To send content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send content items to your Kindle, first ensure firstname.lastname@example.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
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
Email your librarian or administrator to recommend adding this to your organisation's collection.