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Previous studies have examined associations of cardiometabolic factors with depression and cognition separately.
To determine if depressive symptoms mediate the association between cardiometabolic factors and cognitive decline in two community studies.
Data for the analyses were drawn from the Rotterdam Study, the Netherlands (n = 2940) and the Whitehall II study, UK (n = 4469).
Mediation analyses suggested a direct association between cardiometabolic factors and cognitive decline and an indirect association through depression: poorer cardiometabolic status at time 1 was associated with a higher level of depressive symptoms at time 2 (standardised regression coefficient 0.07 and 0.06, respectively), which, in turn, was associated with greater cognitive decline between time 2 and time 3 (standardised regression coefficient of −0.15 and −0.41, respectively).
Evidence from two independent cohort studies suggest an association between cardiometabolic dysregulation and cognitive decline and that depressive symptoms tend to precede this decline.
Studies have suggested both adverse and protective associations of obesity with depressive symptoms. We examined the contribution of environmental and heritable factors in this association. Participants were same-sex twin pairs from two population-based twin cohort studies, the Older Finnish Twin Cohort (n = 8,215; mean age = 44.1) and the US Midlife Development in the United States (MIDUS; n = 1,105; mean age = 45.1). Body mass index (BMI) was calculated from self-reported height and weight. Depressive symptoms were assessed using Beck's Depression Inventory (BDI; Finnish Twin Cohort), and by negative and positive affect scales (MIDUS). In the Finnish Twin Cohort, higher BMI was associated with higher depressive symptoms in monozygotic (MZ) twins (B = 2.01, 95% CI = 1.0, 3.0) and dizygotic (DZ) twins (B = 1.17, 0.5, 1.9) with BMI >22. This association was observed in within-pair analysis in DZ twins (B = 1.47, CI = 0.4, 2.6) but not in within-pair analysis of MZ twins (B = 0.03, CI = -1.9, 2.0). Consistent with the latter result, a bivariate genetic model indicated that the association between higher BMI and higher depressive symptoms was largely mediated by genetic factors. The results of twin-pair analysis and bivariate genetic model were replicated in the MIDUS sample. These findings suggest an association between obesity and higher depressive symptoms, which is largely explained by shared heritable biological mechanisms.
The contribution of education and intelligence to resilience against
age-related cognitive decline is not clear, particularly in the presence
of ‘normal for age’ minor brain abnormalities.
Participants (n = 208, mean age 69.2 years, s.d. = 5.4)
in the Whitehall II imaging substudy attended for neuropsychological
testing and multisequence 3T brain magnetic resonance imaging. Images
were independently rated by three trained clinicians for global and
hippocampal atrophy, periventricular and deep white matter changes.
Although none of the participants qualified for a clinical diagnosis of
dementia, a screen for cognitive impairment (Montreal Cognitive
Assessment (MoCA) <26) was abnormal in 22%. Hippocampal atrophy, in
contrast to other brain measures, was associated with a reduced MoCA
score even after controlling for age, gender, socioeconomic status, years
of education and premorbid IQ. Premorbid IQ and socioeconomic status were
associated with resilience in the presence of hippocampal atrophy.
Independent contributions from a priori risk (age,
hippocampal atrophy) and resilience (premorbid function, socioeconomic
status) combine to predict measured cognitive impairment.
Hypertension is associated with an increased risk of dementia and
depression with uncertain longitudinal associations with brain
To examine lifetime blood pressure as a predictor of brain structure in
A total of 190 participants (mean age 69.3 years) from the Whitehall II
study were screened for hypertension six times (1985–2013). In 2012–2013,
participants had a 3T-magnetic resonance imaging (MRI) brain scan. Data
from the MRI were analysed using automated and visual measures of global
atrophy, hippocampal atrophy and white matter hyperintensities.
Longitudinally, higher mean arterial pressure predicted increased
automated white matter hyperintensities (P<0.002).
Cross-sectionally, hypertensive participants had increased automated
white matter hyperintensities and visually rated deep white matter
hyperintensities. There was no significant association with global or
Long-term exposure to high blood pressure predicts hyperintensities,
particularly in deep white matter. The greatest changes are seen in those
with severe forms of hypertension, suggesting a dose–response
Identifying modifiable risk factors for cognitive decline may inform prevention of dementia.
To examine the combined impact of cigarette smoking and heavy alcohol consumption on cognitive decline from midlife.
Prospective cohort study (Whitehall II cohort) with three clinical examinations in 1997/99, 2002/04 and 2007/09. Participants were 6473 adults (72% men), mean age 55.76 years (s.d. = 6.02) in 1997/99. Four cognitive tests, assessed three times over 10 years, combined into a global z-score (mean 0, s.d. = 1).
Age-related decline in the global cognitive score was faster in individuals who were smoking heavy drinkers than in non-smoking moderate alcohol drinkers (reference group). The interaction term (P = 0.04) suggested that the combined effects of smoking and alcohol consumption were greater than their individual effects. Adjusting for age, gender, education and chronic diseases, 10-year decline in global cognition was −0.42 z-scores (95% Cl −0.45 to −0.39) for the reference group. In individuals who were heavy alcohol drinkers who also smoked the decline was −0.57 z-scores (95% Cl −0.67 to −0.48); 36% faster than the reference group.
Individuals who were smokers who drank alcohol heavily had a 36% faster cognitive decline, equivalent to an age-effect of 2 extra years over 10-year follow-up, compared with individuals who were non-smoking moderate drinkers.
Background: Cardiovascular risk factors and diseases are important etiological factors in depression, particularly late-life depression. Brain changes associated with vascular disease and depression can be detected using magnetic resonance imaging. Using diffusion tensor imaging (DTI), we investigated whether the Framingham Stroke Risk Profile (FSRP), a well-validated risk prediction algorithm, is associated with changes in white-matter connectivity. We hypothesized that depressed participants would show reduced white-matter integrity with higher FSRP, and non-depressed controls (matched for mean vascular risk) would show minimal co-variance with white-matter changes.
Methods: Thirty-six participants with major depression (age 71.8 ± 7.7 years, mean FSRP 10.3 ± 7.6) and 25 controls (age 71.8 ± 7.3 years, mean FSRP 10.1 ± 7.7) were clinically interviewed and examined, followed by 60-direction DTI on a 3.0 Tesla scanner. Image analysis was performed using FSL tools (www.fmrib.ox.ac.uk/fsl) to assess the correlation between FSRP and fractional anisotropy (FA). Voxelwise statistical analysis of the FA data was carried out using Tract Based Spatial Statistics. The significance threshold for correlations was set at p < 0.05 using threshold-free cluster-enhancement. Partial correlation analysis investigated significant correlations in each group.
Results: Participants in the depressed group showed highly significant correlations between FSRP and FA within the body of corpus callosum (r = −0.520, p = 0.002), genu of corpus callosum (r = −0.468, p = 0.005), splenium of corpus callosum (r = −0.536, p = 0.001), and cortico-spinal tract (r = −0.473, p = 0.005). In controls, there was only one significant correlation in the body of corpus callosum (r = −0.473, p = 0.023).
Conclusions: FSRP is associated with impairment in white-matter integrity in participants with depression; these results suggest support for the vascular depression hypothesis.
Studies of diet and depression have focused primarily on individual nutrients.
To examine the association between dietary patterns and depression using an overall diet approach.
Analyses were carried on data from 3486 participants (26.2% women, mean age 55.6 years) from the Whitehall II prospective cohort, in which two dietary patterns were identified: ‘whole food’ (heavily loaded by vegetables, fruits and fish) and ‘processed food’ (heavily loaded by sweetened desserts, fried food, processed meat, refined grains and high-fat dairy products). Self-reported depression was assessed 5 years later using the Center for Epidemiologic Studies – Depression (CES–D) scale.
After adjusting for potential confounders, participants in the highest tertile of the whole food pattern had lower odds of CES–D depression (OR = 0.74, 95% CI 0.56–0.99) than those in the lowest tertile. In contrast, high consumption of processed food was associated with an increased odds of CES–D depression (OR = 1.58, 95% CI 1.11–2.23).
In middle-aged participants, a processed food dietary pattern is a risk factor for CES–D depression 5 years later, whereas a whole food pattern is protective.
Prospective data on the association between common mental disorders and
obesity are scarce, and the impact of ageing on this association is
To examine the association between common mental disorders and obesity
(body mass index 30 kg/m2) across the adult life course.
The participants, 6820 men and 3346 women, aged 35–55 were screened four
times during a 19-year follow-up (the Whitehall II study). Each screening
included measurements of mental disorders (the General Health
Questionnaire), weight and height.
The excess risk of obesity in the presence of mental disorders increased
with age (P = 0.004). The estimated proportion of people
who were obese was 5.7% at age 40 both in the presence and absence of
mental disorders, but the corresponding figures were 34.6% and 27.1% at
age 70. The excess risk did not vary by gender or according to ethnic
group or socioeconomic position.
The association between common mental disorders and obesity becomes
stronger at older ages.
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