Mental Health: A Report of the Surgeon General

among others. Underlying this heterogeneous group of
disorders is a state of heightened arousal or fear in
relation to stressful events or feelings. The biological
manifestations of anxiety, which are grounded in the
"fight-or-flight" response, are unmistakable: they
include surge in heart rate, sweating, and tensing of
muscles. But this is certainly not the whole picture.
Although the full array of biological causes and
correlates of anxiety are not yet in our grasp, numerous
effective treatments for anxiety disorders exist now.
Treatment draws on an assortment of psychosocial and
pharmacological approaches, administered alone or in
combination.

Mood disorders take a monumental toll in human
suffering, lost productivity, and suicide. Moreover,
when unrecognized, they can result in unnecessary
health care use. Mood disorders rank among the top 10
causes of worldwide disability (Murray & Lopez,
1996). Major depression and bipolar disorder are the
most familiar mood disorders, but there are others
including cyclothymia (alternating manic and
depressive states that, while protracted, do not meet
criteria for bipolar disorder) and dysthymia (a chronic,
albeit symptomatically milder formof depression). The
causes of mood disorders are not fully known. They
may be triggered by stressful life events and enduring
stressful social conditions (e.g., poverty and
discrimination). With the exception of bipolar disorder,
they too, like the anxiety disorders, are twice as
common in women as men. One subtype of mood
disorder, seasonal affective disorder, in which episodes
of depression tend to occur in the late fall and winter,
is seven times more common in women than in men
(Blumenthal, 1988). Many psychosocial and genetic
factors interact to dictate the appearance and persis-
tence of mood disorders, according to the biopsycho-
social model presented in Chapter 2.

Mood disorders, like anxiety disorders, can be
treated with a host of effective pharmacological and
psychosocial treatments. Either type of treatment is
effective for about 50 to 70 percent of patients in
outpatient settings (Depression Guideline Panel, 1993).
Severe depression seems to resolve more quickly with
pharmacotherapy (Depression Guideline Panel, 1993)

and may be helped further by multimodal therapy (the
combination of pharmacotherapy and psychotherapy)
(Thase et al., 1997b). Despite the efficacy of treatment,
a surprising fraction of those with mood disorders go
untreated (Katon et al., 1992; Narrow et al., 1993;
Wells et al., 1994; Thase, 1996). The foremost barriers
to treatment include cost, stigma, and problems in the
organization of service systems that contribute to the
underrecognition of these disorders.
Schizophrenia affects about 1 percent of the
population, yet its severity and petsistence reverberate
throughout the mental health service system
Schizophrenia is marked by profound alterations in
cognition and emotion. Symptoms frequently include
hearing internal voices or experiencing other sensations
not connected to an obvious source (hallucinations) and
assigning. unusual significance or meaning to normal
events or holding false personal beliefs (delusions).
The course of illness in schizophrenia is quite variable,
with most people having periods of exacerbation and
remission. Schizophrenia had once been thought to
have a uniformly downhill course, but recent research
dispels this view. Long-term followup studies show
that many individuals with schizophrenia significantly
improve and some recover (Ciompi, 1980; Harding et
al., 1992). Although the causes of schizophrenia are not
fully known, research points to the prominent role of
genetic factors and to the impact of adverse
environmental influences during early brain
development (Tsuang et al., 1991; Weinberger &
Lip&a, 1995; Andreasen, 1997b). New pharmaco-
logical treatments are at least as effective as past
pharmacological treatments with fewer troubling side
effects.

Effective treatment of schizophrenia extends well
beyond pharmacological therapy: it also includes
psychosocial interventions, family interventions, and
vocational and psychosocial rehabilitation. For those
patients who are high service users, treatment should be
coordinated by an interdisciplinary team that provides
high-intensity, community-based services (Lehman &
Steinwachs, 1998a). The prototype for this intensive
case-management approach, which is useful for persons
with other severe and persistent mental disorders as

226


Adults and Mental Health

w,ell. is assertive community treatment, described more
thoroughly later in this chapter. Among the services
included in this approach is substance abuse treatment.
Its inclusion stems from findings that about half of
patients with serious mental disorders (including
schizophrenia) develop alcohol or other drug abuse
problems (Drake & Osher, 1997). Even though research
generated a range of recommendations for effective
treatment of schizophrenia', it is alarming that less than
50 percent of patients actually receive many of the
recommended treatments and that the gap was more
pronounced in African Americans (Lehman &
Steinwachs, 1998b).

The social consequences of serious mental
disorders-family disruption, loss of employment and
housingdan be calamitous. Comprehensive treatment,
which includes services that exist outside the formal
treatment system, is crucial to ameliorate symptoms,
assist recovery, and, to the extent that these efforts are
successful,  redress stigma.  Consumer self-help
programs, family self-help, advocacy, and services for
housing and vocational assistance complement and
supplement the formal treatment system. Many of these
services are operated by consumers, that is, people who
use mental health services themselves.. The logic
behind their leadership in delivery of these services is
that consumers are thought to be capable of engaging
others with mental disorders, serving as role models,
and increasing the sensitivity of service systems to the
needs of people with mental disorders (Mowbray et al.,
1996).

Mental Health in Adulthood

What constitutes mental health during the adult years?
A widely used standard of mental health is the absence
of a defined mental disorder. This standard has its
limitations (discussed later), yet remains useful for
epidemiological purposes. Epidemiology studies
investigate the prevalence of mental disorders within
several time frames: current, the past 12 months, and
across a lifetime. Two well-designed national
epidemiologic surveys estimate that about 80percent of
the adult population of the United States do not have a
mental disorder during a year and hence may be

considered "mentally healthy" (i.e., absence of amental
disorder) during any given year (Regier et al., 1993;
Kessler et al., 1994). Thus, the popular notion that
everyone is "dysfunctional" is far from the truth
(Table 4-l). Yet, from time to time, many adults
experience mental health problems.
Defining mental health by the absence of mental
disorder does not convey the full picture of mental
health. Among its limitations, this definition excludes
adults with mental disorders who function well
between episodes of illness. These people often are
considered by themselves, and by coworkers, friends,
and families, to be "mentally healthy" in spite of a
history of mental illness and the risk of recurrence.
  In addition to the mental health criteria cited
earlier-that is, the successful performance of mental
function, enabling individuals to cope with adversity
and to flourish in their education, vocation, and
personal relationships-a complementary approach
defines the positive features of mental health in terms
of attaining developmental milestones of adulthood, or
in terms of displaying selected personality
characteristics, traits, or attributes. Developmental
theorist Erik Erikson viewed mental health in adulthood
as achieving developmental tasks or milestones.
According to Erikson's formulation and his subsequent
empirical research on adult men, adulthood was the
time for overcoming what he termed "psychosocial
crises," the resolution of which led to satisfactory
interpersonal and sexual relationships and to the pursuit
of broader concerns for society and future generations
(Erikson, 1963; Vaillant, 1977). However, these
milestones, and the developmental theories that
underpin them, have been criticized as reflecting the
norms of European males rather than of women and
other cultures.

Personality Traifs

Mental health and mental illness can be seen as the
product of various personality traits, behavior patterns,
and other characteristics which have roots in the
individual's prior life experiences or biology.

227


Mental Health: A Report of the Surgeon General

Table 4-1. Best estimate 1 -year prevalence based on ECA and NCS, ages 1 B-54

r
//

1

ECA Prevalence (%)     NCS Prevalence (%)

Best Estimate o * (%)

2ny Anxiety Disorder              13.1               18.7              16.4
    Simple Phobia             8.3               8.6              8.3
     Social Phobia             2.0               7.4               2.0
   Agoraphobia     ;:g              3.7              4.9
    GAD                                   3.4               3.4
     Panic Disorder             1.6
   OCD     t:::,*     g,*              1.6
                                                           2.4
    PTSD                                  3.6              3.6
                                         _. ._ ~ r.                     _:-c..       +- _.-a    _   ,_,
                                     Isi-/.. ,:                           i"i*9'1
                                             _*il ,_ "          : .,bAr'#e~uB&a-s. * *a_ ;&r~..s&.,,;' iis%
Any Mood Disorder               7.1               11.1              7.1
    MD Episode              6.5               10.1               6.5
    Unipolar MD              5.3               8.9              6.3
    Dysthymia               1.6               2.5             1.6
    Biopolar I                1.1               1.3               1.1
    Biopolar II                0.6               0.2               0.8

Schizophrenia                  1.3                   -
Nonaffective Psychosis                 -               0.2
Somatization                  0.2                   -
ASP                          2.1                    -
Anorexia Nervosa                0.1                    -
Severe Cognitive Impairment         1.2
                     i .~ /, . . I ." ^              - -9 %
       `- _*`_  j .-ah;- i--`*z         \ `:,.-.~I+
                         a i.iLJ&&iiC*+.J..~~~. ass   `-d&i*~ .d.&m5K- , 1
                                  ,w*~*~"~-pi~ `^.; s-   ,.. .  I-i;.hr ,-a .:.a& _

Any Disorder

19.5               23.4              21 .o

*Numbers in parentheses indicate the prevalence of the disorder without any comorbidity. These rates were calculated using the NCS
data for GAD and PTSD, and the ECA data for OCD. The rates were not used in calculating the any anxiety disorder and any disorder
totals for the ECA and NCS columns. The unduplicated GAD and PTSD rates were added to the best estimate total for any anxiety
disorder (3.3%) and any disorder (1.5%).

`"In developing best-estimate 1 -year prevalence rates from the two studies, a conservative procedure was followed that had previously
been used in an independent scientific analysis comparing these two data sets (Andrews, 1995). For any mood disorder and any anxiety
disorder, the lower estimate of the two surveys was selected, which for these data was the ECA. The best estimate rates for the
individual mood and anxiety disorders were then chosen from the ECA only, in order to maintain the relationships between the individual
disorders. For other disorders that were not covered in both surveys, the available estimate was used.

Key to abbreviations: ECA, Epidemiologic Catchment Area; NCS, National Comorbidity Study; GAD, generalized anxiety disorder;
OCD, obsessive-compulsive disorder; PTSD, post-traumatic stress disorder; MD, major depression: ASP, antisocial personality
disorder.

Source: D. Regier, W. Narrow, & D. Rae, personal communication, 1999

Personality traits are thought to confer either beneficial
or detrimental effects on mental health during adult-
hood. Here too, however, there may be insufficient
attention to gender and culture. The culture-bound
nature of much of behavior has limited widespread
predictive validity of personality research (Mischel &
Shoda, 1968). With this caveat in mind, a brief
summary of healthy and maladaptive characteristics
follows.

Self-Esteem
Self-esteem refers to an abiding set of beliefs about
one's own worth, competence, and abilities to relate to
others (Vaughan & Oldham, 1997). Self-esteem also
has been conceptualized as buffering the individual
from adverse life events. Emotional well-being is often
associated with a slightly positive, yet realistic, outlook
(Alloy & Abramson, 1988). The opposite outlook is

228


characterized by pessimism, demoralization, or minor
5ymptoms of anxiety and depression. One seminal
aspect of self-esteem has garnered much research
attention: self-efficacy (Bandura, 1977). Self-efficacy
is defined as confidence in one's own abilities to cope
\vith adversity, either independently or by obtaining
appropriate assistance from others. Self-efficacy is a
major component of the construct known as resilience
t i.e.. the ability to withstand and overcome adversity).
Other components of resilience include intelligence and
problem solving, although resilience is also facilitated
by having adequate social support (Beardslee &
Vaillant. 1997).

Neuroticism

Neuroticism is a construct that refers to a broad pattern
of psychological, emotional, and psychophysiologic
reactivity (Eysenck & Eysenck,`1975). The opposite of
neuroticism is stability or equanimity, which are major
components of mental health. A high level of
neuroticism is associated with a predisposition toward
recognizing the dangerous, harmful, or defeating.
aspects of a situation and the tendency to respond with
worry, anticipatory anxiety, emotionality, pessimism,
and dissatisfaction. Neuroticism is associated with a
greater risk of early-onset depressive and anxiety
disorders (Clark et al., 1994). Neuroticism also may be
linked to a particular cognitive attributional style in
which life events are perceived to be large in impact
and more difficult to change (Alloy et al., 1984). For
example, this attributional style is embodied by
pessimists who see every setback or failure as lasting
forever, undermining everything, and being their fault
(Seligman, 1991). Neuroticism also is associated with
more rigid or distorted attitudes and beliefs about one's
competence (Beck, 1976).

Avoidance

Avoidance describes an exaggerated predisposition to
withdraw from novel situations and to avoid personal
challenges as threats. This is the behavioral state that
often accompanies the distress of someone who has a
high level of neuroticism and low self-efficacy
(Vaughan & Oldham, 1997). Closely related to the

Adults and Mental Health

characteristics of behavioral inhibition or introversion,
the trait of avoidance appears to be partly inherited and
is associated with shyness, anxiety, and depressive
disorders in both childhood and adult life, as well as the
subsequent development of substance abuse disorders
,(Vaughan & Oldham, 1997; Kagan et al., 1988). The
people with low levels of harm avoidance are described
as "healthy extroverts" and are characterized by
confident, carefree, or outgoing behaviors.

lmpulsivity

Impulsivity is a trait that is associated with poor
modulation of emotions, especially anger, difficulty
delaying gratification, and novelty seeking. There is
some developmental continuity between high levels of
impulsivity in childhood and several adult mental
disorders, including attention deficit hyperactivity
disorder, bipolar disorder, and substance abuse
disorders (Svrakic et al., 1993; Rothbart & Ahadi.
1994). Impulsivity also is associated with physical
abuse (both as victim and, subsequently, as perpetrator)
and antisocial personality traits (Vaughan & Oldham.
1997).

Sociopathy

This set of traits and behaviors refers to the
predisposition to engage in dishonest, hurtful,
unfaithful, and at times dangerous conduct to benefit
one's own ends. The opposite of sociopathy may be
referred to as character or scrupulosity. In its full form,
sociopathy is referred to as antisocial personality
disorder (DSM-IV). Sociopathy is characterized by a
tendency and ability to disregard laws and rules,
difficulties reciprocating within empathic and intimate
relationships, less internalization of moral standards
(i.e., a weaker conscience or superego), and an
insensitivity to the needs and rights of others. People
scoring high in sociopathy often have problems with
aggressivity and are overrepresented among criminal
populations. Although not invariably associated with
criminality, sociopathy is associated with problematic,
unethical, and morally questionable conduct in the
workplace and within social systems. Marked
sociopathy is much more common among men than

229


Mental Health: A Report of the Surgeon General

women, although several other disorders (borderline
and histrionic personality disorders and somatization
disorder) are overrepresented among women within the
same families (Widiger & Costa, 1994).

In summary, *the various traits and behavioral
patterns that epitomize strong mental health do not, of
course, exist in a vacuum: they develop in a social
context, and they underpin people's ability to handle
psychological and social adversity and the exposure to
stressful life events. Furthermore, as reviewed in
Chapter 3, severe or repeated trauma during youth may
have enduring effects on both neurobiological and
psychological development, altering stress responsivity
and adult behavior patterns. Perhaps the best
documented evidence of such enduring effects has been
shown in young adults who experienced severe sexual
or physical abuse in childhood. These individuals
experience a greatly increased risk bf mood, anxiety,
and personality disorders throughout adult life.

Stressful life Events

The most common psychological and social stressors in
adult life include the breakup of intimate romantic
relationships, death of a family member or friend,
economic hardships, racism and discrimination, poor
physical health, and accidental and intentional assaults
on physical safety (Holmes & Rahe, 1967; Lazarus &
Folkman, 1984; Kreiger et al., 1993). Although some
stressors are so powerful that they would evoke
significant emotional distress in most otherwise
mentally healthy people, the majority of stressful life
events do not invariably trigger mental disorders.
Rather, they are more likely to spawn mental disorders
in people who are vulnerable biologically, socially,
and/or psychologically (Lazarus & Folkman, 1984;
Brown & Harris, 1989; Kendler et al., 1995).
Understanding variability among individuals to a
stressful life event is a major challenge to research.
Groups at greater statistical risk include women, young
and unmarried people, African Americans, and
individuals with lower socioeconomic status
Wlbrich et al., 1989; McLeod & Kessler, 1990; Turner
et al., 1995; Miranda & Green, 1999).

Divorce is a common example. Approximately one-
half of all marriages now end in divorce, and about 30
to 40 percent of those undergoing divorce report a
significant increase in symptoms of depression and
anxiety (Brown & Harris, 1989). Vulnerability to
depression and anxiety is greater among those with a
personal history of mental disorders earlier in life and
is lessened by strong social support. For many, divorce
conveys additional economic adversities and the stress
of single parenting. Single mothers face twice the risk
of depression as do married mothers (Brown & Moran,
1997).

The death of a child or spoise during early or
midadult life is much less common than divorce but
generally is of greater potency in provoking emotional
distress (Kim & Jacobs, 1995). Rates of diagnosable
mental disorders during periods of grief are attenuated
by the convention not to diagnose depression during the
first 2 months of bereavement (Clayton & Darvish,
1979). In fact, people are generally unlikely to seek
professional treatment during bereavement unless the
severity of the emotional and behavioral disturbance is
incapacitating.

A majority of Americans never will confront the
stress of surviving a severe, life-threatening accident or
physical assault (e.g., mugging, robbery, rape);
however, some segments of the population, particularly
urban youths and young adults, have exposure rates as
high as 25 to 30 percent (Helzer et al., 1987; Breslau et
al., 199 1). Life-threatening trauma frequently provokes
emotional and behavioral reactions that jeopardize
mental health. In the most fully developed form, this
syndrome is called post-traumatic stress disorder
(DSM-N), which is described later in this chapter.
Women are twice as likely as men to develop post-
traumatic stress disorder following exposure to life-
threatening trauma (Breslau et al., 1998.)
More familiar to many Americans is the chronic
strain that poor physical health and relationship
problems place on day-to-day well-being. Relationship
problems include unsatisfactory intimate relationships;
conflicted relationships with parents, siblings, and
children; and "falling-out" with coworkers, friends, and

230


neighbors. In mid-adult life, the stress of caretaking for
elderly parents also becomes more common.
Relationship problems at least double the risk of
developing a mental disorder, although they are less
immediately threatening or potentially cataclysmic than
divorce or the death of a spouse or child (Brown 8z
Harris, 1989). Finally,.cumulative adversity appears to
be more potent than StreSSfUl events in isolation as a
predictor of psychological distress and mental disorders
(Turner & Lloyd, 1995).

fast Trauma and Child Sexual Abuse
Severe trauma in childhood may have enduring effects
into adulthood (Browne & Finkelhor, 1986). Past
trauma includes sexual and physical abuse, and parental
death, divorce, psychopathology, and substance abuse
(reviewed in Turner & Lloyd, 1995).
  Child sexual abuse is one of the most common
stressors, with effects that persist into adulthood. It
disproportionately affects females. Although
definitions are still evolving, child sexual abuse is often
defined as forcible touching of breasts or genitals or.
forcible intercourse (including anal, oral, or vaginal
sex) before the age of 16 or 18 (Goodman et al., 1997).
Epidemiology studies of adults in varying segments of
the community have found that 15 to 33 percent of
females and 13 to 16 percent of males were sexually
abused in childhood (Polusny & Follette, 1995). A
recent, large epidemiological study of adults in the
general community found a lower prevalence (12.8
percent for females and 4.3 percent for males);
however, the definition of sexual abuse was more
restricted than in past studies (MacMillan et al., 1997).
Sexual abuse in childhood has a mean age of onset
estimated at 7 to 9 years of age (Polusny & Follette,
1995). In over 25 percent of cases of child sexual
abuse, the offense was committed by a parent or parent
substitute (Sedlak & Broadhurst, 1996).
  The long-term consequences of past childhood
sexual abuse are profound, yet vary in expression. They
range from depression and anxiety to problems with
social functioning and adult interpersonal relationships
(Polusny & Follette, 1995). Post-traumatic stress
disorder is a common sequela, found in 33 to 86

Adults and Mental Health

percent of adult survivors of child sexual abuse
(Polusny & Follette, 1995). In a recent review, Weiss
et al. (1999) found that sexual abuse was a specific risk
factor for adult-onset depression and twice as many
women as men reported a history of abuse. Other long-
term effects include self-destructive behavior, social
isolation, poor sexual adjustment, substance abuse, and
increased risk of revictimization (Browne & Finkelhor,
1986; Briere, 1992).

Very few treatments specifically for adult survivors
of childhood abuse have been studied in randomized
controlled trials (IOM, 1998) Group therapy and
Interpersonal Transaction group therapy were found to
be more effective for female survivors than an
experimental control condition that offered a less
appropriate intervention (Alexander et al., 1989,199 1).
In the practice setting, most psychosocial and
pharmacological treatments are tailored to the primary
diagnosis, which, as noted above, varies widely and
may not attend to the special needs of those also
reporting abuse history.

Domestic Violence

Domestic violence is a serious and startlingly common
public health problem with mental health consequences
for victims, who are overwhelmingly female, and for
children who witness the violence. Domestic violence
(also known as intimate partner violence) features a
pattern of physical and sexual abuse, psychological
abuse with verbal intimidation, and/or social isolation
or deprivation. Estimates are that 8 to 17 percent of
women are victimized annually in the United States
(Wilt & Olsen, 1996). Pinpointing the prevalence is
hindered by variations in the way domestic violence is
defined and by problems in detection and
underreporting. Women are often fearful that their
reporting of domestic  violence will precipitate
retaliation by the batterer, a fear that is not unwarranted
(Sisley et al., 1999).

  Victims of domestic violence are at increased risk
for mental health problems and disorders as well as
physical injury and death. Domestic violence is
considered one of the foremost causes of serious injury
to women ages 15 to 44, accounting for about 30

231


Mental Health: A Report of the Surgeon General

percent of all acute injuries to women seen in
emergency departments (Wilt & Olsen, 1996).
According to the U.S. Department of Justice, females
were victims in about 75 percent of the almost 2,000
homicides between intimates in 1996 (cited in Sisley et
al., 1999). The mental healthconsequences of domestic
violence include depression, anxiety disorders (e.g.,
post-traumatic stress disorder), suicide, eating
disorders, and substance abuse (IOM, 1998; Eisenstat
& Bancroft, 1999). Children who witness domestic
violence may suffer acute and long-term emotional
disturbances,  including nightmares,  depression,
learning difficulties, and aggressive behavior. Children
also become at risk for subsequent use of violence
against their dating partners and wives (el-Bayoumi et
al., 1998; NRC, 1998; Sisley et al., 1999).
  Mental health interventions for victims, children,
and batterers are highly important. Individual
counseling and peer support groups are the
interventions most frequently used by battered women.
However, there is a lack of carefully controlled,
methodologically robust studies of interventions and
their outcomes, according to a report by the Institute of
Medicine and National Research Council (IOM, 1998).
A research agenda for violence against women was
developed (IOM, 1996) and has served as an impetus
for an ongoing research program sponsored by the U.S.
Departments of Justice and Health and Human
Services. Clearly, there is an urgent need for
development and rigorous evaluation of prevention
programs to safeguard against intimate partner violence
and its impact on children.

Interventions for Stressful Life Events

232

Stressful life events, even for those at the peak of
mental health, erode quality of life and place people at
risk for symptoms and signs of mental disorders. There
is an ever-expanding list of formal and informal
interventions to aid individuals coping with adversity.
Sources of informal interventions include family and
friends, education, community services, self-help
groups. social support networks, religious and spiritual
endeavors, complementary healers, and physical
activities. As valuable as these activities may be for

promoting mental health, they have received less
research attention than have interventions for mental
disorders. Nevertheless, there are selected interventions
to help people cope with stressors, such as bereavement
programs and programs for caregivers (see Chapter 5)
as well as couples therapy and physical activity.
Couples therapy is the umbrella term applied to
interventions that aid couples in distress. The best
studied interventions are behavioral couples therapy,
cognitive-behavioral couples therapy, and emotion-
focused couples therapy. A recent review. article
evaluated the body of evidence on the effectiveness of
couples therapy and programs ;o. prevent marital
discord (Christensen & Heavey, 1999). The review
found that about 65 percent of couples in therapy did
improve, whereas 35 percent of control couples also
improved. Couples therapy ameliorates relationship
distress and appears to alleviate depression. The gains
from couples therapy generally last through 6 months,
but there are few long-term assessments (Christensen &
Heavey, 1999). Similarly, interventions to prevent
marital discord yield short-term improvements in
marital adjustment and stability, but there is
insufficient study of long-term outcomes. The
prevention programs receiving the most study are the
Couple Communication Program, Relationship
Enhancement, and the Prevention and Relationship
Enhancement Program (Christensen & Heavey, 1999).
Greater research is needed to overcome gaps in
knowledge and to extend findings to a broader array of
programs, to diverse populations of couples, and to a
wider set of outcomes, including effects on children.
  Physical activities are a means to enhance somatic
health as well as to deal with stress. A recent Surgeon
General's Report on Physical Activity and Health
evaluated the evidence for physical activities serving to
enhance mental health (U.S. Department of Health and
Human Services [DHHS], 1996). Aerobic physical
activities, such as brisk walking and running, were
found to improve mental health for people who report
symptoms of anxiety and depression and for those who
are diagnosed with some forms of depression. The
mental health benefits of physical activity for
individuals in relatively good physical and mental


health were not as evident, but the studies did not have
sufficient rigor from which to draw unequivocal
conclusions (DHHS, 1996).

prevention of Mental Disorders
A promising development in prevention of a specific
mental disorder in adults occurred with the publication
of results from the San Francisco Depression Research
Project (Munoz et al., 1995). This study investigated
150 primary care patients who did not meet diagnostic
criteria for depression and who were being seen in a
public clinic for other problems. They were randomized
to either psychoeducation-an 8-week cognitive
behavioral course to help them control and manage
moods--or to a control condition, One year later, those
who received psychoeducation were found to have
developed significantly fewer depression symptoms
than members of the control group. This trial is
noteworthy in two major respects: it was a randomized
controlled trial and its participants were low-income
individuals, with high representation of all major
minority groups. Low-income individuals are
considered a high-risk population because of studies
documenting their higher prevalence of mental
disorders.  This study demonstrated in a
methodologically rigorous fashion that depression may
be preventable in some cases. It serves as a model for
extending the concept of prevention to many mental
disorders. Prevention research is vitally important and
needs to be enhanced.

and without a history of panic disorder), generalized
anxiety disorder, specific phobia, social phobia,
obsessive-compulsive disorder, acute stress disorder,
and post-traumatic stress disorder (DSM-IV). In
addition, there are adjustment disorders with anxious
features, anxiety disorders due to general medical
conditions, substance-induced anxiety disorders, and
the residual category of anxiety disorder not otherwise
specified (DSM-IV).

Anxiety Disorders

233

The anxiety disorders are the most common, or
frequently occurring, mental disorders. They
encompass a group of conditions that share extreme or
pathological anxiety as the principal disturbance of
mood or emotional tone. Anxiety, which may be
understood as the pathological counterpart of normal
fear, is manifest by disturbances of mood, as well as of
thinking, behavior, and physiological activity.

Types of Anxiety Disorders
The anxiety disorders include panic disorder (with and
without a history of agoraphobia), agoraphobia (with

Adults and Mental Health

Anxiety disorders not only are common in the
United States, but they are ubiquitous across human
cultures (Regier et al., 1993; Kessler et al., 1994;
Weissman et al., 1997). In the United States, l-year
prevalence for all anxiety disorders among adults ages
18 to 54 exceeds 16 percent (Table 4-l), and there is
significant overlap or comorbidity with mood and
substance abuse disorders (Regier et al.,  1990;
Goldberg & Lecrubier, 1995; Magee et al., 1996). The
longitudinal course of these disorders is characterized
by relatively early ages of onset, chronicity, relapsing
or recurrent episodes of illness, and periods of
disability (Keller & Hanks, 1994; Gorman & Coplan,
1996; Liebowitz, 1997; Marcus et al., 1997). Although
few psychological autopsy studies of adult suicides
have included a focus on comorbid conditions (Conwell
& Brent, 1995), it is likely that the rate of comorbid
anxiety in suicide is underestimated. Panic disorder and
agoraphobia, particularly, are associated with increased
risks of attempted suicide (Homig & McNally, 1995;
American Psychiatric Association, 1998).

Panic Attacks and Panic Disorder

A panic attack is a discrete period of intense fear or
discomfort that is associated with numerous somatic
and cognitive symptoms (DSM-IV). These symptoms
include palpitations, sweating, trembling, shortness of
breath, sensations of choking or smothering, chest pain,
nausea or gastrointestinal distress, dizziness or
lightheadedness, tingling sensations, and chills or
blushing and "hot flashes." The attack typically has an
abrupt onset, building to maximum intensity within 10
to 15 minutes. Most people report a fear of dying,
"going crazy," or losing control of emotions or
behavior. The experiences generally provoke a strong


Mental Health: A Report of the Surgeon General

urge to escape or flee the place where the attack begins
and, when associated with chest pain or shortness of
breath, frequently results in seeking aid from a hospital
emergency room or other type of urgent assistance. Yet
an attack rarely lasts longer than 30 minutes. Current
diagnostic practice specifies that a panic attack must be
characterized by at least four of the associated somatic
and cognitive symptoms described above. The panic
attack is distinguished from other forms of anxiety by
its intensity and its sudden, episodic nature. Panic
attacks may be further characterized by the relationship
between the onset of the attack and the presence or
absence of situational factors. For example, a panic
attack may be described as unexpected, situationally
bound, or situationally predisposed (usually, but not
invariably occurring in a particular situation). There are
also attenuated or "limited symptom" forms of panic
attacks.

Panic attacks are not always indicative of a mental
disorder, and up to 10 percent of otherwise healthy
people experience an isolated panic attack per year
(Barlow, 1988; Klerman et al., 1991). Panic attacks
also are not limited to panic disorder. They commonly
occur in the course of social phobia, generalized
anxiety disorder, and major depressive disorder
(DSM-IV).

Panic disorder is diagnosed when a person has
experienced at least two unexpected panic attacks and
develops persistent concern or worry about having
further attacks or changes his or her behavior to avoid
or minimize such attacks. Whereas the number and
severity of the attacks varies widely, the concern and
avoidance behavior are essential features. The
diagnosis is inapplicable when the attacks are presumed
to be caused by a drug or medication or a general
medical disorder, such as hyperthyroidism.
Lifetime rates of panic disorder of 2 to 4 percent
and l-year rates of about 2 percent are documented
consistently in epidemiological studies (Kessler et al.,
1994; Weissman et al., 1997) (Table 4-l). Panic
disorder is frequently complicated by major depressive
disorder (50 to 65 percent lifetime comorbidity rates)
and alcoholism and substance abuse disorders (20 to 30
`percent comorbidity) (Keller&Hanks, 1994; Magee et

al., 1996; Liebowitz, 1997). Panic disorder is also
concomitantly diagnosed, or co-occurs, with other
specific anxiety disorders, including social phobia (up
to 30 percent), generalized anxiety disorder (up to 25
percent), specific phobia (up to 20 percent), and
obsessive-compulsive disorder (up to 10 percent)
(DSM-IV). As discussed subsequently, approximately
one-half of people with panic disorder at some point
develop such severe avoidance as to warrant a separate
description, panic disorder with agoraphobia.
Panic disorder is about twice as common among
women as men (American Psychiatric Association,
1998). Age of onset is most common between late
adolescence and midadult life, with onset relatively
uncommon past age 50. There is developmental
continuity between the anxiety syndromes of youth,
such as separation anxiety disorder. Typically, an early
age of onset of panic disorder carries greater risks of
comorbidity, chronicity, and impairment. Panic
disorder is a familial condition and can be
distinguished from depressive disorders by family
studies (Rush et al., 1998).

Agoraphobia

The ancient term agoraphobia is translated from Greek
as fear of an open marketplace. Agoraphobia today
describes severe and pervasive anxiety about being in
situations from which escape might be difficult or
avoidance of situations such as being alone outside of
the home, traveling in a car, bus, or airplane, or being
in a crowded area (DSM-TV).

Most people who present to mental health
specialists develop agoraphobia after the onset of panic
disorder (American Psychiatric Association, 1998).
Agoraphobia is best understood as an adverse
behavioral outcome of repeated panic attacks and the
subsequent worry, preoccupation, and avoidance
(Barlow, 1988). Thus, the formal diagnosis of panic
disorder with agoraphobia was established. However,
for those people in communities or clinical settings
who do not meet full criteria for panic disorder, the
formal diagnosis of agoraphobia without history of
panic disorder is used (DSM-IV).

234


The l-year prevalence of agoraphobia is about 5
percent (Table 4-l). Agoraphobia occurs about two
times more commonly among women than men (Magee
et al., 1996). The gender difference may be attributable
to social-cultural factors that encourage, or permit, the
greater expression of avoidant coping strategies by
women (DSM-IV), although other explanations are
possible.

Specific Phobias

These common conditions are characterized by marked
fear of specific objects or situations (DSM-IV).
Exposure to the object of the phobia, either in real life
or via imagination or video, invariably elicits intense
anxiety, which may include a (situationally bound)
panic attack. Adults generally recognize that this
intense fear is irrational. Nevertheless, they typically
avoid the phobic stimulus or endure exposure with
great difficulty. The most common specific phobias
include the following feared stimuli or situations:
animals (especially snakes, rodents, birds, and dogsj;
insects (especially spiders and bees or hornets);
heights; elevators; flying; automobile driving; water;
storms; and blood or injections.

Approximately 8 percent of the adult population
suffers from one or more specific phobias in 1 year
(Table 4-l). Much higher rates would be recorded if
less rigorous diagnostic requirements for avoidance or
functional impairment were employed. Typically, the
specific phobias begin in childhood, although there is
a second "peak" of onset in the middle 20s of
adulthood (DSM-IV). Most phobias persist for years or
even decades, and relatively few remit spontaneously
or without treatment.

The specific phobias generally do not result from
exposure to a single traumatic event (i.e., being bitten
by a dog or nearly drowning) (Marks, 1969). Rather,
there is evidence of phobia in other family members
and social or vicarious learning of phobias (Cook &
Mineka, 1989). Spontaneous, unexpected panic attacks
also appear to play a role in the development of specific
phobia, although the particular pattern of avoidance is
much more focal and circumscribed.

Adults and Mental Health

Social Phobia

Social phobia, also known as social anxiety disorder,
describes people with marked and persistent anxiety in
social situations, including performances and public
speaking (Ballenger et al., 1998). The critical element
of the fearfulness is the possibiIity of embarrassment or
ridicule. Like specific phobias, the fear is recognized
by adults as excessive or unreasonable, but the dreaded
social situation is avoided or is tolerated with great
discomfort. Many people with social phobia are
preoccupied with concerns that others will see their
anxiety symptoms (i.e., trembling, sweating, or
blushing); or notice their halting or rapid speech; or
judge them to be weak, stupid, or "crazy." Fears of
fainting, losing control of bowel or bladder function, or
having one's mind going blank are also not uncommon.
Social phobias generally are associated with significant
anticipatory anxiety for days or weeks before the
dreaded event, which in turn may further handicap
performance and heighten embarrassment.
  The l-year prevalence of social phobia ranges
from 2 to 7 percent (Table 4-l), although the lower
figure probably better captures the number of people
who experience significant impairment and distress.
Social phobia is more common in women (Wells et al.,
1994). Social phobia typically begins in childhood or
adolescence and, for many, it is associated with the
traits of shyness and social inhibition (Kagan et al.,
1988). A public humiliation, severe embarrassment, or
other stressful experience  may provoke an
intensification of difficulties (Barlow, 1988). Once the
disorder is established, complete remissions are
uncommon without treatment. More commonly, the
severity of symptoms and impairments tends to
fluctuate in relation to vocational demands and the
stability of social relationships. Preliminary data
suggest social phobia to be familial (Rush et al., 1998).

Generalized Anxiety Disorder
Generalized anxiety disorder is defined by a protracted
(16 months' duration) period of anxiety and worry,
accompanied by multiple associated symptoms (DSM-
IV). These symptoms include muscle tension, easy
fatiguability, poor concentration, insomnia, and

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Mental Health: A Report of the Surgeon General

irritability. In youth, the condition is known as
overanxious disorder of childhood. In DSM-IV, an
essential feature of generalized anxiety disorder is that
the anxiety and worry cannot be attributable to the
more focal distress of panic disorder, social phobia,
obsessive-compulsive disorder, or other conditions.
Rather, as implied by the name, the excessive worries
often pertain to many areas, including work,
relationships, finances, the well-being of one's family,
potential misfortunes, and impending deadlines.
Somatic anxiety symptoms are common, as are
sporadic panic attacks.

Generalized anxiety disorder occurs more often in
women, with a sex ratio of about 2 women to 1 man
(Brawman-Mintzer & Lydiard, 1996). The l-year
population prevalence is about 3 percent (Table 4-l).
Approximately 50 percent of cases begin in childhood
or adolescence. The disorder typically runs a
fluctuating course, with periods of increased symptoms
usually associated with life stress or impending
difficulties. There does not appear to be a specific
familial association for general anxiety disorder,
Rather, rates of other mood and anxiety disorders
typically are greater among first-degree relatives of
people with generalized anxiety disorder (Kendler et
al., 1987).

Obsessive-Compulsive Disorder

Obsessions are recurrent, intrusive thoughts, impulses,
or images that are perceived as inappropriate,
grotesque, or forbidden (DSM-IV). The obsessions,
which elicit anxiety and marked distress, are termed
"ego-alien" or "ego-dystonic" because their content is
quite unlike the thoughts that the person usually has.
Obsessions are perceived as uncontrollable, and the
sufferer often fears that he or she will lose control and
act upon such thoughts or impulses. Common themes
include contamination with germs or body fluids,
doubts (i.e., the worry that something important has
been overlooked or that the sufferer has unknowingly
inflicted harm on someone), order or symmetry, or loss
of control of violent or sexual impulses.

Compulsions are repetitive behaviors or mental acts
that reduce the anxiety that accompanies an obsession
or "prevent" some dreaded event from happening
(DSM-IV). Compulsions include both overt behaviors,
such as hand washing or checking, and mental acts
including counting or praying. Not uncommonly,
compulsive rituals take up long periods of time, even
hours, to complete. For example, repeated hand
washing,  intended to remedy anxiety about
contamination,  is a common cause of contact
dermatitis.

Although once thought to be rare, obsessive-
compulsive disorder has now been documented to have
a l-year prevalence of 2.4 percent (Table 4-l).
Obsessive-compulsive disorder is equally common
among men and women.

Obsessive-compulsive disorder typically begins in
adolescence to young adult life (males) or in young
adult life (females) (Burke et al., 1990; DSM-IV). For
most, the course is fluctuating and, like generalized
anxiety. disorder, symptom exacerbations are usually
associated with life stress. Common comorbidities
include major depressive disorder and other anxiety
disorders. Approximately 20 to 30 percent of people in
clinical samples with obsessive-compulsive disorder
report a past history of tics, and about one-quarter of
these people meet the full criteria for Tourette's
disorder (DSM-IV). Conversely, up to 50 percent of
people with Tourette's disorder develop obsessive-
compulsive disorder (Pitman et al., 1987).
Obsessive-compulsive disorder has a clear familial
pattern and somewhat greater familial specificity than
most other anxiety disorders. Furthermore, there is an
increased risk of obsessive-compulsive disorder among
first-degree relatives with Tourette's disorder. Other
mental disorders that may fall within the spectrum of
obsessive-compulsive disorder include trichotillomania
(compulsive hair pulling), compulsive shoplifting,
gambling, and sexual behavior disorders (Hollander,
1996). The latter conditions are somewhat discrepant
because the compulsive behaviors are less ritualistic
and yield some outcomes that are pleasurable or

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gratifying. Body dysmorphic disorder is a more
circumscribed condition in which the compulsive and
obsessive behavior centers around a preoccupation with
one's appearance (i.e., the syndrome of imagined
ugliness) (Phillips, 199 1).

Acute and Post-Traumatic Stress Disorders
Acute stress disorder refers to the anxiety and
behavioral disturbances that develop within the first
month after exposure to an extreme trauma. Generally,
the symptoms of an acute stress disorder begin during
or shortly following the trauma. Such extreme
traumatic events include rape or other severe physical
assault, near-death experiences in accidents, witnessing
a murder, and combat. The symptom of dissociation,
which reflects a perceived detachment of the mind from
the emotional state or even the body, is a critical
feature. Dissociation also is characterized by a sense of
the world as a dreamlike or unreal place and may be
accompanied by poor memory of the specific events,
which in severe form is known as dissociative amnesia.
Other features of an acute stress disorder include
symptoms of generalized anxiety and hyperarousal,
avoidance of situations or stimuli that elicit memories
of the trauma, and persistent, intrusive recollections of
the event via flashbacks, dreams, or recurrent thoughts
or visual images.

If the symptoms and behavioral disturbances of the
acute stress disorder persist for more than 1 month, and
if these features are associated with functional
impairment or significant distress to the sufferer, the
diagnosis is changed to post-traumatic stress disorder.
Post-traumatic stress disorder is further defined in
DSM-IV as having three subforms: acute' (< 3 months'
duration), chronic (2 3 months' duration), and delayed
onset (symptoms began at least 6 months after exposure
to the trauma).

By virtue of the more sustained nature of post-

' The acute subform of post-traumatic stress disorder is distinct
from acute stress.disorder because the latter resolves by the end
of the first month, whereas the former persists until 3 months.
If the condition persists after 3 months duration, the diagnosis is
again changed to the chronic post-traumatic stress disorder
subform (DSM-IV).

Adults and Mental Health

traumatic stress disorder (relative to acute stress
disorder), a number of changes, including decreased
self-esteem, loss of sustained beliefs about people or
society, hopelessness, a sense of being permanently
damaged, and difficulties in. previously established
relationships, are typically observed. Substance abuse
often develops, especially involving alcohol, marijuana,
and sedative-hypnotic drugs.

About 50 percent of cases of post-traumatic stress
disorder remit within 6 months. For the remainder, the
disorder typically persists for years and can dominate
the sufferer's life. A longitu'dinal study of Vietnam
veterans, for example, found 15 percent of veterans to
be suffering from post-traumatic stress disorder 19
years after combat exposure (cited in McFarlane &
Yehuda, 1996). In the general population, the l-year
prevalence is about 3.6 percent, with women having
almost twice the prevalence of men (Kessler et al.,
1995) (Table 4- 1). The highest rates of post-traumatic
stress disorder are found among women who are
victims of crime, especially rape, as well as among
torture and concentration camp survivors (Yehuda,
1999). Overall, among those exposed to extreme
trauma, about 9 percent develop post-traumatic stress
disorder (Breslau et al., 1998).

Etiology of Anxiety Disorders
The etiology of most anxiety disorders, although not
fully understood, has come into sharper focus in the last
decade. In broad terms, the likelihood of developing
anxiety involves a combination of life experiences,
psychological traits, and/or genetic factors. The anxiety
disorders are so heterogeneous that the relative roles of
these factors are likely to differ. Some anxiety dis-
orders, like panic disorder, appear to have a stronger
genetic basis than others (National Institute of Mental
Health [NIMH], 1998), although actual genes have not
been identified. Other anxiety disorders are more
rooted in stressful life events.

It is not clear why females have higher rates than
males of most anxiety disorders, although some
theories have suggested a role for the gonadal steroids.
Other research on women's responses to stress also
suggests that women experience a wider range of life

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Mental Health: A Report of the Surgeon General

events (e.g., those happening to friends) as stressful as
compared with men who react to a more limited range
of stressful events, specifically those affecting
themselves or close family members (Maciejewski et
al., 1999).

What the myriad of anxiety disorders have in
common is a state of increased arousal or fear (Barbee,
1998). Anxiety disorders often are conceptualized as an
abnormal or exaggerated version of arousal. Much is
known about arousal because of decades of study in
animals" and humans of the so-called "fight-or-flight
response," which also is referred to as the acute stress
response. The acute stress response is critical to
understanding the normal response to stressors and has
galvanized research,  but its limitations for
understanding anxiety have come to the forefront in
recent years, as this section later explains.
In common parlance, the term "stress" refers either
to the external stressor, which can be physical or
psychosocial in nature, as well as to the internal
response to the stressor. Yet researchers distinguish the
two, calling the stressor the stimulus and the body's
reaction the stress response. This is an important
distinction because in many anxiety states there is no
immediate external stressor. The following paragraphs
describe the biology of the acute stress response, as
well as its limitations, in understanding human anxiety.
Emerging views about the neurobiology of anxiety
attempt to integrate and understand psychosocial views
of anxiety and behavior in relation to the structure and
function of the central and peripheral nervous system.

Acute Stress Response

When a fearful or threatening event is perceived,
humans react innately to survive: they either are ready
for battle or run away (hence the term "fight-or-flight
response"). The nature of the acute stress response is
all too familiar. Its hallmarks are an almost
instantaneous surge in heart rate, blood pressure,
sweating, breathing, and metabolism, and a tensing of

2 Anxiety is one of the few mental disorders for which animal
models have beendeveloped. Researchers can reproduce some
of the symptoms of human anxiety in animals by introducing
`different types of stressors, either physical or psychosocial.

muscles. Enhanced cardiac output and accelerated
metabolism are essential for mobilizing fast action. The
host of physiological changes activated by a stressful
event are unleashed in part by activation of a nucleus in
the brain stem called the locus ceruleus. This nucleus
is the origin of most norepinephrine pathways in the
brain. Neurons using norepinephrine as their
neurotransmitter project bilaterally from the locus
ceruleus along distinct pathways to the cerebral cortex,
limbic system, and the spinal cord, among other
projections.

Normally, when someone is i? a serene, unstim-
ulated state, the "firing" of neurons in the locus
ceruleus is minimal. A novel stimulus, once perceived,
is relayed from the sensory cortex of the brain through
the thalamus to the brain stem. That route of signaling
increases the rate of noradrenergic activity in the locus
ceruleus, and the person becomes alert and attentive to
the environment. If the stimulus is perceived as a threat,
a more intense and prolonged discharge of the locus
ceruleus activates the sympathetic division of the
autonomic nervous system (Thase & Howland, 1995).
The activation of the sympathetic nervous system leads
to the release of norepinephrine from nerve endings
acting on the heart, blood vessels, respiratory centers,
and other sites. The ensuing physiological changes
constitute a major part of the acute stress response. The
other major player in the acute stress response is the
hypothalamic-pituitary-adrenal axis, which is discussed
in the next section.

In the 198Os, the prevailing view was that excess
discharge of the locus ceruleus with the acute stress
response was a major contributor to the etiology of
anxiety (Coplan & Lydiard, 1998). Yet over the past
decade, the limitations of the acute stress response as a
model for understanding anxiety have become more
apparent. The first and most obvious limitation is that
the acute stress response relates to arousal rather than
anxiety. Anxiety differs from arousal in several ways
(Barlow, 1988; Nutt et al., 1998). First, with anxiety,
the concern about the stressor is out of proportion to
the realistic threat. Second, anxiety is often associated
with elaborate mental and behavioral activities
designed to avoid the unpleasant symptoms of a full-

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Adults and Mental Health

blown anxiety or panic attack. Third, anxiety is usually
longer lived than arousal. Fourth, anxiety can occur
without exposure to an external stressor.

Other limitations of this model became evident
from a lack of support from clinical and basic research
(Coplan 8~ Lydiard, 1998). Furthermore, with its
emphasis on the neurotransmitter norepinephrlne, the
model could not explain why medications that acted on
the neurotransmitter serotonin (the selective serotonin
reuptake inhibitors, or SSRIs) helped to alleviate
anxiety symptoms. In fact, these medications are
becoming the first-line treatment for anxiety disorders
(Kent et al., 1998). To probe the etiology of anxiety,
researchers began to devote their energies to the study
of other brain circuits and the neurotransmitters on
which they rely. The locus ceruleus still participates in
anxiety but is understood to play a lesser role.

New Views About the Anatomical and
Biochemical Basis of Anxiety
An exciting new line of research proposes that anxiety
engages a wide range of neurocircuits. This line of
research catapults to prominence two key regulatory
centers found in the cerebral hemispheres of the
brain-the hippocampus and the amygdala. These
centers,  in turn,  are thought to activate the
hypothalamic-pituitary-adrenocortical (HPA) axis3
(Goddard & Chamey, 1997; Coplan & Lydiard, 1998;
Sullivan et al.,  1998). Researchers have long
established the contribution of the HPA axis to anxiety
but have been perplexed by how it is regulated. They
are buoyed by new findings about the roles of the
hippocampus and the amygdala.

The hippocampus and the amygdala govern
memory storage and emotions, respectively, among
their other functions. The hippocampus is considered
important in verbal memory, especially of time and
place for events with strong emotional overtones
(McEwen, 1998). The hippocampus and amygdala are
major nuclei of the limbic system, a pathway known to

3

Hypothalamus and the pituitary gland, and then the cortex,
or outer layer, of the adrenal gland. Upon stimulation by the
pituitary hormone ACTH, the adrenal cortex releases gluco-
corticoids into the circulation.

underlie emotions. There are anatomical projections
between the hippocampus, amygdala, and hypothal-
alamus (Jacobson & Sapolsky, 1991; Charney &
Deutch, 1996; Coplan & Lydiard, 1998).
Studies of emotional processing in rodents
(LeDoux, 1996; Rogan & LeDoux, 1996; Davis, 1997)
and in humans with brain lesions (Adolphs et al., 1998)
have identified the amygdala as critical to fear
responses. Sensory information enters the lateral
amygdala, from which processed information is passed
to the central nucleus, the major output nucleus of the
amygdala. The central nucleus projects, in turn, to
multiple brain systems involved in the physiologic and
behavioral responses to fear. Projections to different
regions of the hypothalamus activate the sympathetic
nervous system and induce the release of stress
hormones, such as CRH: The production of CRH in
the paraventricular nucleus of the hypothalamus
activates a cascade leading to release of glucocorticoids
from the adrenal cortex. Projections from the central
nucleus innervate different parts of the periaqueductal
gray matter, which initiates descending analgesic
responses (involving the body's endogenous opioids)
that can suppress pain in an emergency, and which also
activates species-typical defensive responses (e.g.,
many animals freeze when fearful).
  Anxiety differs from fear in that the fear-producing
stimulus is either not present or not immediately
threatening, but in anticipation of danger, the same
arousal, vigilance, physiologic preparedness, and
negative affects and cognitions occur. Different types
of internal or external factors or triggers act to produce
the anxiety symptoms of panic disorder, agoraphobia,
post-traumatic stress disorder, specific phobias, and
generalized anxiety disorder, and the prominent anxiety
that commonly occurs in major depression. It is
currently a matter of research to determine whether
dysregulation of these fear pathways leads to the
symptoms of anxiety disorders. It has now been
established, using noninvasive neuroimaging, that the
human amygdala is also involved in fear responses.
Fearful facial expressions have been shown to activate

4 Also known as coriocotropin-releasing factor.

239


Mental Health: A Report of the Surgeon General

the amygdala in MRI studies of normal human subjects
(Breiter et al., 1996). Functional imaging studies in
anxiety disorders, such as PET studies of brain
activation in phobias (Rauch et al., 1993, are also
beginning to investigate the precise neural circuits
involved in the anxiety disorders.
What is especially exciting is that neuroimaging
has furnished direct evidence in humans of the
damaging effects of glucocorticoids. In people with
post-traumatic stress disorder, neuroimaging studies
have found a reduction in the size of the hippocampus.
The reduced volume appears to reflect the atrophy of
dendrites-the receptive portion of nerve cells-in a
select region of the hippocampus. Similarly, animals
exposed to chronic psychosocial stress display atrophy
in the same hippocampal region (McEwen &
Magarinos,  1997). Stress-induced increases in
glucocorticoids are thought to be responsible for the
atrophy (McEwen, 1998). If the hippocampus is
impaired, the individual is thought to be less able to
draw on memory to evaluate the nature of the stressor
(McEwen, 1998).

A/eurofransmitfer Alterations

There are many neurotransmitter alterations in anxiety
disorders. In keeping with the broader view of anxiety,
at least five neurotransmitters are perturbed in anxiety:
serotonin, norepinephrine, gamma-aminobutyric acid
(GABA), corticotropin-releasing hormone (CRH),5 and
cholecystokinin (Coplan & Lydiard 1998; Rush et al.,
1998). There is such careful orchestration between
these neurotransmitters that changes in one
neurotransmitter system invariably elicit changes in
another, including extensive feedback mechanisms.
Serotonin and GABA are inhibitory neurotransmitters
that quiet the stress response (Rush et al., 1998). All of
these neurotransmitters have become important targets
for therapeutic agents either already marketed or in
development (as discussed in the section on treatment
of anxiety disorders).

s CRH may act as a neuromodulator, a neurotransmitter, or a
neurohormone. depending on the pathway.

Psychological Views of Anxiety
There are several major psychological theories of
anxiety: psychoanalytic and psychodynamic theory,
behavioral theories, and cognitive theories (Thorn et
al., 1999). Psychodynamic theories have focused on
symptoms as an expression of underlying conflicts
(Rush et al., 1998; Thorn et al., 1999). Although there
are no empirical  studies to support these
psychodynamic theories, they are amenable to scientific
study (Kandel, 1999) and some therapists find them
useful. For example, ritualistic compulsive behavior
can be viewed as a result ,of a specific defense
mechanism that serves to channel `psychic energy away
from conflicted or forbidden impulses. Phobic
behaviors similarly have been viewed as a result of the
defense mechanism of displacement. From the
psychodynamic perspective, anxiety usually reflects
more basic,  unresolved conflicts  in intimate
relationships or expression of anger.
More recent behavioral theories have emphasized
the importance of two types of learning: classical
conditioning and vicarious or observational learning.
These theories have some empirical evidence to support
them. In classical conditioning, a neutral stimulus
acquires the ability to elicit a fear response after
repeated pairings with a frightening (unconditioned)
stimulus. In vicarious learning, fearful behavior is
acquired by observing others' reactions to fear-
inducing stimuli (Thorn et al., 1999). With general
anxiety disorder, unpredictable positive and negative
reinforcement is seen as leading to anxiety, especially
because the person is unsure about whether avoidance
behaviors are effective.
  Cognitive factors, especially the way people
interpret or think about stressful events, play a critical
role in the etiology of anxiety (Barlow et al., 1996;
Thorn et al., 1999). A decisive factor is the individual's
perception, which can intensify or dampen the
response. One of the most salient negative cognitions
in anxiety is the sense of uncontrollability. It is typified
by a state of helplessness due to a perceived inability to
predict, control, or obtain desired results (Barlow et al.,
1996). Negative cognitions are frequently found in
individuals with anxiety (Ingram et al., 1998). Many

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Adults and Mental Health

,,,odem psychological models of anxiety incorporate
the role of individual vulnerability, which includes both
genetic (Smoller & Tsuang, 1998) and acquired
, Coplan et al.. 1997) predispositions. There is evidence
that vvomen may ruminate more about distressing life
e\`ents compared with men, suggesting that a cognitive
ri>k factor may predispose them to higher rates of
anxiety and depression (Nolen-Hoeksema et al., in
press ).

Treatment of Anxiety Disorders
The anxiety disorders are treated with some form of
counseling or psychotherapy or pharmacotherapy,
either singly or in combination (Barlow & Lehman,
1996: March et al., 1997; American Psychiatric
Association, 1998; Kent et al., 1998).

Counseling and Psychotherapy

Anxiety disorders are responsive to counseling and to
a wide variety of psychotherapies. More severe and
persistent symptoms also may require pharmacotherapy
(American Psychiatric Association, 1998).

During the past several decades, there has been
increasing enthusiasm for more focused, time-limited
therapies that address ways of coping with anxiety
symptoms more directly rather than . exploring
unconscious conflicts or other personal vulnerabilities
(Barlow & Lehman, 1996). These therapies typically
emphasize cognitive and behavioral assessment and
interventions.

The hallmarks of cognitive-behavioral therapies are
evaluating apparent cause and effect relationships
between thoughts, feelings, and behaviors, as well as
implementing relatively straightforward strategies to
lessen symptoms and reduce avoidant behavior
(Barlow, 1988). A critical element of therapy is to
increase exposure to the stimuli or situations that
provoke anxiety. Without such therapeutic assistance,
the sufferer typically withdraws from anxiety-inducing
situations, inadvertently reinforcing avoidant or escape
behavior.

The therapist provides reassurance that the feared
situation is not deadly and introduces a plan to enhance
mastery. This plan may include approaching the feared
situation in a graduated or stepwise hierarchy or
teaching the patient to use responses that dampen
anxiety, such as deep muscle relaxation or coping. One
fundamental principle is that prolonged exposure to a
feared stimulus reliably decreases cognitive and
physiologic symptoms of anxiety (Marks, 1969;
Barlow, 1988). With such experience generally comes
greater self-efficacy and a greater willingness to
encounter other feared stimuli. For panic disorder,
interoceptive training (a type of conditioning
technique) and breathing exercises are often employed
to help the sufferer become more capable of
recognizing and coping with the social cues,
antecedents, or early signs of a panic attack. Cognitive
interventions are used to counteract the exaggerated or
catastrophic thoughts that characterize anxiety. For
treatment of obsessive-compulsive disorder, the
strategy of response prevention must be added to
exposure to ensure that compulsions are not performed
(Barlow, 1988).

There is now extensive evidence that cognitive-
behavioral therapies are useful treatments for a
majority of patients with anxiety disorders (Chambless
et al., 1998). Poorer outcomes are observed, however,
in more complicated patient groups. With obsessive-
compulsive disorder, approximately 20 to 25 percent of
patients are unwilling to participate in therapy (March
et al., 1997). Another major limitation of cognitive-
behavioral therapies is not their effectiveness but,
rather, the limited availability of skilled practitioners
(Ballenger et al., 1998).

It is possible that more traditional forms of therapy
based on psychodynamic or interpersonal theories of
anxiety also may prove to be effective treatments
(Shear, 1995). However, these therapies have not yet
received extensive empirical support. As a result, more
traditional therapies are generally deemphasized in
evidence-based treatment guidelines for anxiety
disorders.

241


Mental Health: A Report of the Surgeon General

Pharmacofherapy

The medications typically used to treat patients with
anxiety disorders are benzodiazepines, antidepressants,
and the novel compound buspirone (Lydiard et al.,
1996). In light of increasing awareness of numerous
neurochemical alterations in anxiety disorders, many
new classes of drugs are. likely to be developed,
expressly targeting CRH and other neuroactive agents
(Nemeroff, 1998).

Benzodiazepines

The benzodiazepines are a large class of relatively safe
and widely prescribed medications that have rapid and
profound antianxiety and sedative-hypnotic effects. The
benzodiazepines are thought to exert their therapeutic
effects by enhancing the inhibitory neurotransmitter
systems utilizing GABA. Benzodiazepines bind to a
site on the GABA receptor and act as receptor agonists
(Perry et al., 1997). Benzodiazepines differ in terms of
potency, pharmacokinetics (i.e., elimination half-life),
and lipid solubility.

The four benzodiazepines currently widely pre-
scribed for treatment of anxiety disorders are diazepam,
lorazepam, clonazepam, and alprazolam. Each is now
available in generic formulations (Davidson, l998).
Among these agents, alprazolam and lorazepam have
shorter elimination half-lives-that is, are removed
from the body more quickly-while diazepam and
clonazepam have a long period of action (i.e., up to 24
hours). Diazepam also has multiple active metabolites,
which increase the risk of "carryover" effects such as
sedation and "hangover." Benzodiazepines that undergo
conjugation appear to have longer elimination time in
women, and oral contraceptive can decrease clearance
(Dawlans, 1995). Since Asians are more likely to
metabolize diazepam more slowly, they may require
lower doses to achieve the same blood concentrations
as Caucasians (Lin et al., 1997).

Benzodiazepines have the potential for producing
drug dependence (i.e., physiological or behavioral
symptoms after discontinuation of use). Shorter acting
compounds have somewhat greater liability because of
more rapid and abrupt onset of withdrawal symptoms.

Because the benzodiazepines do not have strong
antiobsessional effects, their use in obsessive-
compulsive disorder and post-traumatic stress disorder
is generally viewed as palliative (i.e., relieving, but not
eliminating symptoms). Rather, obsessive-compulsive
disorder and post-traumatic stress disorder are more
effectively treated by antidepressants, especially the
SSRIs (as discussed below). When effective,
benzodiazepines should be tapered after several months
of use, although there is a substantial risk of relapse.
Many clinicians favor a combined treatment approach
for panic disorder and generalized inxiety disorder, in
which benzodiazepines are used acutely in tandem with
an antidepressant.  The benzodiazepines are
subsequently tapered as the antidepressant's therapeutic
effects begin to emerge (American Psychiatric
Association, 1998).

Antidepressants

Most antidepressant medications have substantial
antianxiety and antipanic effects in addition to their
antidepressant action (Kent et al., 1998). Moreover, a
large number of antidepressants have antiobsessional
effects (Perry et al., 1997). The observation that the
tricyclic antidepressant imipramine had a different
anxiolytic profile than diazepam helped to differentiate
panic disorder from generalized anxiety disorder and,
subsequently, social phobia.

Clomipramine, a tricyclic antidepressant (TCA)
with relatively potent reuptake inhibitory effects on
serotonin (5HT) neurons, subsequently was found to
be the only TCA to have specific antiobsessional
effects (March et al., 1997). The importance of this
effect on 5-HT was highlighted when the SSRIs
became available. By the late 199Os, it became clear
that all of the SSRIs have antiobsessional effects
(Greist et al., 1995; Kent et al., 1998).

Current practice guidelines rank the TCAs below
the SSRIs for treatment of anxiety disorders because of
the SSRIs' more favorable tolerability and safety
profiles (March et al., 1997; American Psychiatric
Association, 1998; Ballenger et al., 1998;).
Nevertheless, there are patients who respond to the
TCAs after failing to respond to one or more of t.he

242


newer agents. Similarly, although relatively rarely used,
the monoamine oxidate inhibitors (MAOIs) have
significant antiobsessional, antipanic, and anxiolytic
effects (Sheehan et al., 1980; American Psychiatric
Association, 1998). In the United States, the MAOIs
phenelzine. tranylcypromine, and isocarboxazid (which
has not been consistently marketed this decade) are
seldom used unless simpler medication strategies have
failed (American Psychiatric Association, 1998).
The five drugs within the SSRI class-fluoxetine,
sertraline,  paroxetine,  fluvoxamine, and
citalopram-have emerged as the preferred type of
antidepressant for treatment of anxiety disorders
(Westenberg, 1996; Kent et al., 1998). In addition to
well-established efficacy in obsessive-compulsive
disorder, there is convincing and growing evidence of
antipanic and broader anxiolytic effects (American
Psychiatric Association, 1998; Kent et al., 1998).
Treatment of panic disorder often requires lower initial
doses and slower upward titration. By contrast,
treatment for obsessive-compulsive disorder ultimately
may entail higher doses (for example, 60 or 80 mg/day
of fluoxetine or 200 mg per day of sertraline) and
longer durations to achieve desired outcomes (Marchet
al., 1997). As all of the SSRIs are currently protected
by patents, there are no generic forms yet available.
This adds to the direct costs of treatment. Cost may be
offset indirectly, however, by virtue of need for fewer
treatment visits and fewer concomitant medications,
and cost likely will abate when these agents begin to
lose patent protection in a few years.
  Other   newer  antidepressants,  including
venlafaxine, nefazodone, and mirtazapine, also may
have significant antianxiety effects, for which clinical
trials are under way (March et al., 1997; American
Psychiatric Association, 1998). Paroxetine has been
approved by the Food and Drug Administration (FDA)
for social phobia, and sertraline is being developed for
post-traumatic stress disorder. Nefazodone, which also
is being studied in post-traumatic stress disorder, and
mh-tazapine may possess lower levels of sexual side
effects, a problem that complicates longer term
treatment with SSRIs, venlafaxine, TCAs, and MAOIs
(Baldwin & Birtwistle, 1998).

Adults and Mental Health

When effective in treating anxiety, antidepressants
should be maintained for at least 4 to 6 months, then
tapered slowly to avoid discontinuation-emergent
activation of anxiety symptoms (March et al., 1997;
American Psychiatric Association, 1998; Ballenger et
al., 1998). Although less extensively researched than
depression, it is likely that many patients with anxiety
disorders may warrant longer term, indefinite treatment
to prevent relapse or chronicity.

Buspirone

This azopyrine compound is a relatively selective 5-
HT,, partial agonist (Stahl, 1996). It was approved by
the FDA in the mid-1980s as an anxiolytic. However,
unlike the benzodiazepines, buspirone is not habit
forming and has no abuse potential. Buspirone also has
a safety profile comparable to the SSRIs, and it is
significantly better tolerated than the TCAs.
Buspirone does not block panic attacks, and it is
not efficacious as a primary treatment of obsessive-
compulsive disorder or post-traumatic stress disorder
(Stahl, 1996). B uspirone is most useful for treatment of
generalized anxiety disorder, and it is now frequently
used as an adjunct to SSRIs (Lydiardet al., 1996).
Buspirone takes 4 to 6 weeks to exert therapeutic
effects, like antidepressants, and it has little value for
patients when taken on an "as needed" basis.

Combinations of Psychotherapy and Pharmaco-
therapy
Some patients with anxiety disorders may benefit from
both psychotherapy and pharmacotherapy treatment
modalities, either combined or used in sequence
(March et al., 1997; American Psychiatric Association,
1998). Drawing from the experiences of depression
researchers, it seems likely that such combinations are
not uniformly necessary and are probably more cost-
effective when reserved for patients with more
complex, complicated, severe, or comorbid disorders.
The benefits of multimodal therapies for anxiety need
further study.

243


Mental Health: A Report of the Surgeon General

Mood Disorders

In 1 year, about 7 percent of Americans suffer from
mood disorders, a cluster of mental disorders best
recognized by depression or mania (Table 4-l). Mood
disorders are outside the bounds of normal fluctuations
from sadness to elation. They have potentially severe
consequences for morbidity and mortality.
This section covers four mood disorders. As the
predominant mood disorder, major depressive disorder
(also known as unipolar major depression), garners the
greatest attention. It is twice more common in women
than in men, a gender difference that is discussed later
in this section. The other mood disorders covered
below are bipolar disorder, dysthymia, and
cyclothymia.

  Mood disorders rank among the top 10 causes of
worldwide disability (Murray & Lopez, 1996).
Unipolat major depression ranks first, and bipolar
disorder ranks in the top 10. Moreover, disability and
suffering are not limited to the patient. Spouses,
children, parents, siblings, and friends experience
frustration, guilt, anger, financial hardship, and, on
occasion, physical abuse in their attempts to assuage or
cope with the depressed person's suffering. Women
between the ages of 18 and 45 comprise the majority of
those with major depression (Regier et al., 1993).

Depression also has a deleterious impact on the
economy, both in diminished productivity and in use of
health care resources (Greenberg et al., 1993). In the
workplace, depression  is a leading cause of
absenteeism and diminished productivity. Although
only a minority seek professional help to relieve a
mood disorder, depressed people are significantly more
likely than others to visit a physician for some other
reason. Depression-related visits to physicians thus
account for a large portion of health care expenditures.
Seeking another or a less stigmatized explanation for
their difficulties, some depressed patients undergo
extensive and expensive diagnostic procedures and then
get treated for various other complaints while the mood
disorder goes undiagnosed and untreated (Wells et al.,
1989).

Complications and Comorbidities
Suicide is the most dreaded complication of major
depressive disorders. About 10 to 15 percent of patients
formerly hospitalized with depression commit suicide
(Angst et al., 1999). Major depressive disorders
account for about 20 to 35 percent of all deaths by
suicide (Angst et al., 1999). Completed suicide is more
common among those with more severe and/or
psychotic symptoms, with late onset, with co-existing
mental and addictive disorders (Angst et al., 1999), as
well as among those who have experienced stressful
life events, who have medical ill&sses, and who have
a family history of suicidal behavior (Blumenthal,
1988). In the United States, men complete suicide four
times as often as women; women attempt suicide four
times as frequently as do men (Blumenthal, 1988).
Recognizing the magnitude of this public health
problem, the Surgeon General issued a Cull to Action
on Suicide in 1999 (see Figure 4-l). Individuals with
depression also face an increased risk of death from
coronary artery disease (Glassman & Shapiro, 1998).

Mood disorders often coexist, or are comorbid,
with other mental and somatic disorders. Anxiety is
commonly comorbid with major depression. About
one-half of those with a primary diagnosis of major
depression also have an anxiety disorder (Barbee, 1998;
Regier et al., 1998). The comorbidity of anxiety and
depression is so pronounced that it has led to theories
of similar etiologies, which are discussed below.
Substance use disorders are found in 24 to 40 percent
of individuals with mood disorders in the United States
(Merikangas et al., 1998). Without treatment, substance
abuse worsens the course of mood disorders. Other
common comorbidities include personality disorders
(DSM-IV) and medical illness, especially chronic
conditions such as hypertension and arthritis. People
with depression have a high prevalence (65 to 71
percent) of any of eight common chronic medical
conditions (Wells et al., 1991). The mood disorders
also may alter or "scar" personality development.

244


Figure 4-1. Surgeon General's Call to Action to
       Prevent Suicide-1999

.  Suicide is a serious public health problem


   .  31,000 suicides in 1996
   o  500,000 people visit emergency rooms due to
   attempted suicide

.  Suicide rate declined from 12.1 per 100,000 in
  1976 to 10.8 per `100,000 in 1996

o  Rate in adolescents and young adults almost
tripled since 1952
o  Rate is 50 percent higher than the homicide
  rate

I  National Strategy for Suicide Prevention: AIM


   o  Awareness: promote public awareness of
   suicide as.a public health problem
   o  Intervention: enhance services and programs
   o  Methodology: advance the science of suicide
   prevention

.   Risk factors

  o Male gender
   o  Mental disorders, particularly depression and
    substance abuse

  o Prior suicide attempts
   .  Unwillingness to seek help because of stigma
   o  Barriers to accessing mental health treatment
  o Stressful life event/loss
   o  Easy access to lethal methods such as guns


.   Protective factors


   o  Effective and appropriate clinical care for
   underlying disorders
   o  Easy access to care
   o  Support from family, community, and health and
    mental health care staff

Clinical Depression Versus Normal Sadness
People have been plagued by disorders of mood for at
least as long as they have been able to record their
experiences. One of the earliest terms for depression,
"melancholy," literally meaning "black bile," dates
back to Hippocrates. Since antiquity, dysphoric states
outside the range of normal sadness or grief have been
recognized, but only within the past 40 years or so have
researchers had the means to study the changes in
cognition and brain functioning that are associated with
severe depressive states.

Adults and Mental Health

At some time or another, virtually all adult human
beings will experience a tragic or unexpected loss,
romantic heartbreak, or a serious setback and times of
profound sadness, grief, or distress. Indeed, something
is awry if the usual expressions of sadness do not
accompany such situations so common to the human
ConditionAeath of a loved one, severe illness,
prolonged disability, loss of employment or social
status, or a child's difficulties, for example.
What is now called major depressive disorder.
however, differs both quantitatively and qualifativef~
from normal sadness dr grief. Normal states of
dysphoria (a negative or aversive mood state) are
typically less pervasive and generally run a more time-
limited course. Moreover, some of the symptoms of
severe depression, such as anhedonia (the inability to
experience pleasure), hopelessness, and loss of mood
reactivity (the ability to feel a mood uplift in response
to something positive) only rarely accompany "normal"
sadness. Suicidal thoughts and psychotic symptoms
such as delusions or hallucinations virtually always
signify a pathological state.

Nevertheless, many other symptoms commonly
associated with depression are experienced during
times of stress or bereavement. Among them are sleep
disturbances, changes in appetite, poor concentration,
and ruminations on sad thoughts and feelings. When a
person suffering such distress seeks help, the
diagnostician's task is to differentiate the normal from
the pathologic and, when appropriate, to recommend
treatment.

Assessment: Diagnosis and Syndrome
Severity
The criteria for diagnosing major depressive episode,
dysthymia, mania, and cyclothymia are presented in
Tables 4-2 through 4-5. Mania is an essential feature of
bipolar disorder, which is marked by episodes of mania
or mixed episodes of mania and depression. The
reliability of the diagnostic criteria for major depressive
disorder and bipolar disorder is impressive, with greater
than 90 percent agreement reached by independent
evaluators (DSM-IV).

245


Mental Health: A Report of the Surgeon General

Major Depressive Disorder

Major depressive disorder features one or more major
depressive episodes (see Table 4-2), each of which lasts
at least 2 weeks (DSM-IV). Since these episodes are
also characteristic of bipolar disorder, the term "major6
depression" refers to both major depressive disorder
and the depression of bipolar disorder.
The cardinal symptoms of major depressive
disorder are depressed mood and loss of interest or
pleasure. Other symptoms vary enormously. For
example, insomnia and weight loss are considered to be
classic signs, even though many depressed patients gain
weight and sleep excessively. Such heterogeneity is
partly dealt with by the use of diagnostic subtypes (or
course modifiers) with differing presentations and
prevalence. For example, a more severe depressive
syndrome characterized by a constellation of classical
signs and symptoms, called melancholia, is more
common among older than among younger people, as
are depressions characterized by psychotic features
(i.e., delusions and hallucinations) (DSM-IV). In fact,
the presentation  of psychotic features without
concomitant melancholia should always raise suspicion
about the accuracy of the diagnosis (vis-8-vis
schizophrenia or a related psychotic disorder). The so-
called reversed vegetative symptoms (oversleeping,
overeating, and weight gain) may be more prevalent in
women than men (Nemeroff, 1992). Anxiety symptoms
such as panic attacks, phobias, and obsessions also are
not uncommon.

When untreated, a major depressive episode may
last, on average, about 9 months. Eighty to 90 percent
of individuals will remit within 2 years of the first
episode (Kapur & Mann, 1992). Thereafter, at least 50
percent of depressions will recur, and after three or
more episodes the odds of recurrence within 3 years
increases to 70 to 80 percent if the patient has not had
preventive treatment (Thase & Sullivan, 1995). Thus,
for many, an initial episode of major depression will
evolve over time into the more recurrent illness

6 The adjective "major" before the word "depression" denotes
the number of symptoins required for the diagnosis, as distinct,
From a proposed new category of "minor depression," which
requires fewer symptoms (see Chapter 5).

sometimes referred to as unipolar major depression
(Thase & Sullivan, 1995). Each new episode also
confers new risks of chronicity, disability, and suicide.

Dysthymia

Dysthymia is a chronic form of depression. Its early
onset and unrelenting, "smoldering" course are among
the features that distinguish it from major depressive
disorder (DSM-IV). Dysthymia becomes so intertwined
with a person's self-concept or personality that the
individual may be misidentified as "neurotic" (resulting
from unresolved early conflicts expressed through
unconscious personality defenses ,or characterologic
disorders) (Akiskal, 1985). Indeed, the onset of
dysthymia in childhood or adolescence undoubtedly
affects personality development and coping styles,
particularly prompting passive, avoidant, and
dependent "traits."  To avoid the pejorative
connotations associated with the terms "neurotic" and
"characterologic," the term "dysthymia" is used in
DSM-IV as a descriptive, or atheoretical, diagnosis for
a chronic form of depression (see Table 4-3)
(DSM-IV). Affecting about 2 percent of the adult
population in 1 year, dysthymia is defined by its
subsyndromal nature (i.e., fewer than the five persistent
symptoms required to diagnose a major depressive
episode) and a protracted duration of at least 2 years for
adults and 1 year for children. Like other early-onset
disorders, dysthymic disorder is associated with higher
rates of comorbid substance abuse. People with
dysthymia also are susceptible to major depression.
When this occurs, their illness is sometimes referred to
as "double depression," that is, the combination of
dysthymia and major depression (Keller & Shapiro,
1982). Unlike the superimposed major depressive
episode, however, the underlying dysthymia seldom
remits spontaneously. Women are twice as likely to be
diagnosed with dysthymia as men (Robins & Regier,
1991).

Bipolar Disorder

Bipolar disorder is a recurrent mood disorder featuring
one or more episodes of mania or mixed episodes of
mania and depression ( DSM-IV; Goodwin & Jamison,

246


Adults and Mental Health

Table 4-2. DSM-IV criteria for maior dewessive episode

I

4.

B.


C.



D.



E.

Five (or more) of the following symptoms have been present during the same 2.week period and represent a
change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of
interest or pleasure.

Note: Do not include symptoms that are clearly due to a general medical condition, or mood-incongruent
delusions or hallucinations.

(1)

(2)

(3)

(4)
(5)

(6)
(7)

(8)

(9)

depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels
sad'or empty) or observation made by others (e.g., appears tearful). Note: In children and adolescents,
can be irritable mood.

markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day
(as indicated by either subjective account or observation made by others).
significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of body weight in
a month), or decrease or increase in appetite nearly every day. Note: In children, consider failure to
make expected weight gains.                                     .

insomnia or hypersomnia nearly every day.
psychomotor agitation or retardation nearly every day (observable by others, not merely subjective
feelings or restlessness or being slowed down).
fatigue or loss of energy nearly every day.
feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day
(not merely self-reproach or guilt about being sick).
diminished ability to think or concentrate, or indecisiveness, nearly every day (either subjective account
or as observed by others).
recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a
suicide attempt or a specific plan for committing suicide.

The symptoms do not meet criteria for a mixed episode.

The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas
of functioning.

The symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication)
or a general medical condition (e.g.`, hypothyroidism).

The symptoms are not better accounted for by bereavement, i.e., after the loss of a loved one; the symptoms
persist for longer than 2 months or are characterized by marked functional impairment, morbid preoccupation with
worthlessness, suicidal ideation, psychotic symptoms, or psychomotor retardation.

247


Mental Health: A Report of the Surgeon General

Ta

E

_
J.



D.









E.



F.



G.



H.

lble 4-3. DSM-IV diagnostic criteria for Dysthymic Disorder

Depressed mood for most of the day, for more days than not, as indicated either by subjective account or observation
by others, for at least 2 years. Note: In children and adolescents, mood can be irritable and duration must be at
least 1 year.

Presence, while depressed, of two (or more) of the following:

(1)  poor appetite or overeating
(2)  insomnia or hypersomnia
(3)  low energy or fatigue
(4) low self-esteem
(5)  poor concentration or difficulty making decisions
(6) feelings of hopelessness

During the 2-year period (1 year for children or adolescents) of the disturbance, the person has never been without
the symptoms in Criteria A and 6 for more than 2 months at a time.                      .

No major depressive episode has been present during the first 2 years of the disturbance (1 year for children and
adolescents); i.e.! the disturbance is not better accounted for by chronic major depressive disorder, or major
depressive disorder, in partial remission.

Note: There may have been a previous major depressive episode provided there was a full remission (no significant
signs or symptoms for 2 months) before development of the dysthymic disorder. In addition, after the initial 2 years
(1 year in children or adolescents) of dysthymic disorder, there may be superimposed episodes of major depressive
disorder, in which case both diagnoses may be given when the criteria are met for a major depressive episode.

There has never been a manic episode, a mixed episode, or a hypomanic episode, and criteria have never been met
for cyclothymic disorder.

The disturbance does not occur exclusively during the course of a chronic psychotic disorder, such as schizophrenia
or delusional disorder.

The symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a
general medical condition (e.g., hypothyroidism).

The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of
functioning.

1

248


1990). Bipolar disorder' is distinct from major
depressive disorder by virtue of a history of manic or
hypomanic (milder and not psychotic) episodes. Other
differences concern the nature of depression in bipolar
disorder. Its depressive episodes are typically
associated with an earlier age at onset, a greater
likelihood of reversed vegetative symptoms, more
frequent episodes or recurrences, and a higher familial
prevalence (DSM-IV; Goodwin & Jamison, 1990).
Another noteworthy difference between bipolar and
nonbipolar groups is the differential therapeutic effect
of lithium salts, which are more helpful for bipolar
disorder (Goodwin & Jamison, 1990).
Mania is derived from a French word that literally
means crazed or frenzied. The mood disturbance can
range from pure euphoria or elation to irritability to a
labile admixture that also includes dysphoria (Table
4-4). Thought content is usually- grandiose but also can
be paranoid. Grandiosity usually takes the form both of
overvalued ideas (e.g., "My book is the best one ever
written") and of frank delusions (e.g., "I have radio
transmitters implanted in my head and the Martians are
monitoring my thoughts.") Auditory and visual
hallucinations complicate more severe episodes. Speed
of thought increases, and ideas typically race through
the manic person's consciousness. Nevertheless,
distractibility and poor concentration commonly impair
implementation. Judgment also can be severely
compromised; spending sprees, offensive or
disinhibited behavior, and promiscuity or other
objectively reckless behaviors are commonplace.
Subjective energy, libido, and activity typically
increase but a perceived reduced need for sleep can sap
physical reserves.  Sleep deprivation also can
exacerbate cognitive difficulties and contribute to
development of catatonia or a florid, confusional state
known as delirious mania. If the manic patient is
delirious, paranoid, or catatonic, the behavior is
difficult to distinguish from that of a schizophrenic
patient. Clinicians are prone to misdiagnose mania as
schizophrenia in African Americans (Bell & Mehta,

'

Bipolar disorder is also known as bipolar affective disorder and
manic depression.

Adults and Mental Health

198 1). Most people with bipolar disorder have a history
of remission and at least satisfactory functioning before
onset of the index episode of illness.
In DSM-IV, bipolar depressions are divided into
type I (prior mania) and type II (prior hypomanic
episodes only). About 1.1 .percent of the adult
population suffers from the type I form, and 0.6 percent
from the type II form (Goodwin & Jar&on, 1990:
Kessler et al., 1994) (Table 4-5). Episodes of mania
occur, on average, every 2 to 4 years, although
accelerated mood cycles can occur annually or even
more frequently. The type I form of bipolar disorder is
about equally common in men and women, unlike
major depressive disorder, which is more common in

women.

Hypomania, as suggested above, is the sub-
syndromal counterpart of mania (DSM-IV; Goodwin &
Jamison,  1990). By definition, an episode of
hypomania is never psychotic nor are hypomanic
episodes associated with marked impairments in
judgment or performance. In fact, some people with
bipolar disorder long for the productive energy and
heightened creativity of the hypomanic phase.
Hypomania can be a transitional state (i.e., early in
an episode of mania), although at least 50 percent of
those who have hypomanic episodes never become
manic (Goodwin & Jamison, 1990). Whereas a
majority have a history of major depressive episodes
(bipolar type II disorder), others become hypomanic
only during antidepressant treatment (Goodwin &
Jamison, 1990). Despite the relatively mild nature of
hypomania, the prognosis for patients with bipolar type
II disorder is poorer than that for recurrent (unipolar)
major depression, and there is some evidence that the
risk of rapid cycling (four or more episodes each year)
is greater than with bipolar type I (Coryell et al., 1992).
Women are at higher risk for rapid cycling bipolar
disorder than men (Cot-yell et al., 1992). Women with
bipolar disorder are also at increased risk for an episode
during pregnancy and the months following childbirth
(Blehar et al., 1998).

249


Mental Health: A Report of the Surgeon General

Ta

lble 4-4. DSM-IV criteria for manic episode

4.  A distinct period of abnormally and persistently elevated, expansive, or irritable mood, lasting at least 1 week (or any
  duration if hospitalization is necessary).

3.  During the period of mood disturbance, three (or more) of the following symptoms have persisted (four if the mood is
  only irritable) and have been present to a significant degree:

(1)  inflated self-esteem or grandiosity
(2)  decreased need for sleep (e.g., feels rested after only 3 hours of sleep)
(3)  more talkative than usual or pressure to keep talking
(4)  flight of ideas or subjective experience that thoughts are racing
(5)  distractibility (i.e., attention too easily drawn to unimpoitant or irrelevant external stimuli)
(6) increase in goal-directed activity (either socially, at work or school, or sexually) or psyctiomotor agitation

(7)  excessive involvement in pleasurable activities that have a high potential for painful consequences (e.g.,
  engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments)

I

C.  The symptoms do not meet criteria for a mixed episode.

D.  The mood disturbance is sufficiently severe to cause marked impairment in occupational functioning or in USUal
social activities or relationships with others, or to necessitate hospitalization to prevent harm to self or others, or there
  are psychotic features.

E.  The symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication, or
  other treatment) or general medical condition (e.g., hyperthyroidism).

Note: Manic-like episodes that are clearly caused by somatic antidepressant treatment (e.g., medication,
electroconvulsive therapy, light therapy) should not count toward a diagnosis of bipolar I disorder.

able 4-5. DSM-IV diagnostic criteria for Cyclothymic Disorder

4.





3.





cl.









D.



E.



F.

For at least 2 years, the presence of numerous periods with hypomanic symptoms and numerous periods with
depressive symptoms that do not meet criteria for a major depressive episode. Note: In children and adolescents,
the duration must be at least 1 year.

During the above 2-year period (1 year in children and adolescents), the person has not been without the symptoms
in Criterion A for more than 2 months at a time.

No major depressive episode, manic episode, or mixed episode has been present during the first 2 years of the
disturbance.

Note: After the initial 2 years (1 year in children and adolescents) of cyclothymic disorder, there may be
superimposed manic or mixed episodes (in which case both bipolar I disorder and cyclothymic disorder may be
diagnosed) or major depressive episodes (in which case both bipolar II disorder and cyclothymic disorder may be
diagnosed).

The symptoms in Criterion A are not better accounted for by schizoaffective disorder and are not superimposed on
schizophrenia, schizophreniform disorder, delusional disorder, or psychotic disorder not otherwise specified.

The symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a
general medical condition (e.g., hyperthyroidism).
The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of
functioning.

?

250