Associations between sporting physical activity and cognition in mid and later-life: Evidence from two cohorts.

Evidence has linked sporting leisure time physical activity (sporting-LTPA) to healthy cognition throughout adulthood. This may be due to the physiological effects of physical activity (PA), or to other, psychosocial facets of sport. We examined associations between sporting-LTPA and cognition while adjusting for device-measured PA volume devoid of context, both in midlife (N = 4041) participants from the 1970 British Cohort Study and later-life (N = 957) participants from the British Regional Heart Study. Independent of device-measured PA, we identified positive associations between sporting-LTPA and cognition. Sports with team/partner elements were strongly positively associated with cognition, suggesting LTPA context may be critical to this relationship.

Comparison of variance estimators for meta-analysis of instrumental variable estimates.

Background: Mendelian randomization studies perform instrumental variable (IV) analysis using genetic IVs. Results of individual Mendelian randomization studies can be pooled through meta-analysis. We explored how different variance estimators influence the meta-analysed IV estimate. Methods: Two versions of the delta method (IV before or after pooling), four bootstrap estimators, a jack-knife estimator and a heteroscedasticity-consistent (HC) variance estimator were compared using simulation. Two types of meta-analyses were compared, a two-stage meta-analysis pooling results, and a one-stage meta-analysis pooling datasets. Results: Using a two-stage meta-analysis, coverage of the point estimate using bootstrapped estimators deviated from nominal levels at weak instrument settings and/or outcome probabilities ≤ 0.10. The jack-knife estimator was the least biased resampling method, the HC estimator often failed at outcome probabilities ≤ 0.50 and overall the delta method estimators were the least biased. In the presence of between-study heterogeneity, the delta method before meta-analysis performed best. Using a one-stage meta-analysis all methods performed equally well and better than two-stage meta-analysis of greater or equal size. Conclusions: In the presence of between-study heterogeneity, two-stage meta-analyses should preferentially use the delta method before meta-analysis. Weak instrument bias can be reduced by performing a one-stage meta-analysis.

Prospective study of circulating soluble CD40 ligand concentrations and the incidence of cardiovascular disease in a nested prospective case-control study of older men and women.

BACKGROUND: CD40 ligand(CD40L) is implicated in atherosclerotic plaque formation. OBJECTIVES: We investigated prospective associations between circulating soluble CD40L and myocardial infraction (MI) or stroke in an older general population cohort, accounting for established and novel cardiovascular risk factors. METHODS: Baseline serum CD40L (sCD40L) was measured in incident MI (n = 368) and stroke (n = 304) cases and two controls per case, 'nested' in prospective UK studies of 4252 men and 4286 women aged 60-79 years, sampled from general practices in Britain in 1998-2000, with 7-year follow-up for fatal and non-fatal MI and stroke. RESULTS: sCD40L was higher in smokers and negatively associated with lung function and positively associated with total cholesterol and markers of inflammation, but not with other established cardiovascular disease (CVD) risk factors. Geometric mean sCD40L levels did not differ between MI cases and controls (5.94 ng mL(-1) vs. 5.82 ng mL(-1); P = 0.5) or between stroke cases and controls (5.61 ng mL(-1) vs. 5.28 ng mL(-1), P = 0.1). There was no strong evidence for elevated risk of MI or stroke in multivariable models comparing participants in the top to those in the bottom third of sCD40L. Age-adjusted odds ratios (ORs) were 1.39 [95% confidence interval (CI) 0.98, 1.96] for MI and 1.16 (0.78, 1.73) for stroke. These attenuated to 1.24 (95% CI 0.86, 1.79) and 1.18 (0.78, 1.78), respectively, after adjustment for established and novel CVD risk factors. CONCLUSIONS: sCD40L is associated with other inflammatory markers but is not itself a strong independent risk marker for either stroke or MI.

Cotinine-assessed second-hand smoke exposure and risk of cardiovascular disease in older adults.

OBJECTIVES: To examine whether second-hand smoke (SHS) exposure measured by serum cotinine is associated with increased coronary heart disease (CHD) and stroke risk among contemporary older British adults. DESIGN: Prospective population-based study with self-reported medical history and health behaviours. Fasting blood samples were analysed for serum cotinine and cardiovascular disease (CVD) risk markers. SETTING: Primary care centres in 25 British towns in 1998-2001. PATIENTS: 8512 60-79-year-old men and women selected from primary care registers. MAIN OUTCOME MEASURES: Fatal and non-fatal myocardial infarction (MI; n=445) and stroke (n=386) during median 7.8-year follow-up. MAIN EXPOSURE: Observational study of serum cotinine assayed from fasting blood sample using liquid chromatography tandem mass spectrometry method, and self-reported smoking history. RESULTS: Among 5374 non-smokers without pre-existing CVD, geometric mean cotinine was 0.15 ng/ml (IQR 0.05-0.30). Compared with non-smokers with cotinine < or =0.05 ng/ml, higher cotinine levels (0.06-0.19, 0.2-0.7 and 0.71-15.0 ng/ml) showed little association with MI; adjusted HRs were 0.92 (95% CI 0.63 to 1.35), 1.07 (0.73 to 1.55) and 1.09 (0.69 to 1.72), p(trend)=0.69. Equivalent HRs for stroke were 0.82 (0.55 to 1.23), 0.74 (0.48 to 1.13) and 0.69 (0.41 to 1.17), p(trend)=0.065. The adjustment for sociodemographic, behavioural and CVD risk factors had little effect on the results. The HR of MI for smokers (1-9 cigarettes/day) compared with non-smokers with cotinine < or =0.05 ng/ml was 2.14 (1.39 to 3.52) and 1.03 (0.52 to 2.04) for stroke. CONCLUSIONS: In contemporary older men and women, SHS exposure (predominantly at low levels) was not related to CHD or stroke risks, but we cannot rule out the possibility of modest effects at higher exposure levels.

Secondhand smoke (SHS) exposure is associated with circulating markers of inflammation and endothelial function in adult men and women.

AIMS: Secondhand smoke (SHS) exposure is associated with elevated CHD risks. Yet the pathways through which this may operate have not been investigated in epidemiologic studies with objective SHS exposure measures and a wide range of CHD risk factors associated with active smoking. Therefore we investigate associations between SHS exposure and CHD risk factors, to clarify how SHS exposure may raise risk of CHD. METHODS: Cross-sectional population-based study of 5029 men and women aged 59-80 years from primary care practices in Great Britain. Smoking, behavioural and demographic information was reported in questionnaires; nurses made physical measurements and took blood samples for analysis of serum cotinine and markers of inflammation, hemostasis and endothelial dysfunction. RESULTS: Active cigarette smokers had lower albumin and higher triglycerides, CRP, IL-6, white cell count, fibrinogen, blood viscosity, factor VIII, VWF and t-PA than non-smokers. Among non-smokers, serum cotinine levels were independently positively associated with CRP, fibrinogen, factor VIII, VWF and t-PA and inversely associated with albumin, after adjustment for age, gender, social and behavioural factors. The differences in CRP, fibrinogen and albumin between cotinine < or =0.05 and >0.7 ng/ml were one-third to one half the size of differences between cotinine < or =0.05 ng/ml and current smokers, but were of similar magnitude for VWF and t-PA. CONCLUSIONS: Endothelial, inflammatory and haemostatic markers related to CHD risk showed independent associations with SHS exposure in the same direction as those for active smoking. Results aid understanding of the associations between SHS exposure and elevated CHD risks.

Cognitive development in childhood and drinking behaviour over two decades in adulthood.

BACKGROUND/AIMS: Childhood cognition predicts adult morbidity and mortality, potentially working through health behaviours. This study investigates if childhood cognition influences life course (i) non-drinking and (ii) binge drinking and pathways through which this might act-namely, childhood behaviour problems, adult social position and educational qualifications. METHODS: Prospective cohort of British births in March 1958, with information on cognition at 7, 11 and 16 years and alcohol use at 23, 33 and 42 years. Non-drinkers drank "infrequently/on special occasions" or "never". Binge drinkers consumed >or=10 units/occasion (men) and >or=7 units/occasion (women). RESULTS: Lower cognitive ability increased the odds of non-drinking at each adult survey (for example, for men at 42 years OR 1.52 (95% CI 1.34 to 1.72) per SD decrease in 7-year maths). Associations remained after adjustment for pathway factors (i) behaviour problems, (ii) adult social position and (iii) educational qualifications. Decreased ability rank across childhood (7-16 years) also increased odds of non-drinking at 42 years, but the association operated via pathway factors. Lower 7-year ability elevated the odds of 42-year binge drinking, operating via pathway factors. Declining ability rank across childhood also increased the odds of adult binge drinking; associations operated through behavioural problems, adult social position and qualifications. In women, the decline in risk of binge drinking from an age 23-year peak to 42 years was associated with higher 7-year score. CONCLUSIONS: Poorer childhood cognition was associated with non-drinking and binge drinking up to the early 40s. Associations between childhood cognition and drinking status may mediate between childhood cognition and adult health.

Lifecourse socioeconomic predictors of midlife drinking patterns, problems and abstention: findings from the 1958 British Birth Cohort Study.

BACKGROUND: Research suggests that outcomes associated with drinking may differ depending upon patterns of consumption, drinking related symptoms and social problems. This paper investigated socioeconomic predictors (measuring multiple indices, period and consistency of disadvantage) of midlife drinking patterns. METHODS: Socioeconomic information from the 1958 British Birth Cohort Study (n=9146) included: manual socioeconomic position and owner/buyer residential tenure (7, 11, 16, 33 and 42 y), and educational attainment (33 y). At 45 y, the overlap between drinking patterns was explored using the Alcohol Use Disorders Identification Test. Patterns included: 'Moderate-binge' (binge drinkers with low-problem scores, consuming within UK sensible drinking weekly guidelines); Low-Problem Heavy (LPH) drinkers (regardless of binge); 'Problem' (and heavy or binge) and 'Non-/occasional' (< or =monthly) drinkers. These categories were compared to 'Low-risk' drinkers. RESULTS: Socioeconomic disadvantage was consistently associated with moderate-binge, non-/occasional and problem but not LPH drinking. The highest risk was associated with multiple and persistent disadvantage across childhood and adulthood; this risk was partially accounted for education. Non-/occasional and moderate-binge drinking was predicted by disadvantage during childhood alone. The socioeconomic disadvantage of non-/occasional drinkers was not explained by past problem or heavy drinking. CONCLUSIONS: Socioeconomic disadvantage across the lifecourse was consistently linked to specific drinking patterns. Furthermore, associations linking socioeconomic disadvantage with drinking patterns will typically be underestimated if multiple and persistent disadvantage is not investigated. The role of persistent socioeconomic disadvantage in the poor health of non-drinkers and moderate-binge drinkers needs investigation. The findings support current initiatives targeting the reduction of social and individual costs associated with specific drinking patterns.

Adolescent drinking level and adult binge drinking in a national birth cohort.

AIMS: To assess (i) continuities in binge drinking across adulthood and (ii) the association between adolescent drinking level and adult binge drinking. DESIGN: Population-based prospective birth cohort. SETTING: England, Scotland and Wales. PARTICIPANTS: All births during one week in March 1958 (n = 8520 in analysis). MEASUREMENTS: Alcohol consumption reported at 16, 23, 33 and 42 years. Binge drinkers were identified by dividing number of units of alcohol consumed in the last week by usual drinking frequency, with limits of >/=10 units/occasion for men and >/=7 for women. FINDINGS: Four in five cohort members drank alcohol at least twice a month. Prevalences of binge drinking at 23, 33 and 42 years among men were 37%, 28% and 31% and among women 18%, 13% and 14%. Most binge drinkers in adulthood changed drinking status during this period. Nevertheless, binge drinking at age 23 increased the odds of binge drinking at 42 years: odds ratio (OR) 2.10 (95% CI 1.85, 2.39) for men; OR 1.56 (95% CI 1.29,1.89) for women. Women who rarely or never drank aged 16 were less likely than light drinkers (0-2 units/week) to binge drink as adults, OR at 23 years 0.65 (95% CI 0.55, 0.77). Men who were heavier drinkers (>/=7 units/week) at 16 years were more likely than light drinkers to binge drink throughout adulthood; at 42 years, OR 1.64 (95% CI 1.33, 2.08). CONCLUSIONS: Binge drinking is common in British men and women throughout adulthood with continuities between the 20s and 40s. Adolescent drinking has a modest although important association with adult binge drinking.