scholarly journals Association of myocardial infarction with stressful life events and psychiatric symptoms: a population based survey

2011 ◽  
Vol 17 (05) ◽  
pp. 398-403 ◽  
Author(s):  
Z.N. Hatmi ◽  
L.F. Nasiri ◽  
Z. Sodegianmehr ◽  
S. Mirkia ◽  
S. Darbooy
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.


2019 ◽  
Vol 2 (3) ◽  
pp. 12
Author(s):  
Dominique Ashley Bonneville ◽  
Jacqueline Stowkowy ◽  
Kali Brummitt ◽  
Benjamin I Goldstein ◽  
Glenda MacQueen ◽  
...  

Background: Sleep disturbances are common across many mental health disorders, with evidence suggesting a bidirectional relationship. Furthermore, there is evidence of a significant association between sleep disruption and worse symptomology in disorders such as anxiety, depression, and psychosis. Additionally, research has demonstrated the negative impact of stress and stressful life events on psychiatric illness progression. However, little is known about possible links between sleep disturbance and these psychiatric symptoms, ongoing stress, stressful life events and functioning, especially in adolescence and early adulthood, a time when many mental illnesses first begin. Exploring these relationships may allow for a better understanding of the role sleep disruption plays in the early stages of illness. Objective: The objective of this study is to investigate potential correlates of sleep disturbance in youth experiencing subthreshold psychiatric symptoms. Methods: This study included 160 youth, ages 12 to 25 who were help seeking due to experiencing distress, mild symptoms of anxiety or depression, and/or attenuated syndromes such as clinical high risk for psychosis. Youth meeting criteria for full psychiatric diagnoses were excluded. The Pittsburgh Sleep Quality Index was used to assess sleep disruption. A range of clinical symptoms were assessed using the Scale for Assessment of Psychosis-Risk Symptoms, The Calgary Depression Scale for Schizophrenia and the Generalized Anxiety Disorder 7-Item Scale. Current stress was assessed with the Daily Stress Inventory, and the K10 Distress Scale. Past history of major stress was measured with a Childhood Trauma and Abuse Scale, and the Life Events scale. Fourthly, functioning was assessed with the Global Functioning Scale: Social and Role. Results: Global sleep quality was most highly realted to subthreshold symptoms of anxiety (r=0.425, p<0.01), depression (r=0.420, p<0.01), and disorganized symptoms of psychosis (r=0.232, p<0.05). Additionally, global sleep was related to total distress (r=0.356, p<0.01), daily stress (r=0.268, p<0.01), and stressful life events (r=0.291, p<0.01). Social functioning did not reveal any significant correlations with sleep, however, role functioning (r=0.170, p<0.05) did exhibit a relationship with global sleep quality. Finally, bullying (r=0.196, p<0.05) and trauma (r=0.266, p<0.01) were significantly correlated with global sleep quality scores. Conclusion: This study provides early evidence for the interaction that sleep disruption may have with stress, trauma, bullying, and subthreshold psychiatric symptomology in youth. Further research is required to increase the understanding of these relationships early on in youth psychiatric illness progression.


2021 ◽  
Author(s):  
Ludvig Daae Bjørndal ◽  
Eivind Ystrom

Previous studies have found that stressful life events (SLEs) are associated with increased risk of adult depression. However, many studies are observational in nature and limited by methodological issues, such as potential confounding by genetic factors. Genetically informative studies, such as the co-twin control design, can strengthen causal inference in observational research. The co-twin control design involves comparing patterns of associations in the full sample and within dizygotic (DZ) and monozygotic twins (MZ). Discrete-time survival analysis has several benefits and multilevel survival analysis can incorporate frailty terms (random effects) to estimate the components of the biometric model. In the current study, we investigated associations between SLEs and depression risk in a population-based twin sample (N = 2299) with a co-twin control design. Associations were modelled using discrete-time survival analysis with biometric frailty terms. SLE occurrence was associated with increased depression risk. Co-twin control analyses indicated that this association was at least in part due to causal influence of SLE exposure on depression risk for event occurrence across all SLEs and of violent SLEs. Stronger within-pair estimates for economic SLEs compared with the full sample association could have resulted if the full sample association was suppressed or if within-pair estimates were inflated. If the former occurred, economic SLEs may represent particularly important risk factors for depression. A minor proportion of the total genetic risk of depression reflected genetic effects related to SLEs. Our findings have implications for future research on SLEs and depression.


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