Causal Relationship Between Stressful Life Events and the Onset of Major Depression

Kendler, Kenneth S.; Karkowski, Laura M.; Prescott, Carol A.

doi:10.1176/ajp.156.6.837

Cited by 2,074 publications

(1,493 citation statements)

References 29 publications

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“…Parallel to these findings, a growing number of studies demonstrate that many of these stress-induced cellular changes can be reversed by antidepressant treatment (D'Sa and Duman, 2002;Dranovsky and Hen, 2006). It has been argued that these observations are likely to have human relevance as stressful life events are among the most potent factors known to trigger or induce major depressive episodes (Kendler et al, 1999). Thus, these findings contributed to the formulation of a novel concept that structural alterations including suppressed dentate neurogenesis may contribute to the pathogenesis of depression (Manji et al, 2001;Duman, 2004).…”

Section: Introductionmentioning

confidence: 92%

Chronic Social Stress Inhibits Cell Proliferation in the Adult Medial Prefrontal Cortex: Hemispheric Asymmetry and Reversal by Fluoxetine Treatment

Czéh

Müller-Keuker

Ryguła

et al. 2006

Neuropsychopharmacol

314

214

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Profound neuroplastic changes have been demonstrated in various limbic structures after chronic stress exposure and antidepressant treatment in animal models of mood disorders. Here, we examined in rats the effect of chronic social stress and concomitant antidepressant treatment on cell proliferation in the medial prefrontal cortex (mPFC). We also examined possible hemispheric differences. Animals were subjected to 5 weeks of daily social defeat by an aggressive conspecific and received concomitant, daily, oral fluoxetine (10 mg/kg) during the last 4 weeks. Bromodeoxyuridine (BrdU) labeling and quantitative stereological techniques were used to evaluate the treatment effects on proliferation and survival of newborn cells in limbic structures such as the mPFC and the hippocampal dentate gyrus, in comparison with nonlimbic structures such as the primary motor cortex and the subventricular zone. Phenotypic analysis showed that neurogenesis dominated the dentate gyrus, whereas in the mPFC most newborn cells were glia, with smaller numbers of endothelial cells. Chronic stress significantly suppressed cytogenesis in the mPFC and neurogenesis in the dentate gyrus, but had minor effect in nonlimbic structures. Fluoxetine treatment counteracted the inhibitory effect of stress. Hemispheric comparison revealed that the rate of cytogenesis was significantly higher in the left mPFC of control animals, whereas stress inverted this asymmetry, yielding a significantly higher incidence of newborn cells in the right mPFC. Fluoxetine treatment abolished hemispheric asymmetry in both control and stressed animals. These pronounced changes in gliogenesis after chronic stress exposure may relate to the abnormalities of glial cell numbers reported in the frontolimbic areas of depressed patients.

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Section: Introductionmentioning

confidence: 92%

Chronic Social Stress Inhibits Cell Proliferation in the Adult Medial Prefrontal Cortex: Hemispheric Asymmetry and Reversal by Fluoxetine Treatment

Czéh

Müller-Keuker

Ryguła

et al. 2006

Neuropsychopharmacol

314

214

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“…Many studies have examined the relationship between SLEs and the first onset of major depression (e.g., Kendler, Karkowski, & Prescott, 1999;Lewinsohn et al, 1999), and some studies have begun to examine the association between SLEs, either in childhood or adulthood, and the risk for recurrence of depression in particular. In a sample of 3491 individuals, Wainwright and Surtees (2002) examined the relationship between retrospective reports of childhood SLEs and risk for a history of depression in adulthood.…”

Section: Stressful Life Events (Sles)mentioning

confidence: 99%

Risk for recurrence in depression

Burcusa

Iacono

2007

Clinical Psychology Review

816

648

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Depression is a highly recurrent disorder with significant personal and public health consequences. Prevention of recurrence would be extremely desirable, and thus researchers have begun to identify risk factors that are specific to recurrence, which may be different from risk factors for first-onset of depression. Methodological issues in this area of research are briefly reviewed (e.g., the various definitions of "recurrence" and "depression"), followed by a review of studies on specific risk factors, including demographic variables (gender, socio-economic status, marital status), clinical variables (age at first onset, number of prior episodes, severity of first/index episode, comorbid psychopathology), family history of psychopathology, and psychosocial and psychological variables (level of psychosocial functioning, cognitions, personality, social support, and stressful life events). In addition, scar theories are evaluated for their potential to explain how these variables and recurrent depression are linked. Our review suggests that recurrent depression reflects an underlying vulnerability that is largely genetic in nature and that may predispose those high in the vulnerability not only to recurrent depressive episodes, but also to the significant psychosocial risk factors that often accompany recurrent depression.Major depressive disorder is one of the most common forms of psychopathology, one that will affect approximately one in six men and one in four women in their lifetimes . It is also usually highly recurrent, with at least 50% of those who recover from a first episode of depression having one or more additional episodes in their lifetime, and approximately 80% of those with a history of two episodes having another recurrence (American Psychiatric Association, 2000;Kupfer, Frank, & Wamhoff, 1996;Post, 1992). Once a first episode has occurred, recurrent episodes will usually begin within five years of the initial episode (Belsher & Costello, 1988;Lewinsohn, Clarke, Seeley, & Rohde, 1994), and, on average, individuals with a history of depression will have five (Kessler & Walters, 1998) to nine (Kessler, Zhao, Blazer, & Swartz, 1997) separate depressive episodes in their lifetime.Due to the fact that depression can be so recurrent, it can have significant personal and public health consequences. For example, one meta-analysis found that the suicide rate among those with depression is approximately twenty times higher than the rate for the general population (Harris & Barraclough, 1997). In addition, a study of over 3000 adolescents and young adults found that 90% of those with recurrent depression reported "very much" impairment, limiting work productivity and social interactions, and 40% sought professional help as a result (Wittchen, Nelson, & Lachner, 1998). Depression can also have a significant economic impact due to decreased productivity in affected individuals (Klerman & Weissman, 1992); in 1996 the annual direct (e.g., visits to doctors, pharmaceutical costs) and indirect (e.g., time...

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“…125 Research into the role of stressful life events and difficulties in the causation of depression has a long history. 126,127 It has been established that stressful life events (SLE) have a causal role in the genesis of depression, 128 their depressogenic effect is variable and depends on the level of 'contextual threat', 126 they are closely related in time to the onset of depression 129,130 and have stronger effect on first onset of depression than on recurrences. 61 The effect of SLE is not specific to depression as they are also associated with the onset of anxiety disorders, 131 substance abuse, 132 eating disorders 133 and psychosis.…”

Section: Environmental Adversity and Stressorsmentioning

confidence: 99%

The moderation by the serotonin transporter gene of environmental adversity in the aetiology of mental illness: review and methodological analysis

2007

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Causal Relationship Between Stressful Life Events and the Onset of Major Depression

Cited by 2,074 publications

References 29 publications

Chronic Social Stress Inhibits Cell Proliferation in the Adult Medial Prefrontal Cortex: Hemispheric Asymmetry and Reversal by Fluoxetine Treatment

Chronic Social Stress Inhibits Cell Proliferation in the Adult Medial Prefrontal Cortex: Hemispheric Asymmetry and Reversal by Fluoxetine Treatment

Risk for recurrence in depression

The moderation by the serotonin transporter gene of environmental adversity in the aetiology of mental illness: review and methodological analysis

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