they may become upset in situations that
should make them happy.They may also undergo inappropriate shifts in mood. During
a tender conversation with his wife, for example, a man with schizophrenia suddenly
started yelling obscenities at her and complaining about her inadequacies.
In at least some cases, these emotions may be merely a response to other features
of the disorder. Consider a woman with schizophrenia who smiles when told of her
husband’s serious illness. She may not actually be happy about the news; in fact, she
may not be understanding or even hearing it. She could, for example, be responding
instead to another of the many stimuli flooding her senses, perhaps a joke coming from
an auditory hallucination.
362 :1/CHAPTER 12
NegatiVe SyMpiOniS Negative symptoms are those that seem to be “pathologi-
cal deficits,” characteristics that are lacking in an individual. Poverty of speech, blunted and
flat affect, loss of volition, and social withdrawal are commonly found in schizophrenia. Such
deficits greatly affect one’s life and activities.
POVERTY OF SPEECH People with schizophrenia often display alogia, or poverty of
speech, a reduction in speech or speech content. Some people with this negative kind
of formal thought disorder think and say very little. Others say quite a bit but still man-
age to convey little meaning.
BLUNTED AND FLAT AFFECT Many people with schizophrenia have a blunted affect—they
show less anger, sadness, joy, and other feelings than most people. And some show al-
most no emotions at all, a condition known as flat affect. Their faces are still, their
eye contact is poor, and their voices are monotonous. In some cases, people with these
problems may have anhedonia, a general lack of pleasure or enjoyment. In other cases,
however, blunted or flat affect may reflect an inability to express emotions as others do.
One study had participants view very emotional film clips. The
participants with schizophrenia showed less facial expression than
the others; however, they reported feeling just as much positive and
negative emotion and in fact displayed greater skin arousal (Kring
& Neale, 1996).
LOSS OF VOLITION Many people with schizophrenia experience avo-
lition, or apathy, feeling drained of energy and of interest in normal
goals and unable to start or follow through on a course of action.
This problem is particularly common in people who have had
schizophrenia for many years, as if they have been worn down by
it. Similarly, individuals with the disorder may display ambivalence,
or conflicting feelings, about most things. The avolition and am-
bivalence of Richard, the young man you read about earlier, made
eating, dressing, and undressing impossible ordeals for him.
SOCIAL WITHDRAWAL People with schizophrenia may withdraw from
their social environment and attend only to their own ideas and

DSM Checklist
0 110
• I 41,
1. I
1,5
Schizophrenia :11 363
fantasies. Because their ideas are illogical and confused, the withdrawal
has the effect of distancing them still further from reality. The social
withdrawal seems also to lead to a breakdown of social skills, including
the ability to recognize other people’s needs and emotions accurately
(Kurtz & Mueser, 2008; Tenhula & Bellack, 2008).
Psychomotor Symptoms People with schizophrenia sometimes
experience psychomotor symptoms, for example, awkward movements or
repeated grimaces and odd gestures.These unusual gestures often seem to
have a private purpose—perhaps magical.
The psychomotor symptoms of schizophrenia may take certain ex-
treme forms, collectively called catatonia (Weder et al., 2008). People
in a catatonic stupor stop responding to their environment, remaining
motionless and silent for long stretches of time. Recall how Richard
would lie motionless and mute in bed for days. People who display cata-
tonic rigidity maintain a rigid, upright posture for hours and resist efforts
to be moved. Still others exhibit catatonic posturing, assuming awkward,
bizarre positions for long periods of time. Finally, people who display catatonic excite-
ment, a different form of catatonia, move excitedly, sometimes with wild waving of
arms and legs.
What Is the Course of Schizophrenia?
Schizophrenia usually first appears between the person’s late teens and mid-30s (APA,
2000). Although its course varies widely from case to case, many sufferers seem to go
through three phases—prodromal, active, and residual (Hafner & an der Heiden, 2008).
During the prodromal phase, symptoms are not yet obvious, but the individuals are begin-
ning to deteriorate. They may withdraw socially, speak in vague or odd ways, develop
strange ideas, or express little emotion. During the active phase, symptoms become ap-
parent. Sometimes this phase is triggered by stress in the person’s life. For Laura, the
middle-aged woman described earlier, the immediate trigger was the loss of her cher-
ished dog. Finally, many people with schizophrenia eventually enter a residual phase, in
which they return to a prodromal-like level of functioning. The striking symptoms of
the active phase lessen, but some negative symptoms, such as blunted emotions, may re-
main.Although one-quarter or more of patients recover completely from schizophrenia,
the majority continue to have at least some residual problems for the rest of their lives
(Fischer & Carpenter, 2008; Roe & Davidson, 2008).
Each of these phases may last for days or for years. A fuller recovery from schizo-
phrenia is more likely in persons who functioned quite well before the disorder (had
good premorbid functioning) or whose disorder was initially triggered by stress, came on
abruptly, or developed during middle age (Conus et al., 2007). Relapses are apparently
more likely during times of life stress (Bebbington & Kuipers, 2008).
Diagnosing Schizophrenia
DSM-IV-TR calls for a diagnosis of schizophrenia only after symptoms of the disorder
continue for six months or more. In addition, people suspected of having this disorder
must show a deterioration in their work, social relations, and ability to care for them-
selves (see Table 12-1).The DSM distinguishes five types of schizophrenia: disorganized,
catatonic, paranoid, undifferentiated, and residual.
The central symptoms of disovnized type of schizophrenia are confusion, incoherence,
and flat or inappropriate affect.Attention and perception problems, extreme social with-
drawal, and odd mannerisms or grimaces are common. The central feature of catatonic
type of schizophrenia is a psychomotor disturbance of some sort. Some of the people in
this category spend their time in a catatonic stupor, others in the throes of catatonic
excitement. Richard, the unemployed young man who became mute and statue-like,
might receive a diagnosis of this type of schizophrenia.
in n
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People with paranoid type of schizophrenia have an organized system of delusions and
auditory hallucinations that may guide their lives. Laura would receive this diagnosis.
She believed people were out to get her (delusions of persecution) and that people on
television were stealing her ideas (delusions of reference). In addition, she heard noises
from the apartment downstairs and felt “funny sensations” that confirmed her beliefs.
When people with schizophrenia do not fall neatly into one of the other categories,
they are diagnosed with undifferentiated type of schizophrenia. Because this category is
somewhat vague, it has been assigned to a wide assortment of unusual patterns over the
years. Many clinicians believe that it is in fact overused.
When the symptoms of schizophrenia lessen in strength and number yet remain in
a residual form, the patient’s diagnosis is usually changed to residual type of schizophrenia.
As you saw earlier, people with this pattern may continue to display blunted or inap-
propriate emotions, as well as social withdrawal, eccentric behavior, and some illogical
thinking.
Apart from these DSM-IV categories, many researchers believe that a distinction
between so-calledType I andType II schizophrenia helps predict the course of the disor-
der. People with Type I schizophrenia are thought to be dominated by positive symptoms,
such as delusions, hallucinations, and certain formal thought disorders (Crow, 2008,
1995, 1985, 1980). Those with Type II schizophrenia largely display negative symptoms,
such as flat affect, poverty of speech, and loss of volition. Type I patients generally seem
to have a greater likelihood of improvement.
The Clinical Picture of Schizophrenia
Schizophrenia is a disorder in which functioning deteriorates as a result of disturbed
thought processes, distorted perceptions, unusual emotions, and motor abnormali-
ties. Approximately 1 percent of the world’s population suffers from this disorder.
Its symptoms fall into three groupings. Positive symptoms include delusions, certain
formal thought disorders, hallucinations and other disturbances in perception and
attention, and inappropriate affect. Negative symptoms include poverty of speech,
blunted and flat affect, loss of volition, and social withdrawal. The disorder may also
include psychomotor symptoms, collectively called catatonia in their extreme form.
Schizophrenia usually emerges during late adolescence or early adulthood and
tends to progress through three phases: prodromal, active, and residual. DSM-IV-TR
identifies five patterns of schizophrenia: disorganized, catatonic, paranoid, undif-
ferentiated, and residual. Moreover, it is not uncommon for some patients to be
dominated by positive symptoms and others to display more negative ones.
Do Theorists Explain Schizophrenia?
As with many other kinds of disorders, biological, psychological, and sociocultural theo-
rists have each proposed explanations for schizophrenia. So far, the biological explana-
tions have received by far the most research support.This is not to say that psychological
and sociocultural factors play no role in the disorder. Rather, a diathesis- stress relationship
may be at work: People with a biological predisposition will develop schizophrenia only
if certain kinds of events or stressors are also present (Prasad et al., 2009; Glatt, 2008;
Tamminga et al., 2008).
Biological Views
Perhaps the most enlightening research on schizophrenia during the past several decades
has come from genetic and biological studies (Downar & Kapur, 2008; Glatt, 2008).
These studies have revealed the key roles of inheritance and brain activity in the
364 :4/CHAPTER 12

General population
Spouse
First cousin
Uncle/Aunt
Nephew/Niece
Grandchild
Half-sibling
Parent
Sibling
Offspring of one
schizophrenic parent
Fraternal twin
Offspring of two
schizophrenic parents
Identical twin
R
e
la
ti
o
n
s
h
ip
t
o
P
er
so
n
w
it
h
S
c
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iz
o
p
h
re
n
ia

Percentage of Risk
Third-
Degree
Relative
Second-
Degree
Relative
First-
Degree
Relative
46%
48%
• Ir r
•
r t rlinr r. I r. rrrj I ir I rirl –
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Schizophrenia :1/ 365
development of this disorder and have opened the door to
important changes in its treatment.
Genetic Factors Following the principles of the diathesis-.
stress perspective, genetic researchers believe that some people
inherit a biological predisposition to schizophrenia and develop
the disorder later when they face extreme stress, usually during
late adolescence or early adulthood (Glatt, 2008). The genetic
view has been supported by studies of (1) relatives of people
with schizophrenia, (2) twins with this disorder, (3) people with
schizophrenia who are adopted, and (4) genetic linkage and
molecular biology.
ARE RELATIVES VULNERABLE? Family pedigree studies have found
repeatedly that schizophrenia (and other psychotic disorders)
is more common among relatives of people with the disorder
(Tamminga et al., 2008; Higgins & George, 2007). And the
more closely related the relatives are to the person with schizo-
phrenia, the greater their likelihood of developing the disorder
(see Figure 12.2).
IS AN IDENTICAL TWIN MORE VULNERABLE THAN A FRATERNAL TWIN?
Twins, who are among the closest of relatives, have received
particular study by schizophrenia researchers. If both members
of a pair of twins have a particular trait, they are said to be concor-
dant for that trait. If genetic factors are at work in schizophrenia,
identical twins (who share all their genes) should have a higher
concordance rate for this disorder than fraternal twins (who
share only some genes). This expectation has been supported
consistently by research (Higgins & George, 2007; Gottesman,
1991). Studies have found that if one identical twin develops
schizophrenia, there is a 48 percent chance that the other twin will do so as well. If the
twins are fraternal, on the other hand, the second twin has approximately a 17 percent
chance of developing the disorder.
ARE THE BIOLOGICAL RELATIVES OF AN ADOPTEE VULNERABLE? Adoption studies look at adults
with schizophrenia who were adopted as infants and compare them with both their
biological and their adoptive relatives. Because they were reared apart from their bio-
logical relatives, similar symptoms in those relatives would indicate genetic influences.
Conversely, similarities to their adoptive relatives would suggest environmental influ-
ences. Repeatedly, researchers have found that the biological relatives of adoptees with
schizophrenia are more likely to experience schizophrenia or a related disorder (see
Table 12-2 on the next page) than their adoptive relatives (Andreasen & Black, 2006;
Kety, 1988, 1968).
WHAT DO GENETIC LINKAGE AND MOLECULAR BIOLOGY STUDIES SUGGEST? As with bipolar dis-
orders (see Chapter 7), researchers have run studies of genetic linkage and molecular biology
to pinpoint the possible genetic factors in schizophrenia (Glatt, 2008;Walsh et al., 2008).
In one approach, they select large families in which schizophrenia is very common,
take blood and DNA samples from all members of the families, and then compare gene
fragments from members with and without schizophrenia. Applying this procedure to
families from around the world, various studies have identified possible gene defects on
chromosomes 1, 6, 8, 10, 13, 15, 18, and 22 and on the X chromosome, each of which
may help predispose individuals to develop schizophrenia (Folsom et al., 2006; Harrison
& Weinberger, 2005).
These varied findings may indicate that some of the suspected gene sites are cases
of mistaken identity and do not actually contribute to schizophrenia. Alternatively, it
may be that different kinds of schizophrenia are linked to different genes. It is most

Disorder
Schizophrenia
Brief psychotic disorder
Lifetime
Duration Prevalence
6 months or more 1.0%
Less than 1 month Unknown
Key Features
Various psychotic symptoms such as delusions, hallucinations,
disorganized speech, flat or inappropriate affect, and catatonia
Various psychotic symptoms such as delusions, hallucinations,
disorganized speech, flat or inappropriate affect, and catatonia
No minimum length Unknown
such No minimum length Unknown
Psychotic disorder due to a Hallucinations or delusions caused by a medical illness or
general medical condition brain damage
Substance-induced Hallucinations or delusions caused directly by a substance,
psychotic disorder as an abused drug
An Array of Psychotic Disorders
Various psychotic symptoms such as delusions, hallucinations, 1 to 6 months 0.2%
disorganized speech, flat or inappropriate affect, and catatonia
Marked symptoms of both schizophrenia and a mood disorder 6 months or more Unknown
Persistent delusions that are not bizarre and not due to
schizophrenia; persecutory, jealous, grandiose, and somatic
delusions are common
Person adopts delusions that are held by another individual,
such as a parent or sibling; also known as Idle a deux
Schizoaffective disorder
Delusional disorder
Shared psychotic disorder
1 month or more 0.1%
No minimum length Unknown
Schizophreniform disorder
366 ://CHAPTER 12
table:
likely, however, that schizophrenia, like a number of other disorders, is a polygenic disorder,
caused by a combination of gene defects (Tamminga et al., 2008).
How might genetic factors lead to the development of schizophrenia? Research has
pointed to two kinds of biological abnormalities that could conceivably be inherited—
biochemical abnormalities and abnormal brain structure.
odopamine hypothesisoThe theory
that schizophrenia results from excessive
activity of the neurotransmitter dopamine.
oantipsychotic drugsoDrugs that help
correct grossly confused or distorted
thinking.
ophenothiazinesoA group of antihista-
mine drugs that became the first group of
effective antipsychotic medications.
Biochemical Abnormalities As you have read, the brain is made up of neurons
whose electrical impulses (or “messages”) are transmitted from one to another by neu-
rotransmitters.After an impulse arrives at a receiving neuron, it travels down the axon of
that neuron until it reaches the nerve ending.The nerve ending then releases neurotrans-
mitters that travel across the synaptic space and bind to receptors on yet another neuron,
thus relaying the message to the next “station.”This neuron activity is known as “firing.”
Over the past four decades, researchers have developed a dopamine hypothesis to
explain their findings on schizophrenia: Certain neurons that use the neurotransmitter
dopamine fire too often and transmit too many messages, thus producing the symptoms
of the disorder (McGowan et al., 2004). This hypothesis has undergone challenges and
adjustments in recent years, but it is still the foundation for present biochemical ex-
planations of schizophrenia. The chain of events leading to this hypothesis began with
the accidental discovery of antipsychotic drugs, medications that help remove the
symptoms of schizophrenia. The first group of antipsychotic medications, the pheno-
thiazines, were discovered in the 1950s by researchers who were looking for better
antihistamine drugs to combat allergies.Although phenothiazines failed as antihistamines,
their effectiveness in reducing schizophrenic symptoms became obvious, and clinicians
began to prescribe them widely.
Researchers soon learned that these early antipsychotic drugs often produce trouble-
some muscular tremors, symptoms that are identical to the central symptom of Parkinson’s
disease, a disabling neurological illness. This undesired reaction to antipsychotic drugs
offered the first important clue to the biology of schizophrenia. Scientists already knew
that people who suffer from Parkinson’s disease have abnormally low levels of the
neurotransmitter dopamine in some areas of the brain and that lack of dopamine is the

Schizophrenia :11. 367
A CLOSE OCA
Postpartum Psychosis: The Case of Andrea Yates
In the morning of June 20, 2001, the
(nation’s television viewers watched
in horror es officials escorted 36-year-old
Andrea Yates to a police car. Just minutes
before, she had called police and explained
that she had drowned her five children in
the bathtub because “they weren’t develop.
ing correctly” and because she “realized
[she had not been] a good mother to them.”
Homicide sergeant Eric Mehl described how
she twice recounted the order in which the
children had died: first 3-year-old Paul, then
2-year-old Luke, followed by 5-year-old John
and 6-month-old Mary. She then described
how she had had to drag 7-year-old Noah
to the bathroom and how he had come up
twice as he fought for air. Later she told
doctors she wanted her hair shaved so she
could see the number 666—the mark of the
Antichrist—on her scalp (Roche, 2002).
In Chapter 7 you observed that as
many as 80 percent of mothers experience
“baby blues” soon after giving birth, while
between 10 and 30 percent display the
clinical syndrome of postpartum depres-
sion. Yet another postpartum disorder that
has become all too familiar to the public in
recent times, by way of cases such as that
of Andrea Yates, is postpartum psychosis.
Postpartum psychosis affects about 1
to 2 of every 1,000 mothers who have re-
cently given birth. The symptoms apparently
are triggered by the enormous shift in hor-
mone levels that occur after delivery (Black-
more et al., 2008; Nonacs, 2007, 2002).
Within days or at most a few months of
childbirth, the woman develops signs of
losing touch with reality, such as delusions
(for example, she may become convinced
that her baby is the devil); hallucinations
(perhaps hearing voices); extreme anxiety,
confusion, and disorientation; disturbed
sleep; and illogical thoughts (for example,
thoughts about killing herself or her child).
Women with a history of bipolar dis-
order, schizophrenia, or depression are
particularly vulnerable to the disorder
(Read & Purse, 2007; Sit et al., 2006).
In addition, women who have previously
experienced postpartum depression or
postpartum psychosis have an increased
likelihood of developing this disorder after
subsequent births (Nonacs, 2007; Ruta &
Cohen, 1998). Andrea Yates, for example,
had developed signs of postpartum depres-
sion (and perhaps postpartum psychosis)
and attempted suicide after the birth of her
fourth child. At that time, however, she ap-
peared to respond well to a combination
of medications, including antipsychotic
drugs, and so she and her husband later
decided to conceive a fifth child. Although
they were warned that she was at risk for
serious postpartum symptoms once again,
they believed that the same combination
of medications would help if the symptoms
were to recur (King, 2002).
After the birth of her fifth child, the
symptoms did in fact recur, along with fea-
tures of psychosis. Yates again attempted
suicide. Although she was hospitalized
twice and treated with various medications,
her condition failed to improve. Six months
after giving birth to Mary, her fifth child,
she drowned all five of her children.
Most clinicians who are knowledgeable
about this rare disorder agree that Yates
was indeed a victim of postpartum psy-
chosis. Although only a fraction of women
with the disorder actually harm their chil-
dren (estimates run as high as 4 percent),
the Yates case reminds us that such an
outcome is indeed possible (Read & Purse,
2007; Dobson & Sales, 2000). The case
also reminds us that early detection and
treatment are critical.
On March 13, 2002, a Texas jury
found Andrea Yates guilty of murdering her
children and she was sentenced to life in
prison. She had pleaded not guilty by rea-
son of insanity during her trial, but the jury
concluded within hours that despite her
profound disorder, she did know right from
wrong. The verdict itself stirred debate
throughout the United States, but clinicians
and the public alike were united in the be-
lief that, at the very least, the mental health
system had tragically failed this woman
and her five children.
A Texas appeals court later reversed
Yates’s conviction, citing the inaccurate
testimony of a prosecution witness, and on
July 26, 2006, after a new trial, Yates was
found not guilty by reason of insanity and
was sent to a high-security mental health
facility for treatment. In 2007, she was
transferred to a low-security state mental
hospital where she continues to receive
treatment today.

368 ://CHAPTER 12
eatypical antipsychotic drugsoA rela-
tively new group of antipsychotic drugs
whose biological action is different from
that of the traditional antipsychotic drugs.
reason for their uncontrollable shaking. If antipsychotic drugs produce Parkinsonian
symptoms in persons with schizophrenia while removing their psychotic symptoms,
perhaps the drugs reduce dopamine activity. And, scientists reasoned further, if lowering
dopamine activity helps remove the symptoms of schizophrenia, perhaps schizophrenia
is related to excessive dopamine activity in the first place.
Since the 1960s, research has supported and helped clarify the dopamine hypoth-
esis. It has been found, for example, that some people with Parkinson’s disease develop
schizophrenia-like symptoms if they take too much L – dopa, a medication that raises
dopamine levels in patients with that disease (Grilly, 2002).The L-dopa apparently raises
the dopamine activity so much that it produces psychosis. Support has also come from
research on amphetamines, drugs that, as you saw in Chapter 10, stimulate the central
nervous system by increasing dopamine activity in the brain. Clinical investigators have
observed that people who take high doses of amphetamines may develop amphetamine
psychosis — a syndrome very similar to schizophrenia.
Researchers have located areas of the brain that are rich in dopamine receptors and
have found that phenothiazines and other antipsychotic drugs bind to many of these
receptors (Burt et al., 1977; Creese et al., 1977).Apparently the drugs are dopamine an-
tagonists— drugs that bind to dopamine receptors, prevent dopamine from binding there,
and so prevent the neurons from firing (Iversen, 1975). Five kinds of dopamine receptors
have been identified throughout the brain—called the D-1, D-2, D-3, D-4, and D-5
receptors. Phenothiazines bind most strongly to the D- 2 receptors ( Julien, 2008).
These and related findings suggest that in schizophrenia, messages traveling from
dopamine-sending neurons to dopamine receptors on other neurons, particularly to

It’s when I was bitten by a rabid dog. . . When I’m
emotionally upset, I feel as if I am turning into something
else: my fingers go numb, as if I had pins and needles
right in the middle of my hand; I can no longer control
myself. . I get the feeling I’m becoming a wolf. I look
at myself in the mirror and I witness my transformation.
It’s no longer my face; it changes completely. I store, my
pupils dilate, and I feel as if hairs are growing all over my
body, as if my teeth are getting longer. . . feel as if
my skin is no longer mine.
(BENEZECH, EIEWITTE, & BOURGEOIS, 1989)
l ycanthropy, the delusion of being
— an animal, is a rare psychological
syndrome (Nejad, 2007). The word
“lycanthropy” comes from the Greek lykos,
“wolf,” and anthropos, “man.” Accounts
have been found all over the world of
people who take on the characteristics
and behavior of wolves or other animals.
Belief in these tales has persisted for
centuries.
Mention of lycanthropy continues to
produce an image of a werewolf baring
its fangs at a terrified villager on a fog-
shrouded moor. The legend was that the
former had been bitten by another
werewolf in an unbroken chain that
passes on the legacy. But there are
now more reasonable explanations for
this type of behavior. One explanation
is that some people afflicted with lycan-
thropy actually suffer from congenital
generalized hypertrichosis, an extremely
rare disease marked by excessive
amounts of hair on the face and upper
body (Kemp, 2000; Mough, 1995).
Others may suffer from porphyria, an
inherited blood disease whose victims
sprout extra facial hair and are sensitive
to sunlight (Osterweil, 2003). Still another
current explanation ties lycanthropy to a
disturbance in the activity of the temporal
lobe of the brain, which is close to areas
of the brain that may be responsible for
visual hallucinations.
Despite these rational explanations, be-
liefs in werewolves as supernatural beings
are likely to continue for the foreseeable fu-
ture. Tales of demonic possession are more
alluring than histories of congenital disease
or temporal lobe abnormalities. Nor are
publishers or movie producers likely to

say good-bye to such good friends. Old
explanations of lycanthropy may be flawed
scientifically, but the profits they produce
are far from a delusion.

Schizophrenia :ill 369
the D-2 receptors, may be transmitted too easily or too often. This theory is appealing
because certain dopamine neurons are known to play a key role in guiding attention
(Sikstrom & Soderlund, 2007). People whose attention is severely disturbed by exces-
sive dopamine activity might well be expected to suffer from the problems of attention,
perception, and thought found in schizophrenia.
Though enlightening, the dopamine hypothesis has certain problems. The greatest
challenge to it has come with the discovery of a new group of antipsychotic drugs,
referred to as atypical antipsychotic drugs, which are often more effective than
the traditional ones. The new drugs bind not only to D-2 dopamine receptors, like the
traditional antipsychotic drugs, but also to many D-1 receptors and to receptors for
other neurotransmitters such as serotonin (Goldman-Rakic et al., 2004). Thus, it may be
that schizophrenia is related to abnormal activity or interactions of both dopamine and
serotonin and perhaps other neurotransmitters as well, rather than to abnormal dopa-
mine activity alone (Bach, 2007).
Abnormal Brain Structure During the past decade, researchers also have linked
schizophrenia, particularly cases dominated by negative symptoms, to abnormalities in
brain structure (Eyler, 2008;Weyandt, 2006). Using brain scans, they have found, for ex-
ample, that many people with schizophrenia have enlarged ventricles— the brain cavities
that contain cerebrospinal fluid (Cahn et al., 2002; Lieberman et al., 2001). In addition to
displaying more negative symptoms and fewer positive ones, patients who have enlarged
ventricles tend to experience a poorer social adjustment prior to the disorder and greater
cognitive disturbances (Bornstein et a1.,1992).
It may be that enlarged ventricles are actually a sign that nearby parts of the brain
have not developed properly or have been damaged, and perhaps these problems are the
ones that help produce schizophrenia. In fact, studies suggest that some patients with the
disorder also have smaller temporal lobes and frontal lobes than other people, smaller
amounts of cortical gray matter, and, perhaps most important, abnormal blood flow—
either reduced or heightened—in certain areas of the brain (Tamminga et al., 2008;
Higgins & George, 2007). Still other studies have linked schizophrenia to structural
abnormalities of the hippocampus, amygdala, and thalamus (see Figure 12-3).
Viral Problems What might cause the biochemical and structural abnormalities
found in schizophrenia? Various studies have pointed to genetic factors, poor nutrition,
fetal development, birth complications, immune reactions, and toxins (Mum & Cannon,
2008; Bach, 2007). In addition, some investigators suggest that the
brain abnormalities may result from exposure to viruses before birth.
Perhaps the viruses enter the fetus’s brain and interrupt proper brain
development, or perhaps the viruses remain quiet until puberty
or young adulthood, when, activated by changes in hormones or
by another viral infection, they help to bring about schizophrenic
symptoms (Lambert & Kinsley, 2005;Torrey, 2001, 1991).
Some of the evidence for the viral theory comes from animal
investigations, and other evidence is circumstantial, such as the
finding that an unusually large number of people with schizo-
phrenia are born during the winter. The winter birth rate among
people with schizophrenia is 5 to 8 percent higher than among
other persons (Tamminga et al., 2008).This could be because of an
increase in fetal or infant exposure to viruses at that time of year.
More direct evidence comes from studies showing that mothers of
individuals with schizophrenia were more likely to have been ex-
posed to the influenza virus during pregnancy than were mothers
of people without schizophrenia (Brown et al., 2004; Limosin et al.,
2003). And, finally, studies have found antibodies to certain viruses
in the blood of 40 percent of research participants with schizo-
phrenia (Leweke et al., 2004; Torrey et al., 1994). The presence of
Frontal
lobes
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oschizophrenogenic mother•A type
of mother—supposedly cold, domineer-
ing, and uninterested in the needs of
others — who was once thought to cause
schizophrenia in her child.
370 . //CHAPTER 12
such antibodies suggests that these people had at some time been exposed
to those particular viruses.
Together, the biochemical, brain structure, and viral findings are shed-
ding much light on the mysteries of schizophrenia. At the same time, it
is important to recognize that many people who display these biological
abnormalities never develop schizophrenia.Why not? Possibly, as you read
earlier, because biological factors merely set the stage for schizophrenia,
while key psychological and sociocultural factors must be present for the
disorder to appear.
Psychological Views
When schizophrenia investigators began to identify genetic and biologi-
cal factors during the 1950s and 1960s, many clinicians abandoned the
psychological theories of the disorder. During the past decade, however,
the tables have been turned and psychological factors are once again being
considered as important pieces of the schizophrenia puzzle. The leading
psychological theories come from the psychodynamic and cognitive perspectives.
The Psychodynarnic Explanation Freud (1924, 1915, 1914) believed that
schizophrenia develops from two psychological processes: (1) regression to a pre-ego stage
and (2) efforts to reestablish ego control. He proposed that when their world is extremely
harsh or withholding—for example, when parents are cold or unnurturing—people who
develop schizophrenia regress to the earliest point in their development, to the pre-ego
state ofprimary narcissism, in which they recognize and meet only their own needs.Their
near-total regression leads to self-centered symptoms such as neologisms, loose associa-
tions, and delusions of grandeur. Once people regress to such an infantile state, Freud
continued, they then try to reestablish ego control and contact with reality.Their efforts
give rise to yet other schizophrenic symptoms.Auditory hallucinations, for example, may
be an individual’s attempt to substitute for a lost sense of reality.
Years later, noted psychodynamic clinician Frieda Fromm-R.eichmann (1948) elab-
orated on Freud’s notion that cold or unnurturing parents may set schizophrenia in
motion. She described the mothers of people who develop this disorder as cold, domi-
neering, and uninterested in their children’s needs. According to Fromni-Reichmann,
these mothers may appear to be self-sacrificing but are actually using their children to
meet their own needs. At once overprotective and rejecting, they confuse their children
and set the stage for schizophrenic functioning. She called them schizophrenogenic
(schizophrenia-causing) mothers.
Fromm-Reichrnann’s theory, like Freud’s, has received little research support (Willick,
2001). The majority of people with schizophrenia do not appear to have mothers who
fit the schizophrenogenic description. Most of today’s psychodynamic theorists have, in
fact, rejected the views of Freud and Fromm-Reichmann. Although the theorists may
retain some of the early notions (Karon, 2008; Spielrein, 1995), more and more of them
believe that biological abnormalities leave certain persons particularly prone to extreme
regression or other unconscious acts that may contribute to schizophrenia (Berzoff,
Flanagan, & Hertz, 2008).
The Cognitive Explanation A leading cognitive explanation of schizophrenia
agrees with the biological view that during hallucinations and related perceptual diffi-
culties the brains of people with schizophrenia are actually producing strange and unreal
sensations—sensations triggered by biological factors.According to the cognitive expla-
nation, however, further features of the disorder emerge when the individuals attempt
to understand their unusual experiences (Tarrier, 2008;Waters et al., 2007). When first
confronted by voices or other troubling sensations, these people turn to friends and rela-
tives. Naturally, the friends and relatives deny the reality of the sensations, and eventually
the sufferers conclude that the others are trying to hide the truth. They begin to reject
all feedback, and some develop beliefs (delusions) that they are being persecuted (Perez-

Sthizophrenia :ft 371
Alvarez et al., 2008; Bach, 2007). In short, according to this theory, people with schizo-
phrenia take a “rational path to madness” (Zimbardo, 1976).
Researchers have established that people with schizophrenia do indeed experience
sensory and perceptual problems. As you saw earlier, many of them have hallucinations,
for example, and most have trouble keeping their attention focused. But researchers have
yet to provide clear, direct support for the cognitive notion that misinterpretations of
such sensory problems actually produce a syndrome of schizophrenia.
Sociocultural Views
Sociocultural theorists, recognizing that people with mental disorders are subject to a
wide range of social and cultural forces, claim that multicultural factors, social labeling, and
family dysfunctioning all contribute to schizophrenia. At the same time, research has yet
to clarify what the precise causal relationships might be.
Muiticult r l Factors Rates of schizophrenia appear to differ between racial and
ethnic groups, particularly between African Americans and white Americans. As many
as 2.1 percent ofAfrican Americans receive a diagnosis of schizophrenia, compared with
1.4 percent of white Americans (Lawson, 2008; Folsom et al., 2006). Similarly, studies
suggest that African Americans with schizophrenia are overrepresented in state hospitals
(Lawson, 2008; Barnes, 2004). For example, in Tennessee’s state hospitals 48 percent of
those with a diagnosis of schizophrenia are African American, although only 16 percent
of the state population is African American (Lawson, 2008; Barnes, 2004).
It is not clear why African Americans have a higher likelihood than white Americans
of receiving this diagnosis. One possibility is that African Americans are more prone
to develop the disorder. Another possibility is that clinicians from majority groups are
unintentionally biased in their diagnoses of African Americans or misread cultural dif-
ferences as symptoms of schizophrenia (Lawson, 2008; Barnes, 2004).
Yet another explanation for the difference between African Americans and white
Americans may lie in the economic sphere. On average, African Americans are more
likely than white Americans to be poor, and, indeed, when economic differences are
controlled for, the prevalence rates of schizophrenia become closer for the two racial
groups. Consistent with the economic explanation is the finding that Hispanic Ameri-
cans, who are, on average, also economically disadvantaged, also appear to have a higher
likelihood of receiving a diagnosis of schizophrenia than white Americans, although
their diagnostic rate is not as high as that of African Americans (Blow et al., 2004).
It also appears that schizophrenia differs from country to country in key ways. Al-
though the overall prevalence of this disorder is stable—around 1 percent—in countries
across the world, the course and outcome of the disorder may vary considerably. Accord-
ing to a 10-country study conducted by the World Health
Organization (WHO), the 25 million schizophrenic patients
who live in developing countries have better recovery rates
than schizophrenic patients in Western and other developed
countries (Vahia & Vahia, 2008; Jablensky, 2000). During a
two-year observation period, the schizophrenic patients from
developing countries were more likely than those in devel-
oped countries to recover from their disorder and less likely
to experience continuous symptoms, be socially impaired, re-
quire heavy antipsychotic drugs, or require hospitalization.
Some clinical theorists believe that the psychosocial en-
vironments of developing countries tend to be more sup-
portive and therapeutic than those of developed countries,
leading to more favorable outcomes for people with schizo-
phrenia (Vahia & Vahia, 2008; Jablensky, 2000). Developing
countries, for example, seem to provide more family and
social support to people with schizophrenia, make available
more relatives and friends to help care for the individuals, and
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372 ://CHAPTER 12
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*expressed emotion*The general level
of criticism, disapproval, and hostility
expressed in a family. People recovering
from schizophrenia are considered more
likely to relapse if their families rate high
in expressed emotion.
act less judgmental and critical toward persons with schizophrenia. The Nigerian
culture, for example, is generally more tolerant of the presence of voices than are
Western cultures (Matsumoto & Juang, 2008).
Social Labeling Many sociocultural theorists believe that the features of
schizophrenia are influenced by the diagnosis itself (Modrow, 1992). In their opin-
ion, society assigns the label “schizophrenic” to people who fail to conform to
certain norms of behavior. Once the label is assigned, justified or not, it becomes
a self-fulfilling prophecy that leads to the development of many schizophrenic
symptoms.
We have already seen the very real dangers of diagnostic labeling. In the famous
Rosenhan (1973) study, discussed in Chapter 2, eight normal people presented
themselves at various mental hospitals, complaining that they had been hearing
voices utter the words “empty,””hollow,” and “thud.”They were quickly diagnosed
as schizophrenic, and all eight were hospitalized. Although the pseudopatients then
dropped all symptoms and behaved normally, they had great difficulty getting rid
of the label and gaining release from the hospital. They also reported that staff
members treated them as though they were invisible. “A nurse unbuttoned her
uniform to adjust her brassiere in the presence of an entire ward of viewing men.
One did not have the sense that she was being seductive. Rather, she didn’t notice
us.” In addition, the pseudopatients described feeling powerless, bored, tired, and
uninterested. The investigation demonstrates that the label “schizophrenic” can
itself have a negative effect not just on how people are viewed but on how they
themselves feel and behave.
Family Dysfunctioning Many studies suggest that schizophrenia, like a number of
other mental disorders, is often linked to family stress (Boye et al., 2002; Schiffinan et al.,
2002, 2001). Parents of people with this disorder often (1) display more conflict, (2) have
greater difficulty communicating with one another, and (3) are more critical of and
overinvolved with their children than other parents.
Family theorists have long recognized that certain families are high in expressed
emotion—that is, members frequently express criticism, disapproval, and hostility
toward each other and intrude on one another’s privacy. Individuals who are trying
to recover from schizophrenia are almost four times more likely to relapse if they live
with such a family than if they live with one low in expressed emotion (Ritsner &
Gibel, 2007; Nomura et al., 2005). Do such findings mean that family dysfunctioning
helps cause and maintain schizophrenia? Not necessarily. It is also the case that indi-
viduals with schizophrenia greatly disrupt family life. In so doing, they themselves may
help produce the family problems that clinicians and researchers continue to observe
(Barrowclough & Lobban, 2008).
Although the sociocultural causes of schizophrenia, like the psychological causes,
have yet to be fully understood, many clinicians currently believe that such factors play
an important role in the disorder. As we have seen, most hold a diathesis-stress view of
schizophrenia, believing that biological factors set up a predisposition to the disorder,
but that certain kinds of personal, family, or social stress are needed for the syndrome
to spring to life.
How Do Theorists Explain Schizophrenia?
The biological explanations of schizophrenia point to genetic, biochemical, brain
structure, and viral factors. The leading biochemical explanation holds that the
brains of people with schizophrenia experience excessive dopamine activity. Brain-
imaging techniques have also detected abnormal brain structures in many people
with schizophrenia, including enlarged ventricles and abnormal blood flow in

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Schizophrenia :1/ 373
certain parts of the brain. Finally, some researchers believe that schizophrenia is
related to a virus that settles in the fetus and perhaps lies quiet until adolescence or
young adulthood.
The leading psychological explanations for schizophrenia come from the psy-
chodynamic and cognitive models. In influential psychodynamic explanations,
Freud held that schizophrenia involves regression to a state of primary narcissism
and Fromm-Reichmann proposed that schizophrenogenic mothers help produce
this disorder. Today’s psychodynamic theorists believe, however, that the disorder
is caused by a combination of biological and psychodynamic factors. Cognitive
theorists hold that when people with schizophrenia try to understand their strange
biological sensations, they develop delusional thinking.
One sociocultural explanation holds that multicultural differences may influence
the rate and character of schizophrenia, as well as recovery from this disorder. An-
other sociocultural explanation argues that society expects persons who are labeled
as having schizophrenia to behave in certain ways and that these expectations
actually lead to further symptoms. Still other sociocultural theorists point to family
dysfunctioning as a cause of schizophrenia.
Most clinical theorists now agree that schizophrenia can probably be traced to
a combination of biological, psychological, and sociocultural factors. However, the
biological factors have been more precisely identified.
JziM-low Are Schizophrenia and Other
Severe Mental Disorders Treated?
They call us insane—and in reality they are as inconsistent as we are, as flighty and
changeable. This one in particular. One day he derides and ridicules me unmercifully; the
next he talks to me sadly and this morning his eyes misted over with tears as he told me
of the fate ahead. Damn him and all of his wisdom!
He has dinned into my ears a monotonous dirge—”Too Egotistical—too Egotistical—
too Egotistical. Learn to think differently. “—And how can I do it? How—how—can 1 do
it? How the hell can I do it? I have tried to follow his suggestions but have not learned to
think a bit differently. It was all wasted effort. Where has it got me?
(Jefferson, 1948)
With these words, Lara Jefferson, a young woman with schizophrenia, described her
treatment experience in the 1940s. Her pain and frustration were typical of those expe-
rienced by hundreds of thousands of similar patients during that period of
time. In fact, for much of human history, persons with schizophrenia were
considered beyond help.The disorder is still extremely difficult to treat, but
clinicians are much more successful today than they were in the past (Roe
& Davidson, 2008). Much of the credit goes to antipsychotic drugs, medica-
tions that help many people with schizophrenia think clearly and profit
from therapies that previously would have had little effect on them.
To better convey the plight of people with schizophrenia, this chapter
will proceed from a historical perspective. A look at how treatment has
changed over the years will help us understand the nature, problems, and
promise of today’s approaches. As we consider past treatments for schizo-
phrenia, it is important to keep in mind that the label “schizophrenia” was
assigned to most people with psychotic symptoms throughout the twenti-
eth century. Clinical theorists now realize, however, that a number of people
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3 74 ://CHAPTER 12
with psychotic symptoms are in fact displaying a severe form of bipolar disorder or
major depressive disorder and that many such individuals were in past times inaccurately
given a diagnosis of schizophrenia. Thus, our discussions of past treatments for schizo-
phrenia, particularly the failures of institutional care, are as applicable to those other
severe mental disorders as they are to schizophrenia. Indeed, any disorder that includes
psychotic features presents formidable obstacles to treatment, and so even some of our
– —
A – CLO$EP
Hypochondriacs no longer thought they were going to die,
would-be suicides found life acceptable, sufferers from
persecution complex forgot the machinations of imaginary
conspirators. Prefrontal lobotomy, as the operation is
called, was made possible by the localization of fears,
hates, and instincts lin the prefrontal cortex of the brain].
It is fitting, then, that the Nobel Prize in medicine should
be shored by Hess and Moniz. Surgeons now think no
more of operations on the brain than they do of removing
an appendix.
We now know that the lobotomy was
hardly a miracle treatment. Far from “cur-
ing” people with mental disorders, the
procedure left thousands upon thousands
extremely withdrawn, subdued, and even
stuporous. The first lobotomy was per-
formed by Portuguese neuropsychiatrist
Egas Moniz in 1935 (Tierney, 2000). His
particular procedure, called a prefrontal
leukotomy, consisted of drilling two holes
in either side of the skull and inserting an
instrument resembling an icepick into the
brain tissue to cut or destroy nerve fibers.
Moniz believed that severe abnormal
thinking could be changed by cutting the
nerve pathways that carried such thoughts
from one part of the brain to another. In
the 1940s Walter Freeman and his surgi-
cal partner, James Watts, developed a
second kind of psychosurgery called the
transorbital lobotomy, in which the surgeon
inserted a needle into the brain through
the eye socket and rotated it in order to
destroy the brain tissue.
Altogether, an estimated 50,000 peo-
ple in the United States alone received
lobotomies (Johnson, 2005). Why was the
procedure so enthusiastically accepted by
the medical community in the 1940s and
1950s? Neuroscientist Elliot Valenstein
(1986) points first to the extreme over-
crowding in mental hospitals at the time.
This crowding was making it difficult to
maintain decent standards in the hospitals.
Valenstein also points to the personali-
ties of the inventors of the procedure as
important factors. Although these indi-
viduals were gifted and dedicated physi-
cians, Valenstein also believes that their
professional ambitions led them to move
too quickly and boldly in applying the
procedure. Indeed, in 1949 Moniz was
awarded the Nobel Prize for his work.
The prestige of Moniz and Freeman
was so great and the field of neurology
was so small that their procedures drew
little criticism. Physicians may also have
been misled by the seemingly positive
findings of early studies of the lobotomy,
which, as it turned out, were not based
on sound methodology (Swayze, 1995;
Valenstein, 1986).
By the 1950s, better studies revealed
that in addition to having a fatality rate of
1.5 to 6 percent, lobotomies could cause
serious problems such as brain seizures,
huge weight gain, loss of motor coordi-
nation, partial paralysis, incontinence,
endocrine malfunctions, and very poor
intellectual and emotional responsiveness.
Finally, the discovery of effective antipsy-
chotic drugs put an end to this inhumane
treatment for mental disorders (Mashour
et al., 2005).
Today’s psychosurgical procedures are
greatly refined and hardly resemble the
lobotomies of 50 years back. Moreover,
such procedures are considered experimen-
tal and are used only as a last resort in the
most severe cases of obsessive-compulsive
disorder and depression (McNeely et al.,
2008; Anderson & Booker, 2006). Even
so, many professionals believe that any
kind of surgery that destroys brain tissue
is inappropriate and perhaps unethical
and that it keeps alive one of the clinical
field’s most shameful and ill-advised efforts
at cure.
Lobotomy: How Could It Happen?
In 1949 a New York Times article
I reported on a medical procedure
that appeared to offer hope to sufferers of
severe mental disorders:

Schizophrenia :1/ 375
discussions about current approaches to schizophrenia, such as the community mental
health movement, apply to other severe mental disorders as well.
Institutional Care in the Past
For more than half of the twentieth century, most people diagnosed with schizophrenia
were institutionalized in a public mental hospital. Because patients with this disorder
failed to respond to traditional therapies, the primary goals of these establishments were
to restrain them and give them food, shelter, and clothing. Patients rarely saw therapists
and generally were neglected. Many were abused. Oddly enough, this state of affairs
unfolded in an atmosphere of good intentions.
As you read in Chapter 1, the move toward institutionalization in hospitals began in
1793 when French physician Philippe Pinel “unchained the insane” at La Bicetre asylum
and began the practice of “moral treatment.” For the first time in centuries, patients
with severe disturbances were viewed as human beings who should be cared for with
sympathy and kindness.As Pinel’s ideas spread throughout Europe and the United States,
they led to the creation of large mental hospitals rather than asylums to care for those
with severe mental disorders (Goshen, 1967).
These new mental hospitals, typically located in isolated areas where land and labor
were cheap, were meant to protect patients from the stresses of daily life and offer them
a healthful psychological environment in which they could work closely with thera-
pists (Grob, 1966). States throughout the United States were even required by law to
establish public mental institutions, state hospitals, for patients who could not afford
private ones.
Eventually, however, the state hospital system encountered serious problems. Be-
tween 1845 and 1955 nearly 300 state hospitals opened in the United States, and the
number of hospitalized patients on any given day rose from 2,000 in 1845 to nearly
600,000 in 1955. During this expansion, wards became overcrowded, admissions kept
rising, and state funding was unable to keep up.
The priorities of the public mental hospitals, and the quality of care they provided,
changed over those 110 years. In the face of overcrowding and understaffing, the em-
phasis shifted from giving humanitarian care to keeping order. In a throwback to the
asylum period, difficult patients were restrained, isolated, and punished; individual atten-
tion disappeared. Patients were transferred to back wards, or chronic wards, if they failed
to improve quickly (Bloom, 1984). Most of the patients on these wards suffered from
schizophrenia (Hafner & an der Heiden, 1988). The back wards were in fact human
warehouses filled with hopelessness. Staff members relied on straitjackets and handcuffs
to deal with difficult patients. More “advanced” forms of treatment included medical
approaches such as lobotomy.
ostate huspitaisoPublic mental hos-
pitals in the United States, run by the
individual states.
therapy®A humanistic
approach to institutional treatment based
on the belief that institutions can help
patients recover by creating a climate
that promotes self-respect, responsible
behavior, and meaningful activity.
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Institutional Care Takes a Turn for the Better
In the 1950s, clinicians developed two institutional approaches that
finally brought some hope to patients who had lived in institutions
for years: milieu therapy, based on humanistic principles, and the token
economy program, based on behavioral principles. These approaches
particularly helped improve the personal care and self-image of pa-
tients, problem areas that had been worsened by institutionalization.
The approaches were soon adopted by many institutions and are now
standard features of institutional care.
Milieu Therapy In 1953, Maxwell Jones, a London psychiatrist,
converted a ward ofpatients with various psychological disorders into
a therapeutic community, the first application of milieu therapy in a
hospital setting.The principle behind milieu therapy is that institu-
tions can help individuals by creating a social climate, or milieu, that
builds productive activity, self-respect, and a sense of responsibility. In

Ftn. =F I p Olz
°token economy programeA behav-
ioral program in which a person’s
desirable behaviors are reinforced
systematically throughout the day by
the awarding of tokens that can be
exchanged for goods or privileges.
oneuroleptic drugseConventional
antipsychotic drugs, so called because
they often produce undesired effects
similar to the symptoms of neurological
disorders.
376 :Ai/CHAPTER 12
such settings, patients are often given the right to run their own lives and make their own
decisions. They may take part in community government, working with staff members
to set up rules and decide penalties. The atmosphere is one of mutual respect, support,
and openness. Patients may also take on special projects, obs, and recreational activities.
In short, their daily schedule is designed to resemble life outside the hospital.
Since Jones’s pioneering effort, milieu-style programs have been set up in institu-
tions throughout the Western world. The programs vary from setting to setting, but at
a minimum staff members try to encourage interactions (especially group interactions)
between patients and staff, to keep patients active, and to raise patients’ expectations of
what they can accomplish.
Research over the years has shown that patients with severe mental disorders in
milieu hospital programs often improve and that they leave the hospital at higher rates
than patients in programs offering primarily custodial care (Paul, 2000; Paul & Lentz,
1977). Many of these persons remain impaired, however, and must live in sheltered set-
tings after their release. Despite its limitations, milieu therapy continues to be practiced
in many institutions, often combined with other hospital approaches (Gunter, 2005).
Moreover, you will see later in this chapter that many of today’s halfway houses and
other community programs for individuals with severe mental disorders are run in ac-
cordance with the principles of milieu therapy.
The Token Economy In the 1950s, behaviorists discovered that the systematic appli-
cation of operant conditioning techniques on hospital wards could help change the be-
haviors of patients with schizophrenia and other severe mental disorders (Ayllon, 1963;
Ayllon & Michael, 1959). Programs that applied these techniques were called token
economy programs.
In token economies patients are rewarded when they behave acceptably and are not
rewarded when they behave unacceptably.The immediate rewards for acceptable behav-
ior are often tokens that can later be exchanged for food, cigarettes, hospital privileges,
and other desirable items, thus creating a “token economy”Acceptable behaviors likely
to be targeted include caring for oneself and for one’s possessions (making the bed,
getting dressed), going to a work program, speaking normally, following ward rules, and
showing self-control.
Researchers have found that token economies do help reduce psychotic and related
behaviors (Combs et al., 2008; Dickerson et al., 2005). In one early program, Gordon
Paul and Robert Lentz (1977) set up a hospital token economy for 28 patients diag-
nosed with long-term schizophrenia, most of whom improved greatly. After four and a
half years, 98 percent of the patients had been released, mostly to sheltered-care facilities,
compared with 71 percent of patients treated in a milieu program and 45 percent of
patients who received custodial care only.
Despite the effectiveness of token economies, some clinicians have questioned the
quality of the improvements made under such programs. Are behaviorists changing a
patient’s psychotic thoughts and perceptions or simply improving the patient’s ability
to imitate normal behavior? This issue is illustrated by the case of a middle-aged man
named John, who had the delusion that he was the U.S. government (Coiner, 1973).
Whenever he spoke, he spoke as the government. “We are happy to see you….We need
people like you in our service. . . . We are carrying out our activities in John’s body.”
When John’s hospital ward was made into a token economy, the staff members targeted
his delusional statements and required him to identify himself properly to earn tokens.
After a few months on the token economy program, ohn stopped referring to himself
as the government.When asked his name, he would say,”John.”Although staff members
were pleased with his improvement, John himself had a different view of the situation.
In a private discussion he said:
We’re tired of it. Every damn time we want a cigarette, we have to go through their
bullshit. “What’s your name? Who wants the cigarette? Where is the government?”

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Schizophrenia :1/ 377
Today, we were desperate for a smoke and went to Simpson, the damn nurse, and she
made us do her bidding. “Tel/ me your name if you want a cigarette. What’s your name?”
Of course, we said, “John.” We needed the cigarettes. If we told her the truth, no ciga-
rettes. But we don’t have time for this nonsense. We’ve got business to do, international
business, laws to change, people to recruit. And these people keep playing their games.
(Comer; 1973)
Critics of the behavioral approach would argue that John was still delusional and
therefore as psychotic as before. Behaviorists, however, would argue that at the very least,
John’s judgment about the effects of his behavior had improved.
Token economy programs are no longer as popular as they once were, but they are
still used in many mental hospitals, usually along with medication, and in many commu-
nity residences as well (Kopelowicz et al., 2008). The approach has also been applied to
other clinical problems, including mental retardation, delinquency, and hyperactivity, as
well as in other fields, such as education and business (Spiegler & Guevremont, 2003).
Antipsychotic Drugs
Milieu therapy and token economy programs helped improve the gloomy outlook for
patients diagnosed with schizophrenia, but it was the discovery of antipsychotic drugs in
the 1950s that truly revolutionized treatment for this disorder. These drugs eliminate
many of its symptoms and today are almost always a part of treatment.
As we have observed, the discovery of antipsychotic medications dates back to the
1940s, when researchers were developing the first antihistamine drugs to combat allergies.
The French surgeon Henri Laborit soon discovered that one group of antihistamines,
phenothiazines, could also be used to help calm patients about to undergo surgery.
Laborit suspected that the drugs might also have a calming effect on persons with severe
psychological disorders. One of the phenothiazines, chlorpromazine, was eventually tested
on six patients with psychotic symptoms and found to reduce their symptoms sharply.
In 1954, chlorpromazine was approved for sale in the United States as an antipsychotic
drug under the trade name Thorazine.
Since the discovery of the phenothiazines, other kinds of antipsychotic drugs have
been developed. The ones developed throughout the 1960s, 1970s, and 1980s are now
referred to as “conventional” antipsychotic drugs in order to distinguish them from the
“atypical” antipsychotics (also called “second generation” antipsychotic drugs) that have been
developed in recent years.The conventional drugs are also known as neuroleptic drugs
because they often produce undesired movement effects
similar to the symptoms of neurological diseases. As you
saw earlier, the conventional drugs reduce psychotic
symptoms at least in part by blocking excessive activity
of the neurotransmitter dopamine, particularly at the
brain’s dopamine D-2 receptors (Combs et al., 2008;
Julien, 2008).
How Effective Are Antipsychotic Drugs? Re-
search repeatedly has shown that antipsychotic drugs
reduce symptoms in at least 65 percent of patients di-
agnosed with schizophrenia ( Julien, 2008). Moreover,
in direct comparisons the drugs appear to be a more
effective treatment for schizophrenia than any of the
other approaches used alone, such as psychotherapy,
milieu therapy, or electroconvulsive therapy (May,Tuma,
& Dixon, 1981; May & Tuma, 1964). In most cases, the
drugs produce the maximum level of improvement
within the first six months of treatment (Kutscher,

378 ://CHAPTER 12
oextrapyramidal effectse Unwanted
movements, such as severe shaking,
bizarre-looking grimaces, twisting of
the body, and extreme restlessness,
sometimes produced by conventional
antipsychotic drugs.
otardive dyskinesia.Extrapyramidal
effects that appear in some patients after
they have taken conventional antipsy-
chotic drugs for an extended time.
2008); however, symptoms may return if patients stop taking the drugs too soon (Saba
et al., 2007). The antipsychotic drugs, particularly the conventional ones, reduce the
positive symptoms of schizophrenia, such as hallucinations and delusions, more com-
pletely, or at least more quickly, than the negative symptoms, such as flat affect, poverty of
speech, and loss of volition (Combs et al., 2008; Julien, 2008).
Although antipsychotic drugs are now widely accepted, patients often dislike the
powerful effects of the drugs—both intended and unintended—and some refuse to take
them (Saba et at., 2007; Gilmer et al., 2004). But like this man, many are greatly helped
by the medications.

In my case it was necessary to come to terms with a specified drug program. 1 am a legal-
ized addict. My dose: 100 milligrams or Thorazine and 60 milligrams of Stelazine daily.
don’t feel this dope at all, but 1 have been told it is strong enough to flatten a normal per-
son. It keeps me—as the doctors agree—sane and in good spirits. Without the brain candy,
as f call it, I would go—zoom—right back into the bin. I’ve made the institution scene
enough already to be familiar with what it’s like and to know! don’t want to go back.
(Snow, 1976)

s you saw in Chapter 7, depressed
African Americans in the United
States are less likely than depressed
white Americans to be prescribed second-
generation antidepressant drugs, the
newer antidepressants that have fewer
side effects than tricyclics and MAO in-
hibitors (see page 202). Unfortunately, a
similar pattern appears to be at work in
cases of schizophrenia when people are
prescribed atypical antipsychotic medica-
tions, the second-generation antipsychotic
medications that are often more effective
and have fewer undesired effects than con-
ventional antipsychotic medications. The
following racial prescription patterns have
emerged in several studies:
African Americans and Hispanic
Americans with schizophrenia and
other psychotic disorders are signifi-
cantly less likely than white Americans
to be prescribed atypical antipsychotic
drugs (Herbeck et al., 2004; Covell
et al., 2002).
African Americans and Hispanic
Americans with schizophrenia are
much more likely than white Ameri-
cans to be prescribed conventional
antipsychotic drugs (Herbeck et al.,
2004; Covell et al., 2002).
In turn, African American and His-
panic American patients are less likely
to be helped by their antipsychotic
medications and more likely to experi-
ence tardive dyskinesia and extrapy-
ramidal effects in response to their
medications for schizophrenia.
One reason for this racial disparity
may be economic. On average, Afri-
can American and Hispanic American
patients are less likely than white
Americans to have private health insur-
ance or any health insurance at all
(Ni & Cohen, 2004). Schizophrenic
patients without private insurance are more likely to be prescribed con-
ventional antipsychotic medications,
which are much cheaper than atypical
antipsychotics (Herbeck et al., 2004).
Another explanation for this racial
disparity points to the kind of practitio-
ners seen by patients. In general, Afri-
can American and Hispanic American
patients with severe mental disorders
are more likely to have a family physi-
cian rather than a psychiatrist pre-
scribe their psychotropic drugs (Mark
et al., 2002; Pingitore et al., 2001).
It turns out that many family physi-
cians are more inclined to prescribe
conventional antipsychotic drugs than
atypical antipsychotic drugs (Mark et
al., 2003, 2002).
First Dibs on Atypical Antipsychotic Drugs?

Schizophrenia :1/ 379
The Unw. nted Effects of Conventional Antipsychotic Drugs
In addition to reducing psychotic symptoms, the conventional antipsychotic
drugs sometimes produce disturbing movement problems ( Julien, 2008).
These effects are called extrapyramidal effects because they appear to be
caused by the drugs’ impact on the extrapyramidal areas of the brain, areas
that help control motor activity.
The most common extrapyramidal effects are Parleinsonian symptoms,
reactions that closely resemble the features of the neurological disorder
Parkinson’s disease. At least half of patients on conventional antipsychotic
drugs experience muscle tremors and muscle rigidity at some point in their
treatment; they may shake, move slowly, shuffle their feet, and show little
facial expression (Combs et al., 2008). Some also display bizarre movements
of the face, neck, tongue, and back, and a number experience great restless-
ness and discomfort in the limbs.
Whereas most undesired drug effects appear within days or weeks, a
reaction called tardive dyskinesia (meaning “late-appearing movement
disorder”) does not usually unfold until after a person has taken conven-
tional antipsychotic drugs for more than a year.This syndrome may include
involuntary writhing or ticlike movements of the tongue, mouth, face, or whole body;
involuntary chewing, sucking, and lip smacking; and jerky movements of the arms, legs,
or entire body. It is believed that more than 10 percent of the people who take the
conventional drugs for an extended time develop tardive dyskinesia to some degree, and
the longer the drugs are taken, the greater the risk becomes ( Julien, 2008; APA, 2000).
Patients over 50 years of age seem to be at greater risk. Tardive dyskinesia can be dif-
ficult, sometimes impossible, to eliminate (Combs et al., 2008). The longer patients are
on the conventional antipsychotic drugs, the less likely it is that their tardive dyskinesia
will disappear, even when the drugs are stopped ( Julien, 2008).
Today clinicians are more knowledgeable and more cautious
about prescribing conventional antipsychotic drugs than they were
in the past. Previously, when patients did not improve with such a
drug, their clinicians would keep increasing the dose (Kane, 1992);
today a clinician will typically stop the drug. Similarly, today’s clini-
cians try to prescribe the lowest effective dose for each patient and
to gradually reduce or even stop medication weeks or months after
the patient begins functioning normally (Addington Sc Addington,
2008; Kutscher, 2008).
New Antipsychotic Drugs As we saw earlier, “atypical” anti-
psychotic drugs have been developed in recent years (see Table 12-3).
The most effective and widely used of these new drugs are clozapine
(trade name Clozaril), risperidone (Risperdal), olanzapine (Zyprexa),
quetiapine (Seroquel), ziprasidone (Geodon), and aripiprazole (Abilify).
As you have read, the drugs are called atypical because their biological
operation differs from that of the conventional antipsychotic medica-
tions:The atypicals are received at fewer dopamine D-2 receptors and
snore D-1,D -4, and serotonin receptors than the others ( Julien, 2008).
In fact, atypical antipsychotic drugs appear to be more effective
than the conventional drugs, helping as many as 85 percent of persons
with schizophrenia, compared with the 65 percent helped by most of
the conventional drugs ( Julien, 2008). Unlike the conventional drugs,
the new drugs reduce not only the positive symptoms of schizophre-
nia, but also the negative ones (Combs et al., 2008). Another major
benefit of the atypical antipsychotic drugs is that they cause fewer
extrapyramidal symptoms and do not seem to produce tardive dyski-
nesia, although some of them produce significant undesired effects of
their own (Edlinger et al., 2009; Dolder, 2008). Given such advantages,
1- ri if rip €i
Trade Name
Thorazine
Vesprin
Mellaril
Serentil
Stelazine
Prolixin, Permitil
Trilafon
Tindal
Taractan
Navane
Haldol
Loxitane
Mohan, Lidone
Orap
Antipsychotic Drugs
Class/Generic Name
Conventional antipsychotics
Chlorpromazine
Triflupromazine
Thioridazine
Mesoridazine
Trifluoperazine
Fluphenazine
Perphenazine
Acetophenazine
Chlorprothixene
Thiothixene
Haloperidol
Loxapine
Molindone hydrochloride
Pimozide
Atypical antipsychotics
Risperidone
Clozapine
Olanzapine
Quetiapine
Ziprasidone
Aripiprazole

Risperdal
Clozaril
Zyprexa
Serociuel
Geodon
Abirify

380 :// CHAPTER 12
it is not surprising that over half of all medicated patients with schizophrenia now take
the atypical drugs and that these drugs are considered the first line of treatment for the
disorder (Combs et al., 2008; Sajatovic et al., 2008). Moreover, many patients with bi-
polar or other severe mental disorders also seem to be helped by several of the atypical
antipsychotic drugs ( Julien, 2008).
Psychotherapy
Before the discovery of antipsychotic drugs, psychotherapy was not really an option
for people with schizophrenia. Most were too far removed from reality to profit from
it. Today, however, psychotherapy is helpful to many such patients (Kopelowicz et al.,
2008). By helping to relieve thought and perceptual disturbances, antipsychotic drugs
allow people with schizophrenia to learn about their disorder, participate actively
in therapy, think more clearly, and make changes in their behavior (Rosenberg &
Mueser, 2008; Beck et al., 2009). The most helpful forms of psychotherapy include
HOME 1– SEND EXPLORE
Can You Live with the Voices in Your Head?
BY DANIEL B. SMITH, NEW YORK INES, MARCH 25, 2007
,ngelo, a London-born scientist in his early 30s … vividly
recalls the day he began to hear voices. It was Jan. 7,
2001, and he had recently passed his Ph.D. oral exams in chem-
istry at an American university. . . . Angelo was walking home
from the laboratory when, all of a sudden, he heard two voices
in his head. “It was like hearing thoughts in my mind that were
not mine,” he explained recently. “They identified themselves as
Andrew and Oliver, two angels.” … What the angels said, to
Angelo’s horror, was that in the coming days, he would die of
a brain hemorrhage. Terrified, Angela hurried home and locked
himself into his apartment. For three long days he waited out his
fate, at which time his supervisor drove him to a local hospital,
where Angelo was admitted to the psychiatric word. It was his
first time under psychiatric care. He had never heard voices be-
fore. His diagnosis was schizophrenia with depressive overtones.
Angelo remembers his time at the hospital as the deepening
of a nightmare. . . Angelo did not react well to the antipsy-
chotic he’d been prescribed. . . . His voices remained strong
and disturbing. . . . Several days into his stay, Angelo’s parents
flew to the United States from London and took him back home.
More than six years later, Angelo still lives at his parents’
house. He currently takes a cocktail of antidepressants and
antipsychotics, with tolerable side effects. . . . The pills help
Angelo to manage his voices, but they have not been able to
eradicate them. . . . Despite these setbacks, Angelo. . . is eager
to discover new ways to combat his voices. Not long ago, he
found one. In November, his psychologist informed him of a
local support group for people who hear voices, from which he
thought Angelo might benefit. Angelo began to attend the group
late last year.
I first met Angelo at a meeting of the group in mid-January. (I
was given permission to sit in on the condition that I not divulge
the participants’ last names.). . . The gathering was small but
eclectic. In addition to the group’s facilitators—Jo Kutchinsky, an
occupational therapist, and Liana Kaiser, a social-work student—
five men and women assembled in a circle. . . . Besides Angelo,
there was Stewart, . . . Jenny, … Michelle, . . . and David. .
. . . When Kutchinsky opened the meeting by asking each
member to discuss the previous week’s experience hearing
voices, . . . most of the members spoke of their voices in the
way that comedians speak of mothers-in-law: burdensome and
irritating, but an inescapable part of life that you might as well
learn to deal with. When David’s name was called, he lifted his
head and discussed his struggle to accept his voices as part of
his consciousness. “I’ve learned over time that my voices can’t
be rejected,” he said. “No matter what I do, they won’t go
away. I have to find a way to live with them.” Jenny discussed
how keeping busy quieted her voices; she seemed to have taken
a remarkable number of adult-education courses. Michelle ex-
pressed her belief that her voices were nothing more exotic than
powerfully negative thoughts. “Negative thoughts are universal,”
she said. “Everyone has them. Everyone. What matters is how
you cope with them: that’s what counts.”
. . . Afterward I pulled [Angelo] aside and asked him what
he thought. “It’s interesting to hear people’s stories,” he said.
“Before I started coming, I hadn’t realized just how long some
people have suffered. I’ve heard voices for six years. Some
people have heard them for 15 or 20. . It was comforting, he
said, to speak at last with people who understood.
The meeting that I attended in London is one of dozens like
it affiliated with a small but influential grass-roots organization
known as Hearing Voices Network. . . . H.V.N. groups must

Schizophrenia :1/ 381
cognitive-behavioral therapy and two sociocultural interventions—family therapy and
social therapy. Often the various approaches are combined.
Cognitive-Behaviorai Therapy As you read earlier, the cognitive explanation for
schizophrenia starts with the premise that people with this disorder do indeed actually
hear voices (or experience other kinds of hallucinations) as a result of biologically trig-
gered sensations. According to this theory, the journey into schizophrenia takes shape
when individuals try to make sense of these strange sensations and conclude incorrectly
that the voices are coming from external sources, that they are being persecuted, or an-
other such notion.These misinterpretations are essentially delusions.
With this view of hallucinations and delusions in mind, an increasing number of
clinicians now employ a cognitive-behavioral treatment for schizophrenia that seeks
to change how individuals react to their hallucinatory experiences (Morrison, 2008;
Tarrier, 2008). The therapists believe that if individuals can be guided to interpret such
experiences in a more accurate way, they will not suffer the fear and confusion produced
1.•”.•”. ……………. ….. oder …… ■ •• …… ……………. ……….
“And only you can hear this whistle?”
accept all interpretations of auditory hallucinations as equally
valid. If an individual comes to a group claiming that he is hear-
ing the voice of the queen of England, and he finds this belief
useful, no attempt is made to divest him of it, but rather to figure
out what it means to him….
. H.V.N.’s brief „ . can be boiled down to two core posi-
tions. The first is that many more people hear voices, and hear
many more kinds of voices, than is usually assumed. The second
is that auditory hallucination—or “voice-hearing,” H.V.N.’s more
neutral preference—should be thought of not as a pathological
phenomenon in need of eradication but as a meaningful, inter-
pretable experience… .
The concept of “coping” is central to H.V.N., based on its be-
lief that people feel better not when their voices are extinguished
but when the person hearing voices learns to listen to his halluci-
nations without anguish. Jacqui Dillon, the national chairwoman
of H.V.N. . .. has heard voices for more than 30 years. . . But
she no longer heeds their commands or allows them to bother
her.. .
It was just before noon on a mild Friday in January when
the . . . hearing-voices group reconvened after a 15-minute cof-
fee break. . . . The participants were asked to . . . discuss [how
they cope with the voices in their heads]. . . . The coping strate-
gies that followed were … commonsensical lifestyle suggestions
geared toward improving one’s frame of mind, or sanding down
the edges of the experience’s effects. Liana chose “Exercise”;
Jenny chose “Religious Activities”; David chose “Pamper Your-
self.” … The most novel strategy, and the only one that seemed
to cause the group’s members to perk up, came under the
heading of “Mobile Phones.” If you have the temptation to yell
at your voices in public, one suggestion went, you should do
so with a phone to your ear. That way you can feel free to let
loose, and no one who sees you will think you’re crazy. Chris in
particular seemed to cozy to the suggestion. “I sometimes talk to
my voices in public,” he said matter-of-factly. “It’s very upsetting.
I have to bite my knuckles to suppress the urge.”
Participants in H.V.N.’s self-help groups take comfort
from strategies like these…. As for Angelo, his concern is
not to choose one option over another—but only to recover.
“I have found the group interesting,” Angelo wrote via e-mail
three weeks after we met. “It has made me realize that many
voice-hearers have had the problem for many yeors, and that
many . . . are able to hold down a job despite the voices. I
hope to do this myself. Perhaps the right combination of drugs
will make this possible.”
Copyright © 2007 New York Times. All rights reserved. Used by permission.

by delusional misinterpretations. Thus, the therapists use a combination of behavioral
and cognitive techniques:
1. They provide clients with education about the biological causes of
hallucinations.
They help clients learn more about the “comings and goings” of their own
hallucinations and delusions. The individuals learn, for example, to track
which kinds of situations trigger the voices in their heads.
3. The therapists challenge their clients’ inaccurate ideas about the power of
their hallucinations, such as their notions that the voices are all-powerful,
uncontrollable, and must be obeyed.The therapists also have the clients con-
duct behavioral experiments to put such notions to the test.What happens,
for example, if the clients occasionally resist following the orders from their
hallucinatory voices?
4. The therapists teach clients to more accurately interpret their hallucinations.
Clients may, for example, adopt alternative conclusions such as, “It’s not a
real voice, it’s my illness.”
5. The therapists teach clients techniques for coping with their unpleasant sen-
sations (hallucinations).The clients may learn ways to reduce the physical
arousal that accompanies hallucinations–applying special breathing and re-
laxation techniques, for example. Similarly, they may learn to distract them-
selves whenever hallucinations occur (Veiga-Martinez et al., 2008).
These behavioral and cognitive techniques often help schizophrenic individuals gain
more control over their hallucinations and reduce their delusional ideas. But they do not
eliminate the hallucinations. Can anything be done further to lessen the hallucinations’
unpleasant impact? Yes, say new – wave cognitive – behavioral therapists, including practitioners
of Acceptance and Commitment Therapy.
As you read in Chapter 2, new-wave cognitive-behavioral therapists believe that the
most useful goal of treatment is often to help clients accept their streams of problem-
atic thoughts rather than to judge them, act on them, or try to change them (Hayes
et al., 2004; Hayes, 2002). The therapists, for example, help highly anxious individuals
to become simply mindful of the worries that overrun their thinking and to accept such
negative thoughts as but harmless events of the mind (see page 50). Similarly, in cases
of schizophrenia, new-wave cognitive-behavioral therapists try to help clients become
detached and comfortable observers of their hallucinations—merely mindful of the un-
usual sensations and accepting of them—while the individuals otherwise move forward
with the events of their lives (Bach, 2007).
Studies indicate that the various forms of cognitive-behavioral treatment for schizo-
phrenia are often very helpful to clients (Morrison, 2008; Tarrier, 2008). Many clients
who receive such treatments report feeling less distressed by their hallucinations and
display fewer delusions. Indeed, the individuals are often able to shed
the diagnosis of schizophrenia. Rehospitalizations decrease by 50 percent
among clients treated with cognitive-behavioral therapy.
Family Ther py Over 50 percent of persons who are recovering from
schizophrenia and other severe mental disorders live with their families:
parents, siblings, spouses, or children (Barrowclough & Lobban, 2008). Such
situations create special pressures; even if family stress was not a factor in the
onset of the disorder, a patient’s recovery may be influenced greatly by the
reactions of his or her relatives at home.
Generally speaking, persons with schizophrenia who feel positively
toward their relatives do better in treatment (Camacho et al., 2005). As
you saw earlier, recovered patients living with relatives who display high
levels of expressed emotion — that is, relatives who are very critical, emotion-
ally overinvolved, and hostile—–often have a much higher relapse rate than
those living with more supportive relatives (Ritsner & Gibel, 2007; Janicak
382 :// CHAPTER 12

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Social Impact
Schizophrenia :1/ 383
et al., 2001). Moreover, for their part, family members may be upset greatly by the social
withdrawal and unusual behaviors of a relative with schizophrenia (Barrowclough &
Lobban, 2008).
To address such issues, clinicians now commonly include family therapy in their
treatment of schizophrenia, providing family members with guidance, training, practi-
cal advice, psychoeducation about the disorder, and emotional support and empathy
(Kopelowicz et al., 2008; Smerud & Rosenfarb, 2008). In family therapy, relatives de-
velop more realistic expectations and become more tolerant, less guilt-ridden, and more
willing to try new patterns of communication. Family therapy also helps the person
with schizophrenia cope with the pressures of family life, make better use of family
members, and avoid troublesome interactions. Research has found that family therapy—
particularly when it is combined with drug therapy—helps reduce tensions within the
family and so helps relapse rates go down (Barrowclough & Lobban, 2008).
The families of persons with schizophrenia and other severe mental disorders may
also turn to family support groups and family psychoeducational programs for encouragement
and advice (Jewell et al., 2009; Powder, 2004). In such programs, family members meet
with others in the same situation to share their thoughts and emotions, provide mutual
support, and learn about severe mental dysfunctioning.
Socid Therapy Many clinicians believe that the treatment of people with schizo-
phrenia should include techniques that address social and personal difficulties in the
clients’ lives.These clinicians offer practical advice; work with clients on problem solving,
decision making, and social skills; make sure that the clients are taking their medications
properly; and may even help them find work, financial assistance, appropriate health care,
and proper housing (Ridgway, 2008; Sherrer & O’Hare, 2008). Research finds that this
practical, active, and broad approach, called social therapy or personal therapy, does indeed
help keep people out of the hospital (Hogarty, 2002).
The Community Approach
The broadest approach for the treatment of schizophrenia and other severe mental dis-
orders is the community approach. In 1963, partly in response to the terrible conditions in
public mental institutions and partly because of the development of antipsychotic drugs,
the U.S. government ordered that patients be released and treated in the community.
Congress passed the Community Mental Health Act, which provided that patients with
psychological disorders were to receive a range of mental health services—outpatient
therapy, inpatient treatment, emergency care, preventive care, and aftercare—in their
communities rather than being transported to institutions far from home. The act was
aimed at a variety of psychological disorders, but patients diagnosed with schizophrenia,
especially those who had been institutionalized for years, were affected most. Other
countries around the world put similar community treatment programs into action
shortly thereafter (Wiley-Exley, 2007).
Thus began four decades of deinstitutionalization, an exodus of hundreds of
thousands of patients with schizophrenia and other long-term mental disorders from
state institutions into the community. On a given day in 1955 close to 600,000 patients
were living in state institutions; today only around 60,000 patients reside in those set-
tings (Salzer et al., 2006; Torrey, 2001). Clinicians have learned that patients recovering
from severe mental disorders can profit greatly from community programs. As you will
see, however, the actual quality of community care for these people has often been in-
adequate throughout the United States. The result is a “revolving door” syndrome for
many patients: They are released to the community, readmitted to an institution within
months, released a second time, admitted yet again, and so on, over and over (Sadock &
Sadock, 2007; Torrey, 2001).
What Are the Features of Effective Comrnunily Care? People recovering
from schizophrenia and other severe mental disorders need medication, psychotherapy,
help in handling daily responsibilities, guidance in making decisions, training in social
odeinstitutionalizationoThe discharge
of large numbers of patients from long-
term institutional care so that they might
be treated in community programs.

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skills, residential supervision, and vocational counseling—a combination of services
sometimes called assertive community treatment (DeLuca, Moser, & Bond, 2008; Coldwell
& Bender, 2007).Those whose communities help them meet these needs make greater
progress than those living in other communities. Some of the key features of effective
community care programs are (1) coordination of patient services, (2) short-term hos-
pitalization, (3) partial hospitalization, (4) supervised residencies, and (5) occupational
training.
COORDINATED SERVICES When the Community Mental Health Act was first passed, it was
expected that community care would be provided by a community mental health
center, a treatment facility that would supply medication, psychotherapy, and inpatient
emergency care to people with severe disturbances, as well as coordinate the services
offered by other community agencies. When community mental health centers are
available and do provide these services, patients with schizophrenia and other severe dis-
orders often make significant progress (Rapp & Goscha, 2008). Coordination of services
is particularly important for mentally ill chemical abusers (MICAs), patients with psychotic
disorders as well as substance-related disorders (Buckley & Meyer, 2009).
SHORT- TERM HOSPITALIZATION When people develop severe psychotic symptoms, today’s
clinicians first try to treat them on an outpatient basis, usually with a combination of
antipsychotic medication and psychotherapy (Addington & Addington, 2008). If this ap-
proach fails, short- term hospitalization that lasts a few weeks (rather than months or years)
may be tried (Soliman et al., 2008). Soon after the patients improve, they are released for
aftercare, a general term for follow-up care and treatment in the community.
PARTIAL HOSPITALIZATION People’s needs may fall between full hospitalization and outpa-
tient therapy, and so some communities offer day centers or day hospitals, all-day
programs in which patients return to their homes for the night.The day centers provide
patients with daily supervised activities, therapy, and programs to
improve social skills. People recovering from severe mental disor-
ders in day centers often do better than those who spend extended
periods in a hospital or in traditional outpatient therapy (Mayahara
& Ito, 2002; Yoshimasu et al., 2002). Another kind of institution
that has become popular is the semihospital, or residential crisis center:
Semihospitals are houses or other structures in the community that
provide 24-hour nursing care for people with severe mental disor-
ders (Soliman et al., 2008; Torrey, 2001).
SUPERVISED RESIDENCES Many people do not require hospitalization
but, at the same time, are unable to live alone or with their families.
Halfway houses, also known as crisis houses or group homes, often
serve individuals well (Levy et al., 2005). Such residences may shel-
ter between one and two dozen people.The live-in staff usually are
paraprofessionals— lay people who receive training and ongoing su-
pervision from outside mental health professionals. The houses are
usually run with a milieu therapy philosophy that emphasizes mu-
tual support, resident responsibility, and self-government. Research
indicates that halfway houses help many people recovering from
schizophrenia and other severe disorders adjust to community life
and avoid rehospitalization (Hanson et al., 2002; McGuire, 2000).
OCCUPATIONAL TRAINING Paid employment provides income, inde-
pendence, self-respect, and the stimulation of working with others.
It also brings companionship and order to one’s daily life. For these
reasons, occupational training and placement are important services
for people with severe mental disorders (Becker, 2008; DeLuca
et al., 2008).
Many people recovering from such disorders receive occupa-
tional training in a sheltered workshop—a supervised workplace
384 ://CHAPTER 12

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Schizophrenia :1/ 385
for employees who are not ready for competitive or complicated jobs. For some, the
sheltered workshop becomes a permanent workplace. For others, it is an important
step toward better-paying and more demanding employment or a return to a previous
job (Becker, 2008; Chalamat et al., 2005). In the United States, however, occupational
training is not consistently available to people with severe mental disorders (Honberg,
2005; Blyler, 2003).
How Has Community Treatment Failed? There is no doubt that effective
community programs can help people with schizophrenia and other severe mental
disorders recover. However, fewer than half of all the people who need them receive
appropriate community mental health services (Lehman et al., 2004; McGuire, 2000). In
fact, in any given year, 40 to 60 percent of all people with schizophrenia and other severe
mental disorders receive no treatment at all (Wang et al., 2002;Torrey, 2001).Two factors
are primarily responsible: poor coordination of services and shortage of services.
POOR COORDINATION OF SERVICES The various mental health agencies in a community
often fail to communicate with one another (Leshner et al., 1992). There may be an
opening at a nearby halfway house, for example, and the therapist at the community
mental health center may not know about it. In addition, even within a community
agency a patient may not have continuing contacts with the same staff members and
may fail to receive consistent services. Still another problem is poor communication
between state hospitals and community mental health centers, particularly at times of
hospital discharge (Torrey, 2001).
It is not surprising, then, that a growing number of community therapists have be-
come case managers for people with schizophrenia and other severe mental disorders
(Rapp & Goscha, 2008; Sherrer & O’Hare, 2008). Like the social therapists described
earlier, they offer therapy and advice, teach problem-solving and social skills, ensure that
medications are being taken properly, and keep an eye on possible health care needs.
In addition, they try to coordinate available community services, guide clients through
the community system, and, perhaps most importantly, help protect clients’ legal rights.
Many professionals now believe that effective case management is the key to success for
a community program.
SHORTAGE OF SERVICES The number of community programs—from community mental
health centers to halfway houses and sheltered workshops—available to people with
severe mental disorders falls woefully short ( Julien, 2008). In addition, the community
°community mental health center°
A treatment facility that provides medi-
cation, psychotherapy, and emergency
care for psychological problems and
coordinates treatment in the community.
eaftercarecA program of posthospital-
ization care and treatment in the
community.
oday center°A program that offers
hospital-like treatment during the day
only. Also known as a day hospital.
Gila way house°A residence for peo-
ple with schizophrenia or other severe
problems, often staffed by paraprofes-
sionals. Also known as a group home or
crisis house.
°sheltered workshop0A supervised
workplace for people who are not yet
ready for competitive jobs.
case managereA community thera-
pist who offers a full range of services
for people with schizophrenia or other
severe disorders, including therapy,
advice, medication, guidance, and pro-
tection of patients’ rights.

388 ://CHAPTER 12
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How Are Schizophrenia and Other Severe Mental Disorders Treated?
For more than half of the twentieth century, the main treatment for schizophrenia
and other severe mental disorders was institutionalization and custodial care. In
the 1950s two in-hospital approaches were developed, milieu therapy and token
economy programs. They often brought some improvement. The discovery of anti-
psychotic drugs in the 1950s revolutionized the treatment of schizophrenia and
other disorders marked by psychosis. Today they are almost always a part of
treatment. Theorists believe that the first generation of antipsychotic drugs operate
officials continue to press to make it more available. In addition, a number of national in-
terest groups have formed in countries around the world that push for better community
treatment (Frese, 2008; Archibald, 2007; Torrey, 2001). In the United States, for example,
the NationalAiliance on Mental Illness began in 1979 with 300 members and has expanded
to around 220,000 members in more than 1,100 chapters (NAMI, 2008). Made up
largely of relatives of people with severe mental disorders, this group has become both
a source of support for its members and a powerful lobbying force in state legislatures;
additionally, it has pressured community mental health centers to treat more persons
with schizophrenia and other severe mental disorders.
Today community care is a major feature of treatment for people recovering from
severe mental disorders in countries around the world (Wiley-Exley, 2007). Both in the
United States and abroad, well-coordinated community treatment is seen as an impor-
tant part of the solution to the problem of severe mental dysfunctioning (DeLuca et al.,
2008; Rapp & Goscha, 2008).

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by reducing excessive dopamine activity in the brain. These “conventional” anti-
psychotic drugs reduce the positive symptoms of schizophrenia more completely, or
more quickly, than the negative symptoms.
The conventional antipsychotic drugs can also produce dramatic unwanted
effects, particularly movement abnormalities. One such effect, tardive dyskinesia,
apparently occurs in more than 10 percent of the people who take conventional
antipsychotic drugs for an extended time and can be difficult or impossible to
eliminate. Recently, “atypical” antipsychotic drugs have been developed, which
seem to be more effective than the conventional drugs and to cause fewer or no
extrapyramidal effects.
Today psychotherapy is often used successfully in combination with antipsy-
chotic drugs. Helpful forms include cognitive-behavioral therapy, family therapy,
and social therapy.
A community approach to the treatment of schizophrenia and other severe
mental disorders began in the 1960s, when a policy of deinstitutionalization in the
United States brought about a mass exodus of hundreds of thousands of patients
from state institutions into the community. Among the key elements of effective
community care programs are coordination of patient services by a community
mental health center, short-term hospitalization (followed by aftercare), day centers,
halfway houses, and occupational training. However, the quality and funding of
community care for people with schizophrenia and other severe mental disorders
have been inadequate throughout the United States, often resulting in a “revolving
door” syndrome. One result is that many people with such disorders are now home-
less or in jail.

Schizophrenia :1/ 389

PUTTING IT… together
An important Lesson
Schizophrenia—a bizarre and frightening disorder—was studied intensively throughout
the twentieth century. Only since the discovery of antipsychotic drugs, however, have
clinicians acquired practical insight into its causes. As with most other psychologi-
cal disorders, clinical theorists now believe that schizophrenia is probably caused by
a combination of factors. At the same time, researchers have been far more successful
in identifying the biological influences than the psychological and sociocultural ones.
While biological investigations have closed in on specific genes, abnormalities in brain
biochemistry and structure, and even viral infections, most of the psychological and
sociocultural research has been able to cite only general factors, such as the roles of
family conflict and diagnostic labeling. Clearly, researchers must identify psychological
and sociocultural factors with greater precision if we are to gain a full understanding
of the disorder.
The treatment picture for schizophrenia and other disorders marked by psychosis
has also improved in recent decades.After years of frustration and failure, clinicians now
have an arsenal of weapons to use against these disorders—medication, institutional
programs, psychotherapy, and community programs. It has become very clear that anti-
psychotic medications can open the door for recovery, but in most cases other kinds of
treatment are also needed to help the recovery process along. The various approaches
must be combined in a way that meets each individual’s specific needs.
Working with schizophrenia and other severe mental disorders has taught clinicians
an important lesson: No matter how compelling the evidence for biological causa-
tion may be, a strictly biological approach to the treatment of psychological disorders
is a mistake more often than not. Largely on the basis of pharmacological discoveries,
hundreds of thousands of patients with schizophrenia and other severe mental disorders

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390 .//C HAPTER 12
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were released to their communities beginning in the 1960s. Little attention was paid to
the psychological and sociocultural needs of these individuals, and many of them have
been trapped in their pathology ever since. Clinicians must remember this lesson, espe-
cially in today’s climate, when managed care and government priorities often promote
medication as the sole treatment for psychological problems.
When the pioneering clinical researcher Emil Kraepelin described schizophrenia
at the end of the nineteenth century, he estimated that only 13 percent of its victims
ever improved. Today, even with shortages in community care, many more such indi-
viduals show improvement. Certainly the clinical field has advanced considerately since
Kraepelin’s day, yet it still has far to go. It is unacceptable that the majority of people with
this and other severe mental disorders receive few or none of the effective community
interventions that have been developed, worse still that tens of thousands have become
homeless. It is now up to clinical professionals, along with public officials, to address the
needs of all people with schizophrenia and other severe mental disorders.
1. The psychodynamic explanations of

: schizophrenia reflect a long-standing

ce: tradition in the clinical field and in

404 society of pointing to parents as key
causes of mental disorders, even in
cases where evidence is lacking.
Why are parents and family life so
likely to be blamed? p. 370

7;1 than white Americans to receive a

.5- diagnosis of schizophrenia and to be
hospitalized for the disorder. Some

/•• theorists suggest that bias by diag-

7: nosticians may contribute to these
patterns. How and why specifically
might bias produce such race-linked
diagnostic and treatment differences?
pp. 371 -372
3. Why have more people with
schizophrenia than people with
other disorders been the victims
of mistreatment (lobotomy or dein-
stitutionalization, for example)?
pp. 373-388
4. Although both cognitive-behavioral
therapists and self-help programs
such as Hearing Voices Network
believe that people who hallucinate
should “accept” the voices that
spring forth from their brains, there
are differences between the role and
meaning that they each assign to
hallucinations. What are these differ-
ences, and why are they important?
pp. 380-382
5. The public often perceives people
with schizophrenia as dangerous
and violent even though most persons
with this disorder are far from dan-
gerous. Why does the public hold
such a perception, and how can it be
changed? pp. 389, 371
_•••• ■•••••••
2. African Americans are more likely
OF. 1 • • .6″ n • • p w• • .• 00 000 . :• e. • ,• • • 4,..• • • • • ;* a; • …A •
\\■ KEY TEPIS///
schizophrenia, p. 357
psychosis, p. 357
positive symptom, p. 360
delusion, p. 360
formal thought disorder, p. 360
loose associations, p. 360
hallucination, p. 361
inappropriate affect, p. 362
negative symptoms, p. 362
alogicr, p. 362
flat affect, p. 362
avolition, p. 362
psychomotor symptom, p. 363
• •, •, * • • • •
catatonia, p. 363
diathesis-stress relationship, p. 364
polygenic disorder, p. 366
dopamine hypothesis, p. 366
Parkinson’s disease, p. 366
schizophrenogenic mother, p. 370
expressed emotion, p. 372
milieu therapy, p. 375
token economy program, p. 376
conventional antipsychotic drugs, p. 377
atypical antipsychotic drugs, p. 377
extrapyramidol effects, p. 379
tardive dyskinesia, p. 379
P ….off
social therapy, p. 383
deinstitutionalization, p. 383
assertive community treatment, p. 384
community mental health center, p. 384
mentally ill chemical abuser (MICA),
p. 384
aftercare, p. 384
day center, p. 384
halfway house, p. 384
sheltered workshop, p. 384
case manager, p. 385

Schizophrenia 391
0..”
7,2
…-A,
/A!
7-, 2. What are the positive, negative,
A
../..,. and psychomotor symptoms of
/7″.”,… schizophrenia? pp. 360-363
3. What are the five types of schizo-
es: phrenia identified by DSM-1V-TR?
pp. 363-364
40:.
7f. 4. Describe the genetic, biochemical,
Fe. brain structure, and viral explana-
tions of schizophrenia, and discuss
how they have been supported in
.47.0 research. pp. 364-370
pp. 370-372
6. Describe institutional care for
people with schizophrenia and
other severe mental disorders over
the course of the twentieth century.
How effective are the token econ-
omy and milieu treatment
programs? pp. 373-377
7. How do antipsychotic drugs oper-
ate on the brain, and how effective
are they in the treatment of schizo-
phrenia? What are the unwanted
effects of these drugs? pp. 377-380
8. What kinds of psychotherapy seem
to help people with schizophrenia
and other disorders marked by
psychosis? pp. 3 8 0-3 83
9. What is deinstitutionalization?
What features of community care
seem critical for helping people
with schizophrenia and other severe
mental disorders? pp. 383-385
10. How and why has the community
mental health approach been
inadequate for people with severe
mental disorders? pp. 3 85-3 8 8
74: V/2;70121.”; ” • “”e5.07”
,-, •
1. What is schizophrenia, and how 5. What are the key features of the
prevalent is it? What is its rela- psychodynamic, cognitive, multicul-
tion to socioeconomic class and tural, social labeling, and family
gender? pp. 357-358 explanations of schizophrenia?
\\\ r)UIGK r)tili///
‘
Search the Fundamentals of Abnormal Psychology Video Tool Kit
www.worthpublishers.corn/apvtk
A Chapter 12 Video Cases
Hallucinations: ‘The Voices Won’t Leave Me Alone”
A Clinical Picture of Schizophrenia
Postpartum Psychosis: Why Did Andrea Yates Kill Her Children?
Antipsychotic Drugs: Before and After
Treating MICAs: ‘Wild Man of West 96th Street”
John Nash’s Beautiful Mind
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Presentation: Hypothesis Testing and Using Excel to Perform Z Tests

Before we get started, I’d like to review some concepts that you have covered so far in your course reading. First, let’s look at the difference between a population and a sample. A population is the complete set of people, animals or other objects that have something in common. A sample is a subgroup, or small part, of the population. The sample is representative of population, and researchers draw conclusions about a population based on information from a sample. When we talk about populations and samples, there are three concepts that are important to keep in mind. First, the mean for each is represented by a different symbol. Second, the standard deviation for each is also represented by a different symbol. Finally, we can talk about a distribution for a population or a distribution for a sample. Each of these distributions has certain characteristics. For this course, we usually assume that these distributions are normal distributions.

You have also read much about hypothesis testing, and the difference between the null hypothesis and the research, or alternative, hypothesis. The null hypothesis is the one that states that there is no difference between a given value and the corresponding population value itself. It is represented as H sub0. The research, or alternative, hypothesis states that there is some kind of difference between a given value and the corresponding population value itself. There are two important things to remember about the alternative hypothesis. First, it can be either directional or non-directional. A directional hypothesis results in a one-tailed hypothesis test; and a non-directional hypothesis results in a two-tailed hypothesis test. Second, starting now, it will be important to determine the alpha value associated with your hypothesis test. This is equal to the chance of making a Type I error, or rejecting the null hypothesis when it’s actually true. Alpha is always set ahead of time and is usually set to either .05, .01, or .001.

Hypotheses can be written out in words and in symbols. Here, I’m going to show you how to do both. Here is a sample research situation: A middle school counselor has noticed an increase in the number of referrals for ADHD in her school. She wonders whether this number is greater, or higher, than the number of referrals in the general population. She does a review of current research and finds that the general population of middle schools has a mean number of referrals equal to 3 per month and a standard deviation of 1. Based on this information, let’s write out our hypotheses using sentences and then using symbols.

My null hypothesis can be stated as seen here: The number of referrals at this school is equal to or less than the number of referrals in the general population. Using symbols, I can restate the null as seen here (mu is less than or equal to 3). It will help you to remember that the null hypothesis will always contain an equal sign, since it is the statement that there is no difference between your sample and population values—that, in essence, they are equal.

My research hypothesis can be stated as seen here: The number of referrals at this school is greater than the number of referrals in the general population. Using symbols, I can restate the research hypothesis as seen here (mu is greater than 3). This is an example of a directional hypothesis—that is, it predicts that the difference will be in a certain direction. This means that the we would use a one-tailed hypothesis test, seeking for a difference that is greater than the population average. Thus, we will be looking in the right-hand tail of the distribution for our critical values. It will help you to remember that the research hypothesis will never contain an equal sign, since it is the statement that there is some type of difference between your sample and population values—that, in other words, they are not equal. Now that we’ve reviewed some of this basic material, let’s move on to our special topic for this week.

It is usually the case that researchers run studies using a sample of participants instead of one individual. However, most of the work we’ve done up to this point has involved single scores only, such as one person’s number of minutes of exercise, or one person’s SAT score. In these situations, we have tested hypotheses based on a distribution of single scores. However, when we want to look at the performance of a sample compared to the population, we can not test a hypothesis based on a distribution of single scores—rather, we have to look at a distribution of sample means. What does this mean, and why is this true?

Imagine that you are trying to determine how an entire 4th grade class performed on an achievement test as compared to the national average of all 4th grade classes. As we have already learned, the best way to describe a sample of scores is to use summary statistics, such as the mean and standard deviation. So, you compute the mean and standard deviation of your sample 4th grade class. Then, you decide to see how your class did by comparing the mean class score to a distribution of individual children’s scores on the achievement test. What’s wrong with this decision? In everyday language, it’s a meaningless comparison. It would be a bit like using a yardstick to measure the width of a grain of rice. When trying to determine the chance that a certain individual score will occur, it makes sense to look at a distribution of individual scores. However, when trying to determine the chance of a certain mean score occurring that comes from a sample of more than one person, it makes sense to look at a distribution of other mean scores from samples with the same number of individuals in them.

This particular type of distribution is called the distribution of sample means. It is also commonly called the sampling distribution of sample means, or the sampling distribution of the mean. Regardless of what it’s called, however, it is important to remember that each number represented on the distribution is not the score of a single individual, as we have been working with up until now. Each number on the distribution of sample means is the mean of some sample of a given size, like samples consisting of 100 individuals each, for example.

In our example, let’s say our 4th grade class has 31 students. This means that the number or N of our sample is 31. We take the mean achievement test score for this 4th grade class, which turns out to be 89. In order to test how likely it is that this score would occur in the general population, and to test whether our class is at the national average, or is doing better or worse, we now have to compare the mean score of the 4th grade class to an appropriate distribution of sample means. This distribution is the distribution of mean scores of samples of size N = 31.

I want to address one point that often confuses people early on in this process. You might be thinking, “Surely each testing agency doesn’t publish distributions for every possible sample size, like 25 students or 138 students and every number in between. This is true. Any comparison distribution of sample means, at this point in our course, will be one big distribution of the means in the general population, like “4th grade classes”. When we begin our hypothesis test, however, the math that we use to compute certain values for this test takes into account the size of our sample as well as the population values, so you can use the same population information for samples of different sizes. We can use the same population information to ask questions about samples of size 31, like our example 4th grade class, or of size 100. We’ll get into these ideas in more detail later, but it helps to start thinking about it now.

Now that we’ve learned what the distribution of sample means is, let’s look at its characteristics. The following things are always true about any distribution of sample means: the mean of the distribution of sample means is the same as the population mean. The second characteristic explains in more detail what was mentioned in the previous slide about sample sizes. The variance of the distribution of sample means is equal to the population variance divided by the number in the sample, or N. Notice that the variance will change depending on the sample size. This is how we modify the population information to take into account a particular sample size, without constructing hundreds of separate distributions for samples of all possible sizes.

Third, the standard deviation of the distribution of sample means is called the standard error of the mean and is equal to the square root of the variance from number 2. Here you see the standard error of the mean written in two different but equivalent ways. Finally, the shape of the distribution of sample means is normal for samples that are greater than 30 or if the population is known to be normally distributed.

Hypothesis testing using sample means is carried out in much the same way as hypothesis testing for individual scores. The steps remain the same, but some changes need to be made in how we compute and compare scores. First, the comparison distribution becomes the distribution of sample means. It is this distribution that we will use to construct the null hypothesis for any research question. Second, instead of using a simple standard deviation, we have to compute the standard error of the mean, which is basically a standard deviation that takes into account the sample size. Finally, the values used for computing the test statistic will change to reflect our new type of distribution.

The test statistic we will be looking at in this presentation is useful for samples of size 30 or more, when the population information is known. It is called a Z test. Just as a Z score is useful for telling us where an individual score lies along a given distribution, the Z test is a way of doing the same thing, but for sample means instead of individual scores. The formula for calculating Z is very similar to the one you already know, and the steps of the hypothesis testing process remain virtually identical but with different values. Let’s look at how this process works.

Here we see the first two steps of the Z test. First, as before, write out your null and research hypotheses based on your research question. Remember to use evaluators such as “greater than” or “equal to” in your statements. Second, determine the characteristics of your comparison distribution. As we mentioned, the comparison distribution is now the distribution of sample means. Based on what we learned about this distribution, we know that the mean of the distribution of sample means is equal to the population mean, which is normally given. We also know that the standard deviation of the distribution of sample means is the standard error of the mean, so we compute this based on the formula we learned.

Third, we want to determine the cut-off score, or critical value, that marks the rejection region of our hypothesis test. Our final decision to reject the null hypothesis or not depends on where our sample’s mean lies in relation to this cut-off score. (Z stuff here) Fourth, we determine our sample’s score on the comparison distribution (sample’s Z stuff here). Finally, we can put all of our information together and decide whether or not to reject the null hypothesis. If our sample’s Z score lies outside of the cut-off in the expected direction, then we say that our results are unlikely if the null hypothesis were true, so we decide to reject the null hypothesis and support the research, or alternative, hypothesis. If our sample’s Z score lies within the acceptance region, then we decide not to reject the null hypothesis.

A common method used for talking about the significance of results is the p value. You will see this in almost every journal article that reports results of hypothesis tests. Your text briefly introduces you to P values, but let’s look at them a little more closely so that you’ll know what they are and what they mean. You will be required to compute them as part of your Excel homework. If you recall from an earlier presentation, the area under the normal curve is equal to one. We used z scores to compute the percentage or probability of certain values based on this property of the normal curve. If given any value along the curve, you can determine the probability of scores higher than this value, less than this value, or between this value and another value. For example, you may remember that the probability of getting a Z score higher than 0 is equal to 50%, or .5.

P values are exactly this—they represent the probability of a certain score occurring based on a given distribution, in this case the distribution of sample means. Here we see the steps for determining p values. First, determine the cut-off, or critical, p value, which the researcher sets at the beginning of the study. Most critical p values will equal .05, .01, or .001. Second, calculate your sample’s Z score in the usual way. Third, find the probability associated with your Z score using either a Normal Curve Table or a statistics computer program. If your sample result’s p value is less than the critical p value (of .05 or .01), then you can claim that your results are statistically significant. P-values will be covered further in the Excel portion of this presentation.

After you have completed the Z test and computed the p value of your result, you are ready to make a decision about whether to reject the null hypothesis or not. If your results are statistically significant, you can say the following: “Based on these results, we are able to reject the null hypothesis and support the research hypothesis that there is a true difference between the mean of our sample and the population mean.” If your results are not statistically significant, you can say: “Based on these results, there is not enough evidence to support the research hypothesis, so we retain the null hypothesis.”

We are now going to look at performing Z tests in Excel. In order to do this, we are going to use an example research scenario and data set. A family systems psychologist is interested in the amount of television that households in his town watch per day. He knows that the population mean for minutes of television watched per day per household in his state is 20. He wonders whether families in his town watch more television than the general population. He decides to interview a sample of 55 households in his town and record the number of minutes of television watched per day.

The first step is to create a results table in which we can enter the different values necessary to run the hypothesis test and its results. Here you see one such table with many different entries. We will go over these in steps throughout the rest of the presentation.

The first step of any hypothesis testing process is to state the null and alternative, or research, hypotheses. In our Excel table, we will use symbols. This will help us determine whether the test is one- or two-tailed, and if it’s one-tailed, the direction of the predicted difference. The psychologist wants to know whether the minutes of television families in his town watch is greater than the population mean, which is 75 minutes. Restating the question as a hypothesis, the research hypothesis is that families in this town watch more than 75 minutes of television per day. This is shown in the table as “mu is greater than 75.” The null hypothesis is the hypothesis that includes a statement that there is no difference between the two populations. This requires the use of the equal sign. Since our psychologist is only interested in whether the town’s mean is greater than the population mean, the null hypothesis also includes the less than symbol. We can now tell easily from looking at our symbols that our hypothesis is directional—it is only interested in one type of difference, a difference of “greater than 75.” So this tells us that our test is one-tailed. Specifically, we will be interested in the right-hand tail of the distribution, in values that are greater than the mean.

Next, we can fill in the information that we already know based on previous research and given in the research question. Using some of these values, we can compute the standard error of the mean, which is necessary because we are conducting a hypothesis test using the distribution of sample means. The easiest method to do this is to enter a formula manually, and the formula shown is the one we want to use in Excel. To input this formula, click in the desired cell and type the equal sign, then your population standard deviation (in this case, 20), then a forward slash, then the letters “SQRT” followed by the sample size in parentheses, in this case 55. “SQRT” is a function that tells Excel to compute the square root of the number that comes after it.

Hit enter, and the resulting value of about 2.697 shows up. Next, we want to calculate our sample mean and fill in our chosen alpha level. Compute the sample mean in the usual way, calculating the average of the raw sample data using the AVERAGE function. The psychologist wants to test this hypothesis at the .05 level, so we type this in the appropriate cell for the alpha level. Now it is time to compute the critical Z value, or cut-off score, that will mark our rejection region. Since our hypothesis test is one-tailed and is interested in a mean that is greater than the population mean, any Z score that is greater than our critical value will be considered statistically significant.

The Excel function that helps us compute z scores in this manner is the “normsinv” function. This function basically returns the Z score from the standard normal distribution that corresponds to a certain probability. The syntax for the function is “Normsinv” followed by the probability level in parentheses. The probability level has to do with the alpha level. With an alpha equal to .05 and a one-tailed test, there are two options depending on whether the test is left-tailed or right-tailed. If left-tailed, then the probability associated with the test is simply equal to alpha, or .05. However, if the test is right-tailed, the probability must include all of the area under the normal curve up to the last 5% in the tail. This is equal to 1 minus alpha, or .95 in this case. Since our test is right-tailed and our alpha is .05, we want to use a probability of .95 in our formula. It is important to remember this distinction between the two tails when running a hypothesis test. The procedure for a two-tailed test is similar except that you would divide alpha in half, then find the Z score associated with this probability in both tails of the distribution. However, in this section we will focus on one-tailed tests.

The resulting formula is “equals normisinv (.95)”. When we type this in to the appropriate cell, it returns a Z score of 1.64 as seen here. This is our critical value. If our sample’s Z score is greater than 1.64, we will be able to reject the null hypothesis that there is no difference between the means, and accept our research hypothesis that the families in Any Town, USA watch more television per day than families in the general population.

To compute this sample Z score, we type in the Z score formula with the values we already know. This formula is the sample mean minus the population mean divided by the standard error of the mean, just as we went over earlier in the presentation. So, filling in these values in Excel formula style, exactly as shown here, we have our sample Z score of 1.146. Of course, when filling in the formula in Excel, you can simply click on the cells containing the values instead of typing in the values yourself, as we’ve gone over before. We can now compare our two Z scores. Remember that in order to reject the null and support the research hypothesis, our sample’s Z score had to be greater than the critical Z cut-off score. Since 1.146 is not greater than 1.64, we can not reject the null hypothesis because our sample’s score does not lie in the rejection region. We can also say that our research hypothesis is not supported by the data.

Finally, we can calculate p value of our sample and compare it to the pre-determined value of p = .05. With p-values, unlike Z scores, you will always be searching for a sample p value that is less than the critical p-value, whether your test is in the right tail, the left tail, or both tails of the distribution. That is, the one-tailed hypothesis is tested at the .05 level of significance, so if our p value is less than .05, we can consider the results to be statistically significant. Well, we’ve already seen that the Z score of our sample does not support the research hypothesis, so it is pretty much guaranteed that our p value is going to be greater than .05 and not statistically significant. Let’s see if this is the case.

First, enter the critical p value in the appropriate cell as shown. We are running a one-tailed test at the .05 level, so this value is .05. Next, we want to calculate the sample’s p value to see if it is less than the critical p value. As with the Z score, the way this Excel formula is entered depends on which tail of the distribution you are interested in.

The function we want to use to compute our sample’s p value is the “normSdist” function. This function returns the area under the standard normal curve up to a certain Z score. You will recall that a couple of weeks ago you learned how to use the Normal Curve Tables to compute areas or percentages under the normal curve that correspond to certain Z scores. This function does exactly the same thing, but without a normal curve table. If your hypothesis test is left-tailed, the formula is entered as shown, ‘equals normsdist” followed by your sample’s Z score in parentheses. This will give the area under the normal curve that lies to the left of the sample’s Z score. Since our test is right-tailed, however, we are only interested in the area in the tail which is to the right of our sample’s Z score. Because the NormSDist function returns only the area to the left of the Z score, we must subtract the value from one in order to compute the area that is to the right of the Z score. This formula is entered as shown above, with an extra set of parentheses around the entire formula.

So, after entering our formula to compute the p value for a right-tailed test, we find that our sample’s p value is about .126 as shown. Our sample’s p value is greater than .05, not less than or equal to. This means that there is a low chance that our sample came from a distribution that is different from the distribution of the general population. In other words, based on this study, the psychologist can state that the results are not statistically significant and that the mean of minutes of TV watched in his town may not be truly different from the mean of the general population. The null hypothesis is retained, and the research hypothesis is not supported based on the data from this sample.

It is always important to remember that hypothesis tests are statements about the likelihood of certain statements being true or not. The results of hypothesis tests should never be presented as absolutes. Statements like “These results prove the research hypothesis” or “The null hypothesis is false” are not acceptable, because one study or even ten studies does not prove anything beyond the shadow of a doubt when dealing with statistics. Remember that a hypothesis test deals with probabilities, and there is always the possibility of a Type I or Type II error, of accepting or rejecting the wrong hypothesis when the other one is actually true. So be cautious and conscientious when presenting results, using statements like “The evidence supports the research hypothesis” or “Based on these findings, we can not reject the null hypothesis.”

Presentation: Confidence Intervals and Computing Confidence Intervals in Excel

In many instances, you may wish to use information from a sample to estimate a population mean that is unknown. This is how surveys usually work. For example, an organization that polls voters concerning their political opinions is trying to get an idea of the political opinions of the general population based on a smaller sample. This is often done with the presidential approval rating. About 1,000 people provide answers for this survey, and these results are then used to estimate how much the American public in general approves of the president. In this situation, the general approval rating in the population is unknown. The sample information helps provide a basic estimate. When the mean of a population is unknown, it can be proven that the best estimate for this population mean is the sample mean.

However, most social scientists are not comfortable with providing just one number as a point estimate of the population mean. Rather, it is often the case that researchers will report a range of values called a confidence interval. A confidence interval is a range of possible means that is likely to contain the population mean. This range is based on the scores from a sample, so, as you have probably figured out by now, confidence intervals are constructed using the distribution of sample means (which is covered in an earlier presentation). A confidence interval is also useful even if you know the population mean, to see whether or not the confidence interval based on your sample includes the actual population mean or not.

Confidence intervals are bound at the high and low ends by confidence limits. These are the numbers that mark the beginning and end of the interval. Confidence intervals can have different widths depending on how confident you want to be that your range contains the actual population mean: the wider the confidence interval, the more certain you can be that your range of means is likely to contain the population mean. A narrower interval is less likely to contain the true population mean. Why is this true?

Imagine that you are fishing over the side of a boat using a net. In particular, you’ve heard stories about a giant trout that lives in these waters, and you would like to increase your chances of catching this trout among all of the other fish in your net. You have a choice of two nets: one is somewhat large, and the other is really large. Which net is more likely to catch the giant trout among all of the other fish in your net? The larger the net, the more confident you can be that your net might contain that giant trout when you pull it out of the water. Confidence intervals work in basically the same way: the wider the interval, the more likely that it will contain the true population mean among all of the possible means in the interval.

When we construct a confidence interval using the information from a sample, we want to give an idea of the level or amount of confidence we have that our interval might contain the true population mean. In research, it is common to use numbers like 90%, 95% and 99% to talk about confidence intervals. That is, if we construct a 95% confidence interval, roughly speaking, we can say that we are 95% sure that this interval contains the true population mean. It doesn’t necessarily mean that it will. Notice that we are only 95% sure—there is still a 5% chance that our interval will not contain the population mean. Just because we have a bigger net doesn’t guarantee that we will catch the giant fish. Now, if we decided to construct a 99% confidence interval, the chances of our interval containing the population mean increase to the point that we can say we are now 99% sure that our interval contains the population mean. In other words, the 99% confidence interval is wider—it’s the really big net.

Now that we understand basically what a confidence interval is, let’s look at how to construct one. Remember that we are looking at an interval that contains a range of sample means, so we are working with the distribution of sample means. In our first example, the mean presidential approval rating from our sample of 1,000 people would be our starting point. Here you can see all of the information that you need in order to construct a confidence interval: the sample mean, the population standard deviation (which is given), and the desired confidence level. The example values we will use are mean presidential rating of 81, a sigma equal to 3, and a desired confidence level of 95%. In other words, we are constructing a 95% confidence interval.

Once we know these values, the next step is to compute the standard error of the mean, just like we did for the Z test. The formula is given again here. Our standard error of the mean based on our example is equal to 3 divided by 10, or .3. Next, we must compute the lower and upper limits of our confidence interval. Since we are constructing our confidence interval based on our sample mean, the sample mean value will be at the center of the interval. The confidence interval will range a certain distance below and above the sample mean. How far above and below depends on our confidence level. The Z scores that bound the 95% confidence interval are -1.96 and +1.96, and the Z scores that bound the 99% confidence interval are -2.57 and +2.57. To compute the 95% confidence limits, we simply multiply the positive Z score (1.96) by the standard error of the mean (.3). Then we subtract this value from the sample mean for the lower limit, and we add this value to the sample mean for the upper limit, as shown here. For the 99% confidence interval, follow the same steps, but use 2.57 instead of 1.96.

All that remains to do is to make some statement regarding your results. When talking about confidence intervals, it is appropriate to say that they represent the range of possible means likely to include the real population mean. So, after constructing a 95% confidence interval, it is appropriate to say that we can be 95% sure that this range contains the true population mean, but there is always the 5% chance that it doesn’t. The last part of this presentation will be learning how to compute confidence intervals in Excel.

Before we get there, though, I want to tie some things together for you. This week, we have looked at two approaches to answering research questions: hypothesis testing and confidence intervals. Both of these processes deal with samples and populations, using information from these to answer certain research questions. However, each process goes about this in a different way. It is helpful to understand this distinction as you move forward in statistics. When we compute a confidence interval, we first take data from a sample and then make a statement about the population. We are ESTIMATING the population mean based on the sample data. When we perform a hypothesis test (like a Z test), we first make a statement about the population (our hypothesis), and then take data from a sample and decide whether the statement seems reasonable or not. We are using our sample data to TEST our statement about the population. You can see that each of these methods approaches the process from a different end—one starts with the sample, the other starts with the population.

We will be using the same research question and data set that we looked at in the presentation for hypothesis testing and Z tests. To review the information, a family systems psychologist is interested in the amount of television that households in his town watch per day. He knows that the population standard deviation for minutes of television watched per day per household in his state is 20. He decides to interview a sample of 55 households in his town and record the number of minutes of television watched per day. He wants to use this information to construct a 95% confidence interval for mean number of minutes of television watched per day.

Here is a portion of the hypothetical sample data, as well as a table that the psychologist constructed in which to enter his results. The table contains cells for both the information that he already knows as well as the confidence limit information that he will compute in Excel.

We start off by filling in the information that is already known. The sample size is N=55 and the population standard deviation, or sigma, equals 20. Use the Excel AVERAGE function to compute the mean of the sample data, as we have done several times before. Finally, fill in your alpha level. When constructing a confidence interval, alpha is equal to 1 minus your confidence level expressed as a decimal. A 95 % confidence interval expressed as a decimal is .95, so 1 minus .95 equals .05. Put this value into the cell for alpha.

Now it is time to compute the confidence interval. We do this using the Excel function called Confidence. If you paid attention earlier when we went over computing the confidence interval by hand, you may notice that there is something missing from our table. There is no cell for the standard error of the mean or any type of Z score that is used to determine the confidence interval. This is because the Excel Confidence formula computes these values automatically from the given information. Let’s go over how to use this formula. As you can see, the formula requires that we enter alpha, the population standard deviation, and the sample size.

The easiest way to enter these values is to click on each cell in turn, typing a comma between each cell reference. So, first we click in the cell in which we want our value to appear. Type in “equals CONFIDENCE”. Excel will prompt you to enter the arguments for the formula. First, click on the cell containing alpha, then type a comma, then click on the cell containing the sigma value, another comma, and then the cell containing your sample size. Your final formula should appear as shown, with either numbers or the cell references containing the numbers in parentheses.

The resulting value appears in the cell when you press enter. This value represents your margin of error, that is, how far in each direction the confidence interval will extend from the sample mean. In order to actually determine what this interval will look like, we must compute the lower and upper limits. This is done simply by starting with the sample mean and either subtracting or adding the margin of error value to the mean. To compute the lower confidence limit, click in the cell under “lower limit” and type “equals E3-H3” and press enter. For the upper limit, simply type the same formula but change the minus to a plus.

Here we see the final table. Our 95% confidence interval for mean number of minutes of TV watched per day per household ranges from 72.8 minutes to 83.4 minutes. Our family systems psychologist can say that he can be about 95% certain that this range of means contains the true population mean. Remember that this is only an estimate, though, and that there is still a 5% risk that this range does not contain the true population mean.

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CHAPTER 5

•

Hypothesis Tests with Mean

s

of Samples

Chapter Outline

0 The Distribution of Means

1

38

‘ Hypothesis Testing with a

Distributio

n

Advanced Topic Controversy:

Confidence Intervals versus Significance Tests

162

of Means: The Z Test

146

C, Controversy: Marginal

0 Advanced Topic: Confidence

Significance 1

53

Intervals in Research Articles

163

Hypothesis Tests About Means

0 Summary 163

of Samples (Z Tests) and Standard Errors in Research Articles 154

0 Key Terms

164

Advanced Topic: Estimation

,

0 Example Worked-Out Problems 164 0 Practice Problems 1

67

o Chapter Notes

173

Standard Errors, and Confidence Intervals 156

/un c

Chapter 4, we introduced the basic logic of hypothesis testing. The studies we sed as examples had a sample of a single individual. As we noted, however, in

atual practice, psychology research almost always involves a sample of many

individuals. In this chapter, we build on what you have learned so far and consider hypothesis testing with a sample of more than one individual. For example, a social psychologist is interested in the potential effect of perceptions of people’s personality on perceptions of their physical attractiveness. The researcher’s theory predicts that, if a you are told that a person has positive personality qualities (such as kindness, warmth, a sense of humor, and intelligence), you will rate that person as more attrac�tive than if no mention had been made of the person’s personality qualities. From extensive previous research (in which no mention was made of personality qualities),

137

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138

Chapter 5

the researcher has established the population mean and standard deviation of the attractiveness rating of a photo of a particular person. The researcher then recruits a sample of 64 individuals to rate the attractiveness of the person in the photograph. However, prior to rating the person, each individual is told that the person whose photograph they are going to rate has many positive personality qualities. In this chapter, you will learn how to test hypotheses in situations such as those presented in this example, situations in which the population has a known mean and standard deviation and in which a sample has more than one individual. Mainly, this requires examining in some detail a new kind of distribution, called a “distribution of means.” (We will return to this example later in the chapter.)

The

Distribution

of Means

Hypothesis testing in the usual research situation, where you are studying a sample of many individuals, is exactly the same as you learned in Chapter 4—with an important exception. When you have more than one person in your sample, there is a special prob�lem with Step @, determining the characteristics of the comparison distribution. In each of our examples so far, the comparison distribution has been a distribution of individual scores (such as the population of ages when individual babies start walking). A distribution of individual scores has been the correct comparison distribution be�cause we have used examples with a sample of one individual. That is, there has been consistency between the type of sample score we have been dealing with (a score from

one individual) and the comparison distribution (a distribution of individual scores

).

Now, consider the situation when you have a sample of, say, 64 individuals (as in the attractiveness rating example). You now have a group of 64 scores (an attractive�ness rating from each of the 64 people in the study). As you will recall from Chapter 2, the mean is a very useful representative value of a group of scores. Thus, the score you care about when there is more than one individual in your sample is the mean of the group of scores. In this example, you would focus on the mean of the 64 individuals’

scores. If you were to compare the mean of this sample of 64 individuals’ scores to a distribution of a population of individual scores, this would be a mismatch—like comparing apples to oranges. Instead, when you are interested in the mean of a sam�ple of 64 scores, you need a comparison distribution that is a distribution of means of samples of 64 scores. We call such a comparison distribution a distribution of

means.

So, the scores in a distribution of means are means, not scores of individuals.

A distribution of means is a distribution of the means of each of lots and lots of samples of the same size, with each sample randomly taken from the same popula�tion of individuals. (Statisticians also call this distribution of means a sampling dis�tribution of the mean. In this book, however, we use the term distribution of means to keep it clear that we are talking about populations of means, not samples or some

kind of distribution of samples.)

The distribution of means is the correct comparison distribution when there is more than one person in a sample. Thus, in most research situations, determining the characteristics of a distribution of means is necessary for Step @ of the hypothesis

�

testing procedure, determining the characteristics of the comparison

distribution.

distribution of means distribution

of

means of samples of a given size from a population (also called a sampling distrib�ution of the mean); comparison distribu- tion when testing hypotheses involving a single sample of more than one individual.

Building a Distribution of Means

To help you understand the idea of a distribution of means, we consider how you could�build up such a distribution from an ordinary population distribution of individual�scores. Suppose our population of individual scores was of the grade levels of

the

Hypothesis Tests with Means of Samples

139

10,000

0

I

2

1

Grade

M=4.67.

SD2 = .39.

SD= .62.

1_1_

11

I

Grade

Figure 5-1 Distribution of grade levels

among 90,000

Figure 5-2 Distribution of the means of

schoolchildren (fictional data).

three randomly taken samples of two schoolchild�ren’s grade levels each from a population of grade levels of 90,000 schoolchildren (fictional data).

90,000 elementary and junior-high schoolchildren in a particular region. Suppose fur��ther (to keep the example simple) that there are exactly 10,000 children at each grade�level, from first through ninth grade. This population distribution would be rectangular,

with a mean of 5, a variance of 6.67, and a standard deviation of 2.58 (see Figure 5-1).

Next, suppose that you wrote each child’s grade level on a table tennis ball and put all 90,000 balls into a giant tub. The tub would have 10,000 balls with a 1 on them, 10,000 with a 2 on them, and so forth. You stir up the balls in the tub and then take two of them out. You have taken a random sample of two balls. Suppose one ball has a 2 on it and the other has a 9 on it. The mean grade level of this sample of two children’s grade levels is 5.5, the average of 2 and 9. Now you put the balls back, mix up all the balls, and select two balls again. Maybe this time you get two 4s, making the mean of your second sample 4. Then you try again; this time you get a 2

and a 7, making your mean 4.5. So far you have three means: 5.5, 4, and 4.5.

Each of these three numbers is a mean of a sample of grade levels of two school children. And these three means can be thought of as a small distribution in its own right. The mean of this little distribution of means is 4.67 (the sum of 5.5, 4, and 4.5, divided by 3). The variance of this distribution of means is .39 (the variance of 5.5, 4, and 4.5). The standard deviation of this distribution of means is .62 (the square roo

t

of .39). A histogram of this distribution of three means is shown in Figure 5-2.

Suppose you continued selecting samples of two balls and taking the mean of the

numbers on each pair of balls. The histogram of means would continue to grow. Figure 5-3 shows examples of distributions of means varying from a sample with just 50 means, up to a sample with 1,000 means (with each mean being of a sample of two randomly drawn balls). (We actually made the histograms shown in Figure 5-3 using a computer to make the random selections instead of using 90,000 table tennis balls

and a giant tub.)

As you can imagine, the method we just described is not a practical way of de�

termining the characteristics of a distribution of means. Fortunately, however, you can figure out the characteristics of a distribution of means directly, using some sim-ple rules, without taking even one sample. The only information you need is (a) the characteristics of the distribution of the population of individuals and (b) the number of scores in each sample. (Don’t worry for now about how you could know the char- acteristics of the population of individuals.) The laborious method of building up a distribution of means in the way we have just considered and the concise method you will learn shortly give the same result. We have had you think of the process in terms of the painstaking method only because it helps you understand the idea of a distribution

of means.

• ir • la . 41 r-v-r “r

Before moving on to later chap�ters, be sure you fully understand the idea of a distribution of means (and why it is the correct cornpar

son distribution when a saammppllee contains more than one individual). You may need to go through this chapter a couple of times to achieve full understanding of this crucial concept.

Chapter 5

125

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125

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0 75

75

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50

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11 I

1.0 2.0 3.0 4.0 5.0 6.0

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1.0 2.0 3.0 4.0 5.0 6.0 7.0 8.0 9.0

1.0 2.0 3.0 4.0 5.0 6.0 7.0 8.0 9.0

N=50

V=200

N .

400

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1.0 2.0 3.0 4.0 5.0 6.0 7.0 8.0 9.0

N=61

N =800

N = 1000

Figure 5-3 Histograms of means of two grade levels randomly selected from a large

group of students with equal numbers of grades 1 through 9. Histograms are shown for 50 such means, 200 such means, 400 such means, 600 such means, 800 such means, and 1,000 such means. Notice that the histograms become increasingly like a normal curve as the num�ber of means increases.

Determining

the Characteristics of a Distribution of Means

Recall that Step A of hypothesis testing involves determining the characteristics of the comparison distribution. The three key characteristics of the comparison distrib�ution that you need to determine are:

Its mean.

Its spread (which you can measure using the variance and standard deviation).

Its shape.

Notice three things about the distribution of means we built in our example, as shown in Figure 5-3:

1. The mean of the distribution of means is about the same as the mean of the orig�

inal population of individuals (both are 5).

2. The spread of the distribution of means is less than the spread of the distribution

of the pop

ulation of individuals.

3. The shape of the distribution of means is approximately normal.

mean of a distribution of means the

The first two observations, regarding the mean and the spread, are true for all distributions of means. The third, regarding the shape, is true for most distributions of means. These three observations, in fact, illustrate three basic rules you can use to find the mean, the spread (that is, variance and standard deviation), and the shape of any distribution of means without having to write on plastic balls and take endless

mean of a distribution of means of sam�pies of a given size from a population; the same as the mean of the population of individuals.

samples.

Now let’s look at the three rules more closely. The first is for the mean of a distribution of means.

Hypothesis Tests with Means of Samples

141

Rule 1: The mean of a distribution of means is the same as the mean of the population of individuals. Stated as a formula,

�

The mean of a di

�

RA/ = µ

(5-1)

means is equal t(

the population of

pm is the mean of the distribution of means (it uses a Greek letter because the

distribution of means is also a kind of population). }I is the mean of the pop�

ulation of individuals.

Each sample is based on randomly selected individuals from the population of

individuals. Thus, the mean of a sample will sometimes be higher and sometimes�lower than the mean of the whole population of individuals. However, because the�selection process is random and we are taking a very large number of samples, even�

tually the high means and the low means perfectly balance each other out.

In Figure 5-3, as the number of sample means in the distributions of means increases, the mean of the distribution of means becomes more similar to the mean of the population of individuals, which in this example was 5. It can be proven math�ematically that, if you took an infinite number of samples, the mean of the distribu�tion of means of these samples would come out to be exactly the same as the mean

of the distribution of individuals.

The second rule is about spread. Rule 2a is for the variance of a distribution of

means.

Rule 2a: The variance of a distribution of means is the variance of the pop��ulation of individuals divided by the number of individuals in

each sample.

A distribution of means will be less spread out than the distribution of individuals from which the samples are taken. If you are taking a sample of two scores, it is less likely that both scores will be extreme. Further, for a particular random sample to have an extreme mean, the two extreme scores would both have to be extreme in the same direction (both very high or both very low). Thus, having more than a single score in each sample has a moderating effect on the mean of such samples. In any one sample, the extremes tend to be balanced out by a middle score or by an extreme in the opposite direction. This makes each sample mean tend toward the middle and away from extreme values. With fewer extreme means, the variance of the means is

less than the variance of the population of individuals.

Consider again our example. There were plenty of I s and 9s in the population, making a fair amount of spread. That is, about a ninth of the time, if you were taking samples of single scores, you would get a 1 and about a ninth of the time you would get a 9. If you are taking samples of two at a time, you would get a sample with a mean of I (that is, in which both balls were 1s) or a mean of 9 (both balls 9s) much less often. Getting two balls that average out to a middle value such as 5 is much

more likely. (This is because several combinations could give this result-1 and 9, 2

and 8, 3 and 7, 4 and 6, or two 5s).

The more individuals in each sample, the less spread out will be the means of the samples. This is because, the more scores in each sample, the rarer it will be for ex�tremes in any particular sample not to be balanced out by middle scores or extremes in the other direction. In terms of the table tennis balls in our example, we rarely got a mean of 1 when taking samples of two balls at a time. If we were taking three balls at a time, getting a sample with a mean of 1 (all three balls would have to be 1s) is

even less likely. Getting middle values for the means becomes even more likely.

I.LAt mean of a distribution of means. variance o

f a distribution of means

Using samples of two balls at a time, the variance of the distribution of means

came out to about 3.34. This is half of the variance of the population of individuals,�which was 6.67. If we had built up a distribution of means using samples of three

variance of the population divided by the number of scores in each sample

,.

1 42

Chapter 5

balls each, the variance of the distribution of means would have been 2.22. This is�one-third of the variance of our population of individuals. Had we randomly selected�five balls for each sample, the variance of the distribution of means would have been

one-fifth of the variance of the population of individuals.

These examples follow a general rule—our Rule 2a for the distribution of means: the variance of a distribution of means is the variance of the population of individuals divided by the number of individuals in each of the samples. This rule

holds in all situations and can be proven mathematically.

Here is Rule 2a stated as a formula:

�

f a distribution

�

variance of

0-

1

14

—

0′

(5-2)

of individuals

N

number of

each sample.

cr is the variance of the distribution of means (it uses a Greek letter because the distribution of means is also a kind of population). cr2 is the variance of the popula�

tion of individuals, and N is the number of individuals in each sample.

In our example, the variance of the population of individual children’s grade levels was 6.67, and there were two children’s grade levels in each sample. Thus,

When you figure the variance of a distribution of means (4), be sure to divide the population variance (cr2) by the number of individuals in each sample. In many of the exam�ples, you are told the population standard deviation (a), which you will first have to square to find the population variance (cr2); then you can use Formula 5-2 to find the variance of the distribution of means (4).

=

o.2

=

6.67

3.

34

N

2

To use a different example, suppose a population had a variance of 400 and you wanted to know the variance of a distribution of means of 25 individuals each:

=

0-

=

400

16

N

25

The second rule also tells us about the standard deviation of a distribution of

means.

The standard deviation of a distribution of means is the square root of the variance of the distribution of means and also the square root of the result of dividing the variance

Rule 2b: The standard deviation of a distribution of means is the square

root of the variance of the distribution of means. Stated as a formula,

Q

M

Vi

cri

0-

(5-3)

N

of the population of individuals by the number of individuals in each sample.

aM is the standard deviation of the distribution of means. I

The standard deviation of the distribution of means also has a special name of its

(di variance of a distribution of means.

own, the standard error of the mean (SEM), or the standard error (SE), for short. (Thus, aM also stands for the standard error.) It has this name because it tells you how much the means of samples are typically “in error” as estimates of the mean of the population of individuals. That is, it tells you how much the various means in the distribution of means deviate from the mean of the population. We have more to say

standard deviation of a distribution�of means square root of the variance

of a distribution of means; also called

standard error of the mean (SEM) and standard error (SE).

about the standard error later in the chapter.

cr$,

standard deviation of a distribution

Finally, the third rule for finding the characteristics of a distribution of means focuses on its shape.

of means.

standard error of the mean (SEM) same as standard

deviation

of a distribution of means; also called standard error (SE).

Rule 3: The shape of a distribution of means is approximately normal if either�(a) each sample is of 30 or more individuals or (b) the distribution of the�population of individuals is normal. Whatever the shape of the distribution of

standard error (SE) same as standard

deviation of a distribution of means; also�called standard error of the mean (SEM).

the population of individuals, the distribution of means tends to be unimodal and sym��metrical. In the grade-level example, the population distribution was rectangular.

Hypothesis Tests with Means of Samples

143

(It had an equal number at each value.) However, the shape of the distribution of 1,000�sample means (see Figure 5-3) was roughly that of a bell—unimodal and symmetri��cal. Had we taken many more than 1,000 samples, the shape would have been even

more clearly unimodal and symmetrical.

A distribution of means tends to be unimodal because of the same basic process of extremes balancing each other out that we noted in the discussion of the variance: middle scores for means are more likely, and extreme means are less likely. A distribution of means tends to be symmetrical because a lack of symmetry (skew) is caused by extremes. With fewer extremes, there is less asymmetry. In our grade-level example, the distribution of means we built up also came out so clearly symmetrical because the population distribution of individual grade levels was symmetrical. Had the popula�tion distribution of individuals been skewed to one side, the distribution of means

would have still been skewed, but not as much.

The more individuals in each sample, the closer the distribution of means will be to a normal curve. Although the distribution of means will rarely be an exactly normal curve, with samples of 30 or more individuals (even with a nonnormal popu�lation of individuals), the approximation of the distribution of means to a

normal

curve is very close and the percentages in the normal curve table will be extremely

accurate.• (That is, samples that are larger than 30 make for even slightly better ap�

23

proximations, but for most practical research purposes, the approximation with 30 is quite good enough.) Finally, whenever the population distribution of individuals is normal, the distribution of means will be normal, regardless of the number of indi�viduals in each sample.

Summary of Rules and Formulas for Determining

the Characteristics of a Distribution of Means

Rule 1: The mean of a distribution of means is the same as the mean of the population of individuals:

RAI

11

Rule 2a: The variance of a distribution of means is the variance of the pop��ulation of individuals divided by the number of individuals in each sample:

0’2

=

N

Rule 2b: The standard deviation of a distribution of means is the square

root of the variance of the distribution of means:

An

a

vY2M

N

Rule 3: The shape of a distribution of means is approximately normal if�either (a) each sample is of 30 or more individuals or (b) the distribution�of the population of individuals is normal. Figure 5-4 shows these three rules

graphically.

These three rules are based on the central limit theorem, a fundamental principle

in mathematical statistics we mentioned in Chapter 3. A notable strength of the cen�tral limit theorem is that it provides the key characteristics (central tendency, vari�ability, and shape) of a distribution of means for a population with a distribution of any shape.

Chapter 5

�

�

Distribution of Means

Same

Mean

Less

Variance

Normal if population is normal

or regardless of population shape

if samples each contain 30 or

more scores

Figure 5-4 Comparing the distribution of the population of individuals (upper curve)

and the distribution of means (lower curve).

Example of Determining the Characteristics of a Distribution of Means

Think back to the example from the start of the chapter in which students rated the attractiveness of a person in a photograph. Consider the population of students’ rat�ings of the person in the photograph (when students are told nothing about the per�sonality characteristics of the person in the photograph). Suppose the distribution is approximately normal with a mean of 200 and a standard deviation of 48. What will be the characteristics of the distribution of means for samples of 64 students?

Rule 1: The mean of a distribution of means is the same as the mean of the�population of individuals. The mean of the population is 200. Thus, the mean of

the distribution of means will also be 200. That is, p.m = p = 200.

Rule 2a: The variance of a distribution of means is the variance of the popu��lation of individuals divided by the number of individuals in each sample.

The standard deviation of the population of individuals is 48; thus, the variance of the population of individuals is 482, which is 2,304. The variance of the distribution of means is therefore 2,304 divided by 64 (the size of the sample). This comes out to 36. That is, cr2m = o-2/N = 2,304/64 = 36.

Hypothesis Tests with Means of Samples

145

Figure 5-5 Three kinds of distributions: (a) the distribution of a population of individ�

uals, (b) the distribution of a particular sample taken from that population, and (c) the distrib�ution of means.

Rule 2b: The standard deviation of a distribution of means is the square�root of the variance of the distribution of means. The standard deviation

of the distribution of means is the square root of 36, which is 6. That is, = Vo-2m = V36 = 6.

Rule 3: The shape of a distribution of means is approximately normal if either

(a) each sample is of 30 or more individuals or (b) the distribution of the pop�

ulation of individuals is normal. Our situation meets both of these conditions

the sample of 64 students is more than 30, and the population of individuals follows a normal distribution. Thus, the distribution of means will follow a normal curve. (It would have been enough even if only one of the two conditions had been met.)

Review of the Three Kinds of Distributions

We have considered three kinds of distributions: (1) the distribution of a population of individuals, (2) the distribution of a particular sample of individuals from that population, and (3) the distribution of means. Figure 5-5 shows these three kinds of distributions graphically and Table 5-1 describes them.

111111″”1″51177″”m”

Table 5

-1

Comparison of Three Types of Distributions

Particular

Be sure you fully understand the different types of distribution shown in Table 5-1 before you move on to later chapters. To check your understanding, cover up portions of the table and then try to recall the hidden information.

Population’s

Sample’s

Distribution

Distribution

Distribution

of Means

Content

Scores of all individuals

Scores of the individuals

Means of samples randomly

in the population

in a single sample

taken from the population

Shape

Could be any shape; often

Could be any shape

Approximately normal if sam�

normal

pies have _?_.30 individuals in

each or if population is normal

Mean

M = (EX)/

P.m =

Variance

0?

SD2 = [E(X — M)2]/A/

QM = 02/N

Standard

0-

SD = VSD2

QM = V

0m

deviation

146

Chapter 5

�

1. What is a distribution of

means?

2. Explain how you could create a distribution of means by taking a large num�

ber of samples of four individuals each.

3. (a) Why is the mean of the distribution of means the same as the mean of the

population of individuals? (b) Why is the varianc

e of a distribution of means

smaller than the variance of the distribution of the population of individuals?

4. Write the formula for the variance of the distribution of means, and define

each of the symbols.

5. (a) What is the standard error? (b) Why does it have this name?

6. A population of individuals that follows a normal curve has a mean of 60 and

a standard deviation of 10. What are the characteristics of a distribution of means from this population for samples of four each?

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Hypothesis Testing with a Distribution of Means: The Z Test

Now we are ready to turn to hypothesis testing when there is more than one individual�in the study’s sample. The hypothesis testing procedure you will learn is called a Z test.

The Distribution of Means as the Comparison Distribution in Hypothesis Testing

In the usual research situation, a psychologist studies a sample of more than one per��son. In this situation, the distribution of means is the comparison distribution. It�is the distribution whose characteristics need to be determined in Step of the

Hypothesis Tests with Means of Samples

147

BOX 5-1

More About Polls: Sampling Errors and Errors in Thinking About Samples

If you think back to Box 3-3 on surveys and the Gallup poll, you will recall that we left two important questions unanswered about fine print included with the results of a poll, saying something like, “From a telephone poll of 1,000 American adults taken on June 4 and 5. Sampling error ±3%.” First, you might wonder how such small numbers, like 1,000 (but rarely much less), can be used to predict the opinion of the entire U.S. population. Sec-ond, after working through the material in this chapter on the standard deviation of the distribution of means, you may wonder what the term sampling error means when a sample is not randomly sampled but rather selected by

of accuracy. This absolute size determines the impact of�the random errors of measurement and selection. What�remains important is reducing bias or systematic error,

which can be done only by careful planning.

As for the term sampling error, it is worked out ac-cording to past experience with the sampling procedures used. It is given in tables for different sample sizes (usu�ally below 1,000, because that is where error increases

dramatically).

the complicated probability method used for polls.

So the number of people polled is not very important (provided that it is at least 1,000 or so), but what mat-ters very much are the methods of sampling and esti�mating error, which will not be reported in the detail necessary to judge whether the results are reliable. The reputation of the organization doing the survey is prob�ably the best criterion. If the sampling and error-estimating approach is not revealed at all, be cautious. For more information about how polls are conducted, go to � HYPERLINK http://media.gallup.com/PDF/FAQ/HowArePolls ��http://media.gallup.com/PDF/FAQ/HowArePolls � (note that sampling error is referred to as “margin of

Regarding sample size, you know from this chapter that large sample sizes, like 1,000, greatly reduce the standard deviation of the distribution of means. That is, the curve becomes very high and narrow, gathered all around the population mean. The mean of any sample of

that size is very close to being the population mean.

When a sample is only a small part of a very large pop�

ulation, the sample’s absolute size is the only determiner

error” on the Web site).

hypothesis-testing process. The distribution of means is the distribution to which you compare your sample’s mean to see how likely it is that you could have selected a sample with a mean that is extreme if the null hypothesis were true.

Figuring the Z Score of a Sample’s Mean on the Distribution of Means

There can be some confusion in figuring the location of your sample on the compari�son distribution in hypothesis testing with a sample of more than one. In this situation, you are finding a Z score of your sample’s mean on a distribution of means. (Before, you were finding the Z score of a single individual on a distribution of a population of single individuals.) The method of changing the sample’s mean to a Z score is the same as the usual way of changing a raw score to a Z score. However, you have to be careful not to get mixed up because more than one mean is involved. It is important to remember that you are treating the sample mean like a single score. Recall that the ordinary formula (from Chapter 3) for changing a raw score to a Z score is Z=

(X — Mil SD. In the present situation, you are actually using the following formula:

The Z score for the sample’s mean on the distribution of means is the sample’s mean minus the mean of the

distribution of means, divided by the

standard deviation of the distribution of means.

Z

=

M —

(5-4)

QM

For example, suppose your sample’s mean is 18 and the distribution of means

has a mean of 10 and a standard deviation of 4. The Z score of this sample mean is +2.

Using the formula,

Z

=

M

—

µA/

=

18

—

=

=

2

tsM

4

4

Chapter 5

0

�

�

Raw Scores:

,
2

1()

14

Z Scores:

—1

0

+1

+2

t

�

I

18

Figure 5-6 Z score for the mean of a particular sample on the distribution of means.

This is shown in Figure 5-6.

The hypothesis test you are learning in this chapter is called a Z test, because

you figure the Z score for your sample’s mean.

Example

Let’s return again to our example in which a social psychologist is interested in whether being told a person has positive personality qualities increases ratings of the physical attractiveness of that person. The psychologist asks 64 randomly selected students to rate the attractiveness of a particular person in a photograph. Prior to rat�ing the attractiveness of the person, each student is told that the person has positive personality qualities (kindness, warmth, a sense of humor, and intelligence). On a scale of 0 (the lowest possible attractiveness) to 400 (the highest possible attractive�ness), the mean attractiveness rating given by the 64 students is 220. From previous research, the psychologist knows that the attractiveness ratings of the person in the

photograph (when no mention is made of the person’s positive personality qualities)�have a mean of 200 and a standard deviation of 48, and they follow an approximately

normal distribution. This distribution is shown in Figure 5-7a.4

J • a I at r –

Now let’s carry out the Z test by following the five steps of hypothesis testing

As in Chapter 4, Population 2 is the population for the comparison distribution, which is the distribu-tion that shows the population sit uation if the null hypothesis is true.

you learned in Chapter 4:

0 Restate the question as a research hypothesis and a null hypothesis about

the populations. The two populations are these:

Population 1: Students who are told that the person has positive personality

Z test hypothesis-testing procedure in

qualities.

which there is a single sample and the population variance is known.

Population 2: Students in general (who are told nothing about the person’s personality qualities).

Hypothesis Tests with Means of Samples

149

(a)

= 200

a2 = 2.304

a =

48

Test Scores:

260

200

Z Scores:

–1

0

+1

+2

a

�

0 1 2

200 206 212

(c)

M =

220

�

N = 64

220

Figure 5-7 For the fictional study of positive personality qualities and ratings of phys�

ical attractiveness, (a) the distribution of the population of individuals, (b) the distribution of means (the comparison distribution), and (c) the sample’s distribution. The shaded area in the distribution of means is the rejection region—the area in which the null hypothesis will be rejected if the study’s sample mean turns out to be in that area.

The research hypothesis is that the population of students who are told that the person has positive personality qualities will on the average give higher at�tractiveness scores for that person than the population of students who are told nothing about the person’s personality qualities: Ili > 112. The null hypothesis is that Population l’s scores will not on the average be higher than Population 2’s: III I.L2. Note that these are directional hypotheses. The researcher wants to know if being told that the person has positive personality qualities will increase attractiveness scores; a result in the opposite direction would not be relevant to the theory the researcher is testing.

150

Chapter 5

A Determine the characteristics of the comparison distribution. The result of

the study will be a mean of a sample of 64 individuals (students in this case). Thus, the comparison distribution has to be the distribution of means of samples of 64 individuals each. This comparison distribution will have a mean of 200 (the same as the population mean). That is, as we saw earlier in the chapter,

standard deviation of 48 squared); the sample size is 64. Thus, the variance of the distribution of means, o-2m, will be 2,304/64, or 36. The standard deviation of the distribution of means, QM, is the square root of 36, or 6. Finally, because there are more than 30 individuals in the sample, the shape of the distribution of means will be approximately normal. Figure 5-7b shows this distribution of means.

= 200. Its variance will be the population variance divided by the number of

2 is 2,304 (the population individuals in the sample. The population variance, o.,

A Determine the cutoff sample score on the comparison distribution at which

the null hypothesis should be rejected. Let’s assume the researcher decides to use the standard 5% significance level. As we noted in Step 0, the researcher is making a directional prediction. Hence, the researcher will reject the null hy�pothesis if the result is in the top 5% of the comparison distribution. The com�parison distribution (the distribution of means) is a normal curve. Thus, the top 5% can be found from the normal curve table. It starts at a Z of +1.64. This top 5% is shown as the shaded area in Figure 5-7b.

O Determine your sample’s score on the comparison distribution. The result of

the (fictional) study is that the 64 students told that the person has positive per�sonality qualities gave a mean attractiveness rating of 220. (This sample’s distri�bution is shown in Figure 5-7c.) A mean of 220 is 3.33 standard deviations above the mean of the distribution of means:

Z

=

M

—

µM

=

220

—

=

20

3.33

Cr m

6

6

A Decide whether to reject the null hypothesis. We set the minimum Z score t

o

reject the null hypothesis to +1.64. The Z score of the sample’s mean is +3 .33. Thus, the social psychologist can reject the null hypothesis and conclude that the research hypothesis is supported. To put this another way, the result of the Z test is statistically significant at the p < .05 level. You can see this in Figure 5-7b. Note how extreme the sample's mean is on the distribution of means (the distribution that would apply if the null hypothesis were true). The final conclu�sion is that, among students, being told that a person has positive personality qualities does increase the attractiveness ratings of that person. (Results of actual studies show this effect, as well as showing that if you have heard negative in�formation about a person, you then rate them as less physically attractive; e.g., Lewandowski, Aron, & Gee, 2007.)

A Second Example

Suppose a researcher wants to test the effect of a communication skills seminar on�students’ use of verbal fillers during a presentation. Verbal fillers are words such as�”urn,” “uh,” and “you know,” that people commonly use in conversations and when

giving presentations. The researcher conducts a study in which 25 students attend a communication skills seminar and then give a half-hour presentation on a topic of their choice. The presentations are tape-recorded and a research assistant later counts the number of verbal fillers used by each student during his or her presentation. In this fictional example, we assume that the researcher knows from previous studies that students typically use a mean of 53 verbal fillers during a half-hour presentation

Hypothesis Tests with Means of Samples

151

(a)

u = 53

a2=49

Memory Scores 39

67

Z Scores

-2

-1

0

+1

+2

�

T

�

48.8 50.2 51.6

53

54.4 55.8

-3 -2 -1

0

+1 +2

(c)

M=48

N=25

48

Figure 5-8 For the fictional study of the use of verbal filters in a presentation, (a) the

distribution of the population of individuals, (b) the distribution of means (the comparison distribution), and (c) the sample’s distribution. The shaded areas in the distribution of means are the rejection regions—the areas in which the null hypothesis will be rejected if the study’s sample mean turns out to be in that area.

of this kind, with a standard deviation of 7, and the distribution of verbal fillers fol�lows a normal curve (see Figure 5-8a). The 25 students who take the communication skills seminar use a mean of 48 verbal fillers. The researcher wants to carry out the Z test using the 1% significance level, and an effect in either direction would be impor�tant (that is, the researcher is interested in whether the communications seminar could increase or decrease the use of verbal fillers).

0 Restate the question as a research hypothesis and a null hypothesis about

the populations. The two populations are:

Population 1: Students who attend a communication skills seminar. Population 2: Students in general (who do not attend a communication skills seminar).

I =. 2

Chapter 5

The research hypothesis is that the population of students who attend a commu�nication skills seminar will use a different number of verbal fillers during a pre�sentation than students in general: # p.2. The null hypothesis is that Population 1’s scores are on the average the same as Population 2’s: p. = pL2.

A Determine the characteristics of the comparison distribution. This compari�

son distribution is a distribution of means. It has a mean of 53 (the same as the�population mean). Its variance is the population variance divided by 25, the�number of individuals in the sample: crii = 0.2/N =72/2D5 = 49/25 = 1.96;

0M = V1.96 = 1.40. Its shape is normal, since the population of individual verbal filler scores is normally distributed. (Figure 5-8b shows the comparison distribution.)

A Determine the cutoff sample score on the comparison distribution at which

the null hypothesis should be rejected. This is a two-tailed test (the researcher is interested in an effect in either direction) at the overall 1% significance level. Based on the normal curve table for the top and bottom .5%, the cutoffs are +2.57 and —2.57 (see tiny shaded areas in Figure 5-8b).

0 Determine your sample’s score on the comparison distribution. The sample’s

mean was 48 (see Figure 5-8c). This comes out to a Z of —3.57 on the comparison distribution: Z = (M — = (48 — 53)/1.40 = —5/1.40 = —3.57.

A Decide whether to reject the null hypothesis. The Z score of the sample’s

mean is —3.57, which is more extreme than the cutoffs of ±2.57. Thus, the researchers can reject the null hypothesis and conclude that the research hypoth�esis is supported. To put this another way, the result of the Z test is statistically significant at the p < .01 level. You can see this in Figure 5-8b. Note how ex�treme the sample's mean is on the distribution of means (the distribution that would apply if the null hypothesis were true). The final conclusion is that stu�dents' use of verbal fillers during a presentation decreases after attending a com�

munication skills seminar.

When you next give a presentation, ask a friend to count the number of times you use verbal fillers (such as “urn,” “uh,” and “you know”), or tape-record the presenta�tion and count your own verbal fillers. Verbal fillers can be distracting to listeners and may adversely affect the quality of a presentation. Communications specialists rec�ommend replacing verbal fillers with brief pauses (that allow you to gather your thoughts).

�

How are you doing?

1. How is hypothesis testing with a sample of more than one person different

from hypothesis testing with a sample of a single person?

2. How do you find the Z score for the sample’s mean on the distribution of

means?

3. A researcher predicts that showing a certain film will change people’s atti�

tudes toward alcohol. The researchers then randomly select 36 people, show them the film, and give them an attitude questionnaire. The mean score on the attitude test for these 36 people is 70. The score for people in general on this test is 75, with a standard deviation of 12. Using the five steps of hypothesis testing and the 5% significance level, carry out a Z test to see if viewing the film changes people’s attitudes toward alcohol.

Hypothesis Tests with Means of Samples

153

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Controversy: Marginal

Significance

A long-standing controversy regarding significance testing is what to do when a result

does not make the cutoff value at the usual 5% level but comes very close (say, p < .10).

” “approaching significance,” or a “near

This is often called “marginal significance,

significant trend.” A couple of years ago, the controversy was spotlighted on an email listsery for social and personality psychologists. The discussion began when the fol�lowing note was posted by Todd Nelson (California State University at Stanislaw):

Throughout my ph.d. training …it was common parlance to refer to …P-values of�between .05 and .10 as “marginally significant.” It was a very common term in all the

major social psychological journals … and among my professors.

The other day, in a thesis defense I was chairing, I was dumfounded when the other thesis committee members strongly objected to the term “marginally significant”

in the student’s results section… both saying they had NEVER heard of the term (!).

Wanting to make sure I was still on planet Earth, I consulted several statistics and research textbooks in my office, and found a few that referred to “marginal sig�nificance” and several articles by noted statisticians who make the case for discussing

results in the .05—.10 range

…

[H]ave you heard of this term

? Do you use it and teach it? If so, why? If not,

what is your objection?

Almost immediately there were more than 100 responses! First, it quickly be�

“marginally significant” is indeed a

came clear that calling results that are close

common practice in many areas of psychology. As Frank LoSc hiavo (Ohio University) put it, “It sounds like it is the other committee members who are not on Earth.”

i~«

Chapter 5

But it also became clear that while it may be fairly common, many think it is a bad

idea. Charles Stangor (University of Maryland) called it a “completely bogus concept used to make us poor scientists feel better when our results are close but no cigar.” Tricia Yurak (Rowan University) called it “a fudge term that I won’t use” adding that “even if I get a p value of .07, I will report it as not significant.” Richard St. Jean (University of Prince Edward Island) recalls “one of my stats professors said calling a

…

finding marginally significant is like calling a woman marginally pregnant! The princi�

ple is that it is an all or none decision

…

” David Washburn (Georgia State University)

explains the logic: “One decides in advance or by convention to call p < .05 effects [T]erms like 'marginally significant' are counterfactuals—like say�

`significant’

ing you ‘almost did’ something that you didn’t do.” As several of the email posts noted, the argument was spelled out in some detail in an article by Chet Insko (2003; University of North Carolina):

…

null-hypothesis testing depends on traditional two-valued logic. Thus, one either

rejects or fails to reject the null hypothesis, and rejection of the null hypothesis allows for acceptance of the logical contradictory of the null hypothesis, the research hy�pothesis. The crucial point here is that deductive logic is two valued; for example, Socrates is or is not mortal…. A logician would not, for example, conclude that Socrates is marginally mortal. Since null-hypothesis testing depends on logic, only two-valued distinctions can be made, and this, of course, requires a single cut point to differentiate significant test statistics from nonsignificant test statistics. (p. 1331)

However, the majority opinion among those responding was expressed by Warren Thorngate (Carleton University): ” … people who adhere to the ‘0.05 or nothing!’ philosophy either need to be reeducated or enter therapy.” Phoebe Ellsworth (Uni�

versity of Michigan) added that “to act as though there is a gulf between .05 and .06�is not maintaining high standards; it is idiocy.” The point here is that .05 is an arbi�

trary convention. Indeed, many quoted a comment in an influential article by Rosnow and Rosenthal (1989) “… surely God loves the .06 nearly as much as the .05” (p. 1277). In addition, many noted that it is more important to emphasize the size of the effect and the power of the study, issues we consider in the next chapter. Also, several mentioned that such “near significant results” may be appropriate particularly when there are related results that are clearly significant (for example, if a study of the effects on stress is significant when using a questionnaire measure and is also

near significant when using a physiological measure). Finally, quite a few people�emphasized that the acceptability of reporting such results varies considerably

among different specialty areas of psychology.

Hypothesis Tests About Means

of Samples (Z Tests) and Standard Errors in Research Articles

As we have noted several times, research in which there is a known population mean and standard deviation is quite rare in psychology. Thus, you will not often see a Z test in a research article. We have asked you to learn about this situation mainly as a building block for understanding hypothesis testing in more common research situa�

tions. Still, Z tests do show up now and then.

Here is an example. As part of a larger study, Wiseman (1997) gave a loneli�ness test to a group of college students in Israel. As a first step in examining the results, Wiseman checked that the average score on the loneliness test was not sig�nificantly different from a known population distribution based on a large U.S.

Hypothesis Tests with Means of Samples

1

55

study of university students that had been conducted earlier by Russell and col�leagues (1980). Wiseman reported:

. . .

[T]he mean loneliness scores of the current Israeli sample were similar to those

of Russell et al.’s (1980) university sample for both males (Israeli: M = 38.74, SD

9.30; Russell: M = 37.06, SD = 10.91;

1.09, NS) and females (Israeli: M .25, NS). (p. 291)

36.39, SD = 8.87; Russell: M = 36.06, SD = 10.11;

In this example, the researcher gives the standard deviation for both the sample studied (the Israeli group) and the population (the data from Russell). However, in the steps of figuring each Z (the sample’s score on the distribution of means), the re�searcher would have used the standard deviation only of the population. Notice also that the researcher took the nonsignificance of the difference as support for the sam�ple means being “similar” to the population means. However, the researcher was

very careful not to claim that these results showed there was “no difference.”

Of the topics we have covered in this chapter, the one you are most likely to see in a research article is the standard deviation of the distribution of means, used to describe the amount of variation that might be expected among means of samples of a given size from this population. In this context, it is usually called the standard error (SE) or standard error of the mean (SEM). Standard errors are typically shown in research arti�cles as the lines that go above (and sometimes also below) the tops of the bars in a bar graph; these lines are called error bars. For example, Stankiewicz and colleagues (2006) examined how limitations in human perception and memory (and other factors) affect people’s ability to find their way in indoor spaces. In one of their experiments, eight stu�dents used a computer keyboard to move through a virtual indoor space of corridors and hallways shown on a computer monitor. The researchers calculated how efficiently stu�dents moved through the space, with efficiency ranging from 0 (extremely inefficient) to I (extremely efficient). The researchers compared the efficiency of moving through the space when students had a limited view of the space versus when they had a clear (or un�limited) view of the space. Their results, shown in Figure 5-9, include error bars.

1.0 7

0.8 –

0.6 –

T

T

0.4

0.2-I

0.0

Limited View Unlimited View�Viewing Condition

Figure 5-9 The mean navigation efficiency when navigating in the unlimited and lim�

ited viewing condition in Experiment 2. In the limited-view condition, visual information was�available as far as the next intersection (further details were obscured by “fog”). In the unlimited�

view condition, visual information was available to the end of the corridor. Error bars repre�sent 1 standard error of the mean.

Source: Stankiewicz, B. J., Legge, G. E., Mansfield, J. S., & Schlicht, E. J. (2006). Lost in virtual space: Studies in human and ideal spatial navigation. Journal of Experimental Psychology: Human Perception and Performance, 32, 688-704. Copyright © 2006 by the American Psychological Association.

Chapter 5

Error bars on graphs are common in psychology research articles, particularly in the more experimental areas such as perception and cognitive neuroscience.

Advanced Topic: Estimation, Standard Errors, and Confidence Intervals

Hypothesis testing is our main focus in this book. However, there is another kind of statistical question related to the distribution of means that is also important in psychology: estimating the population mean based on the scores in a sample. Tradition�ally, this has been very important in survey research. In recent years it is also becom�ing important in experimental research (e.g., Wilkinson and Task Force on Statistical Inference, 1999) and can even serve as an alternative approach to hypothesis testing.

Estimating the Population Mean When It Is Unknown

When the population mean is unknown, the best estimate of the population mean is the sample mean. In the study of students who were told about a person’s positive personality qualities, the mean attractiveness rating given to that person by the sam�ple of 64 students was 220. Thus, 220 is the best estimate of the mean attractiveness rating that would be given by the unknown population of students who would ever

be told about a person’s positive personality qualities.

How accurate is the sample mean as an estimate of the population mean? A way to get at this question is to ask, “How much do means of samples from a population vary?” Fortunately we have already thought about this question when considering the distribution of means. The variation in means of samples from a population is the vari�ation in the distribution of means. The standard deviation of this distribution of means, the standard error of the mean, is thus a measure of how much the means of samples vary from the overall population mean. (As we noted earlier, just because researchers are often interested in using a mean of a sample to estimate the population mean, this variation in the distribution of means is thought of as “error” and we give the name

“standard error of the mean” to the standard deviation of a distribution of means.)

In our example, the accuracy of our estimate of 220 for the mean of the popula�tion of students who are told about the person’s positive personality qualities is the standard error, which we figured earlier to be 6.

Range of Possible Means Likely to Include the Population Mean

You can also estimate the range of possible means that are likely to include the pop�ulation mean. Consider our estimate of 220 with a standard error of 6. Now follow this closely: suppose you took a mean from our distribution of means; it is 34% likely you would get a mean between 220 (the mean of the distribution of means) and 226 (one standard error above 220). This is because the distribution of means is a normal curve. Thus, the standard error is 1 standard deviation on that curve, and 34% of a normal curve is between the mean and 1 standard deviation above the mean. From this reasoning, we could also figure that another 34% should be between 220 and 214 (1 standard error below 220). Putting this together, we have a region from 214 to 226 that we are 68% confident should include the population mean if our sample was randomly taken from this population. (See Figure 5-10a.)

Hypothesis Tests with Means of Samples

157

I

�

�

—2 —1

0

+1 +2

I

I

204.58 208.24 214

220

226 231.76 235.42

68%

(a)

4

95%

(b)

4

99%

(c)

Figure 5-10 A distribution of means and the (a) 68%, (b) 95%, and (c) 99% confi�

dence intervals for students rating the physical attractiveness of a person after being told that the person has positive personality qualities (fictional data).

This is an example of a confidence interval (usually abbreviated CI). We would call it the “68% confidence interval.” The upper and lower ends of a confidence in�terval are called confidence limits. In this example, the confidence limits for the

68% confidence interval are 214 and 226 (see Figure 5-10a).

Let’s review the logic: based on our knowledge of a sample’s mean, we are try�ing to estimate the mean of the population that sample came from. Our best estimate of the population mean has to be our sample mean. What we don’t know is how good an estimate it is. If sample means from that population could vary a lot, then we can�not be very confident that our estimate is close to the true population mean. But if the sample means are likely all to be very close to the true population mean, we can as�sume our estimate is pretty close. To get a sense of how accurate our estimate is, we can use our knowledge of the normal curve to estimate the range of possible means that are likely to include the population mean. This estimate of the range of means is called a

confidence

interval.

confidence interval (Cl) roughly

speaking, the range of scores (that is, the scores between an upper and lower value) that is likely to include the true popula�

The 95% and 99% Confidence Intervals

tion mean; more precisely, the range of possible population means from which it is not highly unlikely that you could have obtained your sample mean.

Normally, you would want to be more than 68% confident about your estimates.�Thus, when figuring confidence intervals, psychologists use 95% or even 99% con��fidence intervals. These are figured based on the distribution of means for the area

confidence limit upper or lower

value of a confidence interval.

1 >

Chapter 5

that includes the middle 95% or middle 99%. For the 95% confidence interval, you want the area in a normal curve on each side between the mean and the Z score that includes 47.5% (47.5% plus 47.5% adds up to 95%). The normal curve table shows this to be 1.96. Thus, in terms of Z scores, the 95% confidence interval is from -1.96 to +1.96 on the distribution of means. Changing these Z scores to raw scores for the attractiveness ratings example gives an interval of 208.24 to 231.76 (see Figure 5-10b). That is, for the lower confidence limit, ( -1.96)(6) + 220 -11.76 + 220 = 208.24; for the upper confidence limit, (1.96)(6) + 220 11.76 + 220 = 231.76. In sum, based on the sample of 64 students who were told about the person’s positive personality qualities, you can be 95% confident that the true population mean for such students is between 208.24 and 231.76 (see

Figure 5-10b).

For a 99% confidence interval, you use the Z scores for the middle 99% of the normal curve (the part that includes 49.5% above and below the mean). This comes out to ±2.57. Changing this to raw scores, the 99% confidence interval is from

204.58 to 235.42 (see Figure 5-10c).

Notice in Figure 5-10 that the greater the confidence is, the broader is the con�fidence interval. In our example, you could be 68% confident that the true popula�tion mean is between 214 and 226; but you could be 95% confident that it is between 208.24 and 231.76 and 99% confident it is between 204.58 and 235.42. This is a gen�eral principle. It makes sense that you need a wider range of possibility to be more sure you are right.

Steps for Figuring Confidence Limits

There are two steps for figuring confidence limits. These steps assume that the distri�bution of means is approximately a normal distribution.

0 Figure the standard error. That is, find the standard deviation of the distribu�

tion of means in the usual way:

Qz

QM

‘v 2

crm

N

A For the 95% confidence interval, figure the raw scores for 1.96 standard

errors above and below the sample mean; for the 99% confidence interval, figure the raw scores for 2.57 standard errors above and below the sample mean. To figure these raw scores, first multiply 1.96 or 2.57 by the standard error, then add this to the mean for the upper limit and subtract this from the

mean for the lower limit.

In terms of the overall figuring, once you know the standard error, the upper limit of the 95% confidence interval is equal to the sample mean plus 1.96 mul�tiplied by the standard error of the mean: upper limit = M + (1.96)(o- m); the lower limit is the sample mean minus 1.96 multiplied by the standard error: lower limit = M – (1.96)(o-m). For the 99% CI, the computation for the upper limit is: M + (2.57)(crm); the lower 99% CI limit is M – (2.57) (um).

95% confidence interval confidence

interval in which, roughly speaking, there is a 95% chance that the population mean falls within this interval,

Example Let’s find the 99% confidence interval for the verbal fillers example

from earlier in the chapter. Recall that, in that example, the number of verbal fillers�used by students in the general population (that is, students who had not attended a

99% confidence interval confidence

interval in which, roughly speaking, there is a 99% chance that the population mean falls within this interval.

communication skills seminar) was normally distributed with a mean of 53 and a�standard deviation of 7. The 25 students who attended a presentation skills seminar

used a mean of 48 fillers.

Hypothesis Tests with Means of Samples

159

0 Figure the standard error. QM

e) For the 95% confidence interval, figure the raw scores for 1.96 standard

72

mewl w -ir 41 – wi 1

V1.96 = 1.40.

Note that you are figuring the con�fidence interval based on the mean of your sample, not based on the mean oftheknow npopulation.

So,inthecarrentexampleyeaare

figuring the confidence interval around a mean of 48, which was the mean number of fillers used by the 25 students who attended the seminar. The mean number of fillers used by the population of students in general is known (53); so there is no need to figure any kind of confidence interval based on that mean.

N

25

errors above and below the sample mean; for the 99% confidence interval, figure the raw scores for 2.57 standard errors above and below the sample mean. You want the 99% confidence interval. Thus, first multiply 2.57 by 1.40 to get 3.60, which is how far the confidence limit is from the mean. For the upper confidence limit, add this distance to the sample mean: 48 + 3.60 = 51.60.

In terms of the overall calculations, upper limit

M + (2.57)

(o-A,/ = 48 + (2.57)(1.

40)

tract 3.60 (the results of multiplying 2.57 by 1.40) from 48, the mean of the sample, which gives 44.40. In terms of the overall calculations, lower limit

51.60. For the lower confidence limit, sub�

M — (2.57) (1.40) = 44.40.

Thus, based on this sample of 25 students, you can be 99% confident that an interval from 44.40 to 51.60 includes the true population mean.

The Subtle Logic of Confidence Intervals

If you understand the preceding explanation, it will be sufficient for practical purposes in working with confidence intervals. Basically, confidence intervals tell you the range of means that you can be pretty sure include the true population mean. However, if you want to think deeply about the situation, there is a subtle issue about precisely what these numbers mean. (What follows is kind of an “advanced, advanced” topic

section!)

Strictly speaking, consider what we are figuring to be, say, a 95% confidence

interval. We are figuring it as the range of means that are 95% likely to come from a population with a true mean that happens to be the mean of our sample. However, what we really want to know is the range that is 95% likely to include the true popu�lation mean. This we cannot know. That is, we are figuring one thing and really want to know another. Read this paragraph again and think about it. It is easy to miss this

subtle but logically significant twist.

The way this awkward situation has been dealt with traditionally by most re�searchers is just to ignore this subtlety. Researchers who are more sophisticated statisti�

cally are comfortable with the situation by emphasizing that what we actually say is�that we are 95% confident that the true mean is in this range. That is, by using this lan�

guage, we are acknowledging that what we are doing is really a bit backward, but it is the best we can do! “Confidence” is closer to the subjective interpretation of probability we discussed in Chapter 3. In fact, “confidence” is meant to be a slightly vaguer term than probability. Nevertheless, it is not completely vague. What we are doing does have

a solid basis.

Here is how to understand this: suppose in our attractiveness ratings example, the true mean was indeed 220. As we have seen, this would give a 95% confi�dence interval of 208.24 to 231.76, as shown in Figure 5-11a. We don’t know what the true population mean is. But suppose the true population mean was 208.24. The range that includes 95% of sample means from this population’s distribution of means would be from 196.48 to 220.00, as shown in Figure 5-11b. (You can work this out yourself following the two steps for figuring confidence limits.) Similarly, for the population with a mean of 231.76, the range that includes 95% of sample means from this population’s distribution of means is from 220.00 to 243.52, as shown in Figure 5-11c.

Chapter 5

�

�

�

4

(

208.24

231.76

).

4

196.48

(b)

(c)

243.

52

�

220

Figure 5-11 (a) 95% confidence interval based on sample mean of 220 for students

rating the physical attractiveness of a person after being told that the person has positive per�sonality qualities (fictional data); (b) range including 95% of sample means, based on distrib�ution of means shown above it with limb = lower limit of the 95% confidence interval for M = 220; (c) range including 95% of sample means, based on distribution of means above it

with RAI, = upper limit of the 95% confidence interval for M = 220

What this shows is a general principle: for a 95% confidence interval, the lower confidence limit is the lowest possible population mean that would have a 95% probability of including our sample mean; the upper confidence limit is the highest pos�

sible population mean that would have a 95% probability of including our sample mean.

This convoluted logic is a bit like the double-negative logic behind hypothesis testing. This is no accident, since both are making inferences from samples to popu�lations using the same information.

Confidence Intervals and Hypothesis Testing

A practical implication of the link of confidence intervals and hypothesis testing is that you can use confidence intervals to do hypothesis testing! If the confidence in�terval does not include the mean of the null hypothesis distribution, then the result is significant. For example, in the attractiveness ratings study, the 95% confidence in�terval for those who were told that the person has positive personality qualities was from 208.24 to 231.76. However, the population that was told nothing about the per�son’s personality qualities had a mean of 200. This population mean is outside the

range of the confidence interval. Thus, if you are 95% confident that the true range is�208.24 to 231.76 and the population mean for those who were told nothing about the�person’s personality qualities is not in this range, you are 95% confident that that

population is not the same as the one your sample came from.

Another way to understand this is in terms of the idea that the confidence limits are the points at which a more extreme true population would not include your sam�ple mean 95% of the time. The population mean for those who were told nothing

Hypothesis Tests with Means of Samples

161

about the person’s personality qualities was 200. If this were the true mean also for the group that was told about the person’s positive personality qualities, 95% of the time it would not produce a sample mean as high as the one we got.

�

How are you doing

�

�

(

_

(a) What is the best estimate of a popu

lation mean? (b) Why?

(a) What number is used to indicate the accuracy of an estimate of the popu�

lation mean? (b) Why?

3. What is a 95% confidence interval?

4. A researcher predicts that showing a certain film will change people’s atti�

tudes toward alcohol. The researchers then randomly select 36 people, show them the film, and give them an attitude questionnaire. The mean score on the attitude test for these 36 people is 70. The score on this test for people in the general population (who do not see the film) is 75, with a standard devia�tion of 12. (a) Find the best estimate of the mean of people who see the film and (b) its 95% confidence interval. (c) Compare this result to the conclusion you drew for this same situation when you used this example in the How are

you doing? section for hypothesis testing with a distribution of means.

5. (a) Why is it wrong to say that the 95% confidence interval is the region in

which there is a 95% probability of finding the true population mean? (b) What is the basis for our 95% confidence?

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162

Chapter 5

Advanced Topic Controversy: Confidence Intervals versus Significance Tests

You may recall from Chapter 4 that for a number of years there has been a lively de��bate among psychologists about significance testing. Among the major issues in that�debate is a proposal that psychologists should use confidence intervals instead of

significance tests.

Those who favor replacing significance tests with confidence intervals (e.g., Cohen, 1994; Hunter, 1997; Schmidt, 1996) cite several major advantages. First, as we noted above, confidence intervals contain all the key information in a signifi�cance test,5 but also give additional information—the estimation of the range of val�ues that you can be quite confident include the true population mean. A second advantage is that they focus attention on the estimation of effects instead of on hy�pothesis testing. Some researchers argue that the goal of science is to provide numeric estimates of effects (and the accuracy of those estimates), not just decisions as to

whether an effect is different from zero.

Confidence intervals are particularly valuable when the results are not signifi�cant (Frick, 1995). This is, because knowing the confidence interval gives you an idea of just how far from no effect you can be confident that the true mean is to be found. If the results are not significant and the entire confidence interval is near to no effect, you can feel confident that, even if there is some true effect, it is probably small. However, if the results are not significant and the confidence interval, while including no effect, also spreads out to include means far from no effect, it would tell us that the study is really very inconclusive: it is possible that there is little or no ef�

fect, but it is also possible that there is a substantial effect.

A third advantage claimed by proponents of confidence intervals over signifi�cance testing is that researchers are less likely to misuse them. As we noted in Chapter 4, a common error in the use of significance tests is to conclude that a non�significant result means there is no effect. With confidence intervals, it is harder to fall into this kind of error.

In light of these various advantages, the most recent Publication Manual of the American Psychological Association (2001) takes the position that “The use of con�

fidence intervals is . . . strongly recommended” (p. 22).

However, it is still relatively uncommon to find confidence intervals in many

types of psychology research articles. In part, this is probably due to tradition and to�most psychologists having been trained with significance tests and having become

used to them.

Other researchers (e.g., Abelson, 1997; Harris, 1997; Nickerson, 2000) emphasize two reasons for not abandoning significance testing in favor of confidence intervals. First, for some advanced statistical procedures, it is possible to do significance testing but not to figure confidence intervals. Second, just as it is possible to make mistakes with significance tests, it is also possible to make other kinds of mistakes with confidence inter�

vals—especially since most research psychologists are less experienced in using them.

Whatever the outcome of this controversy about confidence intervals, it is valu�able to understand them, since you will run into them occasionally when reading re�

search literature, and you are likely to see them more often in the future. On the other hand, they now appear only occasionally, and there is no sign that they are likely to replace significance testing any time soon. For this reason (and to keep the amount of material to be learned manageable), we have made confidence intervals an ad�vanced topic and decided not to emphasize them in subsequent chapters of this book, which are mainly on significance testing in various types of research situations.

Hypothesis Tests with Means of Samples

163

Advanced Topic: Confidence Intervals in Research Articles

As we noted, confidence intervals (usually abbreviated as CI), while far from stan�

dard, are sometimes reported in research articles. For example, consider a study by�Christakis and Fowler (2007). They studied more than 12,000 people over a 32-year

period to examine whether people’s chances of becoming obese are related to whether they have friends and family who become obese. They reported that “A per�son’s chance of becoming obese increased by 57% (95% confidence interval [CI], 6 to 123) if he or she had a friend who became obese in a given interval” (p. 370). This means that we can be 95% confident that the true increase in obesity risk was between 6% and 123%. As another example, an organizational psychologist might explain that the average number of overtime hours per week worked in a particular industry is 3.7 with a 95% confidence interval of 2.5 to 4.9. This would tell you that the true average

number of overtime hours is probably somewhere between 2.5 and 4.9.

A shortcut that many researchers find helpful in reading research articles that give standard errors but not confidence intervals is that the 95% confidence interval is approximately 2 standard errors in both directions (it is exactly 1.96 SEs) and the 99% confidence interval is approximately 2.5 standard errors in both directions (it is exactly 2.57 SEs).

�

1. When studying a sample of more than one individual, the comparison distribu�

tion in the hypothesis-testing process is a distribution of means. It can be thought�of as what would result from (a) taking a very large number of samples, each of�the same number of scores taken randomly from the population of individuals,

and then (b) making a distribution of the means of these samples.

2. The distribution of means has the same mean as the corresponding population

of individuals. However, it has a smaller variance because the means of samples are less likely to be extreme than individual scores. (In any one sample, extreme scores are likely to be balanced by middle scores or extreme scores in the other direction.) Specifically, the variance of the distribution of means is the variance of the population of individuals divided by the number of individuals in each sam�ple. Its standard deviation is the square root of its variance. The shape of the dis�tribution of means approximates a normal curve if either (a) the samples are each

of 30 or more scores or (b) the population of individuals follows a normal curve.

3. Hypothesis tests with a single sample of more than one individual and a known

population are called Z tests and are done the same way as the hypothesis tests of Chapter 4 (where the studies were of a single individual compared to a popu�lation of individuals). The main exception is that the comparison distribution in a hypothesis test with a single sample of more than one individual and a known

population is a distribution of means

4. There is some controversy about the use of terms such as marginal significance,

approaching significance, and near significant trend to describe results that come close to the significance cutoff value. Critics of these terms note that hypothesis testing is an all or nothing decision. However, other researchers advocate for greater flexibility and point out that the .05 and .01 significance levels are arbi�trary conventions.

164

Chapter 5

5. The kind of hypothesis testing described in this chapter (the Z test) is rarely used

in research practice; you have learned it as a stepping-stone. The standard devi�ation of the distribution of means (the standard error) is commonly used to describe the expected variability of means, particularly in bar graphs in which the standard error may be shown as the length of a line above (and sometimes

below) the top of each bar.

6. ADVANCED TOPIC: The sample mean is the best estimate for the population

mean when the population mean is unknown. The accuracy of the estimate is the standard deviation of the distribution of means (also known as the standard error), which tells you roughly the amount by which means vary. Based on the distribu�tion of means, you can figure the range of possible means that are likely to include the population mean. If we assume the distribution of means follows a normal curve, the 95% confidence interval includes the range from 1.96 standard deviations below the sample mean (the lower confidence limit) to 1.96 standard deviations above the sample mean (the upper confidence limit). Strictly speaking, the 95% confidence interval around a sample mean is the range in which the lower limit is the mean of the lowest population that would have a 95% probability of including a sample with this sample mean, and the upper limit is the corresponding mean of the highest population. The 99% confidence interval includes the range from 2.57 standard deviations below the sample mean (the lower confidence limit) to 2.57

standard deviations above the sample mean (the upper confidence limit).

7. ADVANCED TOPIC: An aspect of the ongoing controversy about significance

tests is whether researchers should replace them with confidence intervals. Propo�nents of confidence intervals argue that they provide additional information, put the focus on estimation, and reduce misuses common with significance tests. Confi�dence intervals have become more common in recent years in psychology research articles, but they are still relatively unusual, in part due to tradition and unfamiliar�ity with them. In addition, opponents of relying exclusively on confidence intervals argue that they cannot be used in some advanced procedures, estimation is not al�ways the goal, and they can have misuses of their own. When confidence intervals are reported in research articles, it is usually with the abbreviation CI.

1

Mon of means (p. 138)

o-m (p. 142)

2

standard error (SE) (p. 142)

f a distribution of means

standard deviation of a distribution

Z test (p. 148)

40)

of means (p. 142)

confidence interval (CI) (p. 157) confidence limit (p. 157)

95% confidence interval (p. 158)�99% confidence interval (p. 158)

1

41)

QM (p. 142)

e of a distribution of means

standard error of the mean (SEM) (p. 142)

41)

I

�

ig the Standard Deviation Distribution of Means

;tandard deviation of the distribution of means for a population with cr 1ple size of 20.

13

Hypothesis Tests with Means of Samples

165

Answer

Using Rules 2a and 2b for the characteristics of a distribution of means: The vari�ance of a distribution of means is the variance of the population of individuals divided by the number of individuals in each sample. The standard deviation of a distribution of means is the square root of the variance of the distribution of means. The variance of the population is 169 (that is, 13 squared is 169); dividing this by 20 gives a variance of the distribution of means of 8.45. The square root of

this, 2.91, is the standard deviation of the distribution of means.

Using the formula,

,72

132

169

QM

�

2.91

N

20

20

Hypothesis Testing with a Sample of More Than One: The Z Test

A sample of 75 was given an experimental treatment and had a mean of 16 on a par�ticular measure. The general population of individuals has a mean of 15 on this measure and a standard deviation of 5. Carry out a Z test using the five steps of hypothesis testing with a two-tailed test at the .05 significance level, and make a drawing of the distributions involved.

Answer

0 Restate the question as a research hypothesis and a null hypothesis about

the populations. The two populations are:

Population 1: Those given the experimental treatment.

Population 2: People in the general population (who are not given the experi�mental treatment).

The research hypothesis is that the population given the experimental treatment�will have a different mean on the particular measure from the mean of people�in the general population (who are not given the experimental treatment):

# The null hypothesis is that the populations have the same mean score�on this measure: pi = 112.

0 Determine

the

characteristics

of

the

comparison

distribution.

0.2

52

= P,

15; um

�

.57; shape is normal (sample

N

75

size is greater than 30).

0 Determine the cutoff sample score on the comparison distribution at which

the null hypothesis should be rejected. Two-tailed cutoffs, 5% significance level, are +1.96 and —1.96.

0 Determine your sample’s score the comparison distribution. Using the

o

n

formula, Z = (M

—

1.44)10- m, Z = (16 — 15)/.57 = 1/.57 = 1.75.

0 Decide whether to reject the null hypothesis. The sample’s Z score of 1.75

is not more extreme than the cutoffs of +1.96; do not reject the null hypothe�sis. Results are inconclusive. The distributions involved are shown in Figure 5-12.

Chapter 5

(a)

15

cy2 = 25

a = 5

Raw Scores: 5

Z Scores: –2

0

+1

+2

�

—

�

�

-2

–1

0

1

2

15

15.57

16.14

(c)

M= 16

�

16

Figure 5-12 Answer to the hypothesis-testing problem in Example Worked-Out Prob�

lems: (a) the distribution of the population of individuals, (b) the distribution of means (the comparison distribution), and (c) the sample’s distribution.

Outline for Writing Essays for Hypothesis-Testing Problems Involving a Single Sample of More Than One and a Known Population (Z Test)

1. Describe the core logic of hypothesis testing in this situation. Be sure to explain

the meaning of the research hypothesis and the null hypothesis in this situation�where we focus on the mean of a sample and compare it to a known population�mean. Explain the concept of support being provided for the research hypothe�

sis when the study results allow the null hypothesis to be rejected.

2. Explain the concept of the comparison distribution. Be sure to mention that,

with a sample of more than one, the comparison distribution is a distribution of�means because the information from the study is a mean of a sample. Mention�that the distribution of means has the same mean as the population mean

Hypothesis Tests with Means of Samples

167

because there is no reason for random samples in the long run to have a differ-ent mean; the distribution of means has a smaller variance (the variance of the population divided by the number in each sample) because it is harder to get ex�treme means than extreme individual cases by chance, and the larger the sam�

I

ples are, the rarer it is to get extreme means.

3. Describe the logic and process for determining (using the normal curve) the cut�

off sample score(s) on the comparison distribution at which the null hypothesis

should be rejected.

4. Describe why and how you figure the Z score of the sample mean on the com�

parison distribution.

5. Explain how and why the scores from Steps e and 0 of the hypothesis-testing

process are compared. Explain the meaning of the result of this comparison with regard to the specific research and null hypotheses being tested.

Advanced Topic: Finding Confidence Intervals

Find the 99% confidence interval for the sample mean in the study just described.

Answer

0 Figure the standard error. The standard error is the standard deviation of the

distribution of means. In the preceding problem, it was .57.

A For the 95% confidence interval, figure the raw scores for 1.96 standard

errors above and below the sample mean; for the 99% confidence interval, figure the raw scores for 2.57 standard errors above and below the sample mean. For the 99% confidence interval, upper limit = M + (2.57)(crM)

16 + (2.57)(.57) = 16 + 1.46 = 17.46; lower limit = M — (2.57)(aM) 16 — (2.57)(.57) = 16 — 1.46 = 14.54. Thus, the 99% confidence interval from 14.54 to 17.46.

i

s

Advanced Topic: Outline for Writing Essays for Finding Confidence Intervals

1. Explain that a confidence interval is an estimate (based on your sample’s mean

and the standard deviation of the distribution of means) of the range of values that�is likely to include the true population mean for the group studied (Population 1).�Be sure to mention that the 95% (or 99%) confidence interval is the range of val�

ues you are 95% (or 99%) confident include the true population mean.

2. Explain that the first step in figuring a confidence interval is to estimate the pop�

ulation mean (for which the best estimate is the sample mean), and figure the

standard deviation of the distribution of means.

3. Mention that you next find the Z scores that go with the confidence interval that

you want.

4. Describe how to change the Z scores to raw scores to find the confidence interval.

�

Practice Proble

These problems involve figuring. Most real-life statistics problems are done on a�computer with special statistical software. Even if you have such software, do these

problems by hand to ingrain the method in your mind.

All data are fictional unless an actual citation is given.

168

Chapter 5

Set I (for Answers to Set I Problems, see pp. 677-678)

1. Why is the standard deviation of the distribution of means generally smaller than

the standard deviation of the distribution of the population of individuals?

2. For a population that has a standard deviation of 10, figure the standard devia�

tion of the distribution of means for samples of size (a) 2, (b) 3, (c) 4, and (d) 9.

3. For a population that has a standard deviation of 20, figure the standard devia�

tion of the distribution of means for samples of size (a) 2, (b) 3, (c) 4, and (d) 9.

4. ADVANCED TOPIC: Figure the 95% confidence interval (that is, the lower and

upper confidence limits) for each part of problem 2. Assume that in each case�the researcher’s sample has a mean of 100 and that the population of individuals

is known to follow a normal curve.

5. ADVANCED TOPIC: Figure the 99% confidence interval (that is, the lower and

upper confidence limits) for each part of problem 3. Assume that in each case�the researcher’s sample has a mean of 10 and that the population of individuals

is known to follow a normal curve.

6. For each of the following samples that were given an experimental treatment,

test whether they are different from the general population: (a) a sample of 10 with a mean of 44, (b) a sample of 1 with a mean of 48. The general population of individuals has a mean of 40, a standard deviation of 6, and follows a normal curve. For each sample, carry out a Z test using the five steps of hypothesis test�ing with a two-tailed test at the .05 significance level, and make a drawing of the distributions involved. (c) ADVANCED TOPIC: Figure the 95% confidence

interval for parts (a) and (b).

7. For each of the following samples that were given an experimental treatment,

test whether they scored significantly higher than the general population: (a) a sample of 100 with a mean of 82, (b) a sample of 10 with a mean of 84. The gen�eral population of individuals has a mean of 81, a standard deviation of 8, and follows a normal curve. For each sample, carry out a Z test using the five steps of hypothesis testing with a one-tailed test at the .01 significance level, and make a drawing of the distributions involved. (c) ADVANCED TOPIC: Figure

the 99% confidence interval for parts (a) and (b).

8. Twenty-five women between the ages of 70 and 80 were randomly selected

from the general population of women their age to take part in a special program to decrease reaction time (speed). After the course, the women had an average reaction time of 1.5 seconds. Assume that the mean reaction time for the general population of women of this age group is 1.8, with a standard deviation of .5 seconds. (Also assume that the population is approximately normal.) What should you conclude about the effectiveness of the course? (a) Carry out a Z test using the five steps of hypothesis testing (use the .01 level). (b) Make a drawing of the distributions involved. (c) Explain your answer to someone who is famil�iar with the general logic of hypothesis testing, the normal curve, Z scores, and probability, but not with the idea of a distribution of means. (d) ADVANCED TOPIC: Figure the 99% confidence interval and explain your answer to some�one who is familiar with the general logic of hypothesis testing, the normal curve, Z scores, probability, and the idea of a distribution of means, but has not

heard of confidence intervals.

9. A large number of people were shown a particular film of an automobile colli�

sion between a moving car and a stopped car. Each person then filled out a ques��tionnaire about how likely it was that the driver of the moving car was at fault,�on a scale from 0 = not at fault to 10 = completely at fault. The distribution of

Hypothesis Tests with Means of Samples

169

ratings under ordinary conditions follows a normal curve with p = 5.5 and Q = .8. Sixteen randomly selected individuals are tested in a condition in which the wording of the question is changed so that the question asks, “How likely is it that the driver of the car who crashed into the other was at fault?” (The differ�ence is that in this changed condition, instead of describing the event in a neutral way, the question uses the phrase “crashed into.”) Using the changed instruc�tion, these 16 research participants gave a mean at-fault rating of 5.9. Did the changed instructions significantly increase the rating of being at fault? (a) Carry out a Z test using the five steps of hypothesis testing (use the .05 level). (b) Make a drawing of the distributions involved. (c) Explain your answer to some�one who has never taken statistics. (d) ADVANCED TOPIC: Figure the 95%

confidence interval.

10. Lee and colleagues (2000) tested a theory of the role of distinctiveness in

face perception. In their study, participants indicated whether they recognized�each of 48 faces of male celebrities when they were shown rapidly on a com�

puter screen. A third of the faces were shown in caricature form, in which facial features were electronically modified so that distinctive features were exaggerated; a third were shown in veridical form, in which the faces were not modified at all; and a third were shown in anticaricature form, in which facial features were modified to be slightly more like the average of the celebrities’ faces. The average percentage correct across their participants is shown in Figure 5-13. Explain the meaning of the error bars in this figure to a person who understands mean, standard deviation, and variance, but nothing

else about statistics.

11. ADVANCED TOPIC: Anderson and colleagues (2000) studied the rate of HIV

testing among adults in the United States and reported one of their findings as�follows: “Responses from the NHIS [National Health Interview Survey] indi�

cate that by 1995, 39.7% of adults (95% CI = 38.8%, 40.5%) had been tested at

least once

” (p. 1090). Explain what “(95% CI = 38.8%, 40.5%)” means to a

person who understands hypothesis testing with the mean of a sample of more than one but who has never heard of confidence intervals.

70

65 –

60

55

50

Anticaricature

Veridical

Caricature

Image Type

Figure 5-13 Identification accuracy as a function of image type. Standard error bars

are shown.

Source: Lee, K., Byatt, G., & Rhodes, G. (2000). Caricature effects, distinctiveness, and identification:�Testing the face-space framework. Psychological Science, 11, 381. Copyright © 2000 by Blackwell

Publishing. Reprinted by permission of Blackwell Publishers Journals.

170

Chapter 5

Set II

12. Under what conditions is it reasonable to assume that a distribution of means

will follow a normal curve?

13. Indicate the mean and the standard deviation of the distribution of means for each of the following situations.

Population

Sample

Size

Mean

Variance

N

(a)

(b)

(C)

(d)

10

(e)

10

(f)

(9)

14. Figure the standard deviation of the distribution of means for a population with a

standard deviation of 20 and sample sizes of (a) 10, (b) 11, (c) 100, and (d) 101.

15. ADVANCED TOPIC: Figure the 95% confidence interval (that is, the lower and

upper confidence limits) for each part of problem 13. Assume that in each case the researcher’s sample has a mean of 80 and the population of individuals is known to follow a normal curve.

16. ADVANCED TOPIC: Figure the 99% confidence interval (that is, the lower and

upper confidence limits) for each part of problem 14. Assume that in each case�the researcher’s sample has a mean of 50 and that the population of individuals

is known to follow a normal curve.

17. For each of the following studies, the samples were given an experimental treat�

ment and the researchers compared their results to the general population. (Assume all populations are normally distributed.) For each, carry out a Z test using the five steps of hypothesis testing for a two-tailed test, and make a draw�ing of the distributions involved. ADVANCED TOPIC: Figure the 95% confi�dence interval for each study.

Sample

Sample

Significance

Population

Size

Mean

Level

cr

N

(a)

36

16

38

.05

(b)

36

16

38

.05

(c)

36

16

38

.05

(d)

36

16

38

.01

(e)

34

16

38

.01

18. For each of the following studies, the samples were given an experimental treat�

ment and the researchers compared their results to the general population. For each, carry out a Z test using the five steps of hypothesis testing for a two-tailed test at the .01 level, and make a drawing of the distributions involved. ADVANCED TOPIC: Figure the 99% confidence interval for each study.

(

Hypothesis Tests with Means of Samples

171

Population

Sample Size

Sample Mean

a

N

(a)

ilj

(b)

(c)

12

(d)

14

100

12

19. A researcher is interested in whether people are able to identify emotions cor�

rectly when they are extremely tired. It is known that, using a particular method of measurement, the accuracy ratings of people in the general population (who are not extremely tired) are normally distributed with a mean of 82 and a vari�ance of 20. In the present study, however, the researcher arranges to test 50 peo�ple who had no sleep the previous night. The mean accuracy for these 50 individuals was 78. Using the .05 level, what should the researcher conclude? (a) Carry out-a Z test using the five steps of hypothesis testing. (b) Make a drawing of the distributions involved. (c) Explain your answer to someone who knows about hypothesis testing with a sample of a single individual but who knows nothing about hypothesis testing with a sample of more than one individual. (d) ADVANCED TOPIC: Figure the 95% confidence interval and explain your an�swer to someone who is familiar with the general logic of hypothesis testing, the normal curve, Z scores, probability, and the idea of a distribution of means, but

who has not heard of confidence intervals.

20. A psychologist is interested in the conditions that affect the number of dreams

per month that people report in which they are alone. We will assume that based on extensive previous research, it is known that in the general popula�tion the number of such dreams per month follows a normal curve, with µ = 5 and o = 4. The researcher wants to test the prediction that the number of such dreams will be greater among people who have recently experienced a trau�matic event. Thus, the psychologist studies 36 individuals who have recently experienced a traumatic event, having them keep a record of their dreams for a month. Their mean number of alone dreams is 8. Should you conclude that people who have recently had a traumatic experience have a significantly dif�ferent number of dreams in which they are alone? (a) Carry out a Z test using the five steps of hypothesis testing (use the .05 level). (b) Make a drawing of the distributions involved. (c) Explain your answer to a person who has never had a course in statistics. (d) ADVANCED TOPIC: Figure the 95% confidence

I

interval.

21. A government-sponsored telephone counseling service for adolescents tested

whether the length of calls would be affected by a special telephone system that had a better sound quality. Over the past several years, the lengths of telephone calls (in minutes) were normally distributed with µ = 18 and o = 8. They arranged to have the special phone system loaned to them for one day. On that day, the mean length of the 46 calls they received was 21 minutes. Test whether the length of calls has changed using the 5% significance level. (a) Carry out a Z test using the five steps of hypothesis testing. (b) Make a drawing of the dis�tributions involved. (c) Explain your answer to someone who knows about hypothesis testing with a sample of a single individual but who knows nothing about hypothesis testing with samples of more than one individual. (d) ADVANCED TOPIC: Figure the 95% confidence interval.

172

Chapter 5

50

�

Young

Old

40

30

20

10

1

0

-10

Neither

Walk

Memory

Both

Task Made More Difficult

Figure 5-14 Dual-task costs in memory as a function of age group and difficulty con�

dition. Error bars represent ± I SEM.

Source: Li, K. Z. H., Lindenberger, U., Freund, A. M., & Baltes, P. B. (2001). Walking while memorizing: Age-related differences in compensatory behavior. Psychological Science, 12, 230-237. Copyright 0 2001 by Blackwell Publishing. Reprinted by permission of Blackwell Publishers Journals.

22. Li and colleagues (2001) compared older (aged 60 to 75) and younger (aged 20

to 30) adults on the impact on memory of making some aspect of what they were doing more difficult. Figure 5-14 shows some of their results. In the figure caption they note that “Error bars represent ±1 SEM” (standard error of the mean). Explain the meaning of this statement, using one of the error bars as an example, to a person who understands mean and standard deviation, but knows

nothing else about statistics.

23. ADVANCED TOPIC: Perna and colleagues (2003) tested whether a stress man�

agement intervention could reduce injury and illness among college athletes. In their study, 34 college athletes were randomly assigned to be in one of two groups: (1) a stress management intervention group: this group received a cog�nitive behavioral stress management (CBSM) intervention during preseason training; (2) a control group: this group did not receive the intervention. At the end of the season, for each athlete, the researchers recorded the number of health center visits (including visits to the athletic training center) and the num�ber of days of illness or injury during the season. The results are shown in Figure 5-15. In the figure caption, the researchers note that the figure show shows the “Mean (+SE)”. This tells you that the line above the top of each bar

represents the standard error. Explain what this means, using one of the error bars as an example, to a person who understands mean and standard deviation, but knows nothing else about statistics.

Hypothesis Tests with Means of Samples

173

5

4

3

2

NOCBSM

=Control

1

I

(

0

Office Visits

Days Out (ill/injured)

Figure 5-15 Mean (+SE) number of accumulated days injured or ill and athletic

training room and health center office visits for cognitive behavioral stress (CBSM) (n = 18) and control groups (n = 16) from study entry to season’s end.

management

Source: Perna, F. M., Antoni, M. H., Baum, A., Gordon, P., & Schneiderman, N. (2003). Cognitive�behavior stress management effects on injury and illness among competitive athletes: A randomized

clinical trial. Annuls of Behavioral Medicine, 25, 66-73. Copyright © Lawrence Erlbaum Associates, Inc. Reprinted with permission.

24. Cut up 90 small slips of paper, and write each number from 1 to 9 on 10 slips

each. Put the slips in a large bowl and mix them up. (a) Take out a slip, write�down the number on it, and put it back. Do this 20 times. Make a histogram, and�figure the mean and the variance of the result. You should get an approximately

rectangular distribution. (b) Take two slips out, figure out their mean, write it

down, and put the slips back.

then figure the mean and the variance of this distribution of means. The variance should be about half of the variance of the distribution of individual scores. (c) Repeat the process again, this time taking three slips at a time. Again, make a histogram and figure the mean and the variance of the distribution of means. The distribution of means of three slips each should have a variance of about a third of the distribution of individual scores. Also note that as the sample size in�creases, your distributions get closer to normal. (Had you begun with a normally distributed distribution of slips, your distributions of means would have been fairly close to normal regardless of the number of slips in each sample.)

6 Repeat this process 20 times. Make a histogram;

�

174

Chapter 5

2. We have ignored the fact that a normal curve is a smooth theoretical distribu�

tion, while in most real-life distributions, scores are only at specific numbers, such as a child being in a particular grade and not in a fraction of a grade. So one difference between our example distribution of means and a normal curve is that the normal curve is smooth. However, in psychology research, even when our measurements are at specific numbers, we usually assume that the underlying

thing being measured is continuous.

3. We have already considered this principle of a distribution of means tending

toward a normal curve in Chapter 3. Though we had not yet discussed the distri�bution of means, we still used this principle to explain why the distribution of so many things in nature follows a normal curve. In that chapter, we explained it as the various influences balancing each other out, to make an averaged influence come out with most of the scores near the center and a few at either extreme. Now we have made the same point using the terminology of a distribution of means. Think of any distribution of individual scores in nature as a situation in which each score is actually an average of a random set of influences on that in�dividual. Consider the distribution of weights of pebbles. Each pebble’s weight is a kind of average of all the different forces that went into making the pebble

have a particular weight.

4. This fictional study would be much better if the researchers also had another

group of students who were randomly assigned to rate the attractiveness of the person after being told nothing about the person’s personality qualities. Relying on the attractiveness ratings for a known population of students is a bit hazardous because the circumstances in the experiment might be somewhat different from that of the usual situation in which students rated the attractiveness of the person. However, we have taken liberties with this example to help introduce the hypothesis-testing process to you one step at a time. In this example and the others in this chapter, we use situations in which a single sample is contrasted with a “known” population. Starting in Chapter 7, we extend the hypothesis-testing procedure to more realistic research situations, those involving more than one group of partic�ipants and those involving populations whose characteristics are not known.

5. Some proponents of confidence intervals over significance testing argue that we should ignore the link with hypothesis testing altogether. This is the most radi�

cal antisignificance-test position. That is, these psychologists argue that our en��tire focus should be on estimation, and significance testing of any kind should�be irrelevant. In Chapter 6, we will discuss the rationale for their position, along

with the counterarguments.

6. Technically, when taking the samples of two slips, this should be done by taking

one, writing it down, putting it back, then taking the next, writing it down, and putting it back. You would consider these two scores as one sample for which you figure a mean. The same applies for samples of three slips. This is called sam�pling with replacement. However, with 90 slips in the bowl, taking two or three slips at a time and putting them back will be a close enough approximation for this exercise and will save you some time.