The influence of psychosocial stress on the course of bipolar disorder has been increasingly recognized. The authors tested hypotheses about both stress and early adversity "sensitization" on the course of bipolar disorder over a one-year period.
The participants were 58 adults (29 male and 29 female) with a diagnosis of bipolar I disorder. They were evaluated every three months for one year. Stressful life events and the presence of early adversity were assessed by structured interview.
There was no significant interaction between stress and episode number in the prediction of bipolar recurrence. The interaction of early adversity severity and stressful life events significantly predicted recurrence in a manner consistent with the sensitization hypothesis. Participants with early adversity reported lower levels of stress prior to recurrence than those without early adversity. Individuals with early adversity also had a significantly younger age of bipolar onset.
The sample size was small and the number of past episodes was determined retrospectively, mainly through self-report.
Severe early adversity may result in a greater effect of stress on bipolar recurrence and earlier onset of bipolar disorder, suggesting the need for further studies of stress mechanisms in bipolar disorder and of treatments designed to intervene early among those at risk.
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"Shapero et al.  observed stress inoculation in humans; among 163 adolescents studied for 3 years, moderate stress during childhood (prior to age 12–13 years) reduced the risk of a depressive response to stress in adolescence (up until age 15–16 years). However, others propose that those exposed to higher levels of stress in early life can become less able to effectively manage subsequent stress, and that this 'stress sensitisation' is associated with a range of psychiatric disorders [20, 21] . Whether inoculation or sensitisation occurs in reaction to stress may be determined by individual differences in glucocorticoid responsivity or innate coping strategies, or by external factors such as support from others. "
[Show abstract][Hide abstract]ABSTRACT: Purpose: Psychological resilience, the ability to manage and quickly recover from stress and trauma, is associated with a range of health and wellbeing outcomes. Resilience is known to relate to personality, self-esteem and positive affect, and may also depend upon childhood experience and stress. In this study, we investigated the role of early-life contributors to resilience and related factors in later life.
Methods: We used data from the 6-Day Sample of the Scottish Mental Survey 1947, an initially representative sample of Scottish children born in 1936. They were assessed on a range of factors between the ages of 11 and 27 years, and resilience and other outcomes at 77 years.
Results: Higher adolescent dependability unexpectedly predicted lower resilience in older-age, as did childhood illnesses, while a count of specific stressors experienced throughout early life significantly predicted higher later-life resilience. We also observed significant cross-sectional correlations between resilience and measures of physical health, mental health, wellbeing and loneliness. Some of the associations between early-life predictors and later-life outcomes were significantly mediated by resilience.
Conclusions: Our results support the hypothesis that stress throughout early life may help to build resilience in later-life, and demonstrate the importance of resilience as a mediator of other influences on health and wellbeing in older age. We suggest that the mechanisms determining how early-life stress leads to higher resilience are worthy of further investigation, and that psychological resilience should be a focus of research and a target for therapeutic interventions aiming to improve older-age health and wellbeing.
Full-text · Article · Feb 2016 · Social Psychiatry and Psychiatric Epidemiology
"Introduction A large body of research has implicated psychological stress in the onset or progression of several disorders, including asthma, cardiovascular disease, certain cancers, and depression (Dienes et al., 2006; Slavich & Irwin, 2014). Because inflammation is involved in many different health outcomes, recent research has examined the role that pro-inflammatory cytokines play in linking stress with poor health (Cohen et al., 2012). "
[Show abstract][Hide abstract]ABSTRACT: Stress is strongly associated with several mental and physical health problems that involve inflammation, including asthma, cardiovascular disease, certain types of cancer, and depression. It has been hypothesized that better cognitive control of emotional information may lead to reduced inflammatory reactivity to stress and thus better health, but to date no studies have examined whether differences in cognitive control predict pro-inflammatory cytokine responses to stress. To address this issue, we conducted a laboratory-based experimental study in which we randomly assigned healthy young-adult females to either an acute emotional stress (emotionally evocative video) or no-stress (control video) condition. Salivary levels of the key pro-inflammatory cytokines IL-1β, IL-6, and IL-8 were measured before and after the experimental manipulation, and following the last cytokine sample, we assessed participants' cognitive control of emotional information using an emotional Stroop task. We also assessed participants' cortisol levels before and after the manipulation to verify that documented effects were specific to cytokines and not simply due to increased nonwater salivary output. As hypothesized, the emotional stressor triggered significant increases in IL-1β, IL-6, and IL-8. Moreover, even in fully adjusted models, better cognitive control following the emotional (but not control) video predicted less pronounced cytokine responses to that stressor. In contrast, no effects were observed for cortisol. These data thus indicate that better cognitive control specifically following an emotional stressor is uniquely associated with less pronounced pro-inflammatory cytokine reactivity to such stress. These findings may therefore help explain why superior cognitive control portends better health over the lifespan.
No preview · Article · Nov 2015 · Stress (Amsterdam, Netherlands)
"In this respect, it should however be realized that the kindling effect has mostly been found after the occurrence of five to seven episodes (Kendler et al. 2000; Kendler and Gardner 2001; Slavich et al. 2011) while we only looked at admissions and the average number of admissions lies between three and four in our sample. Previous studies using the LEDS in bipolar patients (Dienes et al. 2006; Swendsen et al. 1995; Hammen and Gitlin 1997) looking at episodes rather than admissions did not find evidence for either presence or absence of a kindling effect. This is in contrast with findings in unipolar depression, which might be explained by the more complex course of contrasting mood episodes (i.e. "
[Show abstract][Hide abstract]ABSTRACT: Life events play an important role in the onset and course of bipolar disorder. We will test the influence of life events on first and recurrent admissions in bipolar disorder and their interaction to test the kindling hypothesis.
We collected information about life events and admissions across the life span in 51 bipolar patients. We constructed four models to explore the decay of life event effects on admissions. To test their interaction, we used the Andersen-Gill model.
The relationship between life events and admissions was best described with a model in which the effects of life events gradually decayed by 25% per year. Both life event load and recurrent admissions significantly increased the risk of both first and subsequent admissions. No significant interaction between life event load and number of admissions was found.
Life events increase the risk of both first and recurrent admissions in bipolar disorder. We found no significant interaction between life events and admissions, but the effect of life events on admissions decreases after the first admission which is in line with the kindling hypothesis.