Life Events and Depression

Paykel, Eugene S.; Myers, Jerome K.; Dienelt, Marcia N.; Klerman, Gerald L.; Lindenthal, Jacob Jay; Pepper, Max P.

doi:10.1001/archpsyc.1969.01740240113014

Cited by 926 publications

(316 citation statements)

References 13 publications

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“…139 Additionally, an altered HPA axis physiology and dysfunctions of the extrahypothalamic corticotrophin-releasing hormone (CRH) system have been consistently found in subjects with MD. 140 Activation of the HPA axis is one of the best-documented changes in MD.…”

Section: The Inflammatory Hypothesis Of Depressionmentioning

confidence: 99%

The immune-mediated alteration of serotonin and glutamate: towards an integrated view of depression

2007

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Beside the well-known deficiency in serotonergic neurotransmission as pathophysiological correlate of major depression (MD), recent evidence points to a pivotal role of increased glutamate receptor activation as well. However, cause and interaction of these neurotransmitter alterations are not understood. In this review, we present a hypothesis integrating current concepts of neurotransmission and hypothalamus-pituitary-adrenal (HPA) axis dysregulation with findings on immunological alterations and alterations in brain morphology in MD. An immune activation including increased production of proinflammatory cytokines has repeatedly been described in MD. Proinflammatory cytokines such as interleukin-2, interferon-c, or tumor necrosis factor-a activate the tryptophan-and serotonin-degrading enzyme indoleamine 2,3-dioxygenase (IDO). Depressive states during inflammatory somatic disorders are also associated with increased proinflammatory cytokines and increased consumption of tryptophan via activation of IDO. An enhanced consumption of serotonin and its precursor tryptophan through IDO activation could well explain the reduced availability of serotonergic neurotransmission in MD. An increased activation of IDO and its subsequent enzyme kynurenine monooxygenase by proinflammatory cytokines, moreover, leads to an enhanced production of quinolinic acid, a strong agonist of the glutamatergic N-methyl-D-aspartate receptor. In inflammatory states of the central nervous system, IDO is mainly activated in microglial cells, which preferentially metabolize tryptophan to the NMDA receptor agonist quinolinic acid, whereas astrocytes -counteracting this metabolism due to the lack of an enzyme of this metabolism -have been observed to be reduced in MD. Therefore the type 1/type 2 immune response imbalance, associated with an astrocyte/microglia imbalance, leads to serotonergic deficiency and glutamatergic overproduction. Astrocytes are further strongly involved in re-uptake and metabolic conversion of glutamate. The reduced number of astrocytes could contribute to both, a diminished counterregulation of IDO activity in microglia and an altered glutamatergic neurotransmission. Further search for antidepressant agents should take into account anti-inflammatory drugs, for example, cyclooxygenase-2 inhibitors, might exert antidepressant effects by acting on serotonergic deficiency, glutamatergic hyperfunction and antagonizing neurotoxic effects of quinolinic acid. Molecular Psychiatry (2007) 12, 988-1000; doi:10.1038/sj.mp.4002006; published online 24 April 2007 Keywords: major depression; psychoneuroimmunology; IDO; glutamate; immune system; serotonin Glutamate in depressionGlutamatergic neurotransmission is involved in depression and interacts with the serotonergic and noradrenergic systems The common therapeutic mechanism of antidepressant drugs is the enhancement of serotonergic and/or noradrenergic neurotransmission. On the basis of this pharmacological profile of antidepressant drugs, neurochemical research on major depression ...

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Section: The Inflammatory Hypothesis Of Depressionmentioning

confidence: 99%

The immune-mediated alteration of serotonin and glutamate: towards an integrated view of depression

2007

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“…There have been many studies about the relationship between life events and depressive illness symptoms [22][23][24][25]. In our model, we included various other variables simultaneously; however, the relationship showed many complexity-produced interactive effects on the life-stress process.…”

Section: Discussionmentioning

confidence: 99%

The effects of lifestyle and type a behavior on the life-stress process

Maruyama

Morimoto

1997

Environ Health Prev Med

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To evaluate the effects of personal factors such as lifestyle and Thpe A behavior on the life-stress process, we analyzed data randomly collected from 428 metropolitan Tokyo residents. Path analysis techniques were implemented to examine the direct and indirect effects of lifestyle and the Type A behavior pattern between life events, subjective stress and depressive symptoms. The following results were obtained:1. Persons with a healthy lifestyle perceived a lower subjective stress level. 2. Although females with a healthy lifestyle had fewer direct depressive symptoms, males with a healthy lifestyle had fewer indirect depressive symptoms due to alleviation of subjective stress.3. Type A males perceived a lower subjective stress level and Type A females experienced more life events.It is suggested that mental health is modified not only by lifestyle but also by Type A behavior in the life-stress process. In particular, the preservation and promotion of a healthy lifestyle appear to reduce subjective stress and may be an important factor for the improvement of mental ill health.

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“…A single item from a revised version [26] of the Recent Life Change Questionnaire [27] was used to examine family discord during the 6 month period prior to the attempt.…”

Section: Family Discordmentioning

confidence: 99%

Few Sex Differences in Hospitalized Suicide Attempters Aged 70 and Above

Wiktorsson

Sterner

Fässberg

et al. 2017

Preprint

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Relatively little research attention has been paid to sex issues in late life suicidal behaviour.The aim was to compare clinical characteristics of women and men aged 70+ who were hospitalized after a suicide attempt. We hypothesized higher depression and anxiety scores in women, and we expected to find that men would more often attribute the attempt to health problems and compromised autonomy. Participants (56 women and 47 men, mean age 80) were interviewed by a psychologist. In addition to psychiatric and somatic health assessments, participants responded to an open-ended question concerning attributions of the attempt.There were no sex differences in depression and anxiety, but women were more likely to report that they found their situation hopeless (67.9% vs. 43.8%, p = 0.02). At least one serious physical disability was noted in 60.7% of the women and 53.2% of the men (p = 0.55). Proportions attributing their attempt to somatic illness did not differ (women, 14.5% vs. men 17.4%, p = 0.79), and similar proportions attributed the attempt to reduced autonomy (women, 21.8% vs. men, 26.1 %, p = 0.64). The unexpected lack of sex differences might be influenced by cultural context in which sex norms play a part.

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Life Events and Depression

Cited by 926 publications

References 13 publications

The immune-mediated alteration of serotonin and glutamate: towards an integrated view of depression

The immune-mediated alteration of serotonin and glutamate: towards an integrated view of depression

The effects of lifestyle and type a behavior on the life-stress process

Few Sex Differences in Hospitalized Suicide Attempters Aged 70 and Above

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