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The mechanisms linking cardiovascular disease (CVD) and depression are still not established. We investigated the impact of mental vulnerability on the relationship between CVD and depression.
A total of 19,856 individuals from five cohorts of random samples of the background population in Copenhagen were followed from baseline (1983–2011) until 2017 in Danish registries. Additive hazard and Cox proportional hazard models were used to analyze the effects of confounding by mental vulnerability as well as interactions between mental vulnerability and CVD on the risk of depression.
During follow-up, 15.3% developed CVD, while 18.1% experienced depression. A strong positive association between CVD and depression (hazard ratio: 3.60 [95% confidence intervals (CI): 3.30; 3.92]) corresponding to 35.4 (95% CI: 31.7; 39.1) additional cases per 1,000 person-years was only slightly attenuated after adjustment for mental vulnerability in addition to other confounders. Synergistic interaction between CVD and mental vulnerability was identified in the additive hazard model. Due to interaction between CVD and mental vulnerability, CVD was associated with 50.9 more cases of depression per 1,000 person-years among individuals with high mental vulnerability compared with individuals with low mental vulnerability.
Mental vulnerability did not explain the strong relationship between CVD and depression. CVD was associated with additional cases of depression among individuals with higher mental vulnerability indicating that this group holds the greatest potential for intervention, for example, in rehabilitation settings.
Depression and cardiovascular diseases (CVDs) are common diseases and associated in a bidirectional manner.
To examine whether a bidirectional association between CVD and depression could be explained by shared risk factors, misclassification of disease measures or non-response.
A total of 10 population-based cohorts including 93 076 men and women (mean age 54.4 years, s.d. = 9.2) and an additional 10 510 men (mean age 51.2 years, s.d. = 0.3) were followed for subsequent depression, ischaemic heart disease (IHD) and stroke in the Danish National Patient Registry from health examinations between 1982 and 2015 and until end of follow-up in 2017–2018. Exposures were physicians’ diagnoses of IHD, stroke, depression or self-reported chest pain, depression, use of antidepressant medication and the Major Depression Inventory at the time of study entry in the Metropolit study. Associations were analysed using Cox proportional hazard regression with disease as time-dependent variables.
IHD and stroke were associated with subsequent depression (hazard ratio (HR) for IHD: 1.79, 95% CI 1.43–2.23 and HR for stroke: 2.62, 95% CI 2.09–3.29) and the associations were present in both men and women. Adjustment for the shared risk factors socioeconomic status, lifestyle, body mass index, statin use and serum lipids did not change the risk estimates. Furthermore, depression was associated with higher risk of subsequent IHD (HR = 1.63, 95% CI 1.36–1.95) and stroke (HR = 1.94, 95% CI 1.63–2.30). The associations were also present when the analyses were based on self-reported disease measures or restricted to include non-responders.
The bidirectional association between CVD and depression was not explained by shared risk factors, misclassification or non-response.
Depression has been cross-sectionally associated with short telomeres as a measure of biological age. However, the direction and nature of the association is currently unclear.
We examined whether short telomere length is associated with depression cross-sectionally as well as prospectively and genetically.
Telomere length and three polymorphisms, TERT, TERC and OBFC1, were measured in 67306 individuals aged 20–100 years from the Danish general population and associated with register-based attendance at hospital for depression and purchase of antidepressant medication.
Attendance at hospital for depression was associated with short telomere length cross-sectionally, but not prospectively. Further, purchase of antidepressant medication was not associated with short telomere length cross-sectionally or prospectively. Mean follow-up was 7.6 years (range 0.0–21.5). The genetic analyses suggested that telomere length was not causally associated with attendance at hospital for depression or with purchase of antidepressant medication.
Short telomeres were not associated with depression in prospective or in causal, genetic analyses.
No prospective studies have examined the role of C-reactive protein (CRP)
in late-onset bipolar disorder.
We tested the hypothesis that elevated levels of CRP are associated
cross-sectionally and prospectively with late-onset bipolar disorder, and
that such an association possibly is causal.
We performed cross-sectional and prospective analyses with a median
follow-up time of 5.9 years (interquartile range: 4.4– 7.6) in 78 809
individuals from the general population, and used genetic variants
influencing CRP levels to perform a Mendelian randomisation study.
Elevated levels of CRP were associated both cross-sectionally and
prospectively with late-onset bipolar disorder. When CRP was on a
continuous scale, a doubling in CRP yielded an observational odds ratio
for late-onset bipolar disorder of 1.28 (1.08–1.52) with a corresponding
causal odds ratio of 4.66 (0.89–24.3).
Elevated CRP is associated with increased risk of late-onset bipolar
disorder in the general population which was supported by the genetic
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