3
The Etiology of Depression

SUMMARY

Timing and Course of Depression

  • Age of onset of major depression may have both clinical and etiological implications. Clinically, earlier age of onset is associated with a worse course of depression with greater chances of recurrence, chronicity, and impairment. Etiologically, first onset of depression at different ages (e.g., childhood, adolescent, adult, and older adult) may reflect somewhat different causal factors.

  • Many individuals may experience a single, major depressive episode following an acute stressor and recover with little implication for future vulnerability. However, most (50–80 percent) who have one significant episode will have recurrent episodes and intermittent subclinical symptoms, with the risk of recurrence progressively increasing with each episode of major depression.

Biological Factors

  • Genetic, neurological, hormonal, immunological, and neuroendocrinological mechanisms appear to play a role in the development of major depression, and many of these factors center around reactions to stressors and the processing of emotional information. Etiological processes may be modified by gender and developmental factors.



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3 The Etiology of Depression SUMMARY Timing and Course of Depression • Age of onset of major depression may have both clinical and etiological implications. Clinically, earlier age of onset is associ- ated with a worse course of depression with greater chances of recurrence, chronicity, and impairment. Etiologically, first onset of depression at different ages (e.g., childhood, adolescent, adult, and older adult) may reflect somewhat different causal factors. • Many individuals may experience a single, major depressive epi- sode following an acute stressor and recover with little implication for future vulnerability. However, most (50–80 percent) who have one significant episode will have recurrent episodes and intermit- tent subclinical symptoms, with the risk of recurrence progressively increasing with each episode of major depression. Biological Factors • Genetic, neurological, hormonal, immunological, and neuroendo- crinological mechanisms appear to play a role in the development of major depression, and many of these factors center around re- actions to stressors and the processing of emotional information. Etiological processes may be modified by gender and developmen- tal factors. 

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 DEPRESSION IN PARENTS, PARENTING, AND CHILDREN Environmental and Personal Vulnerabilities • Etiological models for depression are largely diathesis-stress models in which stressful experiences trigger depression in those who may be vulnerable due to biological and psychosocial characteristics and circumstances. • Environmental stressors associated with depression include acute life events, chronic stress, and childhood exposure to adversity. Personal vulnerabilities associated with depression include cogni- tive, interpersonal, and personality factors. • Biological, environmental, and personal vulnerabilities interact to contribute to the development of depression and also may be af- fected by depressive states in a bidirectional process. Co-Occurring Disorders • Depression rarely occurs independent of other psychological disor- ders, including anxiety, substance abuse, behavioral, and personal- ity disorders, as well as other medical illnesses. The presence of co-occurring psychological and medical disorders exacerbates the clinical and social consequences of depression, and makes it more challenging to treat. Resilience and Protective Factors • Certain biological, environmental, and personal factors have also been associated with the protection from or the overcoming of risk factors and adverse conditions related to the development of depression. ____________________ The purpose of this chapter is to review what is known or suspected about the causes of depression. Fundamentally, such depressive symptoms as sad mood, pessimism, and lethargy, are universal human experiences and are considered normal reactions to the struggles, disappointments, and losses of everyday life. However, for some individuals, the intensity and persistence of depressive symptoms are not typical, and a challenge for re- searchers has been to understand why some individuals experience marked and enduring depressive reactions and others do not. This chapter discusses some of the characteristics of individuals that may make them vulnerable, as well as the features of environments that are particularly likely to pro- voke depression. The chapter also emphasizes the interplay between persons

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 THE ETIOLOGY OF DEPRESSION and environments—the ways in which, for example, stressors may provoke depression but depression further influences social environments, often a vi- cious cycle that promotes chronic or recurrent depression. A further aspect of this bidirectional influence is the frequent co-occurrence of depression and other disorders, which may complicate its course and treatment. It is noted that some individuals are remarkably resilient in the face of adversity, and a further challenge to the field is to understand such processes. The first topic to address is that not all depressions are alike; therefore, different etiological models and perspectives are likely to apply to different expressions of depressive disorder. TIMING AND COURSE OF DEPRESSIVE DISORDERS Age of onset of major depressive disorder and lifetime course are two fac- tors that have etiological as well as treatment and outcome implications. Age of First Onset First onset can occur at any time. Diagnoses of childhood depression are relatively rare (Birmaher et al., 1996; Egger and Angold, 2006), al- though many preadolescents including preschoolers have significant inter- nalizing symptoms of dysphoria and distress (e.g., Cole et al., 2002; DuBois et al., 1995; Gross et al., 2006). Most diagnosed depressions first appear in adolescence and early adulthood (Andrade et al., 2003; Burke et al., 1990; Kessler et al., 2005)—especially among those born in more recent decades (e.g., Kessler et al., 2003). For example, in recent community studies up to one-third of adolescents met criteria for major depressive disorder (Kessler and Walters, 1998; Lewinsohn, Rohde, and Seeley, 1998). Age of first onset has both clinical and etiological implications. Clini- cally, earlier age of onset of depression is generally thought to be associ- ated with a worse course of depression, with greater chances of recurrence, chronicity, and impairment in role functioning (e.g., Hollon et al., 2006; Zisook et al., 2004). Those with adolescent-onset depression include a sig- nificant proportion among both treatment and community samples who go on to have recurrent episodes and significant impairment (e.g., Hammen, Brennan, and Keenan-Miller, 2008; Lewinsohn et al., 1999, 2000; Pine et al., 1998; Weissman et al., 1999a). Evidence increasingly suggests that childhood, adolescent, adult, and older adult first onsets may reflect different causal factors. Childhood depressions may be a mixture of subgroups: those with true genetically familial early-onset recurrent depression; those exposed to significant psy- chosocial adversity, such as abuse, parental disorder, criminality, and fam- ily disruption who continue to experience social maladjustment and other

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 DEPRESSION IN PARENTS, PARENTING, AND CHILDREN problem behaviors but not depression into adulthood; and some with eventual bipolar disorder (e.g., Harrington et al., 1990; Weissman et al., 1999b). Adolescent-onset depressions are noteworthy for several factors. One is that increasing rates of adolescent depression in recent years (e.g., Kessler et al., 2003) imply, among other things, that the etiology is substantially psychosocial, with significant cultural shifts in recent decades that have created stressful experiences and reduced resources and contribute to de- pressive experiences (e.g., Seligman et al., 1995). Another issue is the enormous divergence in rates of depression for girls and boys beginning in adolescence (e.g., reviewed in Hankin and Abramson, 2001). The dramatic increases in girls’ rates of depression compared with boys’ rates clearly requires etiological models that can explain such differences. For example, different models emphasize genetic (e.g., Silberg, Rutter, and Eaves, 2001), hormonal (e.g., Angold et al., 1999), stress exposure and stress processes (e.g., Rudolph, 2002; Shih et al., 2006), cultural shaping of values and vulnerabilities (Seligman et al., 1995), and gender-based coping strategies (e.g., Nolen-Hoeksema, 1991). Perinatal Depression The childbearing years in general, and those around pregnancy in particular, have attracted special attention with respect to the occurrence of depression and its potential effects on children’s development. A large majority of women experience mild “blues” following delivery of an infant, and between 10 and 20 percent of new mothers experience clinical depres- sion lasting anywhere from several weeks to a year. A smaller proportion, less than 0.5 percent, experience acute psychosis associated with the depres- sion. A recent large-scale epidemiological survey that examined rates of di- agnoses in nonpregnant women compared with past-year pregnant women found no differences overall in mood disorders (Vesga-Lopez et al., 2008). However, the rates of major depression were higher in postpartum women compared with nonpregnant women. For all women pregnant in the past year, their depression was associated with not being married, exposure to trauma and stressful life events in the past year, and overall poor health. The dramatic hormonal changes a woman experiences during and after pregnancy have focused much attention on the biological and hormonal etiological factors of postpartum depression. However, there is widespread agreement that postpartum major depression is not distinct in terms of eti- ology from depression at other times. In addition to biological risk factors, social stressors, family composition, levels of social support, and especially poorer economic circumstances all contribute to the risk of developing postpartum depression (Bloch et al., 2005; Crouch, 1999; Grigoriadis and

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 THE ETIOLOGY OF DEPRESSION Romans, 2006; Hayes, Roberts, and Davare, 2000; Robertson et al., 2004; Segre et al., 2007). Although relatively little research has focused on paternal postpartum depression, the few studies that have report rates among new fathers as lower but not too dissimilar to that of new mothers. Paulson, Dauber, and Lieferman (2006), reporting on depression among two-parent households in a national random sample of over 5,000 families, found rates of depres- sion at 14 percent for mothers and 10 percent for fathers. Fathers’ elevated rates of depressive symptoms and disorders after the birth of a child are associated with stressful adjustments and the quality of their relationship with the mother; mothers’ depression is also a significant predictor of in- creased depression in postpartum fathers (Huang and Warner, 2005; Kim and Swain, 2007). Course of Depression The course of depression may shed light on both treatment and pre- vention concerns and etiological issues. Some individuals may experience a single, major depressive episode in response to an acute stressor, never seek treatment, and, except for impairment associated with the acute episode, recover with little implication for future vulnerability. However, many oth- ers, especially those with sufficient distress and impairment who seek (or should seek) treatment, will have recurrent episodes and possibly significant residual symptoms (e.g., Judd, 1997; Judd et al., 1998; Keller, 1985). Judd (1997) found that 80 percent of patients had at least one recurrence (with an average of 4 episodes) over a few years’ follow-up, and many others had significant even if nondiagnosable symptoms. In an epidemiological study of first episode of depression, more than 50 percent had a recurrence over the multiyear follow-up (Eaton et al., 2008). Moreover, there is evidence that the risk for recurrence progressively increases with each episode of major depression—and decreases as the period of recovery is longer (Solomon et al., 2000). Episodes come closer together over time (Bockting et al., 2006; Kessing et al., 2004; Solomon et al., 2000). As Judd et al. (1998) have documented, impaired functioning in work, family, social, and marital roles persists to a considerable extent even when the individual does not meet the full criteria for a major depressive episode. Thus, recurrent depressive disorders and continuing symptoms are likely to be disruptive of lives and families. Early-onset recurrent depression may reflect a genetic etiology (Holmans et al., 2007), but its progressive nature has also been speculated to indicate a neurobiological process in which early and successive episodes of depres- sion alter the brain and neuroregulatory processes (e.g., Post, 1992). The “kindling” model postulates that successive episodes change the brain in

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 DEPRESSION IN PARENTS, PARENTING, AND CHILDREN ways that reduce the threshold at which stressors may trigger a further episode—possibly to the point of autonomous episodes of depression. A review of studies of stress-depression associations in first and later episodes found some support for the model (Monroe and Harkness, 2005). Truly longitudinal within-person studies to test this hypothesis are quite rare, although one such investigation by Kendler, Thornton, and Gardner (2000) studied nearly 2,400 female twins over 4 waves separated by at least 13 months each. They found evidence of a diminishing association between life events and depression as the person experienced increasing numbers of epi- sodes (up to about 6–8 episodes). They suggested that whether the involved mechanism is biological or psychological, it appears to occur intensively in the first few episodes after initial onset, and then the kindling process slows or stops. The stress-depression relationship not only may vary over time with increasing numbers of episodes but also may differ according to genetic risk for depression (Kendler, Thornton, and Gardner, 2001). Mild, chronic depression—termed dysthymic disorder—may also be very disruptive and enduring. It may be highly predictive of major depres- sive episodes, and, especially if its onset is early in life, it is associated with slow recovery and high rates of relapse or continuing symptoms (Klein, Shankman, and Rose, 2006). Early-onset dysthymic patients had relatively high rates of poor-quality early home environments (Lizardi et al., 1995) and a relatively elevated exposure to early adverse conditions, including physical and sexual abuse, as well as ongoing stressful life conditions (Riso, Miyaktake, and Thase, 2002). Chronic depression is also associated with higher rates of familial depression than is episodic major depression (Klein et al., 2004), which suggests an etiological subtype. Key features of the course of depression have significant implications for families. Most depressions first occur in adolescence and young adult- hood, periods during which critical developmental accomplishments may be disrupted, such as academic attainment and job planning, peer integration and acquisition of effective social skills, and romantic relationship forma- tion. Obviously, childbearing years are affected as well. Young people who are depressed may select into, or default into, problematic environments that are stressful and may further overwhelm impaired coping capabilities. Depression may become recurrent for biological as well as social and psy- chological reasons, and thus it may become harder to manage and treat. All members of the family are affected, and children are the most vulnerable to the negative impact of parental depression. Another important observation that comes from this evidence is that prevention programs may be particu- larly valuable and are probably best targeted at those most vulnerable to depression: those with extensive family history, those with symptoms of de- pression, and those with multiple risk factors for depression (e.g., poverty, exposure to violence, social isolation).

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9 THE ETIOLOGY OF DEPRESSION BIOLOGICAL PERSPECTIVES ON THE ETIOLOGY OF DEPRESSION A complex set of biological processes has been implicated in the eti- ology and course of depression—although such research has not always clarified whether such processes are underlying causal factors, correlates, or consequences of depression. These include interrelated mechanisms of genetic vulnerabilities, brain structure and function, neurotransmitter and neuroendocrine processes, and immune system processes. Discussion of the details and transactions among these processes given the vastly expanding research literature in recent years is beyond the scope of this report (but see Thase, 2008, for a review). Advances have been made in each of these areas as well as in studies of interactions among these biological mecha- nisms and environmental and personal factors that confer increased risk for depression. In light of the heterogeneity of depression, it is not surprising that the research evidence to date has failed to converge on a single set of biological processes that is related to the onset and course of depression. However, evidence supports the role of several important aspects of func- tioning in the brain, the central nervous system, and the periphery. A theme throughout these various lines of research is the importance of considering the interaction between biology and exposure to stress, particularly chronic or recurring stress, in the etiology and course of depression. Genetic Vulnerability It is well known that depression runs in families, a phenomenon impli- cating both genetic and environmental processes. A review of twin studies finds that about one-third of the risk for major depression in adults derives from genetic differences between individuals (Kendler et al., 2006; Sullivan, Neale, and Kendler, 2000). This figure is substantially lower than for some other psychological disorders, such as schizophrenia or bipolar disorder (McGuffin et al., 2003; Sullivan, Kendler, and Neale, 2003). Similarly, the risk of developing major depression increases about 2.5–3 times for those who have a first-degree relative with depression, whereas having a highly threatening life event increases risk from 5 to 16 times in a few months after the event (Kendler, Karkowski, and Prescott, 1998; Sullivan, Neale, and Kendler, 2000). Genetic influences appear to be modified by gender and developmental phase, and they may influence not only internal biological and psychological characteristics but also the nature of the person’s effects on the environment (Kendler et al., 2001, 2006; Kendler and Karkowski- Shuman, 1997; Kendler, Gardner, and Prescott, 2003; Kendler, Gardner, and Lichtenstein, 2008). Several genetic polymorphisms have been linked to increased risk of depression in response to stress. Foremost among these are genes of the

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0 DEPRESSION IN PARENTS, PARENTING, AND CHILDREN serotonin system (5-HT). The neurotransmitter serotonin exerts effects on a broad range of physiological functions, such as emotions, sleep, circadian rhythm, thermoregulation, appetite, aggression, sexual behavior, pain sen- sitivity, and sensorimotor reactivity (e.g., Lucki, 1998; Neumeister, Young, and Strastny, 2004). Deficits in the central 5-HT system, such as reduced 5-HT concentrations, impaired uptake function of the 5-HT transporter, altered 5-HT receptor binding, and tryptophan depletion, have been linked to a number of psychological problems and psychiatric disorders, including depression (Neumeister, Young, and Strastny, 2004). A number of studies have investigated the role of genetic polymor- phisms in the serotonin-related genes in the etiology of depression. Cur- rently, the serotonin transporter (5-HTTLPR) gene is the most promising one. Importantly, Caspi et al. (2003) and Kendler et al. (2005) found that individuals with one or two copies of the short allele of 5-HTTLPR expe- rienced more depressive symptoms and higher rates of major depressive disorder in response to stressful life events than individuals who are homo- zygous for the long allele. These studies are especially noteworthy for their indication that genetic effects on depression may be observed only under conditions of exposure to stressors (see reviews by Uher and McGuffin, 2008; Zammit and Owen, 2006). The effects of the serotonin transporter polymorphism implicated in depression in response to stressful life events may be manifested behaviorally as dysfunctional emotionality in response to stress. As an illustration of the complex transactions among brain functions, genes, and neurotransmitter systems, Hariri et al. (2005) used neuroimaging techniques to explore how individuals with different polymorphisms of the 5-HTTLPR gene responded to an amygdala activation task involving per- ception of fearful and angry faces. They found that normal, never-depressed individuals who had the short allele form of the 5-HTTLPR gene showed amygdala hyperreactivity in response to the emotion-arousing stimuli com- pared with other groups. The results suggest that the serotonin transporter polymorphism is linked to the brain’s processing of emotional threat in- formation. The study is noteworthy for helping to shed further light on neurobiological mechanisms by which stressful environmental experiences eventuate in depression in some people but not others. In addition to the 5-HTTLPR polymorphisms, numerous other sero- tonin system genes have been studied as well as those known to affect the functioning of the hypothalamic-pituitary-adrenal (HPA) axis and other brain regions. Meta-analytic studies of candidate genes and molecular ge- netic genome-wide association studies are increasing throughout the world, but it has been noted by a recent large-sample genome-wide association study of the high heritable human trait of height that they are likely to show what has long been predicted in quantitative genetics: Any relevant

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 THE ETIOLOGY OF DEPRESSION gene will have very small effects, and summing risk across multiple identi- fied genes will yield limited explication of the effects (Weedon et al., 2008). Thus, in view of relatively modest overall heritability of depression, strong environmental effects, and tiny effects of individual genes, it is unlikely that genetic testing will prove to be an effective way to identify those at risk for depression. It has been speculated that “old-fashioned” methods of identifying risk through individual differences in a family history of depression or the personality trait of neuroticism will prove to be superior to molecular genetics (personal communication, Kenneth Kendler, Medi- cal College of Virginia and Virginia Commonwealth University, August 8, 2008). That said, continuing analysis of genetic correlates of depression will doubtlessly contribute valuable information to fuller understanding of the neurobiological mechanisms underlying depression, and it may play a role in the development of pharmacotherapeutic agents. A final note about genetic contributions to depression is the important acknowledgment not only that genetic factors have an impact on internal depressogenic processes but also that gene-environment correlations con- tribute to outcomes. For example, genetic factors may influence a depressed person’s parenting styles as well as the offspring’s heritable traits, so that the child’s genotype and rearing environment are correlated (D’Onofrio et al., 2005, 2006, 2007; Rice, Harold, and Thapar, 2005). Similarly, youth with particular heritable characteristics evoke reactions from oth- ers and select or create experiences that are congruent with their heritable characteristics—processes that might increase the likelihood of depressive outcomes under relevant conditions. Although critically important to full understanding of genetic influences there is relatively sparse research on such mechanisms (personal communication, Sara Jaffe, King’s College Lon- don, August 4, 2008). Neuroendocrine Functioning A dominant model of the neurobiology of depression that has emerged in recent years emphasizes the underlying dysregulation of the body’s response to stress, involving the neuroendocrine system and brain responses (Thase, 2008). Key components are the HPA axis and the related corticotrophin- releasing hormone (CRH) and locus coeruleus-norepinephrine (LC-NE) systems, which include limbic and cortical pathways bidirectionally inter- connected through various neurotransmitter and hormonal circuits (Boyce and Ellis, 2005; Meyer, Chrousos, and Gold, 2001). The primary gluco- corticoid hormone is cortisol, which triggers a cascade of functions that are adaptive in the acute phases of response to stress and which normally resolve quickly through inhibitory feedback processes in the HPA axis. However, failure to normalize, resulting in sustained high cortisol, has

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2 DEPRESSION IN PARENTS, PARENTING, AND CHILDREN deleterious effects, giving rise to physiological changes thought to promote a variety of illnesses. Depression has been linked with elevated cortisol and related neu- rohormones. Numerous studies have indicated higher levels of cortisol and abnormalities in cortisol regulation among depressed compared with nondepressed individuals (e.g., reviewed in Plotsky, Owens, and Nemeroff, 1998; Ribeiro et al., 1993). Furthermore, depressed patients show slower recovery of cortisol levels in response to psychological stress than controls (see meta-analysis by Burke et al., 2005). Individuals who display evidence of abnormal cortisol regulation even after treatment are more likely to relapse and generally have a poorer clinical prognosis than patients whose cortisol functions returned to normal after treatment (e.g., Ribeiro et al., 1993). It appears that sustained hypercortisolism damages the stress system, including death of cells in the hippocampus (Sapolsky, 1996) with general- ized effects on the circuits underlying emotion regulation. It is hypothesized that both genetic and environmental factors account for individual differences in how individuals respond to (and recover from) HPA system activation. Genetic differences in species of animals and non- human primates have been shown to be associated with differences in emo- tional behavior and glucocorticoid responses to stress (e.g., Boyce and Ellis, 2005; Meyer, Chrousos, and Gold, 2001). Human genetic polymorphisms in the glucocorticoid receptor (GR) have been hypothesized as a source of impaired negative feedback regulation contributing to hyperactivity of the HPA-axis in depression (e.g., Holsboer, 2000). Evidence is emerging of GR polymorphisms associated with increased risk of developing major depres- sion (van Rossum et al., 2006) and differences in response to treatment for depression (e.g., Brouwer et al., 2006; van Rossum et al., 2006). Adverse environmental factors, especially those associated with early childhood development (or even prenatal exposure), have attracted consid- erable interest as possible contributors to abnormal biological stress regula- tion. Gold, Goodwin, and Chrousos (1988) speculated that brain circuits associated with stress reactions may have been sensitized as a result of early, acute exposure to stressors, so that in adulthood, depressive reactions to stress may be readily activated by even mild or symbolic representations of early stress precipitants. Evidence supports the impact of prenatal and postnatal stress, as well as disruptions of the parent-child bond, on abnor- malities of HPA functioning in animal and human subjects (reviewed in Heim and Nemeroff, 2001; Kaufman et al., 2000; Meyer, Chrousos, and Gold, 2001; Plotsky, Owens, and Nemeroff, 1998). Meaney, Szyf, and Seckl (2007) also propose epigenetic processes by which maternal adversities affect fetal development mediated by adrenal hormone activity, and gluco- corticoid levels program gene expression in the direction of impaired HPA function and health in offspring. While not specific to depression, the effects

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 THE ETIOLOGY OF DEPRESSION of environmental effects on gene expression in offspring have important implications for depression. Limited but increasing evidence draws links between early adversity, abnormalities of the HPA, CRH, and LC-NE systems, and depression. For example, Essex et al. (2002) assessed cortisol levels in 4.5-year-olds and found that children who had been exposed to maternal stress both in infancy and concurrently had significantly higher levels of cortisol than nonstressed children or those exposed to either but not both periods of ma- ternal stress. Moreover, the children with elevated cortisol had higher rates of behavioral and emotional symptoms (especially internalizing symptoms) approximately 2 years later. Although not specifically about depression, the results are consistent with the idea that early stress exposure predicts elevated cortisol when stress occurs later in life, and the pattern is predictive of later symptomatology (see also Heim et al., 2000, on early abuse expe- riences, depression, and adult HPA axis functioning). Preventing adverse environmental factors in children warrants further attention. Immune System Processes and Depression Spurred in part by the evidence of the strong association between de- pression and coronary heart disease, researchers have begun to examine the potential role of the immune system, and particularly proinflammatory cy- tokines, in the link between stress and depression (e.g., Danese et al., 2008; Miller and Blackwell, 2006). Recent models have proposed that chronic stress activates the immune system in a way that leads to inflammation, and that chronic inflammation in turn leads to symptoms of depression as well as pathological processes underlying heart disease (Miller and Blackwell, 2006). Cytokines are signaling molecules that coordinate inflammation in response to pathogens and include interleukin-1β, interleukin-6 (IL-6), and tumor necrosis factor-α. Among other functions, they direct white blood cells toward infections, signaling them to divide and activating their killing mechanisms. Downstream products of this process, including C-reactive protein (CRP), a molecule produced by the liver in response to IL-6, are used as an index of the inflammatory response. Although the directions of these effects are yet to be disentangled, evi- dence indicates that chronic stress is associated with increased levels of both CRP and depression. Levels of IL-6 and CRP are elevated in individuals exposed to chronic stress (Segerstrom and Miller, 2004). Chronic stressors may prime the immune system to make a heightened response to stress. Alternatively, chronic stress may interfere with the capacity of the immune system to return to baseline after termination of a stressor, perhaps due to dysregulation of the HPA response and the production of glucocorticoids in response to stress (Miller and Blackwell, 2006). The inflammatory re-

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0 DEPRESSION IN PARENTS, PARENTING, AND CHILDREN Gaynes, B.N., Magruder, K.M., Burns, B.J., Wagner, H.R., Yarnall, K.S.H., and Broadhead, W.E. (1999). Does a coexisting anxiety disorder predict persistence of depressive ill- ness in primary care patients with major depression? General Hospital Psychiatry, 2, 158–167. Ge, X., Lorenz, F.O., Conger, R.D., Elder, G.H., and Simons, R.L. (1994). Trajectories of stressful life events and depressive symptoms during adolescence. Developmental Psy- chology, 0, 467–483. Gee, G.C., Spencer, M., Chen, J., Yip, T., and Takeuchi, D.T. (2007). The association between self-reported racial discrimination and 12-month DSM-IV mental disorders among Asian Americans nationwide. Social Science and Medicine, , 1984–1996. Gerlsma, C., Emmelkamp, P.M.G., and Arrindell, W.A. (1990). Anxiety, depression, and per- ception of early parenting: A meta-analysis. Clinical Psychology Review, 0, 251–277. Gibb, B.E., Beevers, C.G., Andover, M.S., and Holleran, K. (2006). The hopelessness theory of depression: A prospective multi-wave test of the vulnerability-stress hypothesis. Cognitive Therapy and Research, 0, 763–772. Gibb, B.E., Butler, A.C., and Beck, J.S. (2003). Childhood abuse, depression, and anxiety in adult psychiatric outpatients. Depression and Anxiety, , 226–228. Gladstone, G.L., and Parker, G.B. (2006). Is behavioral inhibition a risk factor for depression? Journal of Affective Disorders, 9, 85–94. Goering, J., Kraft, J., Feins, J., McInnis, D., Holin, M.J., and Elhassan, H. (1999). Moving to Opportunity for Fair Housing Demonstration Program: Current Status and Initial Findings (accession no. ). Washington, DC: HUD USER. Gold, P.W., Goodwin, F.K., and Chrousos, G.P. (1988). Clinical and biochemical manifesta- tions of depression: Relation to the neurobiology of stress. New England Journal of Medicine, 9, 348–353. Golding, J.M. (1999). Intimate partner violence as a risk factor for mental disorders: A meta- analysis. Journal of Family Violence, , 99–132. Goodman, S.H. (2007). Depression in mothers. Annual Review of Clinical Psychology, , 107–135. Goodman, S.H., and Gotlib, I.H. (1999). Risk for psychopathology in the children of de- pressed mothers: A developmental model for understanding mechanisms of transmission. Psychological Review, 0, 458–490. Grigoriadis, S., and Romans, S. (2006). Postpartum psychiatric disorders: What do we know and where do we go? Current Psychiatry Reviews, 2, 151–158. Gross, D., Fogg, L., Young, M., Ridge, A., Cowell, J., Richardson, R., and Sivan, A. (2006). The equivalence of the Child Behavior Checklist/1½–5 across parent race/ethnicity, in- come level, and language. Psychological Assessment, , 313–323. Gross, J.J. (2001). Emotion regulation in adulthood: Timing is everything. Current Directions in Psychological Science, 0, 214–219. Hammen, C. (1991a). Depression Runs in Families: The Social Context of Risk and Resilience in Children of Depressed Mothers. New York: Springer-Verlag. Hammen, C. (1991b). Generation of stress in the course of unipolar depression. Journal of Abnormal Psychology, 00, 555–561. Hammen, C. (2005). Stress and depression. Annual Review of Clinical Psychology, , 293–319. Hammen, C. (2006). Stress generation in depression: Reflections on origins, research, and future directions. Journal of Clinical Psychology, 2, 1065–1082. Hammen, C., and Brennan, P.A. (2002). Interpersonal dysfunction in depressed women: Impairments independent of depressive symptoms. Journal of Affective Disorders, 2, 145–156.

OCR for page 73
09 THE ETIOLOGY OF DEPRESSION Hammen, C., Brennan, P., and Keenan-Miller, D. (2008). Patterns of adolescent depression to age 20: The role of maternal depression and youth interpersonal dysfunction. Journal of Abnormal Child Psychology, , 1189–1198. Hammen, C., Henry, R., and Daley, S.E. (2000). Depression and sensitization to stressors among young women as a function of childhood adversity. Journal of Consulting and Clinical Psychology, , 782–787. Hankin, B.L., and Abramson, L.Y. (2001). Development of gender differences in depression: An elaborated cognitive vulnerability-transactional stress theory. Psychological Bulletin, 2, 773–796. Hankin, B.L., Abramson, L.Y., Miller, N., and Haeffel, G.J. (2004). Cognitive vulnerability- stress theories of depression: Examining affective specificity in the prediction of depres- sion versus anxiety in three prospective studies. Cognitive Therapy and Research, 2, 309–345. Hariri, A.R., Drabant, E.M., Munoz, K.E., Kolachana, B.S., Mattay, V.S., Egan, M.F., and Weinberger, D.R. (2005). A susceptibility gene for affective disorders and the response of the human amygdala. Archives of General Psychiatry, 2, 146–152. Harkness, K.L., Bruce, A.E., and Lumley, M.N. (2006). The role of childhood abuse and neglect in the sensitization to stressful life events in adolescent depression. Journal of Abnormal Psychology, , 730–741. Harrington, R., Fudge, H., Rutter, M., Pickles, A., and Hill, J. (1990). Adult outcomes of childhood and adolescent depression: I. Psychiatric status. Archives of General Psychia- try, , 465–473. Hasin, D.S., Goodwin, R.D., Stinson, F.S., and Grant, B.F. (2005). Epidemiology of major depressive disorder: Results from the national epidemiologic survey on alcoholism and related conditions. Archives of General Psychiatry, 2, 1097–1106. Hayes, M., Roberts, S., and Davare, A. (2000). Transactional conflict between psychobiology and culture in the etiology of postpartum depression. Medical Hypotheses, , 7–17. Heilemann, M.V., Coffey-Love, M., and Frutos, L. (2004). Perceived reasons for depression among low income women of Mexican descent. Archives of Psychiatric Nursing, , 185–192. Heim, C., and Nemeroff, C.B. (2001). The role of childhood trauma in the neurobiology of mood and anxiety disorders: Preclinical and clinical studies. Biological Psychiatry, 9, 1023–1039. Heim, C., Newport, D.J., Heit, S., Graham, Y.P., Wilcox, M., Bonsall, R., Miller, A.H., and Nemeroff, C.B. (2000). Pituitary-adrenal and autonomic responses to stress in women after sexual and physical abuse in childhood. Journal of the American Medical Associa- tion, 2, 592–597. Hiott, A., Grzywacz, J., Arcury, T., and Quandt, S. (2006). Gender differences in anxiety and depression among immigrant Latinos. Families, Systems and Health, 2, 137–146. Hollon, S.D., Shelton, R.C., Wisniewski, S., Warden, D., Biggs, M.M., Friedman, E.S., Husain, M., Kupfer, D.J., Nierenberg, A.A., Petersen, T.J., Shores-Wilson, K., and Rush, A.J. (2006). Presenting characteristics of depressed outpatients as a function of recurrence: Preliminary findings from the STAR*D clinical trial. Journal of Psychiatric Research, 0, 59–69. Holmans, P., Weissman, M.M., Zubenko, G.S., Scheftner, W.A., Crowe, R.R., DePaulo, J.R., Jr., Knowles, J.A., Zubenko, W.N., Murphy-Eberenz, K., Marta, D.H., Boutelle, S., McInnis, M.G., Adams, P., Gladis, M., Steele, J., Miller, E.B., Potash, J.B., MacKinnon, D.F., and Levinson, D.F. (2007). Genetics of recurrent early-onset major depression (GenRED): Final genome scan report. American Journal of Psychiatry, , 248–258.

OCR for page 73
0 DEPRESSION IN PARENTS, PARENTING, AND CHILDREN Holmes, S.J., and Robins, L.N. (1987). The influence of childhood disciplinary experience on the development of alcoholism and depression. Journal of Child Psychology and Psychiatry, 2, 399–415. Holmes, S.J., and Robins, L.N. (1988). The role of parental disciplinary practices in the devel- opment of depression and alcoholism. Psychiatry: Journal for the Study of Interpersonal Processes, , 24–36. Holsboer, F. (2000). The corticosteroid receptor hypothesis of depression. Neuropsychophar- macology, 2, 477–501. Howren, M., Lamkin, D., and Suls, J. (2009). Associations of depression with C-reactive protein, IL-1, and IL-6: A meta-analysis. Psychosomatic Medicine, , 171–186. Huang, C.C., and Warner, L.A. (2005). Relationship characteristics and depression among fathers with newborns. Social Service Review, 9, 95–118. Hughes, M.E., Waite, L., LaPierre, T., and Luo, Y. (2007). All in the family: The impact of caring for grandchildren on grandparents’ health. Journal of Gerontology, 2B, S108– S119. Jaser, S.S., Langrock, A.M., Keller, G., Merchant, M.J., Benson, M., Reeslund, K., Champion, J.E., and Compas, B.E. (2005). Coping with the stress of parental depression II: Adoles- cent and parent reports of coping and adjustment. Journal of Clinical Child and Adoles- cent Psychology, , 193–205. Joorman, J. (2008). Cognitive aspects of depression. In I. Gotlib and C. Hammen (Eds.), Handbook of Depression (2nd ed., pp. 298–321). New York: Guilford Press. Judd, L.L. (1997). The clinical course of unipolar major depressive disorders. Archives of General Psychiatry, , 989–991. Judd, L.L., Akiskal, H.S., Maser, J.D., Zeller, P.J., Endicott, J., Coryell, W., Paulus, M.P., Kunovac, J.L., Leon, A.C., Mueller, T.I., Rice, J.A., and Keller, M.B. (1998). A prospec- tive 12-year study of subsyndromal and syndromal depressive symptoms in unipolar major depressive disorders. Archives of General Psychiatry, , 694–700. Katon, W. (2003). Clinical and health services relationships between major depression, depres- sive symptoms, and general medical illness. Biological Psychiatry, , 216–226. Kaufman, J., Plotsky, P.M., Nemeroff, C.B., and Charney, D.S. (2000). Effects of early adverse experiences on brain structure and function: Clinical implications. Biological Psychiatry, , 778–790. Keller, M.B. (1985). Chronic and recurrent affective disorders: Incidence, course, and influenc- ing factors. In D. Kemali and G. Recagni (Eds.), Chronic Treatments in Neuropsychiatry (pp. 111–120). New York: Raven Press. Kendler, K.S., and Karkowski-Shuman, L. (1997). Stressful life events and genetic liability to major depression: Genetic control of exposure to the environment? Psychological Medicine, 2, 539–547. Kendler, K.S., Bulik, C., Silberg, J., Hettema, J., Myers, J., and Prescott, C. (2000). Childhood sexual abuse and adult psychiatric and substance use disorders in women: An epidemio- logical and co-twin control analysis. Archives of General Psychiatry, , 953–959. Kendler, K.S., Gardner, C.O., and Lichtenstein, P. (2008). A developmental twin study of symptoms of anxiety and depression: Evidence for genetic innovation and attenuation. Psychological Medicine, 0, 1–9 [E pub]. Kendler, K.S., Gardner, C.O., and Prescott, C.A. (2002). Toward a comprehensive develop- mental model for major depression in women. American Journal of Psychiatry, 9, 1133–1145. Kendler, K.S., Gardner, C.O., and Prescott, C.A. (2003). Personality and the experience of environmental adversity. Psychological Medicine, , 1193–1202. Kendler, K.S., Gardner, C.O., and Prescott, C.A. (2006). Toward a comprehensive devel- opmental model for major depression in men. American Journal of Psychiatry, , 115–124.

OCR for page 73
 THE ETIOLOGY OF DEPRESSION Kendler, K.S., Gardner, C.O., Gatz, M., and Pedersen, N.L. (2007). The sources of comorbid- ity between major depression and generalized anxiety disorder in a Swedish national twin sample. Psychological Medicine, , 453–462. Kendler, K.S., Gardner, C.O., Neale, M.C., and Prescott, C.A. (2001). Genetic risk factors for major depression in men and women: Similar or different heritabilities and same or partly distinct genes? Psychological Medicine, , 605–616. Kendler, K.S., Gatz, M., Gardner, C., and Pedersen, N. (2006). A Swedish National Twin Study of Lifetime Major Depression. American Journal of Psychiatry, , 109–114. Kendler, K.S., Karkowski, L.M., and Prescott, C.A. (1998). Stressful life events and major depression: Risk period, long-term contextual threat, and diagnostic specificity. Journal of Nervous and Mental Disease, , 661–669. Kendler, K.S., Karkowski, L.M., and Prescott, C.A. (1999). Causal relationship between stressful life events and the onset of major depression. American Journal of Psychiatry, , 837–841. Kendler, K.S., Kessler, R.C., Walters, E.E., MacLean, C., Neale, M.C., Heath, A.C., and Eaves, L.J. (1995). Stressful life events, genetic liability, and onset of an episode of major depres- sion in women. American Journal of Psychiatry, 2, 833–842. Kendler, K.S., Kuhn, J., and Prescott, C.A. (2004). The interrelationship of neuroticism, sex, and stressful life events in the prediction of episodes of major depression. American Journal of Psychiatry, , 631–636. Kendler, K.S., Kuhn, J.W., Vittum, J., Prescott, C.A., and Riley, B. (2005). The interaction of stressful life events and a serotonin transporter polymorphism in the prediction of epi- sodes of major depression: A replication. Archives of General Psychiatry, 2, 529–535. Kendler, K.S., Thornton, L.M., and Gardner, C.O. (2000). Stressful life events and previous episodes in the etiology of major depression in women: An evaluation of the “kindling” hypothesis. American Journal of Psychiatry, , 1243–1251. Kendler, K.S., Thornton, L.M., and Gardner, C.O. (2001). Genetic risk, number of previous depressive episodes, and stressful life events in predicting onset of major depression. American Journal of Psychiatry, , 582–586. Kendler, K.S., Thornton, L.M., and Prescott, C.A. (2001). Gender differences in the rates of exposure to stressful life events and sensitivity to their depressogenic effects. American Journal of Psychiatry, , 587–593. Kessing, L.V., Hansen, M.G., Andersen, P.K., and Angst, J. (2004). The predictive effect of episodes on the risk of recurrence in depressive and bipolar disorders: A lifelong perspec- tive. Acta Psychiatrica Scandinavica, 09, 339–344. Kessler, R.C. (1997). The effects of stressful life events on depression. Annual Review of Psychology, , 191–214. Kessler, R.C., and Magee, W.J. (1993). Childhood adversities and adult depression: Basic pat- terns of association in a US national survey. Psychological Medicine, 2, 679–690. Kessler, R.C., and Walters, E.E. (1998). Epidemiology of DSM-III-R major depression and minor depression among adolescents and young adults in the National Comorbidity Survey. Depression and Anxiety, , 3–14. Kessler, R.C., Berglund, P., Demler, O., Jin, R., Koretz, D., Merikangas, K.R., Rush, A.J., Walters, E.E., and Wang, P.S. (2003). The epidemiology of major depressive disorder: Results from the National Comorbidity Survey Replication (NCS-R). Journal of the American Medical Association, 29, 3095–3105. Kessler, R.C., Berglund, P., Demler, O., Jin, R., Merikangas, K.R., and Walters, E.E. (2005). Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Archives of General Psychiatry, 2, 593–602. Kessler, R.C., Davis, C.G., and Kendler, K.S. (1997). Childhood adversity and adult psychi- atric disorder in the U.S. National Comorbidity Survey. Psychological Medicine, 2, 1101–1119.

OCR for page 73
2 DEPRESSION IN PARENTS, PARENTING, AND CHILDREN Kessler, R.C., Nelson, C.B., McGonagle, K.A., Liu, J., Swartz, M., and Blazer, D.G. (1996). Comorbidity of DSM-III-R major depressive disorder in the general population: Results from the U.S. National Comorbidity Survey. British Journal of Psychiatry, (Suppl.), 17–30. Kim, P., and Swain, J.E. (2007). Sad dads: Paternal postpartum depression. Psychiatry, , 36–47. Klein, D.N. (2003). Patients’ versus informants’ reports of personality disorders in predicting 7½-year outcome in outpatients with depressive disorders. Psychological Assessment, , 216–222. Klein, D.N., and Shih, J.H. (1998). Depressive personality: Associations with DSM-III-R mood and personality disorders and negative and positive affectivity, 30-month stability, and prediction of course of Axis I depressive disorders. Journal of Abnormal Psychology, 0, 319–327. Klein, D.N., Shankman, S.A., and Rose, S. (2006). Ten-year prospective follow-up study of the naturalistic course of dysthymic disorder and double depression. American Journal of Psychiatry, , 872–880. Klein, D.N., Shankman, S.A., Lewinsohn, P.M., Rohde, P., and Seeley, J.R. (2004). Family study of chronic depression in a community sample of young adults. American Journal of Psychiatry, , 646–653. Kobak, R., Sudler, N., and Gamble, W. (1991). Attachment and depressive symptoms during adolescence: A developmental pathways analysis. Development and Psychopathology, , 461–474. Kwak, K. (2003). Adolescents and their parents: A review of intergenerational family relations for immigrant and non-immigrant families. Human Development, , 115–136. Lau, J.Y.F., Rijsdijk, F., and Eley, T.C. (2006). I think, therefore I am: A twin study of attribu- tional style in adolescents. Journal of Child Psychology and Psychiatry, , 696–703. Lewinsohn, P.M., Rohde, P., and Seeley, J.R. (1998). Major depressive disorder in older ado- lescents: Prevalence, risk factors, and clinical implications. Clinical Psychology Review, , 765–794. Lewinsohn, P.M., Rohde, P., Klein, D.M., and Seeley, J.R. (1999). Natural course of adolescent major depressive disorder: I. Continuity into young adulthood. Journal of the American Academy of Child and Adolescent Psychiatry, , 56–63. Lewinsohn, P.M., Rohde, P., Seeley, J.R., Klein, D.N., and Gotlib, I.H. (2000). Natural course of adolescent major depressive disorder in a community sample: Predictors of recurrence in young adults. American Journal of Psychiatry, , 1584–1591. Lizardi, H., Klein, D.N., Ouimette, P.C., Riso, L.P., Anderson, R.L., and Donaldson, S.K. (1995). Reports of the childhood home environment in early-onset dysthymia and epi- sodic major depression. Journal of Abnormal Psychology, 0, 132–139. Lovejoy, C.M., Graczyk, P.A., O’Hare, E., and Neuman, G. (2000). Maternal depression and parenting behavior: A meta-analytic review. Clinical Psychology Review, 20, 561–592. Lucki, I. (1998). The spectrum of behaviors influenced by serotonin. Biological Psychiatry, , 151–162. Maciejewski, P.K., Prigerson, H.G., and Mazure, C.M. (2001). Sex differences in event-related risk for major depression. Psychological Medicine, , 593–604. MacMillan, H.L., Fleming, J.E., Streiner, D.L., Lin, E., Boyle, M.H., Jamieson, E., Duku, E.K., Walsh, C.A., Wong, M.Y.-Y., Beardslee, W.R. (2001). Childhood abuse and life- time psychopathology in a community sample. American Journal of Psychiatry, , 1878–1883. Malik, N., Boris, N., Heller, S., Harden, B., Squires J., Chazan-Cohen, R., Beeber, L.S., Kaczynski, K.J. (2007). Risk for maternal depression and child aggression in Early Head Start families: A test of ecological models. Infant Mental Health Journal, 2, 171–191.

OCR for page 73
 THE ETIOLOGY OF DEPRESSION Masten, A. (2007). Resilience in developing systems: Progress and promise as the fourth wave rises. Development and Psychopathology, 9, 921–930. Mathews, A., and MacLeod, C. (2005). Cognitive vulnerability to emotional disorders. Annual Review of Clinical Psychology, , 167–195. Mathews, C.A., and Reus, V.I. (2001). Assortative mating in the affective disorders: A system- atic review and meta-analysis. Comprehensive Psychiatry, 2, 257–262. Mazure, C.M. (1998). Life stressors as risk factors in depression. Clinical Psychology: Science and Practice, , 291–313. McGonagle, K.A., and Kessler, R.C. (1990). Chronic stress, acute stress, and depressive symp- toms. American Journal of Community Psychology, , 681–706. McGuffin, P., Rijsdijk, F., Andrew, M., Sham, P., Katz, R., and Cardno, A. (2003). The heri- tability of bipolar affective disorder and the genetic relationship to unipolar depression. Archives of General Psychiatry, 0, 497–502. McGuire, S., Manke, B., Saudino, K.J., Reiss, D., Hetherington, E.M., and Plomin, R. (1999). Perceived competence and self-worth during adolescence: A longitudinal behavioral ge- netic study. Child Development, 0, 1283–1296. Meany, M.J., Szyf, M., and Seckl, J.R. (2007). Epigenetic mechanisms of perinatal program- ming of hypothalamic-pituitary-adrenal function and health. Trends in Molecular Medi- cine, , 269–277. Melartin, T.K., Rytsala, H.J., Leskela, U.S., Lestela-Mielonen, P.S., Sokero, T.P., and Isometsa, E.T. (2002). Current comorbidity of psychiatric disorders among DSM-IV major depres- sive disorder patients in psychiatric care in the Vantaa Depression Study. Journal of Clinical Psychiatry, , 126–134. Meyer, S.E., Chrousos, G.P., and Gold, P.W. (2001). Major depression and the stress system: A life span perspective. Development and Psychopathology, , 565–580. Miller, G.E., and Blackwell, E. (2006). Turning up the heat: Inflammation as a mechanism linking chronic stress, depression, and heart disease. Current Directions in Psychological Science, , 269–272. Mineka, S., Watson, D., and Clark, L.A. (1998). Comorbidity of anxiety and unipolar mood disorders. Annual Review of Psychology, 9, 377–412. Moffitt, T.E., Harrington, H., Caspi, A., Kim-Cohen, J., Goldberg, D., Gregory, A.M., and Poulton, R. (2007). Depression and generalized anxiety disorder: Cumulative and se- quential comorbidity in a birth cohort followed prospectivity to age 32 years. Archives of General Psychiatry, , 651–660. Monroe, S.M., and Harkness, K.L. (2005). Life stress, the “kindling” hypothesis, and the recurrence of depression: Considerations from a life stress perspective. Psychological Review, 2, 417–445. Muntaner, C., Eaton, W.W., Miech, R., and O’Campo, P. (2004). Socioeconomic position and major mental disorders. Epidemiologic Reviews, 2, 53–62. Musselman, D.L., Betan, E., Larsen, H., and Phillips, L.S. (2003). Relationship of depression to diabetes types 1 and 2: Epidemiology, biology, and treatment. Biological Psychiatry, , 317–329. Neiderhiser, J.M., and McGuire, S. (1994). Competence during middle childhood. In J.C. DeFries, R. Plomin, and D.W. Fulker (Eds.), Nature and Nurture During Middle Child- hood (pp. 141–151). Malden, MA: Blackwell. Neiss, M.B., Sedikides, C., and Stevenson, J. (2006). Genetic influences on level and stability of self-esteem. Self and Identity, , 247–266. Neumeister, A., Young, T., and Stastny, J. (2004). Implications of genetic research on the role of the serotonin in depression: Emphasis on the serotonin type 1A receptor and the serotonin transporter. Psychopharmacology, , 512–524.

OCR for page 73
 DEPRESSION IN PARENTS, PARENTING, AND CHILDREN Newton-Howes, G., Tyrer, P., and Johnson, T. (2006). Personality disorder and the outcome of depression: Meta-analysis of published studies. British Journal of Psychiatry, , 13–20. Nolen-Hoeksema, S. (1991). Responses to depression and their effects on the duration of depressive episodes. Journal of Abnormal Psychology, 00, 569–582. Nolen-Hoeksema, S. (2000). The role of rumination in depressive disorders and mixed anxi- ety/depressive symptoms. Journal of Abnormal Psychology, 09, 504–511. Nolen-Hoeksema, S., and Girgus, J.S. (1994). The emergence of gender differences in depres- sion during adolescence. Psychological Bulletin, , 424–443. Nolen-Hoeksema, S., Morrow, J., and Fredrickson, B.L. (1993). Response styles and the dura- tion of episodes of depressed mood. Journal of Abnormal Psychology, 02, 20–28. O’Campo, P., and Yonas, M. (2005). Health of economically deprived populations in cities. In S. Galea and D. Vlahov (Eds.), Handbook of Urban Health: Populations, Methods, and Practice (pp. 43–61). New York: Springer Science and Business Media Publishers. O’Campo, P., Ahmad, F., and Cyriac, A. (2008). Chapter 12: Role of healthcare profession- als in preventing and intervening on IPV. In J. Keeling and T. Mason (Eds.), Domestic Violence: A Multi-professional Approach for Health Professionals (pp. 107–115). Maid- enhead, UK: Open University Press. O’Campo, P., Salmon, C., and Burke, C. (2009). Neighbourhoods and mental well-being: What are the pathways? Health and Place, , 56–68. Panzarine, S., Slater, E., and Sharps, P. (1995). Coping, social support, and depression symp- toms in adolescent mothers. Journal of Adolescent Health, , 113–119. Parker, G., and Gladstone, G.L. (1996). Parental characteristics as influences on adjustment in adulthood. In G.R. Pierce, B.R. Sarason, and I.G. Sarason (Eds.), Handbook of Social Support and the Family (pp. 195–218). New York: Plenum Press. Paulson, J., Dauber, S., and Leiferman, J. (2006). Individual and combined effects of post- partum depression in mothers and fathers on parenting behavior. Pediatrics, , 659–668. Phinney, J.S., Ong, A., and Madden, T. (2000). Cultural values and intergenerational value dis- crepancies in immigrant and nonimmigrant families, Child Development, , 528–539. Pinderhughes, E.E., Dodge, K.A., Bates, J.E., Pettit, G.S., and Zelli, A. (2000). Discipline responses: Influences of parents’ socioeconomic status, ethnicity, beliefs about parenting, stress, and cognitive-emotional processes, Journal of Family Psychology, , 380–400. Pine, D.S., Cohen, P., Gurley, D., Brook, J., and Ma, Y. (1998). The risk for early-adulthood anxiety and depressive disorders in adolescents with anxiety and depressive disorders. Archives of General Psychiatry, , 56–64. Plotsky, P.M., Owens, M.J., and Nemeroff, C.B. (1998). Psychoneuroendocrinology of de- pression: Hypothalamic-pituitary-adrenal axis. Pediatric Clinics of North America, 2, 293–307. Post, R.M. (1992). Transduction of psychosocial stress into the neurobiology of recurrent affective disorder. American Journal of Psychiatry, 9, 999–1010. Rajaratnam, J.K., O’Campo, P., Caughy, M.O., and Muntaner C. (2008). The effect of social isolation on depressive symptoms varies by neighborhood characteristics: A study of an urban sample of women with preschool aged children. International Journal of Mental Health and Addiction, , 464–475. Rao, U., Hammen, C., and Daley, S.E. (1999). Continuity of depression during the transition to adulthood: A 5-year longitudinal study of young women. Journal of the American Academy of Child and Adolescent Psychiatry, , 908–915. Reid, V., and Meadows-Oliver, N. (2007). Postpartum depression in adolescent mothers: An integrative review of the literature. Journal of Pediatric Health Care, 2, 289–298.

OCR for page 73
 THE ETIOLOGY OF DEPRESSION Ribeiro, S.C.M., Tandon, R., Grunhaus, L., and Greden, J.F. (1993). The DST as a predic- tor of outcome in depression: A meta-analysis. American Journal of Psychiatry, 0, 1618–1629. Rice, F., Harold, G.T., and Thapar, A. (2005). The link between depression in mothers and offspring: An extended twin analysis. Behavior Genetics, , 565–577. Riso, L.P., Miyatake, R.K., and Thase, M.E. (2002). The search for determinants of chronic depression: A review of six factors. Journal of Affective Disorders, 0, 103–115. Robbins, T.W. (2005). Controlling stress: How the brain protects itself from stress. Nature Neuroscience, , 261–262. Robertson, E., Grace, S., Wallington, T., and Stewart, D.E. (2004). Antenatal risk factors for postpartum depression: A synthesis of recent literature. General Hospital Psychiatry, 2, 289–295. Rohde, P., Lewinsohn, P.M., and Seeley, J.R. (1991). Comorbidity of unipolar depression: II. Comorbidity with other mental disorders in adolescents and adults. Journal of Abnormal Psychology, 00, 214–222. Rossi, A., Marinangeli, M.G., Butti, G., Scinto, A., Di Cicco, L., Kalyvoka, A., and Petruzzi, C. (2001). Personality disorders in bipolar and depressive disorders. Journal of Affective Disorders, , 3–8. Rudolph, K.D. (2002). Gender differences in emotional responses to interpersonal stress dur- ing adolescence. Journal of Adolescent Health, 0(Suppl. 1), 3–13. Rudolph, K.D., and Hammen, C. (1999). Age and gender as determinants of stress exposure, generation, and reactions in youngsters: A transactional perspective. Child Development, 0, 660–677. Rugulies, R. (2002). Depression as a predictor for coronary heart disease: A review and meta- analysis. American Journal of Preventive Medicine, 2, 51–61. Rush, A.J., Zimmerman, M., Wisniewski, S.R., Fava, M., Hollon, S.D., Warden, D., Biggs, M.M., Shores-Wilson, K., Shelton, R.C., Luther, J.F., Thomas, B., and Trivedi, M.H. (2005). Comorbid psychiatric disorders in depressed outpatients: Demographic and clini- cal features. Journal of Affective Disorders, , 43–55. Sanderson, W.C., Beck, A.T., and Beck, J.S. (1990). Syndrome comorbidity in patients with major depression or dysthymia: Prevalence and temporal relationships. American Journal of Psychiatry, , 1025–1028. Santor, D.A., Bagby, R.M., and Joffe, R.T. (1997). Evaluating stability and change in personal- ity and depression. Journal of Personality and Social Psychology, , 1354–1362. Sapolsky, R.M. (1996). Why stress is bad for your brain. Science, 2, 749–750. Scher, C.D., Ingram, R.E., and Segal, Z.V. (2005). Cognitive reactivity and vulnerability: Em- pirical evaluation of construct activation and cognitive diatheses in unipolar depression. Clinical Psychology Review, 2, 487–510. Schmitz, N., Kugler, J., and Rollnik, J. (2003). On the relation between neuroticism, self- esteem, and depression: Results from the National Comorbidity Survey. Comprehensive Psychiatry, , 169–176. Segerstrom, S.C., and Miller, G.E. (2004). Psychological stress and the human immune system: A meta-analytic study of 30 years of inquiry. Psychological Bulletin, 0, 601–630. Segre, L., O’Hara, M., Arndt, S., and Stuart, S. (2007). The prevalence of postpartum depres- sion. Social Psychiatry and Psychiatric Epidemiology, 2, 316–321. Seligman, M.E.P., Reivich, K., Jaycox, L., and Gillham, J. (1995). The Optimistic Child. New York: Houghton Mifflin. Shankman, S.A., and Klein, D.N. (2002). The impact of comorbid anxiety disorders on the course of dysthymic disorder: A 5-year prospective longitudinal study. Journal of Affec- tive Disorders, 0, 211–217.

OCR for page 73
 DEPRESSION IN PARENTS, PARENTING, AND CHILDREN Shattell, M.M., Smith, K.M., Quinlan-Colwell, A., and Villalba, J.A. (2008). Factors contrib- uting to depression in Latinas of Mexican origin residing in the United States: Implica- tions for nurses. Journal of the American Psychiatric Nurses Association, , 193–204. Shea, M.T., Pilkonis, P.A., Beckham, E., Collins, J.F., Elkin, I., Sotsky, S.M., and Docherty, J.P. (1990). Personality disorders and treatment outcome in the NIMH treatment of depres- sion collaborative research program. American Journal of Psychiatry, , 711–718. Shea, M.T., Widiger, T.A., and Klein, M.H. (1992). Comorbidity of personality disorders and depression: Implications for treatment. Journal of Consulting and Clinical Psychology, 0, 857–868. Sherbourne, C.D., Hays, R.D., and Wells, K.B. (1995). Personal and psychosocial risk factors for physical and mental health outcomes and course of depression among depressed patients. Journal of Consulting and Clinical Psychology, , 345–355. Shih, J.H., Eberhard, N.K., Hammen, C., and Brennan, P.A. (2006). Differential exposure and reactivity to interpersonal stress predict sex differences in adolescent depression. Journal of Clinical Child and Adolescent Psychology, , 103–115. Silberg, J.L., Rutter, M., and Eaves, L. (2001). Genetic and environmental influences on the temporal association between earlier anxiety and later depression in girls. Biological Psychiatry, 9, 1040–1049. Singer, G.H.S. (2006). Meta-analysis of comparative studies of depression in mothers of children with and without developmental disabilities. American Journal on Mental Re- tardation, , 155–169. Solomon, D.A., Keller, M.B., Leon, A.C., Mueller, T.I., Lavori, P.W., Shea, M.T., Coryell, W., Warshaw, M., Turvey, C., Maser, J.D., and Endicott, J. (2000). Multiple recurrences of major depressive disorder. American Journal of Psychiatry, , 229–233. Southwick, S.M., Vythilingham, M., and Charney, D.S. (2005). The psychobiology of depres- sion and resilience to stress: Implications for prevention and treatment. Annual Review of Clinical Psychology, , 255–291. Spangler, D.L., Simons, A.D., Monroe, S.M., and Thase, M.E. (1996). Gender differences in cognitive diathesis-stress domain match: Implications for differential pathways to depres- sion. Journal of Abnormal Psychology, 0, 653–657. Stein, M.B., Fuetsch, M., Muller, N., Hofler, M., Lieb, R., and Wittchen, H.-U. (2001). Social anxiety disorder and the risk of depression: A prospective community study of adoles- cents and young adults. Archives of General Psychiatry, , 251–256. Sullivan, P.F., Kendler, K.S., and Neale, M.C. (2003). Schizophrenia as a complex trait: Evidence from a meta-analysis of twin studies. Archives General Psychiatry, 0, 1187–1192. Sullivan, P.F., Neale, M.C., and Kendler, K.S. (2000). Genetic epidemiology of major depres- sion: Review and meta-analysis. American Journal of Psychiatry, , 1552–1562. Suls, J., and Bunde, J. (2005). Anger, anxiety, and depression as risk factors for cardiovascular disease: The problems and implications of overlapping affective dispositions. Psychologi- cal Bulletin, , 260–300. Swendsen, J.D., and Merikangas, K.R. (2000). The comorbidity of depression and substance use disorders. Clinical Psychology Review, 20, 173–189. Targosz, S., Bebbington, P., Lewis, G., Brugha, T., Jenkins, R., Farrell, M., and Meltzer, H. (2003). Lone mothers, social exclusion and depression. Psychological Medicine, , 715–722. Tennant, C. (2002). Life events, stress and depression: A review of the findings. Australian and New Zealand Journal of Psychiatry, , 173–182. Thase, M. (2008). Neurobiological aspects of depression. In I. Gotlib and C. Hammen (Eds.), Handbook of Depression (2nd ed., pp. 187–217). New York: Guilford Press. Tse, W.S., and Bond, A.J. (2004). The impact of depression on social skills. Journal of Nervous and Mental Disease, 92, 260–268.

OCR for page 73
 THE ETIOLOGY OF DEPRESSION Uher, R., and McGuffin, P. (2008). The moderation by the serotonin transporter gene of environmental adversity in the aetiology of mental illness: Review and methodological analysis. Molecular Psychiatry, , 131–146. Van Os, J., and Jones, P.B. (1999). Early risk factors and adult person-environment relation- ships in affective disorder. Psychological Medicine, 29, 1055–1067. Van Rossum, E.F.C., Binder, E.B., Majer, M., Koper, J.W., Ising, M., Modell, S., Salyakina, D., Lamberts, S.W., and Holsboer, F. (2006). Polymorphisms of the glucocorticoid receptor gene and major depression. Biological Psychiatry, 9, 681–688. Van Voorhees, B.W., Walters, A.E., Prochaska, M., and Quinn, M.T. (2007). Reducing health disparities in depressive disorders outcomes between non-Hispanic whites and ethnic minorities: A call for pragmatic strategies over the life course. Medical Care Research and Review, , 157S–194S. Vesga-Lopez, O., Blanco, C., Keyes, K., Olfson, M., Grant, B.F., and Hasin, D.S. (2008). Psychiatric disorders in pregnant and postpartum women in the United States. Archives of General Psychiatry, , 805–815. Wade, T.D., and Kendler, K.S. (2000). Absence of interactions between social support and stressful life events in the prediction of major depression and depressive symptomatology in women. Psychological Medicine, 0, 965–974. Wang, J.L. (2004). The difference between single and married mothers in the 12-month prevalence of major depressive syndrome, associated factors and mental health service utilization. Social Psychiatry and Psychiatric Epidemiology, 9, 26–32. Watson, D., and Clark, L.A. (1984). Negative affectivity: The disposition to experience aver- sive emotional states. Psychological Bulletin, 9, 465–490. Weedon, M.N., Lango, H., Lindgren, C.M., Wallace, C., Evans, D.M., Mangino, M., Freathy, R.M., Perry, J.R., Stevens, S., Hall, A.S., Samani, N.J., Shields, B., Prokopenko, I., Farrall, M., Dominiczak, A., Johnson, T., Bergmann, S., Beckmann, J.S., Vollenweider, P., Waterworth, D.M., Mooser, V., Palmer, C.N., Morris, A.D., Ouwehand, W.H., Zhao, J.H., Li, S., Loos, R.J., Barroso, I., Deloukas, P., Sandhu, M.S., Wheeler, E., Soranzo, N., Inouye, M., Wareham, N.J., Caulfield, M., Munroe, P.B., Hattersley, A.T., McCarthy, M.I., and Frayling, T.M. (2008). Genome-wide association analysis identifies 20 loci that influence adult height. Nature Genetics, 0, 575–583. Weissman, M.M., Wolk, S., Goldstein, R.B., Moreau, D., Adams, P., Greenwald, S., Klier, C.M., Ryan, N.D., Dahl, R.E., and Wickramaratne, P. (1999a). Depressed adolescents grown up. Journal of the American Medical Association, 2, 1707–1713. Weissman, M.M., Wolk, S., Wickramaratne, P., Goldstein, R.B., Adams, P., Greenwald, S., Ryan, N.D., Dahl, R.E., and Steinberg, D. (1999b). Children with prepubertal-onset major depressive disorder and anxiety grown up. Archives of General Psychiatry, , 794–801. Whisman, M.A. (2001). The association between depression and marital dissatisfaction. In S.R.H. Beach (Ed.), Marital and Family Processes in Depression: A Scientific Foundation for Clinical Practice (pp. 3–24). Washington, DC: American Psychological Association. Whisman, M.A., and Bruce, M.L. (1999). Marital dissatisfaction and incidence of major depressive episode in a community sample. Journal of Abnormal Psychology, 0, 674–678. Whisman, M.A., Uebelacker, L.A., and Weinstock, L.M. (2004). Psychopathology and mari- tal satisfaction: The importance of evaluating both partners. Journal of Consulting and Clinical Psychology, 2, 830–838. Yates, W., Mitchell, J., Rush, A.J., Trivedi, M.H., Wisniewski, S.R., Warden, D., Hauger, R.B., Fava, M., Gaynes, B.N., Husain, M.M., and Bryan, C. (2004). Clinical features of depressed outpatients with and without co-occurring general medical conditions in the STAR*D. General Hospital Psychiatry, 2, 421–429.

OCR for page 73
 DEPRESSION IN PARENTS, PARENTING, AND CHILDREN Zammit, S., and Owen M.J. (2006). Stressful life events, 5-HTT genotype and risk of depres- sion. British Journal of Psychiatry, , 199–201. Zimmerman, M., Chelminski, I., and McDermut, W. (2002). Major depressive disorder and axis I diagnostic comorbidity. Journal of Clinical Psychiatry, , 187–193. Zisook, S., Rush, A.J., Albala, A., Alpert, J., Balasubramani, G.K., Fava, M., Husain, M., Sackeim, H., Trivedi, M., and Wisniewski, S. (2004). Factors that differentiate early vs. later onset of major depression disorder. Psychiatry Research, 29, 127–140. Zlotnick, C., Kohn, R., Keitner, G., and Della Grotta, S.A. (2000). The relationship between quality of interpersonal relationships and major depressive disorder: Findings from the National Comorbidity Survey. Journal of Affective Disorders, 9, 205–215. Zuckerman, M., and Cloninger, C.R. (1996). Relationships between Cloninger’s, Zuckerman’s, and Eysenck’s dimensions of personality. Personality and Individual Differences, 2, 283–285.