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Symptoms of anxiety and depression across adulthood and blood pressure in late middle age: the 1946 British birth cohort.

ABSTRACT: Previous studies testing the hypothesis that symptoms of anxiety and depression increase blood pressure (BP) levels show inconsistent and limited findings. We examined the association between those symptoms across adult life and BP in late middle age.Using data from 1683 participants from the MRC NSHD, we investigated associations between affective symptoms at ages 36, 43, 53 and 60-64 years and SBP and DBP at age 60-64. Multivariable linear regression was used to examine the effect on BP of affective symptoms at each age separately and as a categorical cumulative score based on the number of times an individual was classified as a 'case'. Models were adjusted for sex, BMI, educational attainment, socio-economic position, heart rate, lifestyle factors and antihypertensive treatment.In fully adjusted models, we observed lower SBP in study members with case-level symptoms at one to two time-points [-1.83?mmHg; 95% confidence interval (CI) -3.74 to 0.01] and at three to four time-points (-3.93?mmHg; 95% CI -7.19 to -0.68) compared with those never meeting case criteria suggesting a cumulative inverse impact of affective symptoms on SBP across adulthood (P value for trend 0.022). Sex and BMI had a large impact on the estimates while not other confounders. Potential mediators such as heart rate and lifestyle behaviours had a little impact on the association. SBP at age 36 and behavioural changes across adulthood, as additional covariates, had a little impact on the association. A similar but weaker trend was observed for DBP.A cumulative effect of symptoms of anxiety and depression across adulthood results in lower SBP in late middle age that is not explained by lifestyle factors and antihypertensive treatment. Mechanisms by which mood may impact BP should be investigated.

SUBMITTER: Tikhonoff V

PROVIDER: S-EPMC4166011 | biostudies-literature | 2014 Aug

REPOSITORIES: biostudies-literature

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Symptoms of anxiety and depression across adulthood and blood pressure in late middle age: the 1946 British birth cohort.

Tikhonoff Valérie V Hardy Rebecca R Deanfield John J Friberg Peter P Kuh Diana D Muniz Graciela G Pariante Carmine M CM Hotopf Matthew M Richards Marcus M

Journal of hypertension 20140801 8

<h4>Objective</h4>Previous studies testing the hypothesis that symptoms of anxiety and depression increase blood pressure (BP) levels show inconsistent and limited findings. We examined the association between those symptoms across adult life and BP in late middle age.<h4>Methods</h4>Using data from 1683 participants from the MRC NSHD, we investigated associations between affective symptoms at ages 36, 43, 53 and 60-64 years and SBP and DBP at age 60-64. Multivariable linear regression was used ...[more]

PMID: 24906173

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Project description:BackgroundMidlife hypertension confers increased risk for cognitive impairment in late life. The sensitive period for risk exposure and extent that risk is mediated through amyloid or vascular-related mechanisms are poorly understood. We aimed to identify if, and when, blood pressure or change in blood pressure during adulthood were associated with late-life brain structure, pathology, and cognition.MethodsParticipants were from Insight 46, a neuroscience substudy of the ongoing longitudinal Medical Research Council National Survey of Health and Development, a birth cohort that initially comprised 5362 individuals born throughout mainland Britain in one week in 1946. Participants aged 69-71 years received T1 and FLAIR volumetric MRI, florbetapir amyloid-PET imaging, and cognitive assessment at University College London (London, UK); all participants were dementia-free. Blood pressure measurements had been collected at ages 36, 43, 53, 60-64, and 69 years. We also calculated blood pressure change variables between ages. Primary outcome measures were white matter hyperintensity volume (WMHV) quantified from multimodal MRI using an automated method, amyloid-β positivity or negativity using a standardised uptake value ratio approach, whole-brain and hippocampal volumes quantified from 3D-T1 MRI, and a composite cognitive score-the Preclinical Alzheimer Cognitive Composite (PACC). We investigated associations between blood pressure and blood pressure changes at and between 36, 43, 53, 60-64, and 69 years of age with WMHV using generalised linear models with a gamma distribution and log link function, amyloid-β status using logistic regression, whole-brain volume and hippocampal volumes using linear regression, and PACC score using linear regression, with adjustment for potential confounders.FindingsBetween May 28, 2015, and Jan 10, 2018, 502 individuals were assessed as part of Insight 46. 465 participants (238 [51%] men; mean age 70·7 years [SD 0·7]; 83 [18%] amyloid-β-positive) were included in imaging analyses. Higher systolic blood pressure (SBP) and diastolic blood pressure (DBP) at age 53 years and greater increases in SBP and DBP between 43 and 53 years were positively associated with WMHV at 69-71 years of age (increase in mean WMHV per 10 mm Hg greater SBP 7%, 95% CI 1-14, p=0·024; increase in mean WMHV per 10 mm Hg greater DBP 15%, 4-27, p=0·0057; increase in mean WMHV per one SD change in SBP 15%, 3-29, p=0·012; increase in mean WMHV per 1 SD change in DBP 15%, 3-30, p=0·017). Higher DBP at 43 years of age was associated with smaller whole-brain volume at 69-71 years of age (-6·9 mL per 10 mm Hg greater DBP, -11·9 to -1·9, p=0·0068), as were greater increases in DBP between 36 and 43 years of age (-6·5 mL per 1 SD change, -11·1 to -1·9, p=0·0054). Greater increases in SBP between 36 and 43 years of age were associated with smaller hippocampal volumes at 69-71 years of age (-0·03 mL per 1 SD change, -0·06 to -0·001, p=0·043). Neither absolute blood pressure nor change in blood pressure predicted amyloid-β status or PACC score at 69-71 years of age.InterpretationHigh and increasing blood pressure from early adulthood into midlife seems to be associated with increased WMHV and smaller brain volumes at 69-71 years of age. We found no evidence that blood pressure affected cognition or cerebral amyloid-β load at this age. Blood pressure monitoring and interventions might need to start around 40 years of age to maximise late-life brain health.FundingAlzheimer's Research UK, Medical Research Council, Dementias Platform UK, Wellcome Trust, Brain Research UK, Wolfson Foundation, Weston Brain Institute, Avid Radiopharmaceuticals.

Project description:Investigating associations between metabolites and late midlife cognitive function could reveal potential markers and mechanisms relevant to early dementia. Here, we systematically explored the metabolic correlates of cognitive outcomes measured across the seventh decade of life, while untangling influencing life course factors. Using levels of 1019 metabolites profiled by liquid chromatography-mass spectrometry (age 60-64), we evaluated relationships between metabolites and cognitive outcomes in the British 1946 Birth Cohort (N = 1740). We additionally conducted pathway and network analyses to allow for greater insight into potential mechanisms, and sequentially adjusted for life course factors across four models, including sex and blood collection (Model 1), Model 1 + body mass index and lipid medication (Model 2), Model 2 + social factors and childhood cognition (Model 3) and Model 3 + lifestyle influences (Model 4). After adjusting for multiple tests, 155 metabolites, 10 pathways and 5 network modules were associated with cognitive outcomes. Of the 155, 35 metabolites were highly connected in their network module (termed 'hub' metabolites), presenting as promising marker candidates. Notably, we report relationships between a module comprised of acylcarnitines and processing speed which remained robust to life course adjustment, revealing palmitoylcarnitine (C16) as a hub (Model 4: β = -0.10, 95% confidence interval = -0.15 to -0.052, P = 5.99 × 10-5). Most associations were sensitive to adjustment for social factors and childhood cognition; in the final model, four metabolites remained after multiple testing correction, and 80 at P < 0.05. Two modules demonstrated associations that were partly or largely attenuated by life course factors: one enriched in modified nucleosides and amino acids (overall attenuation = 39.2-55.5%), and another in vitamin A and C metabolites (overall attenuation = 68.6-92.6%). Our other findings, including a module enriched in sphingolipid pathways, were entirely explained by life course factors, particularly childhood cognition and education. Using a large birth cohort study with information across the life course, we highlighted potential metabolic mechanisms associated with cognitive function in late midlife, suggesting marker candidates and life course relationships for further study.

Project description:ObjectiveTo examine whether different lifetime patterns of cigarette smoking are associated with chronic widespread pain (CWP) and chronic regional pain (CRP) at age 68.DesignProspective cohort study.SettingEngland, Scotland and Wales.ParticipantsUp to 2347 men and women from the Medical Research Council National Survey of Health and Development, who have been followed up since birth in 1946 and provided sufficient information on cigarette smoking across adulthood to be classified as never smoker, predominantly non-smoker, predominantly smoker or lifelong smoker and pain assessment at age 68.Primary outcome measuresPain was self-reported at age 68, and CWP was defined according to American College of Rheumatology criteria. Participants who reported having pain for ≥3 months but who did not meet the CWP definition were classified as having CRP; those who reported pain which had lasted for <3 months were classified as 'other' pain. No pain was the reference group.ResultsFindings from multinomial logistic regression models indicated that compared with never smokers, predominantly non-smokers, predominantly smokers and lifelong smokers all had an increased risk of CWP; relative risk ratios=1.70(95% CI 1.16 to 2.49); 2.10(95% CI 1.34 to 3.28) and 1.88(95% CI 0.99 to 3.57), respectively, after adjusting for sex, own occupational class, educational level, body mass index, leisure time physical activity, alcohol intake, long-standing illness and symptoms of anxiety and depression. No association was observed between smoking history and CRP or other pain.ConclusionsThese results suggest that exposure to cigarette smoking at any stage in adulthood was associated with higher risk of CWP in later adulthood; highlighting the ongoing importance of smoking prevention programmes. It also suggests that assessment of lifetime smoking behaviour may be more useful in identifying those at greater risk of CWP in later life than assessment of current smoking status.

Project description:BackgroundFew studies have examined the impact of childhood obesity on later kidney disease, and consequently, our understanding is very limited.Study designLongitudinal population-based cohort.Setting & participantsThe Medical Research Council National Survey of Health and Development, a socially stratified sample of 5,362 singletons born in 1 week in March 1946 in England, Scotland, and Wales, of which 4,340 were analyzed.PredictorEarly-life overweight latent classes (never, prepubertal only, pubertal onset, or always), derived from repeated measurements of body mass index between ages 2 and 20 years.Outcomes & measurementsThe primary outcome was chronic kidney disease (CKD), defined as creatinine- or cystatin C-based estimated glomerular filtration rate (eGFRcr and eGFRcys, respectively) <60 mL/min/1.73 m² or urine albumin-creatinine ratio (UACR) ≥3.5 mg/mmol measured at age 60-64 years. Associations were explored through regression analysis, with adjustment for socioeconomic position, smoking, physical activity level, diabetes, hypertension, and overweight at ages 36 and 53 years.Results2.3% of study participants had eGFRcr <60 mL/min/1.73 m², 1.7% had eGFRcys <60 mL/min/1.73 m², and 2.9% had UACR ≥3.5 mg/mmol. Relative to being in the never-overweight latent class, being in the pubertal-onset- or always-overweight latent classes was associated with eGFRcys-defined CKD (OR, 2.04; 95% CI, 1.09-3.82). Associations with CKD defined by eGFRcr (OR, 1.27; 95% CI, 0.71-2.29) and UACR (OR, 1.33; 95% CI, 0.70-2.54) were less marked, but in the same direction. Adjustment for lifestyle and health factors had little impact on effect estimates.LimitationsA low prevalence of CKD resulted in low statistical power. No documentation of chronicity for outcomes. All-white study population restricts generalizability.ConclusionsBeing overweight in early life was found to be associated with eGFRcys-defined CKD in later life. The associations with CKD defined by eGFRcr and UACR were less marked, but in the same direction. Reducing or preventing overweight in the early years of life may significantly reduce the burden of CKD in the population.

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Symptoms of anxiety and depression across adulthood and blood pressure in late middle age: the 1946 British birth cohort.

Publications

Symptoms of anxiety and depression across adulthood and blood pressure in late middle age: the 1946 British birth cohort.

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