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REDUCING RISKS FOR Mental Disorders: FRONTIERS FOR PREVENTIVE INTERVENTION RESEARCH 6 Risk and Protective Factors for the Onset of Mental Disorders During the past 30 years a growing body of research has elucidated some of the risk factors that predispose children and adults to mental disorder. Recent research has also helped to change the concept of a risk factor from a fixed, specific circumstance or life stress to a broader, more general phenomenon that may be modifiable, or malleable, and related to a developmental phase (Avison, 1992). These findings have led to a shift in risk factor research in both emphasis and complexity. Risk factors are those characteristics, variables, or hazards that, if present for a given individual, make it more likely that this individual, rather than someone selected at random from the general population, will develop a disorder (Werner and Smith, 1992; Garmezy, 1983). To qualify as a risk factor, therefore, a variable must be associated with an increased probability of disorder and must antedate the onset of disorder. Variables that may be risk factors at one life stage may or may not put an individual at risk at a later stage of development. Risk factors can reside with the individual or within the family, community, or institutions that surround the individual. They can be biological or psychosocial in nature. Some risk factors play a causal role, although this may not be known prior to an intervention study. Others merely mark or identify the potential for a disorder rather than cause the disorder, and for these, therefore, malleability is not an issue. For example, unusual eye movement is often associated with and predates schizophrenia. Its presence increases the likelihood that an individual will develop schizophrenia, but any efforts to alter such eye movements
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REDUCING RISKS FOR Mental Disorders: FRONTIERS FOR PREVENTIVE INTERVENTION RESEARCH would be fruitless-for preventing schizophrenia because it is not thought to have a causal role. The committee uses the term marker for both biological and psychosocial risk factors of this sort. Incorporated into this definition of risk factor is the concept of vulnerability, which is a predisposition to a specific disease process. Vulnerability traits are identifiable and measurable (and may sometimes be referred to as markers). They are not intrinsically the disease, but they may be necessary for a specific mental disorder to develop. Having vulnerability traits may increase an individual's risk for developing a disorder, but other risk factors also may be necessary for the illness to be expressed. For years, mental health workers devoted their energies to the study of maladaptation and incompetence (Garmezy, 1983) as attempts were made to identify patterns of functioning in childhood that might portend the future development of mental disorders. Rutter (1985b) described this preoccupation as a “regrettable tendency to focus gloomily on the ills of mankind and all that can and does go wrong. ” But not everyone with risk factors goes on to develop a mental disorder, and the importance of protective factors is becoming more recognized. Recently, research has been directed toward understanding why some children appear to be resilient, and why they come to maturity relatively unscathed by the organic and psychosocial insults that prevent so many of their peers from achieving optimal intellectual, social, and emotional functioning (Werner and Smith, 1992). Werner and Smith (1992) defined resilience as “an unusual or marked capacity to recover from or successfully cope with significant stresses, of both internal and external origin.” Theoretical explanations for the phenomenon of resilience (Rutter, 1985b; Garmezy, 1983) involve the interaction of risk factors, including individual vulnerability, and protective factors to explain why some are spared and others are not. Vulnerable individuals are considered to be those who, by virtue of genetic predisposition, chronic illness, hardship, deprivation, or abuse, are more susceptible to life stressors than others. Thus “they are at risk for failure to master, mature and adapt” (O'Grady and Metz, 1987). Rutter (1985b) defined protective factors as “those factors that modify, ameliorate or alter a person's response to some environmental hazard that predisposes to a maladaptive outcome.” Protective factors seemingly function in a catalytic fashion. They do not necessarily foster normal development in the absence of risk factors, but they may make an appreciable difference on the influence exerted by risk factors. Protective factors also can reside with the individual or the family, community, or institutions and can be biological or psychosocial in nature.
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REDUCING RISKS FOR Mental Disorders: FRONTIERS FOR PREVENTIVE INTERVENTION RESEARCH Reviews of community surveys and longitudinal epidemiological studies have emphasized that each mental disorder is likely to have multiple risk factors (Hawkins, Catalano, and Miller, 1992; Werner and Smith, 1992; Offord, Boyle, and Racine, 1989; Rutter, 1989; Offord, Boyle, Szatmari, Rae Grant, Links, Cadman et al., 1987). Thus, in order to look for possible opportunities for intervention, it is necessary to identify as many risk and protective factors that impinge on individuals at different stages of development as possible. The process of critically examining risk factor research on mental disorders is part of the foundation for preventive interventions. Not all evidence from risk research is conclusive enough to warrant the design of a preventive intervention. Even where the evidence is strong, it is still worth seeking other potential markers and causal risk factors because targeting multiple risks may increase the success of a preventive intervention program. This chapter examines the factors that current research indicates may potentially operate to predispose or protect against the occurrence of mental disorders. The examination proceeds first within a categorical framework organized around the five major mental disorders that are used as illustrations throughout this report—Alzheimer's disease, schizophrenia, alcohol abuse and dependence, depressive disorders, and conduct disorder. Because these are disorders in which the relative potential contribution of biological risk factors (including genetic vulnerability) and psychosocial risk factors (including individual, family, and community issues) varies greatly, as a group they provide an opportunity for a review of a wide range of diverse risk factors and the interplay among them. The discussion then moves away from a focus on specific disorders to a broad view of general risk and protective factors that are common to many disorders and dysfunctional states. The sequence of the disorders has been reversed in this chapter and emphasizes the range of risk factors along a continuum from heavily biological to heavily psychosocial. ALZHEIMER'S DISEASE Studies of epidemiology, biochemistry, pathology, and genetics have uncovered several biological risk factors related to Alzheimer's disease (AD), and there is limited evidence for the role of some psychosocial factors, particularly level of education. This section reviews knowledge about biological and psychosocial risk and protective factors for Alzheimer's disease and then discusses their implications for research and for prevention.
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REDUCING RISKS FOR Mental Disorders: FRONTIERS FOR PREVENTIVE INTERVENTION RESEARCH Biological Risk Factors Genetic Vulnerability Over the past decade, evidence that genetic factors play a major role in vulnerability to AD has accumulated. In a distinct minority of cases, AD begins early, in the fourth or fifth decade, rather than the more typical onset after age 70 or 75. This early onset, “presenile” form often clusters in families in a pattern consistent with inheritance of a single gene of major effect. (The pattern is most consistent with “autosomal dominant” inheritance, whereby 50 percent of the children of an affected parent are expected to inherit such a gene and develop the disease.) Breitner and colleagues have raised the question whether the absence of a familial pattern in the senile form of AD may be an artifact of “bias of ascertainment” (Breitner, Folstein, and Murphy, 1986a; Breitner, Murphy, and Folstein, 1986b). Because many first-degree relatives may have died of other causes before living through the period of risk, their loss leads to underestimates of the number who actually carry the gene. Using AD patients identified in nursing homes, Breitner and colleagues attempted to estimate the true prevalence among first-degree relatives (siblings and children) by taking a careful family history in a subpopulation marked by language disorders. If family history was ruled out only for cases in which both parents lived to at least age 85, they found that the risk for AD in first-degree relatives of AD patients approached 50 percent, consistent with autosomal dominant inheritance, even in cases of late onset (Breitner et al., 1986a; Breitner et al., 1986b). European case-control studies, however, showed that although family history was an important risk factor, it did not account for all cases (van Duijn, Clayton, Chandra, Fratiglioni, Graves, Heyman et al., 1991). It is clear that there are several genetic forms of AD, but it is also clear that there are cases of “sporadic” AD that are not inherited. The relative prevalence of genetic and sporadic forms is subject to considerable debate among investigators. Investigators have turned to genetic studies, not only to identify the molecular events underlying AD, but also to ascertain the importance of environmental factors more precisely. Twin Studies. Twin studies could theoretically be particularly useful in sorting among genetic and nongenetic contributions to the genesis of AD (Murphy and Breitner, 1992). One case report describes identical twins, only one of whom developed AD over a 20-year follow-up period (Renvoize, Mindham, Stewart, McDonald, and Wallace, 1986). This case
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REDUCING RISKS FOR Mental Disorders: FRONTIERS FOR PREVENTIVE INTERVENTION RESEARCH of apparent twin discordance must be interpreted with some caution, however, as previous reports of discordance have proved to be premature. In one pair of identical twins initially reported as discordant, the second twin developed AD 13 to 15 years after her twin sister (Cook, Schneck, and Clark, 1981). AD in both twins could be a mere coincidence, or it could reflect factors that caused the age of onset to differ by more than a decade despite a genetic predisposition to AD. In surveys of twin studies, the age of onset may differ by as much as a decade between identical twins (Li, Silverman, and Mohs, 1991; Breitner, Murphy, Folstein, and Magruder-Habib, 1990; Nee, Eldridge, Sunderland, Thomas, Katz, Thompson et al., 1987). Because identical twins share their genes, if both do not develop AD, this is strong evidence of nongenetic factors. At the very least, when the age of onset is different for a pair of identical twins, it indicates that environmental factors influence when symptoms begin, suggesting that prevention might work by delaying onset. In one twin study, for example, investigators found that symptoms of dementia began later among female than male twin pairs, an intriguing finding that merits further inquiry (Nee et al., 1987). The differing ages of onset between a pair of identical twins imply that even genetic factors underlying AD may be malleable to environmental interventions. Breitner notes that delaying onset of AD by only five years would reduce its clinical impact by half, because onset is typically delayed until late in life (Breitner, 1991). If the disease began five years later, many individuals would die before showing symptoms. Finding strategies to delay onset is thus a primary focus of epidemiological and other biomedical research. Twin studies to date have been hampered by a bias, because the twins studied are likely to have volunteered. A more reliable population-based study that should not suffer from this flaw is under way, using a twin registry of U.S. veterans. This data set includes a heavy predominance of males, and clinical data are incomplete. This study cannot verify the preliminary finding that age of onset differs between the sexes, but its analysis should nonetheless illuminate the importance of many other nongenetic factors among identical and fraternal twins (Breitner, Welsh, Magruder-Habib, Churchill, Robinette, Folstein et al., 1990). Studies of Down's Syndrome. Down's syndrome (DS), the most common genetically identified cause of mental retardation, has provided another line of evidence supporting genetic factors in the risk for AD (Coyle, Oster-Granite, and Gearhart, 1986). DS, or trisomy 21, results from having three copies, instead of the normal two, of all or part of
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REDUCING RISKS FOR Mental Disorders: FRONTIERS FOR PREVENTIVE INTERVENTION RESEARCH chromosome 21, especially the distal end of its long arm. Thus DS does not result from “mutant genes” but rather from the altered gene expression from an abnormal gene copy number. Post mortem studies indicate that virtually all DS individuals develop the neuropathology of AD by the time they reach their fourth decade. The distribution and density of the pathological stigmata in DS brains are indistinguishable from AD. Furthermore, the DS brains with AD exhibit the same selective vulnerability of nerve cell populations. Nevertheless, some older DS individuals do not exhibit the cognitive deterioration expected on the basis of the microscopic findings in brain tissue, and thus do not fulfill the standard criteria for “dementia,” which by definition entails cognitive decline. Molecular Studies of Amyloid. Recent molecular biological studies have begun to shed light on the cellular processes leading to AD pathology by focusing upon amyloid (Mueller-Hill and Beyreuther, 1989). Amyloid in the senile plaque is an obvious target for analysis, because the density of senile plaques correlates both with cognitive impairment and with biochemical deficits in AD. Amyloid has been purified to homogeneity from the brains of individuals with AD or DS/AD, demonstrating that it is a peptide of approximately 42 amino acids. From the sequence of amino acids in amyloid, it is possible through molecular biological methods to clone the gene that contains the amyloid sequence. These studies demonstrate that amyloid is a breakdown by-product of a much larger protein (designated amyloid precursor protein, or APP) that is normally expressed on the surface of many cells in the body, but especially nerve cells in the brain's cerebral cortex. The gene encoding the APP protein is located on the long arm of chromosome 21 and can be processed inside cells into at least four proteins of varying length. A critical question concerns the mechanisms that favor a breakdown pathway for APP that generates amyloid (Hardy and Higgins, 1992). In the case of DS, the three copies of the APP gene, due to its presence on chromosome 21, could result in a marked overexpression of APP in brain. As a consequence, amyloid might accumulate in the DS brain much more rapidly than normal. In AD, an aberrant enzyme that degrades or modifies APP and its metabolites could play a role. There are many possible explanations for how amyloid deposition relates to disease, and this will be a main target for AD research in coming years. Preclinical studies suggest that aberrant addition of phosphate groups to the APP protein favors a metabolic route that generates amyloid instead of protein cleavage. One strategy for prevention focuses on delaying the degradation of APP. If amyloid accumulation is indeed a
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REDUCING RISKS FOR Mental Disorders: FRONTIERS FOR PREVENTIVE INTERVENTION RESEARCH cause of cell death, then slowing its accumulation could delay this, and presumably also the onset of clinical dementia. Genetic Mutations. An obvious possible cause of abnormal disposition of APP is an alteration of the DNA constituting its gene—a mutation. Indeed, several families with autosomal dominant forms of presenile AD have been shown to have just such a mutation, localized to a specific position (codon 717) of the APP gene (Goate, Chartier-Harlin, Mullan, Brown, Crawford, Fidani et al., 1991). In other cases, a different mutation, at codon 670/671, has been found in the same gene, again associated with AD (Mullan, Crawford, Axelman, Houlden, Lilius, Winblad, and Lannfelt, 1992). Another mutation complex, affecting codons 713 and 715, was found in a 64-year-old woman with AD, but also in her 88-year-old mother and four siblings, all of whom were older than 62 and clinically unaffected (Carter, Desmarais, Bellis, Campion, Clerget-Darpoux, Brice et al., 1992). The significance of this double mutation is thus unclear, and it may represent a mere coincidence. Mutations in the APP account for only a very small percentage of early-onset familial AD cases, although they strongly suggest that the APP gene can be functionally related to AD in these few cases. This seems likely to prove but the first of many molecular aberrations that can lead to AD. Genetic Heterogeneity. There appear to be multiple genes that can cause AD in different families. The first report of linkage between AD and DNA markers appeared in 1987, implicating a region on chromosome 21, and was later confirmed by other groups (St. George-Hyslop, Haines, Farrer, Polinsky, Van Broeckhoven and Goate, 1990; St. George-Hyslop, Tanzi, Polinsky, Haines, Nee, Watkins et al., 1987). In addition to the very small fraction of familial cases associated with a mutation of the gene encoding the APP protein on chromosome 21 (Schellenberg, Anderson, O'dahl, Wisjman, Sadovnick, Ball et al., 1991), there is also evidence of a gene elsewhere on the same chromosome (Goate, Haynes, Owen, Farrall, James, Lai et al., 1989; St. George-Hyslop et al., 1987). Most of the evidence for another chromosome 21 gene, however, comes from a large Italian family that shows even stronger evidence of a gene on chromosome 14. A second chromosome 21 AD gene, in addition to the APP gene, is thus possible but by no means certain. A second gene on chromosome 21 may also modify the action of the APP gene or another gene, and hence show genetic linkage. It was already clear in 1988 that the molecular defect among several different families with an inherited form of AD resided on sites other
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REDUCING RISKS FOR Mental Disorders: FRONTIERS FOR PREVENTIVE INTERVENTION RESEARCH than chromosome 21 (Schellenberg, Bird, Wijsman, Moore, Boehnke, Bryant et al., 1988). Since that time, evidence has accumulated for another possible gene on chromosome 19 in a few families (Corder, Saunders, Strittmater, Schmechel, Gaskell, Small et al., 1993; Pericak-Vance, Bebout, Gaskell, Yamaoka, Hung, Alberts, and Walker, 1991), and a more common gene defect, perhaps accounting for most families with early onset, on chromosome 14 (Mullan, Houlden, Windelspecht, Fidani, Lombardi, Diaz et al., 1992; St. George-Hyslop, Haines, Rogaev, Mortilla, Vaula, Pericak-Vance et al., 1992; Van Broeckhoven, Backhovens, Cruts, DeWinter, Bruyland, Cras, and Martin, 1992). A few large families, called the Volga Germans for their common pattern of ethnic migration from Germany to Russia and thence to the United States early in this century, also have an inherited form of AD. In the Volga German families, the inheritance pattern is not consistent with any of the chromosomal locations associated with other families. This suggests one or more as yet undiscovered genes associated with AD or a mixture of genes on different chromosomes in the same family. Continuing Investigation. Viewed in aggregate, these studies indicate that AD is a common disorder with genetic heterogeneity, meaning that several genetic defects can cause a clinically and neuropathologically similar syndrome. AD can result from mutation in the APP gene, may possibly follow from overexpression of APP due to gene triplication (DS), and clearly can also be caused by mutations elsewhere in the human genome. AD may develop from one or more genes on chromosome 21 (the APP gene and perhaps one other), a gene on chromosome 14, perhaps another on chromosome 19, and one or more genes among the Volga German families. Because of the complexity of APP metabolism, there is reason to expect that mutations of genes encoding for enzymes that process amyloid protein could cause an accelerated rate of accumulation of amyloid, leading to AD. The clinical and pathological features of AD may also appear in response to entirely different biochemical defects not yet discovered. Those studying familial forms of AD hope to identify and isolate specific gene defects, which would lead to the protein those genes encode, and to possible clues about the causes of Alzheimer 's disease. The common conception that genetic disorders are resistant to intervention has proved untrue in many disorders. There are dietary treatments for phenylketonuria, and many genetic disorders require an environmental trigger. Twin studies, genetic linkage studies, and searches for specific genes not only provide logical paths for scientific
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REDUCING RISKS FOR Mental Disorders: FRONTIERS FOR PREVENTIVE INTERVENTION RESEARCH investigation toward a causal explanation of AD, but also may provide clues for prevention, depending on what the genes do. Genetic studies to date have solidly established the role of genetic factors, but the implications for prevention are not yet clear. History of Head Trauma A history of head trauma has appeared as a risk factor for AD in several epidemiological studies (Henderson, Jorm, Korten, Creasey, McCusker, Broe et al., 1992; Mortimer, van Duijn, Chandra, Fratiglioni, Graves, Heyman et al., 1991; Graves, White, Koepsell, Reifler, van Belle, Larson, and Raskind, 1990; Amaducci, Fratiglioni, Rocca, Fieschi, Livrea, Pedone et al., 1986; French, Schuman, Mortimer, Hutton, Boatman, and Christians, 1985; Mortimer, French, Hutton, and Schuman, 1985; Heyman, Wilkinson, Stafford, Helms, Sigmon, and Weinberg, 1984). Recent studies show correlations with nonfamilial cases of AD, rather than familial cases (Henderson et al., 1992; Mortimer et al., 1991), suggesting it is an independent risk factor and may or may not contribute to dementia through an entirely different causal pathway from that of the genetic forms. These studies have rekindled interest in trauma as a cause of AD. A clinical syndrome, dementia pugilistica, has long been described in the clinical literature (Mendez, 1993). Microscopic plaques and tangles are found at autopsy, but they are distributed more widely than in typical AD. Dementia pugilistica is most likely to occur among those who sustain repeated closed head injuries, especially boxers. Dementia typically begins several years after exposure to trauma. It is most common among those with a history of vascular disease, alcoholism, or low IQ (Mendez, 1993). Recent studies show a correlation between severe head injury and presence of plaques, which appear in one of three individuals subjected to repeated head trauma such as boxing (Clinton, Ambler, and Roberts, 1991; Roberts, Allsop, and Bruton, 1989). Prevention of head trauma is itself a laudable goal. Head trauma can be reduced by use of seat belts and air bags in automobiles, wearing helmets while riding motorcycles or bicycles, and reducing exposure to events likely to result in trauma (e.g., boxing), and other measures. The immediate benefits include reduced risk of spinal cord injury and acute brain injury. Trauma, including head trauma, is a major cause of premature mortality, especially among young adults. Preventing AD several years hence may be but an additional, delayed, benefit from measures commendable in their own right. The association between
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REDUCING RISKS FOR Mental Disorders: FRONTIERS FOR PREVENTIVE INTERVENTION RESEARCH repeated head trauma and dementia suggests that the sport of boxing carries a significant long-term risk. Medical Risk Factors, Including Thyroid Disorders Several other risk factors have been identified by one or more epidemiological studies. However, a recent study concluded that despite enormous efforts to gather clinical data on a large number of subjects, “ we have been unable to identify any important candidate [medical] risk factors that may account for a substantial proportion of the cases of AD occurring in the community” (Kokmen, Beard, Chandra, Offord, Schoenberg, and Ballard, 1991). But there may be one exception. A recent review of several studies corroborated previous reports of an association with thyroid disorders (Breteler, van Duijn, Chandra, Fratiglioni, Graves, Heyman et al., 1991; Treves, 1991), although the effect was much smaller than that of family history or head trauma. Maternal Age at Time of Birth An even weaker association was found between AD and maternal age at time of birth, with AD prevalence increased among those born to either unusually young or unusually old mothers (Rocca, van Duijn, Chandra, Fratiglioni, Graves, Heyman et al., 1991). These preliminary results suggest future research directions. Psychosocial Risk and Protective Factors Educational Level Several studies have shown a higher prevalence of dementia among those with less education, although findings are not entirely consistent from study to study. Projections of AD prevalence in the United States in 2050 yield estimates of 10.3 million cases of probable AD if the trend to increased education in the U.S. population is taken into account, but 15.4 million without this adjustment factor for education (Evans, Scherr, Cook, Albert, Funkenstein, Smith et al., 1990). Studies in Italy and China show more dementia among the less educated (Rocca, Bonaiuto, Lippi, Luciani, Turtu, Cavarzeran et al., 1990; Zhang, Katzman, Salmon, Jin, Cai, Wang et al., 1990; Amaducci et al., 1986), similar to previous North American and European studies. One recent community survey in Baltimore, Maryland, however, found the opposite effect, with higher AD prevalence among the more educated (Folstein, Bassett, Anthony,
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REDUCING RISKS FOR Mental Disorders: FRONTIERS FOR PREVENTIVE INTERVENTION RESEARCH Romanoski, and Nestadt, 1991). This effect was relatively weak and depended on a small number of cases in the higher-educated categories, and thus should be interpreted with some caution. Katzman (1993) recently reviewed the literature on education and Alzheimer's disease, observing that several epidemiological criteria of causality have been met, but he still urges caution in interpreting results. He concluded that if education has the effect of increasing synaptic density in some brain regions, and if it is indeed loss of cells in these regions that predisposes to clinical dementia, then the epidemiological and biological data could be integrated into a plausible theory. The effect of education would not be to alter the underlying biological cause of cell loss, but rather to delay its clinically detectable effects, so that dementia does not ensue for an additional five or so years. Smoking Epidemiological case-control studies looking for associations between AD and smoking over the past decade have produced conflicting results. Graves and colleagues recently reported a meta-analysis of data from eight of these studies, which individually had reached different conclusions (Graves, van Duijn, Chandra, Fratiglioni, Heyman, Jorm et al., 1991). The reanalysis of pooled data disclosed a statistically significant inverse correlation between smoking and AD prevalence —that is, those who smoked more were less likely to have AD. The analysis included one study that had found a positive correlation (higher prevalence of AD among smokers), but the population in this study was unusual and even when cases from this study were included, the meta-analysis reached the same conclusion of an inverse correlation. An association between reduced AD prevalence and smoking is an intriguing lead. It has some biological plausibility because nicotine, an active agent in tobacco products, binds to the acetylcholine receptors, whose loss is associated with AD. It is thus not unreasonable to postulate that smoking might delay onset of symptoms. Against this, however, the studies did not show a later onset in smoking than nonsmoking cases of AD, although one of the component studies from the Netherlands did find that when two or more family members developed AD, one of whom smoked and the others not, the onset was later for the smokers. This was based on a very small number of cases and is thus only a tantalizing but uncorroborated finding. The authors of the meta-analysis urge caution in interpreting the findings, as there are many possible confounding factors that could be controlled only by prospective longitudinal population-based studies, rather than case
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Representative terms from entire chapter: