Journal of Clinical Child & Adolescent Psychology

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Early Detection and Prevention of Mental Health

Problems: Developmental Epidemiology and
Systems of Support

E. Jane Costello

To cite this article: E. Jane Costello (2016) Early Detection and Prevention of Mental Health
Problems: Developmental Epidemiology and Systems of Support, Journal of Clinical Child &
Adolescent Psychology, 45:6, 710-717, DOI: 10.1080/15374416.2016.1236728

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Journal of Clinical Child & Adolescent Psychology, 45(6), 710–717, 2016
Published with License by Taylor & Francis Group
ISSN: 1537-4416 print/1537-4424 online
DOI: 10.1080/15374416.2016.1236728

Early Detection and Prevention of Mental Health

Problems: Developmental Epidemiology and Systems
of Support
E. Jane Costello
Department of Psychiatry and Behavioral Sciences, Duke University

This article reviews the role of developmental epidemiology in the prevention of child and
adolescent mental disorders and the implications for systems of support. The article distinguishes
between universal or primary prevention, which operates at the level of the whole community to
limit risk exposure before the onset of symptoms, and secondary or targeted prevention, which
operates by identifying those at high risk of developing a disorder. It discusses different aspects of
time as it relates to risk for onset of disease, such as age at first exposure, duration of exposure, age
at onset of first symptoms, and time until treatment. The study compares universal and targeted
prevention, describing the systems needed to support each, and their unintended consequences.

In this article we discuss how epidemiology, the study of TYPES OF PREVENTION

patterns of illness in time and space, can help to prevent
mental health problems by preventing either their occur-
rence or their causes. Preventing something is usually easier
if we can reliably detect the problem, or its cause, or both.
We tend to assume, probably with reason, that it is better to
detect a problem or its cause earlier rather than later in the
course of the disorder and that that systems of support will
be strengthened if detection occurs early. A case can be
made against this argument for early intervention (think of
all those tonsillectomies and umbilical hernia operations
later shown to be a complete waste of resources). But until
proven otherwise, epidemiology is ethically bound to oper-
ate on the assumption that early detection is a service that it
can and should provide to the health care system.
© E. Jane Costello
This is an Open Access article. Non-commercial re-use, distribution, and
reproduction in any medium, provided the original work is properly attributed,
cited, and is not altered, transformed, or built upon in any way, is permitted.
The moral rights of the named author(s) have been asserted.
Correspondence should be addressed to E. Jane Costello, Department of
Psychiatry and Behavioral Sciences, Suite, 22, 905 W Main St, Durham NC
27701. E-mail: jcostell@psych.duhs.duke.edu
Color versions of one or more of the figures in the article can be found
online at www.tandfonline.com/hcap.
What should we be trying to prevent? Of course we want to
prevent disease, but disease has many precursors, consisting
both of early symptoms and of risk factors that increase the
likelihood of disease. Public health has tried to create a man-
ageable taxonomy of risk by classifying exposures according
to the level of response best designed to prevent either risk or
disease (Gordon, 1983; Mrazek & Haggerty, 1994; Rothman
& Greenland, 1998). At the most extreme level (“indicated”
prevention) we enforce treatment, or even lock people away, to
prevent their harming others or themselves. Isolating or quar-
antining cases for the safety of the community has been used
for centuries to limit the spread of infectious diseases; psychia-
try is one of the few areas of chronic disease medicine that still
has recourse to this type of prevention.
“Targeted” prevention projects are designed for individuals
who have symptoms of a disorder or a clearly recognized
risk factor (e.g., parental bereavement as a risk factor for depres-
sion; Sandler et al., 2010). “Universal” or “primary” prevention
describes public health activities designed to reduce risk for the
whole population In this article we present the case that most
mental health problems are prevented by aspects of the way we
live that have little to do with identification, treatment, or
“targeted prevention” at the level of existing symptoms.
Epidemiology can be used to identify ordinary everyday aspects
of life, like having two parents or being born full-term, which
we don’t think of as mental health interventions but which can
be shown to be protective. Sometimes, however, the good-
 MENTAL HEALTH PROBLEM DETECTION AND PREVENTION
enough system of daily life fails. At that point, epidemiology
can be used to identify who needs care, of what kind, and to
monitor the adequacy and effectiveness of that care. Taken
together, these functions of epidemiology help to answer ques-
tions about the extent to which systems of support for the basic
aspects of life are cost-effective for preventing mental illness,
compared with the more focused systems of care that we bring
into play when things go wrong. Many of the articles in this
special issue take as their focus various emotional and beha-
vioral problems for which specialized systems of care have been
devised. Here, the concern is rather how many of those pro-
blems might never have developed in the first place given a solid
groundwork of support. It turns out that not only do many kinds
of primary prevention avoid the costs of screening and the pain
of stigma but they often prevent a wide range of health and
developmental problems, in addition to mental illness, and so
can be highly cost-effective.
EPIDEMIOLOGY AND PREVENTION
As its name implies, epidemiology grew out of the struggle to
prevent the epidemics of infectious diseases that swept coun-
tries and continents well into the first half of the 20th century.
The job for infectious disease epidemiology is to discover
patterns of disease in time and space that could explain why
some people become sick and others do not. Understanding
patterns of transmission enables systematic interventions to
break the chain—from stagnant water to malaria, or unpasteur-
ized milk to tuberculosis. The century up to World War II was a
time of many famous victories against infectious diseases.
The challenge for the past half century, however, has been
how to prevent not infectious or communicable diseases so
much as chronic or episodic or noncommunicable diseases,
mental illnesses among them. In the case of infectious diseases
we now generally know the germs that cause them and can
employ a fairly simple two-pronged attack: to exterminate the
germs and to eliminate the environments in which they breed.
So the old “systems of care” for infectious diseases—the
plague hospitals and tuberculosis infirmaries—have dwindled
to a small fraction of the health care system, and funding goes
almost entirely to early universal prevention via inoculation
against these diseases. Much of the cost of primary prevention
is borne by nonmedical services like the Environmental
Protection Agency, the schools, and the local water boards.
At present, the picture for mental health is very different.
We are still at the stage of discovering the “patterns of
disease in time and space” that may help to identify major
risk exposures. On the whole, the “one bug–one drug”
model that defeated many infectious diseases does not fit
mental illnesses (syphilis, caused by the spirochete
Treponema pallidum, is no longer treated as a psychiatric
disorder). This has the corollary that experimental methods
such as case-control designs for identifying causal factors
rarely work either. Even if we have a causal hypothesis we
711
cannot, for example, randomly assign newborn infants to
nurturing versus nonnurturing mothers. To chart a course
between true causes and confounders, epidemiologists often
have to rely on observational methods or at best quasi-
experiments (Cook & Shadish, 1994).
TYPES OF PREVENTION FOR CHRONIC DISEASE
In line with the well-established sequence of prevention levels,
the sequence of interventions runs from health promotion,
through universal prevention, to selective (high-risk) preven-
tion, to indicated prevention (Weisz, Sandler, Durlak, & Anton,
2005). Different writers have slightly different emphases, but
the general principles are similar. Briefly, health promotion
enables people to increase control over their health and its
determinants (World Health Organization, 2005); primary or
universal prevention aims to enable people to escape disease
by either avoiding exposure to risk factors or being able to resist
it after exposure; secondary or targeted prevention aims to
minimize harm from disease exposure by preventing full-
blown disease; and tertiary prevention aims to restore function-
ing and reduce disease-related complications, relapse, or spread
to others. A key difference among them is that different levels of
prevention have different target populations. Health promotion
and universal prevention focus on the entire population, either
throughout the life course (e.g., food safety regulations) or at a
particular developmental stage (e.g., safe car seats for infants).
Targeted prevention has at its focus those identified as at risk for
a disease, either because of symptoms (e.g., depression identi-
fied by screening) or because of some kind of risk exposure
(e.g., parental bereavement). Indicated prevention or “Treatment
as Prevention” as advocated for the prevention of HIV/AIDS
(http://www.who.int/hiv/pub/mtct/programmatic_update_tasp/)
looks to clinical treatment both to reduce relapse rates and to
prevent the spread of the disease to others (e.g., antiretroviral
treatment for HIV/AIDS). This review concentrates on the pros
and cons of the more common universal versus targeted pre-
vention strategies, although we need to remember that psychia-
try still use tertiary “treatment as prevention” in the form of
incarceration and compulsory hospitalization of children and
adolescents who might harm themselves or others.
Preventing Symptoms or Preventing Exposure
As noted in the discussion of infectious disease epidemiology,
once a causal pathway to disease has been identified, preventive
strategies may focus on exposure to risk, or on dealing with the
first symptoms of disease (or both). The former (universal
prevention) covers everyone in the population, whereas the
latter (targeted prevention) is restricted to high-risk or potential
cases. Arguments about the cost-effectiveness of each type of
prevention strategy have been made for decades (Mrazek &
Haggerty, 1994). It is likely that the balance depends on the type
of illness and the population in question (Eaton et al., 2002). For
712 COSTELLO
example, evidence that low birth weight is a strong predictor of
female adolescent depression (Bohnert & Breslau, 2008;
Costello, Worthman, Erkknali, & Angold, 2007; but see
Vasiliadis et al., 2008) supports the case for universal preven-
tion, whereas prevention of depression following bereavement
makes more sense only after bereavement has occurred (Haine,
Ayers, Sandler, & Wolchik, 2008).
Infectious disease epidemiology has mainly concentrated
on universal approaches to prevention: for example, ensur-
ing that children are inoculated; cleaning up water, food,
and air; and setting safety standards for cars and toys. Even
the chronic diseases that are the main causes of mortality
today are being approached using universal prevention
methods: exercise, diet, smoking reduction.
What are the universal prevention programs that would
prevent mental illness? Interesting to note, the work to evaluate
these has hardly begun (Durlak, Weissberg, Dymnicki, Taylor,
& Schellinger, 2011; Koenen et al., 2009). Lists of exposures
that might respond to universal interventions have been pro-
posed (Eaton et al., 2002), but the evidence for them is based
on common sense more than on research, and there are few
tests of the relative efficacy of universal versus targeted ver-
sions of the same or similar interventions. Several studies have
suggested that, just as environmental effects on psychopathol-
ogy may have a stronger effect at the most stressed end of the
distribution (Lee, Kosterman, McCarty, Hill, & Hawkins,
2012), an intervention to relieve a particular stress may also
be most effective at that level (Costello, Compton, Keeler, &
Angold, 2003). For example, an income supplement led to
lower levels of behavioral problems in children whose families
were moved out of poverty by the supplement but had no effect
on the (already low) levels of behavioral problems in those
who were never poor (Costello et al., 2003). The types of
exposure that might respond to primary prevention include
poor diet, lack of physical exercise (Koenen et al., 2009),
poverty (Lee et al., 2012), and low birth weight (Bohnert &
Breslau, 2008; Sonuga-Barke & Halperin, 2010). All of these
exposures are also associated with a range of other chronic
diseases. This raises questions such as, Does a particular pre-
ventive intervention prevent more than one disorder? How
does this affect the cost–benefit calculations for the interven-
tion? In the example of the income supplement described
earlier, subsequent studies showed that supplementing family
income reduced substance use and abuse several years later,
when the children had left home (Costello, Erkanli, Copeland,
& Angold, 2010). It also increased the chance of completing
high school, reduced minor crime (Akee, Costello, Copeland,
Keeler, & Angold, 2010), and slowed the rate of obesity
problems (Akee, Simeonova, Copeland, Angold, & Costello,
2013). Thus, a single intervention applied to a whole popula-
tion had a wide range of positive effects.
An advantage of universal prevention is precisely that it
is universal; there is no need to screen or select and there-
fore there are no screening costs, as there often are for
secondary prevention. Another advantage is that it avoids
the stigma associated with being picked out for “anger
management class” or “fat camp.” For tertiary prevention,
someone—parent or teacher usually—has to identify a pro-
blem or symptom and seek help, which brings its own
problems. For example, in a study with more than 20,000
assessments of children made by the children themselves
and a parent (Costello et al., 1996), when a child reported
one of nine symptoms of depression, the parent reported the
same symptom between 0% and 29% of the time. This
means that at best 71% of child-reported symptoms were
missed; in the case of cognitive problems, psychomotor
agitation, and anhedonia, the parent never identified cases
reported by the child. Given that even the most highly
developed instruments to identify child and adolescent
psychopathology, whether screening questionnaires or
interviews, are of only moderate test–retest and interrater
reliability (Angold et al., 2012), the probability that the
children in need of care will be correctly identified is low.
Unfortunately, primary care physicians have an even worse
record for case-identification (Dulcan et al., 1990).
If one is making a case for primary or universal preven-
tion, one has to address the question of systems of support.
It is a waste of effort, as well as arguably unethical, to
identify cases for which no treatment is available. The
standard systems of care for children (medical and psychia-
tric specialty services, educational, juvenile justice, and
social services; Burns et al., 1995)) cannot provide income
supplements or a healthy diet, although they can certainly
do much to reduce low birth weight and improve facilities
for exercise. But, perhaps more important, primary preven-
tion of this kind can help to bring different branches of
medicine and service providers together to share resources
and lobby together for more. For example, reducing the
proportion of low birth weight children also lightens the
burden of special needs children on educational services. On
the other hand, it can often happen that an intervention puts
demands on one part of the system (e.g., improving antena-
tal care) but brings benefits only later to another part of the
system (e.g., reducing special education service needs). So,
institutional pressures can work against otherwise rational
reallocation of resources.
RISK, EXPOSURE, AND THE MEANING OF TIME
Many questions about early detection and prevention can be
answered only by methods that take into account temporal
characteristics of risk factors, including age at onset and the
“dose” or level of exposure over time. To be most effective,
systems of support need to be sensitive both to children’s
developmental needs and to the developmental course of
risk exposure.
Age at first exposure, time since first exposure, duration
of exposure, and intensity of exposure are all interrelated
aspects of timing that may have different implications for
 MENTAL HEALTH PROBLEM DETECTION AND PREVENTION
prevention. In addition, every attempt to prevent illness is
an implicit or explicit test of a causal hypothesis, and the
timing of preventive interventions adds another level of
causal questioning. The kinds of questions we are thinking
of include the following:
● Does physical abuse by parental figures cause psychia-
tric disorders in children? Is a single blow a sufficient
cause or does abuse have to go on for a period of time,
or happen at a certain level of severity, before it con-
stitutes a risk factor? Are children of different ages or
developmental stages differentially vulnerable to phy-
sical abuse as a risk factor? What risks are associated
with removing children of different ages from home
because of physical abuse?
● Why are depressive disorders rare in both prepubertal girls
and boys but much more common in postpubertal girls?
What causes the observed sex difference to develop? Is it
associated with hormonal, morphological, or social
changes occurring around puberty? Why is earlier-than-
average maturation apparently a positive event for
boys but a negative one, associated with increased risk of
behavioral and school problems, for girls?
The answers to such questions imply different assump-
tions about the causal role of timing, intensity, and duration.
Here we offer a few examples of the impact on psychiatric
disorder of different aspects of development: (a) age at first
exposure, (b) time since first exposure, (c) duration of
exposure, and (d) intensity of exposure. We then consider
the implications for support systems.
The importance of age at first exposure has been studied
most intensively of all the aspects of risk over time in child
psychopathology because of the theoretical importance
attached to early experiences in the Freudian and other
psychodynamic models of development. For example,
researchers investigating the role of attachment in children’s
development have concentrated on the very early months
and years of life as the crucial period during which the
inability to form one or more such relationships may have
damaging effects that last into childhood and perhaps even
into adulthood (Sroufe, 1988). The critical date of onset of
risk appears to occur after 6 months, but the duration of the
risk period is not yet clear. Hay (1985) presented evidence
that maternal depression, which presumably interferes with
mothers’ ability to form normal relationships with their
infants, affects motor development if it occurs during the
1st year of life, and language development but not motor
development if it occurs during the 2nd year of life. This is
a case where age at first exposure appears to interact with
the developmental processes most salient at a particular age.
In another example of the importance of timing, Rutter
(1985) pointed out that once children have achieved urinary
continence at around age 2, there is a period of risk for
relapse into incontinence that appears to coincide with
713
starting school. Once this period of risk is over, the chance
of developing enuresis is very slight. In this case, age at
exposure is clearly the critical developmental risk factor,
because it is very rare for a parallel increase in functional
enuresis to occur at later times of stress, such as moving to
middle or high school, and there is no delay between the
stress and the symptoms.
Timing of exposure has rarely been treated separately in
studies of child psychopathology. Brown and Harris (1978),
in their work on the social origins of depression, argued that
women who lost their mother in the first decade of life were
more vulnerable as adults to depressive episodes in the face
of severe life events. However, theirs was a retrospective
study that did not address the question of whether these
women were also at greater risk of depressive episodes dur-
ing later childhood and adolescence. It is not clear whether
the crucial factor was the length of time since exposure to the
risk factor of the mother’s death, or the age of the child at the
time of exposure, or some combination of the two.
Timing of puberty has emerged as an important aspect of
risk in relation to both depression and behavioral problems.
In a longitudinal study that measured not only age at
menarche but also morphological development, Tanner sta-
ging (Marshall & Tanner, 1969), and levels of gonadal and
steroidal hormones, it was clear that it was high levels of
estrogen and testosterone, not timing of puberty, that pre-
dicted adolescent depression (Angold, Costello, Erkanli, &
Worthman, 1999). However, there are many studies show-
ing that girls who are early in developing the morphological
signs of puberty, indexed by Tanner stage or menarche, are
at risk for behavioral problems, especially if they have
unsupportive families (Costello, Sung, Worthman, &
Angold, 2007; Ge, Brody, Conger, & Murry, 2002; Ge,
Conger, & Elder, 1996; Magnusson, Stattin, & Allen, 1985).
Sometimes duration of exposure may be a more powerful
predictor of later harm than timing. For example, Copeland,
Wolke, Angold, and Costello (2013) found that the number of
years over which children reported being bullied was a stronger
predictor of poor adult outcomes than the timing of the experi-
ence (e.g., childhood, adolescence, or both.) In a longitudinal
study from New Zealand, Moffitt (1990) found that children
identified at age 13 as both delinquent and hyperactive had
experienced significantly more family adversity (poverty, poor
maternal education and mental health), consistently from the
age of 7, than children who were only delinquent or only
hyperactive at age 13. The most striking increase in the
antisocial behavior of ADD+delinquent boys diagnosed at age
13 occurred between the ages of 5 and 7, when they attained a
mean antisocial rating that was not reached by other delinquent
boys until 6 years later. School entry and reading failure coin-
cided temporally with this exacerbation of antisocial behavior.
These data suggest that the problem behavior of this group,
despite being generally persistent, is responsive to experience.
The data also reveal a key point of vulnerability that could be a
target for intervention: reading readiness.
714 COSTELLO
Another example comes from the Great Smoky
Mountains Study. Children who had been assessed over an
8-year period were classified into four groups on the basis of
their body mass index (a ratio of weight to height) at each
assessment: no obesity (72.8%), childhood-only obesity
(5.1%), adolescent-only obesity (7.5%), and chronic obesity
(14.8%). Only the chronically obese group was at increased
risk of psychiatric disorder (Mustillo et al., 2003). This is an
example of duration of exposure as the key risk character-
istic. It is also an example of the impact of intensity of
exposure because no effects were found of overweight that
fell just below the threshold of obesity.
Intensity of exposure to lead (Needleman & Bellinger,
1991) provides an example of a definite dose–response
relationship. Needleman and Bellinger (1991) divided den-
tine lead levels into six classes, from less than 5.1 parts per
million to more than 27 parts per million, and showed a
highly significant effect of dose on teachers’ ratings of
children’s functioning on a wide range of intellectual and
behavioral tasks. Another aspect of intensity is the number
of different risk factors to which a child is exposed (Seifer,
Sameroff, Baldwin, & Balwin, 1989). Most children appear
to be able to cope with a single adverse circumstance, but
rates of psychopathology rise sharply in children exposed to
several adverse circumstances or events (Seifer et al., 1989).
However, Rutter (1985) and others have pointed out that
children exposed to one risk factor are at increased risk of
exposure to others (e.g., no father in the home and poverty)
and that the dose–response relationship to an increasing
number of different risk factors is not a simple linear one
These examples show that it is possible to design studies
that at least begin to allow us to tease out the respective roles
played by time since first exposure, age or developmental
stage at first exposure, duration of exposure, and intensity of
exposure. Multistage models of risk, which have been devel-
oped to address the complexities of causality in chronic
disease, are one way of putting the pieces together. Several
such models have been proposed, particularly in the context
of carcinogenesis (Peto, 1984), and have been reviewed in
terms of developmental psychopathology (Pickles, 1993).
Statistical techniques for exploring causality in such multi-
stage models have made great strides recently (Robins,
1997). The challenge is to incorporate all the various aspects
of risk into a single model and distinguish the ones that carry
the tune from those that are just noise.
EARLY DETECTION OF MENTAL HEALTH
PROBLEMS AND SYSTEMS OF SUPPORT
Is early detection in the form of detection of the first
symptoms likely to be beneficial? Do our treatments work
well when employed with symptomatic but subsyndromal
cases? Is a system of support that focuses on early interven-
tion a good use of resources?
Figure 1 shows the mean age at onset of a range of
disorders, using repeated assessments up to age 21 in a
representative population sample of children (National
Institute of Medicine, 2009). The mean age at onset of the
first symptom, in children who would eventually get a
diagnosis of that disorder, preceded the full diagnosis by
about two years. Sometimes the first symptom and full
disorder occurred almost simultaneously (attention deficit/
hyperactivity disorder, anxiety disorders), whereas in other
disorders (oppositional defiant disorder, conduct disorder,
depression) there was a time gap of about three years.
This implies that for many psychiatric disorders there is
time to identify early symptoms and intervene.
It is also the case that many children who experience one
or two symptoms never develop a full disorder. In the study
from which the figure comes, for example, there were 10
times as many observations including one or more symp-
toms of depression as there were cases of depression
(N = 3,924 with one or more symptoms; N = 278 with a
full diagnosis). But the mean age at onset of the first
symptom was almost two years earlier in the children who
eventually developed a full diagnosis (12.5 vs. 14.4). This
suggests that really early intervention (e.g., when prepuber-
tal children showed even one symptom of depression) could
identify the children most likely to go on to a full diagnosis.
FIGURE 1 Age at onset of first symptom and of full psychiatric disorder, by
age 21. Data from the Great Smoky Mountains Study. Note. ADHD = attention
deficit/hyperactivity disorder; ODD = oppositional defiance disorder; CD =
conduct disorder. Reproduced with permission from the National Institute of
Medicine (2009). Preventing Mental, Emotional, and Behavioral Disorders
Among Young People: Progress and Possibilities. Committee on Prevention of
Mental Disorders and Substance Abuse Among Children, Youth, and Young
Adults: Research Advances and Promising Interventions. Washington, DC:
The National Academies Press. © [Rightsholder]. Reproduced by permission
of National Academy of Medicine. Permission to reuse must be obtained from
the rightsholder.
 MENTAL HEALTH PROBLEM DETECTION AND PREVENTION
EARLY DETECTION, PREVENTION, AND THE
SERVICE SYSTEM
Universal and targeted prevention make very different
demands on those whose job it is to reduce the rate of
onset of mental disorders. They also identify different
kinds of people, with different skills, as the key interveners.
Targeted Prevention and the Service System
In the past two decades a whole new prevention industry has
emerged in the United States, complete with master’s,
doctoral, and postdoctoral training programs; professional
societies and journals; and expert lobbyists at state and
federal levels. This is understandable, because targeted pre-
vention is a complicated and expensive activity. First, it is
necessary to decide what disorders or disabilities are to be
prevented. This requires a taxonomy agreed to and shared
across the prevention community. Second, prevention provi-
ders need to work toward one or more recognized prevention
programs or strategies, a process that requires controlled
trials, tests of generalizability from one site to another, and
all the accoutrements of clinical research. In fact, targeted
prevention may be even more complex than clinical treatment
because it requires the interveners to go out and find subjects
with whom to work, rather than waiting for them to walk
through the clinic door. So, targeted prevention requires
methods for identifying potential cases. People normally in
contact with children in the community—parents and tea-
chers most obviously—need to be trained and helped to
identify subjects for intervention, and if necessary “screen-
ing” measures must be developed and tested. “Screening” can
mean case identification, if the signs are clear enough, but
more often the term is used to mean picking possible cases
out of a general population, with the concomitant risk of false
positives and false negatives. Targeted prevention is often
advocated as being less expensive to implement than
universal prevention, but it is important to bear in mind that
screening implies at least some level of involvement with
everyone in the target population, which entails its own costs.
Next, to be successful, targeted prevention mandates a
service system that can provide effective interventions,
available on a scale that matches the need identified in the
screening phase. It is unethical to arouse the awareness of
needs that cannot be met.
The processes involved in targeted prevention are listed here
at some length because of the widely held assumption that
targeted intervention is more efficient and cost-effective than
primary or universal intervention. This may be true, but targeted
prevention carries very considerable costs that will have to be
paid by someone. Also to be considered are the costs to those
identified as being “labelled,” correctly or incorrectly, and the
potential damage to those incorrectly missed in the screening
stage. In sum, “targeting” is neither cost-free nor entirely benign.
715
Universal Prevention and the Service System
Primary or universal prevention programs generally need a
different set of service systems, most of which have not been
established, or exist in bits and pieces across the field of public
health. As with targeted prevention, it is helpful to have a clearly
defined target, which means a taxonomy, such as those of the
Diagnostic and Statistical Manual of Mental Disorders (5th ed.;
DSM–5; American Psychiatric Association) or International
Classification of Diseases. Second, some method is needed to
monitor the effect of a prevention program at the population
level. These have been set up in some countries, through orga-
nizations such as the Centers for Disease Control and Prevention
in the United States, or using national case registers such as
those in force in the Scandinavian countries. Evaluation is often
the weak point of universal prevention programs; for example,
the vast system of health visitors, operating for more than a
century in the United Kingdom with the goal of educating
mothers and protecting young children, has hardly been evalu-
ated at all (Laming, 2009). Another example is the provision of
specialty mental health and counseling services to school-age
children. There is good evidence that these services reach more
children than any other form of mental health care (Brener,
Martindale, & Weist, 2001; Burns et al., 1995), but we know
very little about their effectiveness.
In other areas of health it is very clear that universal
prevention has been extraordinarily effective, for example,
in lowering infant and child mortality and morbidity and
improving healthy physical development. There is also indir-
ect evidence that mean intelligence levels have increased
dramatically in the past 100 years, at a far faster speed than
could be attributable to evolutionary selection (Flynn, 1984).
No such data are available for mental health. The second step
for instituting universal systems of mental health care is
clearly a national (and eventually international) surveillance
system that can monitor need for services and change in
demand.
It is likely that when and if such systems were to be set
up, we should find that some of the universal health care
programs already in place have a marked effect on chil-
dren’s mental health. Prenatal care and nutrition is an
obvious example, given the evidence for the damage that
can be caused by low birth weight (Costello, Worthman,
et al., 2007; Sommerfelt, Troland, Ellertsen, & Markestad,
1996; Szatmari, Saigal, Rosenbaum, Campbell, & King,
1990). Mandated screening for hearing and visual deficits
is another example. Programs that affect whole commu-
nities, such as the removal of lead from the environment,
have effects on both behavioral and cognitive development
(Needleman & Bellinger, 1991).
It is nevertheless the case that, despite what universal
prevention has done to protect them, far too many children
have psychiatric disorders. For example, our 20-year pro-
spective study of a community sample found that by age
21 more than 50% of the participants had experienced at
716 COSTELLO
least one DSM-IV (American Psychiatric Association, 1994)
psychiatric disorder, and a further 10%–15% had significant
functional impairment associated with psychiatric symptoms
(Copeland, Shanahan, Costello, & Angold, 2011). Other
longitudinal studies show similar results(Jaffee, Harrington,
Cohen, & Moffitt, 2005). Barely one in four received any
specialty mental health care, and those who did waited 2 or
3 years for services (Burns et al., 1995; Costello, He,
Sampson, Kessler, & Merikangas, 2013).
CONCLUSIONS
Returning to the title, “Early Detection and Prevention of
Mental Health Problems: The Role of Developmental
Epidemiology in Planning Systems of Support,” the role of
developmental epidemiology in the prevention of metal dis-
order has both optimistic and pessimistic sides. In the case of
targeted prevention we can be optimistic because, as other
articles in this issue show, preventive interventions can be
effective, and the systems needed to bring them to scale—
screening, training of field staff, destigmatization of mental
illness—have been worked out at least in principle (of interest,
a lot of the work has been done in the context of global mental
health; Collins et al., 2011; Patel, Flisher, Hetrick, & McGorry,
2007). Pessimism is induced by the high cost of instrument and
program development and by the likely service gap that will
yawn when screening reveals the true numbers of children in
need of clinical care.
In the case of universal prevention, we can be more opti-
mistic that programs already in the field, and well accepted by
almost everyone, will be shown to yield mental health benefits
that have not yet been evaluated. Pessimistically, we note the
high rate of (largely untreated) mental disorder in the popula-
tion and the lack of surveillance systems that can track the
effects of existing or new programs.
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