Article

The stress sensitization hypothesis: Understanding the course of bipolar disorder

Department of Psychology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Journal of Affective Disorders (Impact Factor: 3.38). 11/2006; 95(1-3):43-9. DOI: 10.1016/j.jad.2006.04.009
Source: PubMed

ABSTRACT

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.

Download full-text

Full-text

Available from: Risha Henry
    • "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)
  • Source
    • "In spite of these limitations, we believe that impulsivity, involving poorly regulated action, is persistent and stable in bipolar disorder and may be one of the basic mechanisms of the illness. One way to explain this is through the mechanism of behavioral sensitization by which a recurrent course of bipolar disorder, or bipolar disorder complicated by co-morbidity or substance use disorders, could lead over time to more severe impulsivity even outside of manic episodes and in the euthymic state [40]. However, bipolar disorder also has a state-dependent impulsivity component that correlates positively with manic symptoms and negatively with depressive symptoms. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective To review scores on measures of impulsivity in remitted bipolar disorder. Data source We used keywords “impulsivity and bipolar”; “impulsivity and mania” to narrow down our search on Medline, EMBASE and Psychinfo to include those studies that had reported impulsivity scores using validated and reliable assessment measures in remitted bipolar disorder (Both I & II). We searched all English language studies from 1990 to October 2012. Study Selection 19 reports met the inclusion criteria and were reviewed by two abstractors independently. Data abstraction We generated weighted mean differences (WMDs) from pooled data using RevManager 5.0 from Cochrane analysis. Results The Barratt Impulsivity Scale (BIS) 11 was the instrument most commonly used. 19 studies met inclusion criteria, of which 2 were excluded due to incomplete data. A WMD of 12.8 was observed for BIS 11 total scores, 4.3 on the motor component, 4.1 on the cognitive and 7.6 on the non-planning components of the BIS 11 respectively. Conclusion Impulsivity is significantly higher in remitted bipolar patients than normal controls. Non-planning impulsivity is a key domain affected in bipolar disorder, which may represent a stable trait.
    Full-text · Article · Oct 2014 · Comprehensive Psychiatry
  • Source
    • "History of depression as a risk factor for heightened vulnerability and treatment resistance Depression is a recurrent condition, in which each episode increases the probability of a further episode (American Psychiatric Association, 2000; Solomon et al., 2000). However, there are many studies demonstrating that the association between severe stress and depression decreases with each successive episode, as minor stress episodes may by now be a sufficient trigger (Dienes et al., 2006; Stroud et al., 2008; Morris et al., 2010; Slavich et al., 2011). For example, a study of over 2000 women reported that over the first six episodes of depression the likelihood of an episode occurring in any given month increased 15-fold, but at the same time, the association with a stressful life event decreased by 75% (Kendler et al., 2000). "
    [Show abstract] [Hide abstract]
    ABSTRACT: The first half of this paper briefly reviews the evidence that (i) stress precipitates depression by damaging the hippocampus, leading to changes in the activity of a distributed neural system involving, inter alia, the amygdala, the ventromedial and dorsolateral prefrontal cortex, the lateral habenula and ascending monoamine pathways, and (ii) antidepressants work by repairing the damaged hippocampus, thus restoring the normal balance of activity within that circuitry. In the second half of the paper we review the evidence that heightened vulnerability to depression, either because of a clinical history of depression or because of the presence of genetic, personality or developmental risk factors, also confers resistance to antidepressant drug treatment. Thus, although antidepressants provide an efficient means of reversing the neurotoxic effects of stress, they are much less effective in conditions where vulnerability to depression is elevated and the role of stress in precipitating depression is correspondingly lower. Consequently, the issue of vulnerability should feature much more prominently in antidepressant research. Most of the current animal models of depression are based on the induction of a depressive-like phenotype by stress, and pay scant attention to vulnerability. As antidepressants are relatively ineffective in vulnerable individuals, this in turn implies a need for the development of different clinical and preclinical methodologies, and a shift of focus away from the current preoccupation with the hippocampus as a target for antidepressant action in vulnerable patients.
    Full-text · Article · Sep 2014 · Behavioural Pharmacology
Show more