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Depression in Parents, Parenting, and Children: Opportunities to Improve Identification, Treatment, and Prevention 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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Depression in Parents, Parenting, and Children: Opportunities to Improve Identification, Treatment, and Prevention 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 cognitive, interpersonal, and personality factors. Biological, environmental, and personal vulnerabilities interact to contribute to the development of depression and also may be affected by depressive states in a bidirectional process. Co-Occurring Disorders Depression rarely occurs independent of other psychological disorders, including anxiety, substance abuse, behavioral, and personality 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 researchers 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 provoke depression. The chapter also emphasizes the interplay between persons
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Depression in Parents, Parenting, and Children: Opportunities to Improve Identification, Treatment, and Prevention and environments—the ways in which, for example, stressors may provoke depression but depression further influences social environments, often a vicious 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 factors 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), although many preadolescents including preschoolers have significant internalizing 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. Clinically, earlier age of onset of depression is generally thought to be associated 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 significant 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 psychosocial adversity, such as abuse, parental disorder, criminality, and family disruption who continue to experience social maladjustment and other
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Depression in Parents, Parenting, and Children: Opportunities to Improve Identification, Treatment, and Prevention 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 depressive 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 depression lasting anywhere from several weeks to a year. A smaller proportion, less than 0.5 percent, experience acute psychosis associated with the depression. A recent large-scale epidemiological survey that examined rates of diagnoses 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 etiology 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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Depression in Parents, Parenting, and Children: Opportunities to Improve Identification, Treatment, and Prevention 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 depression 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 increased 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 prevention 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 others, 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 depression 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: Opportunities to Improve Identification, Treatment, and Prevention 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 episodes (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 depressive 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 adulthood, 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 formation. 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 psychological 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 particularly valuable and are probably best targeted at those most vulnerable to depression: those with extensive family history, those with symptoms of depression, and those with multiple risk factors for depression (e.g., poverty, exposure to violence, social isolation).
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Depression in Parents, Parenting, and Children: Opportunities to Improve Identification, Treatment, and Prevention BIOLOGICAL PERSPECTIVES ON THE ETIOLOGY OF DEPRESSION A complex set of biological processes has been implicated in the etiology 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 mechanisms 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 functioning 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 implicating 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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Depression in Parents, Parenting, and Children: Opportunities to Improve Identification, Treatment, and Prevention 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 sensitivity, 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 polymorphisms in the serotonin-related genes in the etiology of depression. Currently, 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 experienced more depressive symptoms and higher rates of major depressive disorder in response to stressful life events than individuals who are homozygous 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 perception 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 compared with other groups. The results suggest that the serotonin transporter polymorphism is linked to the brain’s processing of emotional threat information. 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 serotonin 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 genetic 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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Depression in Parents, Parenting, and Children: Opportunities to Improve Identification, Treatment, and Prevention gene will have very small effects, and summing risk across multiple identified 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, Medical 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 contribute 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 others 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 London, 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 interconnected through various neurotransmitter and hormonal circuits (Boyce and Ellis, 2005; Meyer, Chrousos, and Gold, 2001). The primary glucocorticoid 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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Depression in Parents, Parenting, and Children: Opportunities to Improve Identification, Treatment, and Prevention deleterious effects, giving rise to physiological changes thought to promote a variety of illnesses. Depression has been linked with elevated cortisol and related neurohormones. 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 generalized 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 nonhuman primates have been shown to be associated with differences in emotional 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 depression (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 considerable interest as possible contributors to abnormal biological stress regulation. 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 abnormalities 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 glucocorticoid 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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Depression in Parents, Parenting, and Children: Opportunities to Improve Identification, Treatment, and Prevention 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 maternal 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 experiences, 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 depression and coronary heart disease, researchers have begun to examine the potential role of the immune system, and particularly proinflammatory cytokines, 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, evidence 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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Depression in Parents, Parenting, and Children: Opportunities to Improve Identification, Treatment, and Prevention 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 illness in primary care patients with major depression? General Hospital Psychiatry, 21, 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 Psychology, 30, 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, 64, 1984–1996. Gerlsma, C., Emmelkamp, P.M.G., and Arrindell, W.A. (1990). Anxiety, depression, and perception of early parenting: A meta-analysis. Clinical Psychology Review, 10, 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, 30, 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, 17, 226–228. Gladstone, G.L., and Parker, G.B. (2006). Is behavioral inhibition a risk factor for depression? Journal of Affective Disorders, 95, 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. 8771). Washington, DC: HUD USER. Gold, P.W., Goodwin, F.K., and Chrousos, G.P. (1988). Clinical and biochemical manifestations of depression: Relation to the neurobiology of stress. New England Journal of Medicine, 319, 348–353. Golding, J.M. (1999). Intimate partner violence as a risk factor for mental disorders: A meta-analysis. Journal of Family Violence, 14, 99–132. Goodman, S.H. (2007). Depression in mothers. Annual Review of Clinical Psychology, 3, 107–135. Goodman, S.H., and Gotlib, I.H. (1999). Risk for psychopathology in the children of depressed mothers: A developmental model for understanding mechanisms of transmission. Psychological Review, 106, 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, income level, and language. Psychological Assessment, 18, 313–323. Gross, J.J. (2001). Emotion regulation in adulthood: Timing is everything. Current Directions in Psychological Science, 10, 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, 100, 555–561. Hammen, C. (2005). Stress and depression. Annual Review of Clinical Psychology, 1, 293–319. Hammen, C. (2006). Stress generation in depression: Reflections on origins, research, and future directions. Journal of Clinical Psychology, 62, 1065–1082. Hammen, C., and Brennan, P.A. (2002). Interpersonal dysfunction in depressed women: Impairments independent of depressive symptoms. Journal of Affective Disorders, 72, 145–156.
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