| 1. |
- Crawford, Andrew A., et al.
(författare)
-
Morning plasma cortisol as a cardiovascular risk factor : findings from prospective cohort and Mendelian randomization studies
- 2019
-
Ingår i: European Journal of Endocrinology. - : Bioscientifica. - 0804-4643 .- 1479-683X. ; 181:4, s. 429-438
-
Tidskriftsartikel (refereegranskat)abstract
- Objective: The identification of new causal risk factors has the potential to improve cardiovascular disease (CVD) risk prediction and the development of new treatments to reduce CVD deaths. In the general population, we sought to determine whether cortisol is a causal risk factor for CVD and coronary heart disease (CHD).Design and methods: Three approaches were adopted to investigate the association between cortisol and CVD/CHD. First, we used multivariable regression in two prospective nested case-control studies (total 798 participants, 313 incident CVD/CHD with complete data). Second, a random-effects meta-analysis of these data and previously published prospective associations was performed (total 6680 controls, 696 incident CVD/CHD). Finally, one- and two-sample Mendelian randomization analyses were performed (122,737 CHD cases, 547,261 controls for two-sample analyses).Results: In the two prospective nested case-control studies, logistic regression adjusting for sex, age, BMI, smoking and time of sampling, demonstrated a positive association between morning plasma cortisol and incident CVD (OR: 1.28 per 1 SD higher cortisol, 95% CI: 1.06-1.54). In the meta-analysis of prospective studies, the equivalent result was OR: 1.18, 95% CI: 1.06-1.31. Results from the two-sample Mendelian randomization were consistent with these positive associations: OR: 1.06, 95% Cl: 0.98-1.15.Conclusions: All three approaches demonstrated a positive association between morning plasma cortisol and incident CVD. Together, these findings suggest that elevated morning cortisol is a causal risk factor for CVD. The current data suggest strategies targeted at lowering cortisol action should be evaluated for their effects on CVD.
|
|
| 2. |
- Lynch, Rebekka, et al.
(författare)
-
Lifetime exposure to violence and other life stressors and hair cortisol concentration in women
- 2022
-
Ingår i: Stress. - : Informa UK Limited. - 1025-3890 .- 1607-8888. ; 25:1, s. 48-56
-
Tidskriftsartikel (refereegranskat)abstract
- Women are exposed to a variety of life stressors, particularly violence, during their lifetime which increases the risk of developing various psychiatric and somatic diseases, with the dysregulated secretion of cortisol as one potential biological mechanism. We examined the association between violence and other life stressors and hair cortisol concentration (HCC) in a population of urban women. We included 470 adult women (age = 21-86 years) attending the Cancer Detection Clinic in Iceland. The Life Stressor Checklist-Revised (LSC-R; 30-items) was used to assess exposure. HCC was measured with liquid chromatography coupled with tandem mass spectrometry. We used linear regression models to assess the association between life stressors and log-transformed HCC. The median HCC (pg/mg) in the study population was 4.9 (range 0.6-616.6). HCC was not associated with background covariates, including age (p = 0.868), education level (p = 0.824), marital status (p = 0.545), income (p = 0.363), occupation (p = 0.192), but associated with current smoking (p = 0.013). We noted a 3.3% (95% CI: 0.17-6.6%) associated increase in HCC per endorsed life stressor after adjusting for age and smoking, while non-violent life stressors were not associated with HCC. Per endorsed violence item, we observed a 10.2% (95% CI: 1.4-19.7%) associated increase in HCC after age and smoking adjustment. Women with lifetime exposure to both physical and sexual violence presented with higher HCC than unexposed women (p = 0.010), after age and smoking adjustment. Lifetime exposure to violence was associated with higher levels of HCC in a community sample of women. These findings need confirmation with prospective studies.
|
|
| 3. |
- Schindler, Lena, et al.
(författare)
-
Cognitive functioning in posttraumatic stress disorder before and after cognitive-behavioral therapy
- 2020
-
Ingår i: Journal of Anxiety Disorders. - : Elsevier BV. - 0887-6185. ; 74
-
Tidskriftsartikel (refereegranskat)abstract
- Although substantial evidence suggests altered executive functioning and autobiographical memory in posttraumatic stress disorder (PTSD), the clinical significance of these findings remains unclear. Here, we investigated the effects of cognitive-behavioral therapy (CBT) on different aspects of cognitive functioning (working memory, interference susceptibility, conflict adaptation, autobiographical memory) in PTSD patients in a pre-post control group design with a nested cross-sectional element. Cross-sectional analyses at baseline were conducted on 58 PTSD patients, 39 traumatized (TC), and 45 non-traumatized controls (NTC). Intervention effects were investigated before and after 25 CBT sessions in 25 PTSD and 34 untreated NTC individuals assessed in parallel. At baseline, PTSD patients showed higher conflict adaptation than the NTC group and less autobiographical memory specificity than both control groups, suggesting particularly the latter to be a correlate of PTSD. No consistent evidence for treatment-induced improvements in cognitive functioning emerged on the group level or from associations between intra-individual clinical and cognitive changes. Analyses on the role of cognitive functioning on subsequent treatment effects revealed a predictive effect of backward digit span on CBT-induced reductions of depressiveness, but no other significant effects. Our findings highlight the need for further research to identify more relevant predictors of differential treatment response.
|
|
| 4. |
- Schindler, Lena, et al.
(författare)
-
Lifetime Trauma History and Cognitive Functioning in Major Depression and Their Role for Cognitive-Behavioral Therapy Outcome
- 2021
-
Ingår i: Clinical Psychology in Europe. - : Leibniz Institute for Psychology (ZPID). - 2625-3410. ; 3:3
-
Tidskriftsartikel (refereegranskat)abstract
- Background: While cognitive-behavioral therapy (CBT) is the gold-standard psychological treatment for major depression (MD), non-response and lacking stability of treatment gains are persistent issues. Potential factors influencing treatment outcome might be lifetime trauma history and possibly associated primarily prefrontal-cortex- and hippocampus-dependent cognitive alterations. Method: We investigated MD and healthy control participants with (MD+T+, n = 37; MD-T+, n = 39) and without lifetime trauma history (MD+T-, n = 26; MD-T-, n = 45) regarding working memory, interference susceptibility, conflict adaptation, and autobiographical memory specificity. Further, MD+T+ (n = 21) and MD+T- groups (n = 16) were re-examined after 25 CBT sessions, with MD-T- individuals (n = 34) invited in parallel in order to explore the stability of cognitive. This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International License, CC BY 4.0, which permits unrestricted use, distribution, and reproduction, provided the original work is properly cited. alterations and the predictive value of lifetime trauma history, cognitive functioning, and their interaction for treatment outcome. Results: On a cross-sectional level, MD+T+ showed the highest conflict adaptation, but MD+T- the lowest autobiographical memory specificity, while no group differences emerged for working memory and interference susceptibility. Clinical improvement did not differ between groups and cognitive functioning remained stable over CBT. Further, only a singular predictive association of forward digit span, but no other facets of baseline cognitive functioning, lifetime trauma history, or their interaction with treatment outcome emerged. Discussion: These results indicate differential roles of lifetime trauma history and psychopathology for cognitive functioning in MD, and add to the emerging literature on considering cognitive, next to clinical remission as a relevant treatment outcome.
|
|
