The Core Sciences: Contributions and Frontiers
Research on the prevention of mental disorders, like all research, should be grounded in a rigorous scientific tradition. If prevention research can build on past contributions and integrate an immense amount of new knowledge from a wide range of core sciences, it will be able to expand its frontiers and open up new possibilities for intervention. Two broad areas of science provide the knowledge base for research on the prevention of mental disorders—the behavioral sciences, in which the study of mental disorders has its historical roots, and the biological sciences, which have begun to provide insights into these disorders more recently.
The boundaries between the behavioral and biological sciences should not be viewed as rigid and distinct. Interdisciplinary investigations that incorporate principles and findings from both the behavioral and the biological perspectives have vital implications for research on the prevention of mental disorders. The frontiers for the field of prevention can be moved forward through appropriate theoretical integration. In the sections that follow, this chapter presents four of these integrative core sciences as illustrations—neuroscience, genetics, epidemiology, and developmental psychopathology—to highlight how they have contributed and will continue to contribute to preventive intervention research.
Neuroscience research encompasses the acquisition of knowledge about fundamental biological processes of the brain and nervous system
and about the pathophysiology of neurological disease processes, including cellular mechanisms underlying etiology, course, and outcome. Knowledge about these biological processes can lead to the design of strategies aimed at treating specific symptoms and disorders and evaluating the efficacy and limitations of those treatments. Such understanding also can be important in framing and implementing a rational prevention strategy. The more that is known about etiology, the more possible it becomes to target preventive interventions to intervene in causal chains.
Neuroscience research varies in scope from highly theoretical to practical application, but, in general, the neuroscience research supported by the National Institutes of Health (NIH) takes a more disease-oriented focus, whereas the research supported by the National Science Foundation (NSF) focuses on acquiring basic knowledge about the functioning of the nervous system. The strategic value of having these complementary approaches is well recognized, but merits reaffirmation: knowledge from research in basic science is essential for applied investigations. Using worms or grasshoppers to study how nerve cells grow, differentiate, and reach their targets, and investigating the interaction between genetic and environmental factors in these processes, provides a simpler model system for understanding how more complex systems function.
Neuroscience research has provided important insights into how mental disorders arise. The discovery of chemical neurotransmission more than 70 years ago can be taken as the beginning of the modern neuroscience era. Prior to this discovery, understanding of the brain was limited to knowledge of its anatomy. Now, however, the functional relationship between certain classes of transmitters and specific neurons, the nature of transmitter receptors, and the consequences of receptor activation are being studied. Specific data are being gathered that define conditions in which channels will open or close, calcium will enter the cell or be excluded, and genes will be activated or silenced.
The basic function of nerve cells is to transmit information. Once chemical neurotransmitters are released, they act on neighboring cells to excite or inhibit them. There is a highly precise interaction between the neurotransmitter and a specific receptor protein on the target cell that regulates the latter's response, yet a single neurotransmitter can affect multiple receptors. For example, the neurotransmitter serotonin, which is important in both depression and schizophrenia, acts on at least 11 different specific serotonin receptors, and the neurotransmitter gamma-amino butyric acid (GABA) may act on as many as 100. These receptors differ slightly in their molecular structure and in the target functions
they regulate, and are dispersed among cell clusters throughout the brain, thus providing great diversity in the cellular response to a single neurotransmitter. Serotonin released from a group of neurons may excite some neighboring cells and inhibit others, with gradations of activation and inhibition depending on the diversity of receptors it acts upon. There are also differences in where the receptors are found on a given cell, how avidly they respond to the transmitter, how long they respond, and what other cellular processes they regulate.
The production, liberation, and inactivation of neurotransmitters are highly regulated biological processes. Elucidating the mechanisms underlying these processes has contributed to the discovery of drugs used with varying degrees of success to treat schizophrenia, major depressive disorder, bipolar disorder, anxiety disorders, including obsessive compulsive disorder, and other conditions. Recent advances in molecular biology have led to an increase in our understanding of the scope and complexity of neuronal function. The practical outcome so far has been the discovery of new classes of drugs, such as the calcium channel blockers.
One goal of current research is to provide even greater effectiveness of drug therapy by increasing the number of cellular targets for drug action. These may include more receptor-subtype-specific agents, as well as drugs that act on ion channels (that regulate the influx and afflux of charged molecules) and protein kinases (that add phosphate groups to proteins), all of which are steps between the receptor and the cellular response to its activation. The potential implications of this research for indicated preventive interventions may be considerable if the medications are found to be safe enough to justify their use with high-risk individuals who have developed early signs and symptoms of a disorder.
Research into the genetic causes of disease is among the most active and exciting areas of biomedical investigation.* Within the next several years, genetic research promises to make substantial contributions to our understanding of mental disorders.
Genetic influences are quite relevant to prevention research. First, the accumulated results in genetic research have provided convincing evidence of the role of genetic factors both in normal variations in
Portions of this section were based on a commissioned paper by M. Rutter, available as indicated in Appendix D.
psychological functioning and in psychopathology (Loehlin, 1992; Plomin, 1990, 1986; Rutter, Bolton, Harrington, Le Couteur, Macdonald, and Simonoff, 1990; Rutter, Macdonald, Le Couteur, Harrington, Bolton, and Bailey, 1990; Vandenberg, Singer, and Pauls, 1986). Heritability estimates for most mental disorders tend to be in the 30 to 60 percent range, so the genetic component, although not overwhelming, is by no means trivial. Second, interaction between environmental influences and genetic factors will be clearer as research gradually elucidates the specific impact of genes on mental functioning. Genetic studies have the power to be highly informative about developmental processes and psychopathological mechanisms (Rutter, Simonoff, and Silberg, in press; Rutter, Silberg, and Simonoff, 1993; Rutter, 1991). Because an understanding of such processes and mechanisms is crucial for the most effective planning of interventive measures, genetic research and genetic knowledge are potentially very valuable to prevention as well as treatment. Current and potential contributions to prevention center on the following topics:
Nature of disorders. When planning preventive interventions, knowledge about the nature of the disorders to be prevented may often be helpful; genetic research findings can be useful in that connection. First, they may point to basic causal processes. Second, they can indicate which disorders are, and which are not, continuous with normally distributed characteristics. Third, disorders may come about through several rather different mechanisms, and genetics research may be helpful in determining which mechanism applies in each case.
In the future, research will seek to understand whether disease-specific genetic alleles controlling receptor-mediated processes lead to mental disorders. If this is found to be true, the initial application of this knowledge will be to screen individuals bearing the disease-specific allele so that earlier, and hopefully more effective, preventive strategies can be implemented. Some of these indicated preventive interventions may be pharmacological, but rich opportunities also exist for psychosocial interventions.
An example of such an opportunity may exist with infantile autism, a severe developmental disorder that strikes in infancy and leads to profound cognitive and social impairment. Autism represents a disturbance in the development of the brain centers that mediate language and information processing. One goal of research in autism is to identify a reliable marker for the disorder that will enable high-risk individuals to be identified in early infancy. Indicated prevention strategies, such as language and social skills training, could then be implemented to take
advantage of the great plasticity of the brain in early childhood. One hypothesis of this research is that immature, still developing brain centers could be stimulated to acquire the function of the centers that are developmentally impaired, thus delaying or even eliminating the emergence of autism. This notion arises directly from the concept of sensitive periods, that is, periods in development during which relevant stimuli and transactions must occur or development is irreversibly altered, an important principle derived from basic research in developmental neurobiology.
Mechanisms of genetic risk. In the past, much genetic research in the field of psychopathology has been concerned with quantifying the genetic contribution to overall population variance. In themselves, however, heritability estimates are not particularly useful because they carry no information about the mechanisms involved in genetic risk. Understanding genetic mechanisms is crucial for most effective interventions. Phenylketonuria constitutes an obvious example of a disorder in which such an understanding has led to an extremely effective environmental preventive intervention (low phenylalanine diet in childhood). Thus a disorder that is genetic nevertheless leads to disabilities that are environmentally preventable.
There is a rapidly growing body of evidence that major genes play a contributory role, as part of multifactorial inheritance, in a range of complex human diseases, including diabetes, heart disease, and hypertension (Weatherall, 1992). The value of these studies is that they are beginning to identify the mode of operation of genetic risk (Kurtz, 1992). Cambien and colleagues have reported that a deletion polymorphism in the gene encoding the angiotensin converting enzyme (ACE) may be a risk factor for myocardial infarction in a specific subgroup of individuals (Cambien, Poirer, Lecerf, Evans, Cambou, Arveiler et al., 1992). If confirmed, this particular finding could mean that genotyping could be used to identify people for whom administration of an ACE inhibitor might prevent recurrent myocardial infarction. The implication of this work, particularly for mental disorders, is that for most conditions we must move from thinking about a single cause of a disease (genetic or environmental) to thinking about how we may elucidate possible risk mechanisms. Examples relevant to mental disorders include the role genetic factors play in alcohol dependence, depressive disorders, physiological reactivity, temperamental characteristics, and emotional and conduct disturbances.
Testing for environmental effects. Traditionally, studies examining differences between identical and fraternal twins have been classified as genetic research. However, when the phenotype being studied is a
behavior, these studies provide the most satisfactory way of quantifying the strength of environmental effects. Other types of studies that have provided useful information include adoption studies; studies of various classes of relatives, using path models; and experimental studies, including experiments of nature, in which individuals are exposed to changing environments.
As Plomin and Bergman (1991) pointed out, the fact that a variable is labeled as “environmental” does not mean that its effects are environmentally mediated; many supposedly “environmental” measures actually index genetic, as well as environmental, influences. This point is best seen with the many risk factors that are based on someone's personal characteristics or behavior, such as low intelligence, aggressiveness, and behavioral inhibition. These involve a genetic component as well, and it is necessary to determine whether the psychiatric risk reflects genetic or environmental mediation.
Individual differences in environmental effects. One of the most important recent findings from behavioral genetics research with twins has been the demonstration that, for many aspects of normal and abnormal psychosocial development, nonshared environmental effects tend to be substantially more important than shared ones in quantifying variability in outcomes (Plomin and Daniels, 1987). Shared risk factors that apply to the family as a whole, such as family discord or poverty, are indeed relevant, but they are likely to impinge on different children in the same family to varying degrees or in different ways, that is, to have nonshared effects. If we are to understand how such environmental risk factors operate, we must investigate the processes on a person-specific basis and not simply assume a uniform impact.
Relative differences between siblings in how they are treated in a home may be more important than the absolute level of this treatment in the home (Dunn and Plomin, 1990). That is, what appears to be a shared risk factor within the family may actually be an unshared risk factor, with its concomitant unshared effect, for, perhaps, only one child in the family. For example, it may be that it is less important whether parents respond to their children in a generally warm, or strict, or harsh fashion than whether one child in the family is consistently dealt with less warmly, or more strictly, or more harshly than his or her brothers and sisters. In other words, scapegoating or favoritism may be the operative risk factor (Boer and Dunn, 1992).
Attention needs to be paid to shared and unshared risk and protective factors and shared and unshared effects outside, as well as inside, the family. The body of evidence that school influences have effects on children's behavior and scholastic attainments (Maughan, in press;
Mortimore, in press) is particularly pertinent because it provides a setting for potential prevention that applies to all children. Peer group and community influences are also relevant (Quinton, in press; Reiss, in press).
Individual differences in exposure to risk factors. During the last decade, behavioral geneticists have drawn attention to the various ways in which gene-environment interactions can arise. They have argued that, to a great extent, individuals shape and select their environments and that genetic factors play a part in this process (Scarr, 1992; Scarr and McCartney, 1983). Many nongeneticists have been reluctant to accept this possibility and have interpreted the suggestion as an argument against taking measures to improve environmental conditions. This suggests a point that may be vital to planning effective interventions, namely, that individuals vary greatly in their exposure to risk factors in their environments (Rutter and Rutter, 1993). Psychosocial stresses and adversities are not randomly distributed, and it is essential that we understand how those individual differences in risk exposure come about. This issue has not been addressed in any intensive and systematic manner, but we need to learn why some individuals suffer a host of environmental adversities, whereas others go through life with a string of generally positive experiences. Individual differences in environmental risk exposure should be treated as dependent, as well as independent, variables.
Misleading environmental assumptions. Up until 10 or 20 years ago, there was a widespread assumption that birth trauma was an important environmental cause of brain damage and therefore a common cause of mental retardation and cerebral palsy (Hardy, 1965). More recent findings have forced a reassessment of this belief and now indicate that in most cases the causal factors operated at a much earlier stage in gestation (Nelson and Ellenberg, 1986). Nevertheless, there is still a tendency to treat obstetric complications as though they were only environmental risk factors. Recent evidence suggests that the process may also work the other way around: genetic or chromosomal abnormalities in the fetus may predispose to obstetric complications. For example, studies in children with Down's syndrome have indicated that the genetic abnormality is associated with a substantially increased risk of obstetric complications (Bolton and Holland, in press). This appreciation has also led to a reevaluation of the etiological role of obstetric complications in autism.
Genetic counseling. Most medical genetic counseling has been based on the various patterns of risk associated with different types of genetic disorders: autosomal dominant, autosomal recessive, and so
forth. But advances in molecular genetics now enable us to provide individualized risk information and not just actuarial probabilities. Genetic counseling is no longer confined to advising people about the risks involved if they have children or the risk involved in a particular pregnancy. It may now involve decisions on whether to take preventive action with people who are known to be at genetic risk through mechanisms involving susceptibility to environmental factors.
Gene therapy. Gene therapy may become a possibility with some applications in the field of mental disorders. Some therapy is currently feasible in conditions caused by a single gene of major effect. Most mental disorders, however, involve multiple genes. It is now possible in tissue culture cells, and in limited cases in animals, to modify the expression of mutant genes and alter their pathologic outcome. This capability will only grow over the coming years, and the advent of gene therapy has led to a parallel realization of the ethical dilemmas it engenders. There is now growing agreement that somatic gene therapy to treat a disease, in which the genes of body (e.g., muscle) cells are modified, is ethical in certain circumstances. In contrast, there is currently an active debate over whether modification of genes in the germline cells (sperm and ova) can be considered ethical in any circumstances.
Epidemiology also can take a developmental and integrative perspective on the etiology and course of psychopathology. Epidemiology is the study of the distribution of disorders in populations. Epidemiologists prefer to study well-defined populations, including community samples. The differential distribution of disorders is reported as incidence and prevalence of specified disorders. Incidence refers to the rate at which new cases of the disorder arise. Prevalence is the proportion of the population with the disorder. The prevalence of a disorder is a function not only of incidence but also of duration. Disorders can vary in duration from brief to lifelong. Point prevalence is the proportion in the population at a given point in time who have the disorder. Point prevalence is most useful for estimating need for services. Lifetime prevalence (sometimes called the proportion of survivors affected, or PSA) is the proportion of the population who, at some time during their lives up to the present, have had the disorder. Lifetime prevalence is most useful to those with interest in genetics. But because not everyone surveyed will have lived through the age of risk at the time of the interview, lifetime prevalence estimates are considered conservative.
Preventive interventions are directed toward reducing incidence, whereas treatment interventions seek to reduce prevalence by early detection and reduction of duration by effective intervention to reverse the symptoms and reduce the likelihood of relapse. Without effective treatment interventions, early case identification will have the paradoxical effect of increasing prevalence by increasing the count of a disorder that will then have lengthy duration because it is untreatable.
Epidemiological research has produced data on differential incidence and prevalence by demographic factors such as age, gender, educational level, employment status, ethnicity, and socioeconomic level; environmental factors such as hazardous conditions, toxic substances, stressful environments, availability of resources or supports, and ease of availability of drugs, alcohol, guns, and cars; personal attributes such as temperament, attractiveness, intelligence, and prior individual experience; and biological attributes such as genetics, health status, and other biological vulnerability.
Throughout epidemiological research, there is a common goal of identifying risk factors. There are two major research strategies for ascertaining the relation of risk factors to subsequent disorders. They are the case-control and the cohort designs. Case-control studies are often an initial and exploratory step in the identification of risk. An observed condition or disorder within an individual is called a “case.” The cases are then compared with “controls,” that is, similar individuals who do not have the disorder. On the basis of existing knowledge and reasonable hypotheses about antecedents, the cases and controls are compared retrospectively across a number of salient dimensions. This approach is often followed by a prospective cohort study, in which a group of persons who all have the antecedents of interest (that is, the risk factors) but do not have the condition or disorder of interest are compared with a group of persons who have neither the antecedents nor the disorder. These cohort studies yield actual estimates of the risk of disorder that follows a particular event or set of events.
Epidemiological studies of the occurrence of differential distribution of disorders across the population have yielded valuable data on both the origins and the life course of mental disorders. In studying the origins of a mental disorder, a prospective longitudinal design is particularly powerful. Epidemiological research designs that sample a range of populations and use repeated measurements permit inferences about causality. For some rare disorders and for disorders with onset in later life, case-control studies are the only practical method.
Two refinements of the concept of risk allow comparisons of various factors as they influence the development of disorder. One important
refinement is relative risk. Relative risk is the ratio of incidence for a given disorder in an exposed population to the incidence in an unexposed population. For example, the risk of death by lung cancer might be 15 times higher among smokers than among nonsmokers—a relative risk of 15. Relative risk is obtained in a cohort study and can be approximated in a case-control study.
A second measure linked to risk is attributable risk. Attributable risk is the maximum proportion of cases that would be prevented if an intervention were 100 percent effective in eliminating the risk factor. Attributable risk combines information on relative risk with information on the prevalence of the exposure, in order to help judge which risk factor to target in trying to eliminate the disorder. The formula is p(r − 1)/[p(r − 1) + 1], where p is prevalence of exposure and r is relative risk (Mausner and Kramer, 1985). If the relative risk of lung cancer for smokers versus nonsmokers is 15, as above, and the prevalence of smoking is about 50 percent, then the proportion of cases of lung cancer attributable to smoking, that is, the attributable risk, is approximately 88 percent.
Data on prevalence and on attributable risk are especially germane to research on the prevention of mental disorders. To acquire these data, diverse strategies of research are needed. The prevalence of the disorder is required in order to assess its impact on the population. Prevalence is obtained efficiently from a cross-sectional survey. The attributable risk for a range of risk factors is required in order to select interventions that will have the most powerful effect. Attributable risk probably is most efficiently obtained via the case-control strategy.
An even more recent frontier is the conceptualization of the age of onset for specific disorders. Determination of age of onset is required in order to time the intervention appropriately, that is, before the first incidence of a disorder or problem. Decisions as to when to target a high-risk population can be guided by epidemiological data regarding the range and mean age of onset in a population. Age of onset is best obtained from a longitudinal study of a cohort from the general population. Recognizing the importance of such data, the committee commissioned new analyses of data from the Epidemiologic Catchment Area study. The conceptualizations and methods used in these analyses, and the resulting fresh perspectives they permit, are presented in Chapter 5.
Many scientific areas of study with links to prevention research have their origin in the behavioral and social sciences. Developmental psychopathology is one of these areas. (See Box 4.1 for other illustrations.)
Illustrations from the Behavioral and Social Sciences
Many theoretical concepts originating in the behavioral sciences have relevance to research on prevention of mental disorders. These include self-esteem, regulation of emotions, attribution, cultural and gender-based diversity, social networks, community context, and ecological perspectives. Other concepts are presented here as illustrations of specific areas of study that have had—and will continue to have —an impact on the conceptual design of prevention studies.
Psychological stress is associated with a variety of negative effects on health, although the specific mechanisms for this relationship are not well understood. Recent research in psychoneuroimmunology (Ader, Felten, and Cohen, 1991) has suggested that stress can directly affect interactions between the central nervous system and the immune system. Studies of the neuroendocrine correlates of stress, for example, may lead to a better understanding of the physiological pathways by which environmental stressors affect personal health (IOM, 1989, 1984, 1982b; CBASSE, 1988).
Social support mechanisms appear to perform an essential function in several areas, including increasing or decreasing an individual's sensitivity to certain stressors, increasing or decreasing an individual's likelihood of using or abstaining from drugs, and increasing compliance with therapeutic regimes. The quantity and quality of social support networks are also thought to have a role in the onset and course of mental disorders, including depression and schizophrenia. One line of inquiry has examined how perceptions of personal control mediate the effects of social networks on health outcomes, a factor that appears to be far more significant than has been recognized by health care providers (CBASSE, 1988; IOM, 1984, 1982a).
Analysis of the usage of health care delivery systems is also relevant to prevention. Research on the role of health maintenance organizations (HMOs), for example, has indicated that certain forms of public and private subsidies of diagnostic and preventive health care practices affect the use of such services by individuals and groups. Data from these studies strongly suggest that the delivery of health care services for the general population could be greatly improved by subsidizing expanded preventive interventions for people at risk for certain health disorders, although the economic and social consequences of such targeted practices have yet to be determined (CBASSE, 1988).
Interpersonal transaction research in recent years has defined a complex interplay among expectancies, self-concepts, and motives. For example, hostile acts are often stimulated and guided by expectations of aggression that may be influenced by early childhood experiences. If the individual has experienced aggressive behavior in the past, his or her perceptions may be negatively distorted, rather than assuming ambiguous acts to be benign or accidental (CBASSE, 1993, 1988; Dodge, Bates, and Pettit, 1990).
Attachment theory postulates that early relationships between infants and their caregivers, usually their mothers, have a critical role in the infants' later development, especially in social relationships. Infants show attachment behavior by seeking comfort and protection, and caregivers' responses dem-
onstrate the quality of their sensitivity and responsivity. Mother-child pairs differ in their interactive styles, and there has been considerable research in the last 15 years, based on early work by Ainsworth and colleagues on the measurement and classification of these differences and their links to later behaviors (Ainsworth, Blehar, Waters, and Well, 1978). This theory has direct relevance to prevention and indeed has been applied in programs designed to enhance healthy parent-infant relationships. For example, a preventive intervention designed by Erickson, Korfmacher, and Egeland (1992) targeted prospective mothers in “a special window of opportunity” around the birth of their first child with the aim of having an impact on the mother's view of herself and her child as well as their relationship.
Self-efficacy theory is based on the premise that individuals who have a sense of control over their environment will live a more active and self-determined life. Perceived self-efficacy appears to be highly correlated with a wide range of health behaviors, affecting the onset, course, and sequelae of both mental and physical disorders (Schwarzer, 1992). For example, perceived self-efficacy is related to the appraisal and management of stressful experiences, to the onset of depressive symptoms, to problem-solving strategies that might influence decisions regarding use of cigarettes, to the alleviation of inappropriate fears of individuals recovering from heart attacks, and to the self-management capabilities of patients with chronic illnesses. A sense of self-efficacy is enhanced as individuals learn how to influence the risk factors and stressful experiences in their lives by setting attainable goals, enlisting incentives and social supports to sustain their efforts for behavior changes, and developing self-regulatory capabilities required for sustaining the new behavior over an extended period (Bandura, 1992).
Its developmental life span perspective reflects the impact of biological and psychological changes in the individual, and it provides the opportunity for an integrated empirical application of advances in other core sciences, including neuroscience, genetics, and epidemiology. In 1984, developmental psychopathology was defined by Sroufe and Rutter as “the study of the origins and course of individual patterns of behavioral maladaptation” (Sroufe and Rutter, 1984, p. 18). However, developmental psychopathologists are as interested in individuals who do not develop disorders despite severe adversity as in those who do succumb to illness. They also study children who appear emotionally healthy early in life, but develop mental disorders in adulthood. Prospective longitudinal risk research is at the heart of this new discipline; prospective designs help define etiologies and pathways for illness, illuminating changes in risk and protective factors for individuals over time. The task is complex. “Links between earlier adaptation and later pathology generally will not be simple or direct. It will be necessary to understand both individual patterns of adaptation with
respect to salient issues of a given developmental period and the transaction between prior adaptation, maturational change, and subsequent environmental challenges” (Sroufe and Rutter, 1984, p. 17). Such a perspective provides a comfortable home for true integration of biological and behavioral influences.
Developmental psychopathology may indeed be the core integrative discipline for the knowledge base for preventive intervention research. Certainly its concepts, principles, and goals are similar to those in prevention. These concepts include risk and protective factors, precursors, sequelae, competence/incompetence, developmental antecedents of disorders, age-defined adaptation, resilience, and predictability. Sroufe and Rutter (1984) believed not only that the information gained from longitudinal risk research could yield valuable information for preventive interventions, but also that prevention was one of the central justifications for the existence of this special discipline. Developmentally based preventive interventions, moreover, have the potential to serve as tests of theory (Cicchetti and Toth, 1992).
Two examples highlight the research developments in developmental psychopathology. First, low birthweight and premature birth have long been thought to be risk factors associated with increased rates of behavioral and emotional symptoms. Early reports of these associations were largely retrospective and descriptive in nature, but with prospective longitudinal studies in many different disciplines the evidence is more sound. For example, Rose and colleagues reported that very low birthweight premature infants manifested more behavior problems than full-term infants at three and six years (Rose, Feldman, Rose, Wallace, and McCarton, 1992). Also, the overall prevalence of clinically significant problems in the low-birthweight premature infants increased with age: at age three, 30 percent had problems; by age six, 50 percent of them did. Studies such as this one add credence to the beliefs that some such infants are at risk not only for cognitive impairment but also for behavioral dysfunction and that the problems are not transient in nature. Other studies, however, have not shown such pessimistic outcomes, thereby raising research questions regarding degrees of risk and the role of protective factors.
Second, developmental approaches to depression—including epidemiology, risk and protective factors, precursor symptoms, onset, course, and sequelae—are needed across the life span. For example, during the transition to parenthood, depression can be a serious problem; about 10 percent of postpartum women develop a depressive disorder severe enough that it interferes with daily functioning (Campbell and Cohn, 1991; O'Hara, Zekoski, Phillips, and Wright, 1990).
Campbell and colleagues found that even though most postpartum depressions tend to be brief, they can last as long as two years; even those women whose depressive episode abates are likely to continue to experience more subtle difficulties (Campbell, Cohn, Flanagan, Popper, and Meyers, 1992). These problems eventually are reflected in the mother-infant relationship. In Campbell's study the infants of depressed mothers received less appropriate and less responsive care and more negative and rejecting care than the comparison group at two months. The impact of maternal depression on the infant's development can be seen quite early. Field (1992) found that these infants can develop a “depressed mood style” as early as three months and that this mood state persists over the first year of life if the mother's depression persists. By the end of the first year, this mood has affected both physical growth and scores on the Bayley Scales of Infant Development. There is also some evidence that by 11 to 17 months of age, infants of depressed mothers exhibit reduced activity in the right frontal area of the brain (Dawson, Klinger, Panagiotides, Spieker, and Frey, 1992). This finding raises the possibility that maternal behavior can influence not only an infant's developing psychosocial areas of functioning but also the development of the central nervous system.
Maternal depression is not the only, and perhaps not even the most frequent, risk factor for the development of depression during childhood. For example, other forms of parental psychopathology and child maltreatment, and especially the interactive effects when both risk factors are present, also significantly increase the likelihood that a child will become depressed in middle childhood (Downey and Walker, 1992; Toth, Manly, and Cicchetti, 1992).
The rate of depression rises overall between childhood and adolescence. In a sample of 3,519 8- to 16-year-old psychiatric patients, both boys and girls had increasing rates of depression across this age range, with no gender difference in rates before age 11 (Angold and Rutter, 1992). However, by age 16 girls were twice as likely as boys to have significant depressive symptomatology. When age was controlled for, pubertal status had no effect on depression scores. Depressed girls are at high risk for multiple problems, including early pregnancy. The babies of these girls can be, in turn, at risk for developing a similar affective style.
These two examples—low-birthweight premature births and depression—highlight new directions and frontiers for research in developmental psychopathology. First, there is value in understanding age variations in susceptibility to a wide range of phenomena, including low birthweight, parental psychopathology, brain injury, attachment prob-
lems, and hospital admissions. Second, it is essential to learn about continuities and discontinuities in development and about normal variation so that researchers can begin to clarify when preventive interventions are not warranted as well as when they are. Third, there is much more to understand about indirect causal chain processes, mechanisms, and biological and environmental interactions. Finally, there is a need to assess risk factors and the effects of intervention across multiple age periods in each individual and across generations, such as both mothers and their infants.
FINDINGS AND LEADS
There is an increasing tendency within the biological and behavioral sciences to appreciate the complexity and interplay of genetic and environmental interactions. There has been some movement away from the traditional nature-nurture dichotomy toward a recognition that genetic inheritance (the genotype) provides a reaction range within which the environment can have some impact on the characteristic that is expressed (the phenotype).
An understanding of etiology can contribute to the conceptualization and implementation of rational preventive interventions. Research in the core sciences to uncover the wide range of biopsychosocial etiological factors in mental illness is therefore critical to the long-term success of the prevention research initiative. Such basic scientific research endeavors have been the building blocks for the knowledge base on which prevention research has developed.
Many of the interdisciplinary areas of investigation with relevance to prevention research have independently recognized the utility of a developmental focus. These areas include neuroscience, genetics, epidemiology, and developmental psychopathology. From this developmental focus has arisen the concept of sensitive periods.
Eventually, it may become possible to determine the precise mechanisms by which environmental risk factors operate. In attempting to ascertain the relative contributions of the biological and environmental influences on expressed behavior or attributes, a number of paradigms have been useful, including twin, adoption, and experimental studies. In the absence of sound knowledge on risk mechanisms, there is some danger that prevention measures may be either wrongly targeted or so diffuse that they do not bring the expected benefits.
There is considerable evidence that people act in ways that influence the level of risk in the environments they experience. What is less certain is the genetic influence in this process. Genetic influences on behavior
may heighten or lower the likelihood of risk exposure. Investigations into genetic influences should lead to increased understanding as to how individual differences in environmental risk exposure come about.
In the field of genetics, research findings are accumulating rapidly. Some of these are relevant to traditional genetic disorders that have psychiatric implications (e.g., mental retardations, Huntington 's disease), but many have considerable value for the broader range of common, multifactorial mental disorders in which genetic factors play a variably prominent role, such as alcohol dependence and depressive disorder. To a limited extent, available genetic data have preventive implications in the area of genetic counseling, but, to a much greater extent, the findings identify the potential importance of environmental preventive interventions for individuals who are known to be at genetic risk through mechanisms involving vulnerability to environmental factors.
Effective and efficient research on prevention of mental disorders requires that certain data on the epidemiology of the disorders be available—specifically, incidence, prevalence, relative risk, attributable risk, and age of onset. Such data are needed across the life span for an integrative, developmental understanding of mental disorders.
Research studies on risk factors in the interdisciplinary area of developmental psychopathology have the potential for developing into preventive interventions targeting these risk factors with developmentally appropriate timing.
Much can be learned from studies of individuals who do not develop mental disorders despite being at high risk as well as studies of individuals who appear emotionally healthy while young but develop mental disorders in adulthood.
Contributions from areas of investigation rooted in the behavioral sciences offer substantial leads for research on the prevention of mental disorders. These include the impact of psychological stress on health; the role of social support mechanisms in decreasing risk factors and enhancing protective factors; usage of health care delivery systems; the relationship between theoretical concepts such as attachment, self-esteem, and self-efficacy and later social relationships and health behaviors; and the importance of social frames of reference, including race, culture, gender, and community context.
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