The psychosocial context of bipolar disorder: environmental, cognitive, and developmental risk factors

In this article, we review empirical research on the role of individuals' current environmental contexts, cognitive styles, and developmental histories as risk factors for the onset, course, and expression of bipolar spectrum disorders. Our review is focused on the following over arching question: Do psychosocial factors truly contribute risk to the onset, course, or expression of bipolar disorders? As a secondary issue, we also address whether the psychosocial risks for bipolar disorders are similar to those for unipolar depression. We begin by discussing the methodological requirements for demonstrating a psychosocial risk factor and the challenges posed by bipolar spectrum disorders for psychosocial risk research. Next, we review the extant studies on the role of recent life events and supportive and non-supportive social interactions (current environment) in bipolar disorders, as well as psychosocial treatments designed to remediate these current environmental factors. We then review the role of cognitive styles featured as vulnerabilities in theories of unipolar depression as risk factors for bipolar disorder alone and in combination with life events, including studies of cognitive-behavioral therapies for bipolar disorder. Finally, we review studies of parenting and maltreatment histories in bipolar disorders. We conclude with an assessment of the state of the psychosocial risk factors literature in bipolar disorder with regard to our guiding questions.     

The search for determinants of chronic depression: a review of six factors

While strides have been made in the classification, assessment and identification of chronic depression, there remains a limited understanding of the factors underlying chronicity. This review focuses on six putative determinants of chronic depression: developmental factors, personality and personality disorders, psychosocial stressors, comorbid disorders, biological factors and cognitive factors. The strongest support was found for the role of developmental factors in the chronicity of depression. Some support was found for the role of chronic stressors and certain personality features such as stress reactivity. Few other factors found support. The determinants of chronic depression do not differ qualitatively from acute depression. Rather, the development of chronic depression may involve increased levels of childhood adversity, protracted environmental stress and heightened stress reactivity. However, it is difficult to determine to what extent these putative determinants might reflect retrospective bias in data collection, or even parental reaction to children with subthreshold depressive traits. Detailed etiological models await further research attention to understudied areas and improved research designs. Suggestions for future research include greater specification of criteria for chronicity, use of more appropriate comparison groups and longer term prospective follow-up studies.     

Stress and memory bias interact to predict depression in multiple sclerosis

This study is an investigation of the moderating effect of cognitive schema on the relationship between stress and depression in individuals with multiple sclerosis (MS). In the study, the authors employed a performance-based measure of affective memory bias and a self-report measure of everyday stress to assess both direct and interactive effects of cognitive schema and stress on depression in individuals with MS. The specific hypotheses were that high stress would be more highly associated with depression if an individual also demonstrated a bias for negative information, but that a bias for positive information may buffer against the effects of stress on depression. Results supported the hypotheses, demonstrating a significant effect of the interaction and differential effects of stress based on the direction of memory bias. Implications for understanding depression in MS are discussed, as well as dominant theories of adult depression in the general population. The results are also discussed as a potential contradiction to A. T. Beck's (1967, 1976) developmental hypothesis of cognitive schemas.     

Remitted depression studies as tests of the cognitive vulnerability hypotheses of depression onset: a critique and conceptual analysis

Investigations of cognitive patterns among individuals who have recovered from a depressive episode (i.e., remitted depressives) have figured importantly in evaluations of the validity of the vulnerability hypotheses of the cognitive theories of depression. However, we suggest that remitted depression studies as typically conducted and interpreted are inadequate tests of the cognitive vulnerability hypotheses of depression onset for four reasons: (1) remitted depression studies are based on the erroneous assumption that cognitive vulnerability should be an immutable trait; (2) remitted depression studies use a logically "backward" participant selection strategy in which participants are selected on the basis of the "dependent" variable (depression) and then compared on the "independent" variable (cognitive vulnerability), which is likely to result in heterogeneity of cognitive vulnerability among both the remitted depressed as well as the nondepressed groups given the causal relations specified in the cognitive theories of depression; (3) many remitted depression studies have ignored the possible activating role of stress in the cognitive vulnerability-stress theories, particularly Beck's theory, and thus, may attempt to assess cognitive vulnerability at a time when it is not operative (i.e., priming hypothesis); and (4) remitted depression studies inappropriately use postmorbid participants to test causal hypotheses, and therefore, are ambiguous about whether negative cognitive styles observed in remitted depressed persons are vulnerabilities as opposed to consequences of depression (i.e., scar hypothesis). As a remedy, we advocate the use of a theory-guided behavioral high-risk strategy to more adequately test the cognitive vulnerability hypotheses of depression onset.     

Prevention of bipolar disorder in at-risk children: theoretical assumptions and empirical foundations

This article examines how bipolar symptoms emerge during development, and the potential role of psychosocial and pharmacological interventions in the prevention of the onset of the disorder. Early signs of bipolarity can be observed among children of bipolar parents and often take the form of subsyndromal presentations (e.g., mood lability, episodic elation or irritability, depression, inattention, and psychosocial impairment). However, many of these early presentations are diagnostically nonspecific. The few studies that have followed at-risk youth into adulthood find developmental discontinuities from childhood to adulthood. Biological markers (e.g., amygdalar volume) may ultimately increase our accuracy in identifying children who later develop bipolar I disorder, but few such markers have been identified. Stress, in the form of childhood adversity or highly conflictual families, is not a diagnostically specific causal agent but does place genetically and biologically vulnerable individuals at risk for a more pernicious course of illness. A preventative family-focused treatment for children with (a) at least one first-degree relative with bipolar disorder and (b) subsyndromal signs of bipolar disorder is described. This model attempts to address the multiple interactions of psychosocial and biological risk factors in the onset and course of bipolar disorder.     

Sleep Dysfunction Prior to the Onset of Schizophrenia: A Review and Neurodevelopmental Diathesis–Stress Conceptualization

Sleep dysfunction is a pervasive symptom in schizophrenia, yet little is known regarding the extent to which problematic sleep is present prior to illness onset. Results from an online database search targeting genetic high‐risk, clinical high‐risk, and retrospective studies of patients with schizophrenia prior to onset suggest that abnormalities in sleep dysfunction precede schizophrenia onset. Further, a host of proximal factors such as neural structures, endocrine function, and cognitive performance holds promise for improving our conceptualization of sleep dysfunction. However, support is preliminary, and extensive new research in this area is essential. Drawing from this review, a neurodevelopmental diathesis–stress model is posited to highlight potential research targets and mechanisms through which vulnerability, biological/psychosocial stress, and adolescent neuromaturational factors may contribute to both sleep dysfunction and development of psychosis in at‐risk youth.     

Psychosocial aspects of assessment and treatment of irritable bowel syndrome in adults and recurrent abdominal pain in children

This article presents a selective review of psychosocial research on irritable bowel syndrome (IBS) in adults and on a possible developmental precursor, recurrent abdominal pain (RAP), in children. For IBS the authors provide a summary of epidemiology, of the psychological and psychiatric disturbances frequently found among IBS patients, and of the possible role of early abuse in IBS. A review of the psychosocial treatments for IBS finds strong evidence to support the efficacy of hypnotherapy, cognitive therapy, and brief psychodynamic psychotherapy. The research relating RAP to IBS is briefly reviewed, as is the research on its psychological treatment. Cognitive-behavioral therapy that combines operant elements and stress management has the strongest support as a treatment for RAP.     

Maternal postpartum stress and toddler developmental delays: Results from a multisite study of racially diverse families

Maternal psychosocial stress during pregnancy can adversely influence child development, but few studies have investigated psychosocial stress during the postpartum period and its association with risk of toddler developmental delays. Moreover, given the expanding diversity of the U.S. population, and well-documented health and stress disparities for racial and ethnic minorities, research examining the effect of postpartum stress on risk of developmental delays in diverse populations is of critical importance. In this study, data from the Community Child Health Network provided the opportunity to test maternal postpartum stress as a predictor of toddler risk of developmental delay in a sample of African American, Latina and non-Hispanic White women and their toddlers (N = 1537) recruited in urban, suburban, and rural communities. Postpartum maternal stress over 1 year was operationalized as perceived stress, life events, and negative impact of life events. Regression results revealed higher risk of developmental delays in toddlers whose mothers experienced more negative life events, greater negative impact of events, and higher perceived stress over the year. Prenatal stress, pregnancy/birth complications, and postpartum depression did not explain these associations. Maternal postpartum stress may contribute to increased risk for developmental delays and is an important target for psychosocial intervention.     

Severe melancholic depression is more vulnerable than non-melancholic depression to minor precipitating life events

BACKGROUND: The present study examines the moderating role of global depression severity on the relation of melancholic versus non-melancholic depression to severe and non-severe levels of stress. METHOD: A community sample of 50 women with unipolar major depressive disorder, of which 54% met Research Diagnostic Criteria for melancholic depression, were interviewed regarding stressful life events experienced prior to onset. Events were coded as severe or non-severe based on the rigorous Bedford College contextual rating system. RESULTS: Greater severity of depression was related to a higher likelihood of a severely stressful event prior to onset only for women with non-melancholic major depression. By contrast, greater severity of depression was related to a higher likelihood of a non-severe, more minor, stressful event prior to onset only for women with melancholic major depression. LIMITATIONS: The present study was limited by its use of a female volunteer sample, which might not be entirely representative of the population of individuals with major depression. In addition, the study employed a cross-sectional design, which limits conclusions relating to the causal relation of stress to melancholic versus non-melancholic depression. CONCLUSIONS: Far from being autonomous of stress, individuals with severe melancholic depression may be especially sensitive to stress, such that their episodes are influenced by more minor stressors than those of individuals with non-melancholic depression.     

Preconception origins of perinatal maternal mental health

Perinatal maternal symptoms of depression and anxiety compromise psychosocial function and influence developmental outcomes in the offspring. The onset of symptoms remains unclear with findings that suggest a preconceptual origin. We addressed this issue with a prospective analysis of anxiety and depressive symptom profiles from preconception through to parturition. Women were recruited into a preconception study to assess (a) variation in symptom levels of depression and anxiety from pre- to post-conception and (b) if the symptom network profiles of depression and anxiety change from pre-conception to post-conception. A within-subject intraclass correlation analyses revealed that symptoms of depression or anxiety in the preconception phase strongly predicted those across pregnancy and into the early postnatal period. The symptom network analysis revealed that the symptom profiles remained largely unchanged from preconception into the second trimester. Our findings suggest that for a significant portion of women, maternal mental health remains stable from preconception into pregnancy. This finding highlights the need for early intervention studies on women’s mental health to be targeted during the preconception period and to be extended across the population.

     

Early childhood adversity and adolescent depression: the mediating role of continued stress

BACKGROUND: While various conceptualizations of the link between childhood adversity and later depression have been offered, most have not accounted for the possibility that early adversity predicts continuing stress proximal to depression onset. Thus, the present study tested the possible mediating role of recent stress in the association between early adversity and depression in late adolescence.METHOD: Study questions were examined in a longitudinal community sample of 705 youth who were contemporaneously assessed for early adversity exposure prior to age 5 years, chronic and episodic stress at age 15 years, and major depression prior to age 15 years and between 15 and 20 years. RESULTS: Total youth stress burden at age 15 years mediated the effect of early adversity on depression between ages 15 and 20 years, and none of the observed relationships were moderated by onset of depression prior to age 15 years. CONCLUSIONS: These findings suggest that continued stress exposure proximal to depression onset largely accounts for the association between early adversity and depression in late adolescence. Intervention should thus focus on disrupting the continuity of stressful conditions across childhood and adolescence. Future studies of the neurobiological and psychosocial mechanisms of the link between early experiences and depression should explore whether the effects of early experiences are independent of continuing adversity proximal to depressive onset.     

Alterations induced by gestational stress in brain morphology and behaviour of the offspring.

Retrospective studies in humans suggest that chronic maternal stress during pregnancy, associated with raised plasma levels of CRH, ACTH and cortisol may increase the likelihood of preterm birth, developmental delays and behavioural abnormalities in the children. In adulthood, it may contribute to the significant association between the incidence of schizophrenia, increased left or mixed handedness, reduction in cerebral asymmetry and anomalies in brain morphology. Our studies and others have shown that prenatal stress in rats can mimic these developmental and behavioural alterations. These rats show a reduced propensity for social interaction, increased anxiety in intimidating or novel situations and a reduction in cerebral asymmetry and dopamine turnover, consistent with those in schizophrenic humans. Prenatally-stressed (PS) rats also show behaviour consistent with depression, including a phase-shift in their circadian rhythm for corticosterone, sleep abnormalities, a hedonic deficit and greater acquisition of learned helplessness under appropriate conditions. These behavioural abnormalities are associated with impaired regulation of the hypothalamic-pituitary-adrenal axis response to stress and increased CRH activity. PS males may show demasculinisation and feminisation of their sexual behaviour. The developmental and behavioural abnormalities in PS offspring could occur through sensitisation of the foetal brain by maternal stress hormones to the action of glucocorticoid and CRH and to neurotransmitters affected by them. This may have long-lasting consequences and could explain the precipitation of depressive symptoms or schizophrenia by psychosocial stress in later life. The character of the behavioural abnormalities probably depends on the timing of the maternal stress in relation to development of the particular neuronal systems.     

A cognitive vulnerability-stress perspective on bipolar spectrum disorders in a normative adolescent brain, cognitive, and emotional development context

Why is adolescence an "age of risk" for onset of bipolar spectrum disorders? We discuss three clinical phenomena of bipolar disorder associated with adolescence (adolescent age of onset, gender differences, and specific symptom presentation) that provide the point of departure for this article. We present the cognitive vulnerability-transactional stress model of unipolar depression, evidence for this model, and its extension to bipolar spectrum disorders. Next, we review evidence that life events, cognitive vulnerability, the cognitive vulnerability-stress combination, and certain developmental experiences (poor parenting and maltreatment) featured in the cognitive vulnerability-stress model play a role in the onset and course of bipolar disorders. We then discuss how an application of the cognitive vulnerability-stress model can explain the adolescent age of onset, gender differences, and adolescent phenomenology of bipolar disorder. Finally, we further elaborate the cognitive vulnerability-stress model by embedding it in the contexts of normative adolescent cognitive (executive functioning) and brain development, normative adolescent development of the stress-emotion system, and genetic vulnerability. We suggest that increased brain maturation and accompanying increases in executive functioning along with augmented neural and behavioral stress-sensitivity during adolescence combine with the cognitive vulnerability-stress model to explain the high-risk period for onset of bipolar disorder, gender differences, and unique features of symptom presentation during adolescence.     

Stress, immunity and illness--a review

Psychological factors have long been thought to play a contributing role in either the predisposition, onset or course of various physical illnesses. Recently, rapid advances in immunology have created interest in the interaction between psychosocial factors, behaviour and the immune system. This paper reviews some of the models proposed to explain the relationship between psychological variables and physical illness and presents evidence for a contribution of psychological factors to certain illnesses in which abnormalities in immunologic state are thought to be important. From a somewhat different perspective, animal studies have demonstrated complex effects of stress, on disease susceptibility. Recent human studies have demonstrated consistent immunologic changes in people undergoing acute naturally occurring psychological stress such as bereavement or an important examination. In humans, the effects of chronic stress may be different from acute stress, corresponding to the findings in animals. Abnormalities in immunologic functioning and physical illness are reviewed for different psychiatric disorders--depression, anorexia nervosa and schizophrenia; depression is the only disorder which consistently demonstrated immunologic changes. Possible mechanisms for the stress/immune-change relationship are suggested.     

Severe life events predict specific patterns of change in cognitive biases in major depression

BACKGROUND: A long-standing debate concerns whether dysfunctional cognitive processes and content play a causal role in the etiology of depression or more simply represent correlates of the disorder. There has been insufficient appreciation in this debate of specific predictions afforded by cognitive theory in relation to major life stress and changes in cognition over time. In this paper we present a novel perspective for investigating the etiological relevance of cognitive factors in depression. We hypothesize that individuals who experienced a severe life event prior to the onset of major depression will exhibit greater changes in dysfunctional attitudes over the course of the episode than will individuals without a severe life event. METHOD: Fifty-three participants diagnosed with major depression were assessed longitudinally, approximately 1 year apart, with state-of-the-art measures of life stress and dysfunctional attitudes. RESULTS: Depressed individuals with a severe life event prior to episode onset exhibited greater changes in cognitive biases over time than did depressed individuals without a prior severe event. These results were especially pronounced for individuals who no longer met diagnostic criteria for major depression at the second assessment. CONCLUSIONS: Specific patterns of change in cognitive biases over the course of depression as a function of major life stress support the etiological relevance of cognition in major depression.     

Brain maturational processes and delayed onset in schizophrenia.

The central feature of schizophrenia is its onset in adolescence. Although this clinical observation is consistent with the view that schizophrenia may be a neurodevelopmental disorder, debate has focused on when the proposed brain maturational deviations may begin and what might be the nature of such defective development. Conflicting models of this illness (e.g., the early and late neurodevelopmental models) have been proposed. In this paper, we will first review concepts from basic developmental neurobiology pertinent to these issues; we then summarize aspects of the neurobiology of schizophrenia that have a particular bearing on the adolescent onset of this illness. We propose that the schizophrenic syndrome may result from early brain adversity and late maturational processes of brain development interacting with adverse humoral, biochemical, and psychosocial factors during adolescence and early adulthood. The onset of schizophrenia in adolescence may be related to the "plasticity switch" secondary to the peripubertal brain maturational changes, perhaps involving an alteration in glutamate receptor function. This loss of plasticity could result in social and nonsocial cognitive deficits that are central to the pathophysiology of schizophrenia; the vulnerable person may therefore utilize prepubertal processing styles that are insufficient to the adaptive and "gistful" abstraction requirements of adult cognition. Schizophrenia onset might occur in the context of psychosocial developmental challenges to a delayed social cognitive capacity among neurodevelopmentally compromised individuals. We review therapeutic implications as well as testable predictions generated by this model, and discuss research strategies that might further our understanding of the brain maturational abnormalities in schizophrenia.     

Internet-based interventions for traumatic stress-related mental health problems: A review and suggestion for future research

Exposure to potentially traumatic events is a common occurrence. Most individuals exposed to such an event are resilient or recover rapidly, although some individuals develop psychological problems that warrant treatment. However, a small percentage of individuals seek traditional treatment, thereby calling for novel approaches or methodologies of treatment. The present paper provides a comprehensive and critical review of the extant literature on computerized and internet-based interventions (IBIs) for traumatic stress-related conditions (i.e., panic disorder, posttraumatic stress disorder/complicated grief, depression, comorbid anxiety and depression, alcohol abuse, smoking cessation). Generally, computerized or IBIs for depression and anxiety are yielding effect sizes that are comparable to traditional psychosocial treatment. Interventions aimed at alcohol and smoking cessation generally have lower effect sizes than do IBIs for anxiety and depression. Most interventions reviewed in this paper included common components (e.g., were developed through a cognitive behavioral framework and included psychoeducation, cognitive restructuring, goal setting, exposure). Therefore, it is possible that these shared features may in part account for symptom reduction. Little is known regarding mechanisms of change. Future directions for novel web-based approaches to treatment are provided.     

Biologically based treatment approaches to the patient with resistant perinatal depression

This study aims to summarize the current state of knowledge regarding approaches to treatment-resistant depression in pregnancy and the postpartum period and to develop algorithms for ante- and postnatal management in cases of refractory major depression. PubMed, Scopus, Google Scholar, and the Cochrane Library databases were searched without temporal restriction. Search terms included pregnancy and depression, perinatal depression, postnatal depression, treatment resistance and depression, antipsychotics and pregnancy, antidepressants and pregnancy, and mood stabilizers and pregnancy. Abstracts were reviewed for relevance, and further articles were obtained from bibliographic citations. There is a significant subpopulation of patients in pregnancy and postpartum whose depressive symptoms do not respond to first-line treatments. No research studies have focused specifically on this population. Data extracted from studies on women with depressive symptoms in pregnancy suggest that in the absence of evidence on which to base clinical decisions, many are receiving combinations of psychotherapeutic medications that have not been specifically studied for use in pregnancy. Antidepressant use in pregnancy is well studied, but studies specifically addressing the case of the patient who does not respond to first-line treatments are absent. Research in this area is urgently needed. The authors review a number of possible therapeutic approaches to treatment-resistant depression in pregnancy and the postpartum period.     

Dehydroepiandrosterone in the nucleus accumbens is associated with early onset of depressive-behavior: a study in an animal model of childhood depression

Although the monoamine theory of depression is well studied, regarding childhood depression it is poorly supported. Antidepressant treatments affecting the monoaminergic system fail to ameliorate childhood depression in the same manner that they affect adult depression. The present study used the Flinders sensitive line (FSL) rat, a well-investigated genetic animal model of depression and Sprague-Dawley (SD) rats as controls. We co-measured monoamines and dehydroepiandrosterone (DHEA) levels in the nucleus accumbens on postnatal day 1, in prepubertal rats (35 days), and adult rats (4 months) in order to examine developmental characteristics in the monoamine systems. The results suggest that there are different ontogenetic patterns of monoaminergic activity in FSL and SD rats. While monoamine levels were different only in adulthood, FSL rats exhibited lower DHEA levels already in prepubertal childhood. These differences may be relevant to the poor response to antidepressant drugs observed in depressed children and suggest DHEA as a new marker for childhood depression.     

Major depression in panic disorder: role of recent life events

The authors assessed life events during the year before the onset of panic disorder in 57 panic patients with a lifetime history of major depression. Compared with a group of 43 panic patients without major depression, the group with depression had experienced more severe events. The clinical and theoretical implications of these results are discussed in the context of current concepts regarding the role of recent life events in comorbidity of panic disorder and major depression.