scholarly journals Childhood adversity, adult stressful life events, and risk of past-year psychiatric disorder: a test of the stress sensitization hypothesis in a population-based sample of adults

2011 ◽  
Vol 52 (6) ◽  
pp. e11 ◽  
Author(s):  
K.A. McLaughlin ◽  
K.J. Conron ◽  
S.J. Gilman ◽  
K.C. Koenen
2009 ◽  
Vol 40 (10) ◽  
pp. 1647-1658 ◽  
Author(s):  
K. A. McLaughlin ◽  
K. J. Conron ◽  
K. C. Koenen ◽  
S. E. Gilman

BackgroundChildhood adversity (CA) is associated with adult mental disorders, but the mechanisms underlying this association remain inadequately understood. Stress sensitization, whereby CA increases vulnerability to mental disorders following adult stressful life events, has been proposed as a potential mechanism. We provide a test of the stress sensitization hypothesis in a national sample.MethodWe investigated whether the association between past-year stressful life events and the 12-month prevalence of major depression, post-traumatic stress disorder (PTSD), other anxiety disorders, and perceived stress varies according to exposure to CA. We used data from the National Epidemiological Survey of Alcohol and Related Conditions (NESARC) (n=34 653).ResultsPast-year stressful life events were associated with an increased risk of major depression, PTSD, anxiety disorders, and perceived stress. However, the magnitude of the increased risk varied according to respondents' history of CA. For example, past-year major stressors were associated with a 27.3% increase in the 12-month risk of depression among individuals with ⩾3 CAs and a 14.8% increased risk among individuals without CAs. Stress sensitization effects were present for depression, PTSD, and other anxiety disorders in women and men, although gender differences were found in the threshold of past-year stress needed to trigger such effects. Stress sensitization was most evident among individuals with ⩾3 CAs.ConclusionsCA is associated with increased vulnerability to the deleterious mental health effects of adult stressors in both men and women. High levels of CA may represent a general diathesis for multiple types of psychopathology that persists throughout the life course.


2019 ◽  
Author(s):  
David G. Weissman ◽  
Hilary K. Lambert ◽  
Alexandra M. Rodman ◽  
Matthew Peverill ◽  
Margaret A. Sheridan ◽  
...  

AbstractOBJECTIVEStressful life events are more likely to trigger depression among individuals exposed to childhood adversity. However, the mechanisms underlying this stress sensitization remain largely unknown. Any such mechanism must be altered by childhood adversity and interact with recent stressful life events, magnifying their association with depression. This study investigated whether reduced hippocampal and amygdala volumes are mechanisms of stress sensitization following childhood violence exposure.METHODSA sample of 149 youth (aged 8-17 years), with (N=76) and without (N=73) exposure to physical abuse, sexual abuse, or domestic violence participated. Participants completed a structural MRI scan and were assessed for symptoms of depression. Approximately two years later, stressful life events were assessed along with depression symptoms in 120 participants (57 violence-exposed).RESULTSChildhood violence exposure was associated with smaller hippocampal and amygdala volumes. Stressful life events occurring during the follow-up period predicted worsening depression over time, and this association was magnified among those with smaller hippocampal and amygdala volumes. Significant moderated mediation models revealed indirect effects of violence exposure on increasing depression over time through hippocampal and amygdala volumes, particularly among youths who experienced more stressful life events.CONCLUSIONSThese results provide novel evidence for reduced hippocampal and amygdala volumes as mechanisms of stress sensitization to depression following exposure to violence. These findings suggest that hippocampal and amygdala-mediated emotional and cognitive processes may contribute to vulnerability to stressful life events following childhood violence exposure.


2013 ◽  
Vol 26 (1) ◽  
pp. 147-154 ◽  
Author(s):  
Anna Sundström ◽  
Michael Rönnlund ◽  
Rolf Adolfsson ◽  
Lars-Göran Nilsson

ABSTRACTBackground:The impact of stressful life events as a risk factor of dementia diseases is inconclusive. We sought to determine whether stressful negative life events are associated with incidental dementia in a population-based study with long-term follow-up. We also tested the hypothesis that the occurrence of positive life events could mitigate or overcome the possible adverse effects of negative life events on dementia conversion.Methods:The study involved 2,462 dementia-free participants aged 55 years and older. Information on life events was ascertained at baseline from a comprehensive Life Event Inventory, which included 56 questions about specific life events. For each life event, the emotional impact (both positive and negative) and emotional adjustment were asked for.Results:During follow-up, 423 participants developed dementia; of these, 240 developed Alzheimer's disease (AD). Cox regression analysis showed no association between the total number of negative life events and the incidence of dementia when adjusted solely for age and gender (hazard ratio = 0.97, 95% CI = 0.92–1.02), or with multiple adjustments for a range of covariates (hazard ratio = 0.96, 95% CI = 0.91–1.01). Similarly, neither emotional impact nor emotional adjustment to these life events was associated with incident dementia. A separate analysis of AD did not alter the results.Conclusions:The result of this population-based study finds no association between negative or positive life events and dementia. Accordingly, our results reject the hypothesis that stressful life events trigger the onset of dementia diseases.


2004 ◽  
Vol 34 (8) ◽  
pp. 1475-1482 ◽  
Author(s):  
KENNETH S. KENDLER ◽  
JONATHAN W. KUHN ◽  
CAROL A. PRESCOTT

Background. In animals, early trauma can produce long-lasting changes in sensitivity to the pathogenic effects of stress. To explore whether similar processes occur in humans, we examine whether childhood sexual abuse (CSA) in women alters sensitivity in adulthood to the depressogenic effects of stressful life events (SLEs).Method. A history of CSA was obtained from a population-based sample of 1404 female adult twins. Cox Proportional hazard models were used to predict onsets of episodes of DSM-III-R major depression (MD) in the past year from previously assessed levels of neuroticism (N), CSA and past-year SLEs scored on long-term contextual threat.Results. In the best-fit model, onset of MD was predicted by CSA, SLEs and N. Individuals with CSA (and especially with severe CSA) had both an overall increased risk for MD and a substantially increased sensitivity to the depressogenic effects of SLEs. A ‘dose–response’ relationship between severity of CSA and sensitivity to SLEs was clearer in those with low to average levels of N than in those with high levels of N.Conclusion. As documented with physiological responses to a standardized laboratory stressor, CSA increases stress sensitivity in women in a more naturalistic setting. Both genetic and early environmental risk factors can produce long-term increase in the sensitivity of individuals to depressogenic life experiences.


2016 ◽  
Vol 21 (4) ◽  
pp. 544-555 ◽  
Author(s):  
Rita Fjeldsted ◽  
Thomas William Teasdale ◽  
Martin Jensen ◽  
Annette Erlangsen

1996 ◽  
Vol 26 (6) ◽  
pp. 1239-1252 ◽  
Author(s):  
D. L. Foley ◽  
M. C. Neale ◽  
K. S. Kendler

SynopsisThis study investigates the basis of individual variation in exposure to stressful life events (SLEs). A population based sample of 547 MZ and 390 DZ female–female twin pairs, aged between 17 and 55 years, were surveyed by two structured interviews, separated by at least 1 year, that enquired about SLEs experienced during the preceding 12 months. Data were analysed with a model that resolves occasion specific (‘random’) versus enduring (‘stable’) influences on SLEs. The latter is partitioned into that due to genetic, familial environmental and unique environmental factors. We demonstrate that both random factors and stable individual differences underlie variation in self-reported exposure to SLEs. For most network events this stable variance makes a relatively small contribution to the total variance in SLEs exposure and is almost entirely due to genetic or familial environmental effects. Stable individual differences are more important determinants of personal SLEs, and these reflect both familial factors as well as previous experiences unshared by relatives.


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