To examine the relation between IQ in childhood and vegetarianism in adulthood.
Prospective cohort study in which IQ was assessed by tests of mental ability at age 10 years and vegetarianism by self-report at age 30 years.
8170 men and women aged 30 years participating in the 1970 British cohort study, a national birth cohort.
Main outcome measures
Self-reported vegetarianism and type of diet followed.
366 (4.5%) participants said they were vegetarian, although 123 (33.6%) admitted eating fish or chicken. Vegetarians were more likely to be female, to be of higher social class (both in childhood and currently), and to have attained higher academic or vocational qualifications, although these socioeconomic advantages were not reflected in their income. Higher IQ at age 10 years was associated with an increased likelihood of being vegetarian at age 30 (odds ratio for one standard deviation increase in childhood IQ score 1.38, 95% confidence interval 1.24 to 1.53). IQ remained a statistically significant predictor of being vegetarian as an adult after adjustment for social class (both in childhood and currently), academic or vocational qualifications, and sex (1.20, 1.06 to 1.36). Exclusion of those who said they were vegetarian but ate fish or chicken had little effect on the strength of this association.
Higher scores for IQ in childhood are associated with an increased likelihood of being a vegetarian as an adult.
There is some evidence to suggest that obesity is a risk factor for the development of depression, although this is not a universal finding. This discordance might be ascribed to the existence of a ‘healthy obese phenotype’– that is, obesity in the absence of the associated burden of cardio-metabolic risk factors. We examined whether the association of obesity with depressive symptoms is dependent on the individual’s metabolic health. Participants were 3851 men and women (aged 63.0 ± 8.9 yrs, 45.1% men) from the English Longitudinal Study of Ageing, a prospective study of community dwelling older adults. Obesity was defined as body mass index ≥ 30 kg/m2. Based on blood pressure, HDL-cholesterol, triglycerides, glycated haemoglobin, and C-reactive protein, participants were classified as ‘metabolically healthy’ (0 or 1 metabolic abnormality) or ‘unhealthy’ (≥ 2 metabolic abnormalities). Depressive symptoms were assessed at baseline and at 2 years follow up using the 8-item Centre of Epidemiological Studies Depression (CES-D) scale. Obesity prevalence was 27.5%, but 34.3% of this group was categorized as metabolically healthy at baseline. Relative to non-obese healthy participants, after adjustment for baseline CES-D score and other covariates, the metabolically unhealthy obese participants had elevated risk of depressive symptoms at follow-up (odds ratio [OR] = 1.50, 95% CI, 1.05–2.15), although the metabolically healthy obese did not (OR = 1.38, 95% CI, 0.88–2.17). The association between obesity and risk of depressive symptoms appears to be partly dependent on metabolic health, although further work is required to confirm these findings.
C-reactive protein (CRP) is associated with the risk of cardiovascular disease (CVD); whether the effects are modified by diabetes status still is unclear. This study investigated these issues and assessed the added value of CRP to predictions.
RESEARCH DESIGN AND METHODS
Participants were drawn from representative samples of adults living in England and Scotland. Cox proportional hazards regression models were used to relate baseline plasma CRP with all-cause and CVD mortality during follow-up in men and women with and without diabetes. The added value of CRP to the predictions was assessed through c-statistic comparison and relative integrated discrimination improvement.
A total of 25,979 participants (4.9% with diabetes) were followed for a median of 93 months, during which period there were 2,767 deaths (957 from CVD). CRP (per SD loge) was associated with a 53% (95% CI 43–64) and 43% (38–49) higher risk of cardiovascular and all-cause mortality, respectively. These associations were log linear and did not differ according to diabetes status (both P ≥ 0.08 for interaction), sex, and other risk factors. Adding CRP to conventional risk factors improved predictions overall and separately by diabetes status but not for CVD mortality, although such improvements only were marginal based on several discrimination statistics.
The association between CRP and CVD was similar across diabetes status, and the effects are broadly similar across levels of other conventional risk factors.
Background: It has been suggested that dietary patterns are associated with future risk of depressive symptoms. However, there is a paucity of prospective data that have examined the temporality of this relation.
Objective: We examined whether adherence to a healthy diet, as defined by using the Alternative Healthy Eating Index (AHEI), was prospectively associated with depressive symptoms assessed over a 5-y period.
Design: Analyses were based on 4215 participants in the Whitehall II Study. AHEI scores were computed in 1991–1993 and 2003–2004. Recurrent depressive symptoms were defined as having a Center for Epidemiologic Studies Depression Scale score ≥16 or self-reported use of antidepressants in 2003–2004 and 2008–2009.
Results: After adjustment for potential confounders, the AHEI score was inversely associated with recurrent depressive symptoms in a dose-response fashion in women (P-trend < 0.001; for 1 SD in AHEI score; OR: 0.59; 95% CI: 0.47, 0.75) but not in men. Women who maintained high AHEI scores or improved their scores during the 10-y measurement period had 65% (OR: 0.35%; 95% CI: 0.19%, 0.64%) and 68% (OR: 0.32%; 95% CI: 0.13%, 0.78%) lower odds of subsequent recurrent depressive symptoms than did women who maintained low AHEI scores. Among AHEI components, vegetable, fruit, trans fat, and the ratio of polyunsaturated fat to saturated fat components were associated with recurrent depressive symptoms in women.
Conclusion: In the current study, there was a suggestion that poor diet is a risk factor for future depression in women.
It has been hypothesized that one way in which lower socioeconomic status (SES) affects health is by increasing the rate of biological aging. A widely used marker of biological aging is telomere length. Telomeres are structures at the ends of chromosomes that erode with increasing cell proliferation and genetic damage. We aimed to identify, through systematic review and meta-analysis, whether lower SES (greater deprivation) is associated with shorter telomeres. Thirty-one articles, including 29 study populations, were identified. We conducted 3 meta-analyses to compare the telomere lengths of persons of high and low SES with regard to contemporaneous SES (12 study populations from 10 individual articles), education (15 study populations from 14 articles), and childhood SES (2 study populations from 2 articles). For education, there was a significant difference in telomere length between persons of high and low SES in a random-effects model (standardized mean difference (SMD) = 0.060, 95% confidence interval (CI): 0.002, 0.118; P = 0.042), although a range of sensitivity analyses weakened this association. There was no evidence for an association between telomere length and contemporaneous SES (SMD = 0.104, 95% CI: −0.027, 0.236; P = 0.119) or childhood SES (SMD = −0.037, 95% CI: −0.143, 0.069; P = 0.491). These results suggest weak evidence for an association between SES (as measured by education) and biological aging (as measured by telomere length), although there was a lack of consistent findings across the SES measures investigated here.
biological aging; review, systematic; socioeconomic status; telomere length
The adverse effects of advancing maternal age on offspring's health and development are well understood. Much less is known about the impact of paternal age.
We explored paternal age-offspring cognition associations in 772 participants from the West of Scotland Twenty-07 study. Offspring cognitive ability was assessed using Part 1 of the Alice Heim 4 (AH4) test of General Intelligence and by reaction time (RT).
There was no evidence of a parental age association with offspring RT. However, we observed an inverse U-shaped association between paternal age and offspring AH4 score with the lowest scores observed for the youngest and oldest fathers. Adjustment for parental education and socioeconomic status somewhat attenuated this association. Adjustment for number of, particularly older, siblings further reduced the scores of children of younger fathers and appeared to account for the lower offspring scores in the oldest paternal age group.
We observed a paternal age association with AH4 but not RT, a measure of cognition largely independent of social and educational experiences. Factors such as parental education, socioeconomic status and number of, particularly older, siblings may play an important role in accounting for paternal age-AH4 associations. Future studies should include parental intelligence.
To examine the association of early adulthood blood pressure with CVD mortality, while accounting for middle-age hypertension.
Elevated blood pressure in middle-age is an established CVD risk factor, but evidence for association with measurements earlier in life is sparse.
HAHS is a cohort study of 18,881 male university students who had blood pressure measured at university entry (1914 –1952; mean age 18.3 years) and who responded to a questionnaire mailed in 1962/1966 (mean age 45.8 years) in which physician-diagnosed hypertension status was reported. Study members were subsequently followed for mortality until the end of 1998.
Following adjustment for age, BMI, smoking and physical activity at college entry, compared to men who were normotensive according to JNC-7 criteria (<120/<80mmHg) there was an elevated risk of CHD mortality (1,917 deaths) in those who were pre-hypertensive (120–139/80–89 mmHg) (hazards ratio; 95% confidence intervals: 1.21; 1.07, 1.36), stage 1 (140–159/90–99 mmHg) (1.46; 1.25, 1.70), and stage 2 hypertensive (≥160/≥100 mmHg) (1.89; 1.46, 2.45), incremental across categories (ptrend<0.001). After additional account for middle-age hypertension, estimates were somewhat attenuated but the pattern remained. Similar associations were apparent for total and CVD but not stroke mortality.
Higher blood pressure in early adulthood was associated with elevated risk of mortality from all-causes, CVD and CHD, but not stroke several decades later. Effects largely persisted after taking account of mediation by middle-age hypertension. Thus, the long-term benefits of blood pressure lowering in early adulthood are promising but supporting trial data are required.
blood pressure; cardiovascular disease mortality; epidemiology; blood pressure; lifecourse
A potential role for cardiovascular disease (CVD) risk factors in the aetiology of suicide has not been comprehensively examined. In addition to being small in scale and poorly characterized, existing studies very rarely sample Asian populations in whom risk factor–suicide relationships may plausibly differ to Caucasian groups. We examined the association between a series of CVD risk factors and future mortality from suicide.
Methods and results
The Korean Cancer Prevention Study is a prospective cohort study comprising 1 234 927 individuals (445 022 women) aged 30–95 years with extensive measurement of established CVD risk factors at baseline and subsequent mortality surveillance. Fourteen years of follow-up gave rise to 472 deaths (389 in men and 83 in women) from suicide. After adjustment for a range of covariates, in men, smoking hazard ratio; 95% CI: (current vs. never: 1.69; 1.27, 2.24), alcohol intake (1–24 g/day vs. none: 1.29; 1.00, 1.66), blood cholesterol (≥240 vs. <200 mg/dL: 0.54; 0.36, 0.80), body mass index (underweight vs. normal weight: 2.08; 1.26, 3.45), stature [quartile 1(lowest) vs. 4: 1.68; 1.23, 2.30], socioeconomic status [quartile 1(lowest) vs. 4: 1.65; 1.21, 2.24], and martial status (unmarried vs. other: 1.60; 0.83, 3.06) were related to suicide mortality risk. These associations were generally apparent in women, although of lower magnitude. Exercise and blood pressure were not associated with completed suicide.
In this cohort of Korean men and women, a series of CVD risk factors were associated with an elevated risk of future suicide mortality.
Cardiovascular disease; Risk factors; Epidemiology; Suicide
Background Adult height is known to be inversely related to coronary heart disease (CHD) risk. We sought to investigate transgenerational influence of parental height on offspring’s CHD risk.
Methods Parents took part in a cardiorespiratory disease survey in two Scottish towns during the 1970s, in which their physical stature was measured. In 1996, their offspring were invited to participate in a similar survey, which included an electrocardiogram recording and risk factor assessment.
Results A total of 2306 natural offspring aged 30–59 years from 1456 couples were subsequently flagged for notification of mortality and followed for CHD-related hospitalizations. Taller paternal and/or maternal height was associated with socio-economic advantage, heavier birthweight and increased high-density lipoprotein cholesterol in offspring. Increased height in fathers, but more strongly in mothers (risk ratio for 1 SD change in maternal height = 0.85; 95% confidence interval: 0.76 to 0.95), was associated with a lower risk of offspring CHD, adjusting for age, sex, other parental height and CHD risk factors.
Conclusion There is evidence of an association between taller parental, particularly maternal, height and lower offspring CHD risk. This may reflect an influence of early maternal growth on the intrauterine environment provided for her offspring.
Coronary heart disease; mortality; intergenerational; height
This glossary provides a guide to some concepts, findings and issues of discussion in the new field of research in which intelligence test scores are associated with mortality and morbidity. Intelligence tests are devised and studied by differential psychologists. Some of the major concepts in differential psychology are explained, especially those regarding cognitive ability testing. Some aspects of IQ (intelligence) tests are described and some of the major tests are outlined. A short guide is given to the main statistical techniques used by differential psychologists in the study of human mental abilities. There is a discussion of common epidemiological concepts in the context of cognitive epidemiology.
Published work assessing psychosocial stress (job strain) as a risk factor for coronary heart disease is inconsistent and subject to publication bias and reverse causation bias. We analysed the relation between job strain and coronary heart disease with a meta-analysis of published and unpublished studies.
We used individual records from 13 European cohort studies (1985–2006) of men and women without coronary heart disease who were employed at time of baseline assessment. We measured job strain with questions from validated job-content and demand-control questionnaires. We extracted data in two stages such that acquisition and harmonisation of job strain measure and covariables occurred before linkage to records for coronary heart disease. We defined incident coronary heart disease as the first non-fatal myocardial infarction or coronary death.
30 214 (15%) of 197 473 participants reported job strain. In 1·49 million person-years at risk (mean follow-up 7·5 years [SD 1·7]), we recorded 2358 events of incident coronary heart disease. After adjustment for sex and age, the hazard ratio for job strain versus no job strain was 1·23 (95% CI 1·10–1·37). This effect estimate was higher in published (1·43, 1·15–1·77) than unpublished (1·16, 1·02–1·32) studies. Hazard ratios were likewise raised in analyses addressing reverse causality by exclusion of events of coronary heart disease that occurred in the first 3 years (1·31, 1·15–1·48) and 5 years (1·30, 1·13–1·50) of follow-up. We noted an association between job strain and coronary heart disease for sex, age groups, socioeconomic strata, and region, and after adjustments for socioeconomic status, and lifestyle and conventional risk factors. The population attributable risk for job strain was 3·4%.
Our findings suggest that prevention of workplace stress might decrease disease incidence; however, this strategy would have a much smaller effect than would tackling of standard risk factors, such as smoking.
Finnish Work Environment Fund, the Academy of Finland, the Swedish Research Council for Working Life and Social Research, the German Social Accident Insurance, the Danish National Research Centre for the Working Environment, the BUPA Foundation, the Ministry of Social Affairs and Employment, the Medical Research Council, the Wellcome Trust, and the US National Institutes of Health.
The search for biomarkers of aging (BoAs) has been largely unsuccessful to-date and there is widespread skepticism about the prospects of finding any that satisfy the criteria developed by the American Federation of Aging Research. This may be because the criteria are too strict or because a composite measure might be more appropriate. Telomere length has attracted a great deal of attention as a candidate BoA. We investigate whether it meets the criteria to be considered as a single biomarker of aging, and whether it makes a useful contribution to a composite measure.
Using data from a large population based study, we show that telomere length is associated with age, with several measures of physical and cognitive functioning that are related to normal aging, and with three measures of overall health. In the majority of cases, telomere length adds predictive power to that of age, although it was not nearly as good a predictor overall. We used principal components analysis to form two composites from the measures of functioning, one including telomere length and the other not including it. These composite BoAs were better predictors of the health outcomes than chronological age. There was little difference between the two composites.
Telomere length does not satisfy the strict criteria for a BoA, but does add predictive power to that of chronological age. Equivocal results from previous studies might be due to lack of power or the choice of measures examined together with a focus on single biomarkers. Composite biomarkers of aging have the potential to outperform age and should be considered for future research in this area.
Little is known about psychological risk factors in cerebrovascular disease. We examined the association between psychological distress and risk of death due to cerebrovascular disease.
We obtained data from 68 652 adult participants of the Health Survey for England (mean age 54.9 [standard deviation 13.9] yr, 45.0% male sex) with no known history of cardiovascular diseases at baseline. We used the 12-item General Health Questionnaire (GHQ-12) to assess the presence of psychological distress. We followed participants for eight years for cause-specific death using linkage to national registers.
There were 2367 deaths due to cardiovascular disease during follow-up. Relative to participants with no symptoms of psychological distress (GHQ-12 score 0) at baseline, people with psychological distress (GHQ-12 score ≥ 4, 14.7% of participants) had an increased risk of death from cerebrovascular disease (adjusted hazard ratio [HR] 1.66, 95% confidence interval [CI] 1.32–2.08) and ischemic heart disease (adjusted HR 1.59, 95% CI 1.34–1.88). There was also evidence of a dose–response effect with increasing GHQ-12 score (p for trend < 0.001 in all analyses). Associations were only marginally attenuated after we adjusted for possible confounders, including socioeconomic status, smoking and use of antihypertensive medications.
Psychological distress was associated with increased risk of death due to cerebrovascular disease in a large population-representative cohort. These data suggest that the cardiovascular effects of psychological distress are not limited to coronary artery disease.
The authors aggregated the results of observational studies examining the association between long working hours and coronary heart disease (CHD). Data sources used were MEDLINE (through January 19, 2011) and Web of Science (through March 14, 2011). Two investigators independently extracted results from eligible studies. Heterogeneity between the studies was assessed using the I2 statistic, and the possibility of publication bias was assessed using the funnel plot and Egger's test for small-study effects. Twelve studies were identified (7 case-control, 4 prospective, and 1 cross-sectional). For a total of 22,518 participants (2,313 CHD cases), the minimally adjusted relative risk of CHD for long working hours was 1.80 (95% confidence interval (CI): 1.42, 2.29), and in the maximally (multivariate-) adjusted analysis the relative risk was 1.59 (95% CI: 1.23, 2.07). The 4 prospective studies produced a relative risk of 1.39 (95% CI: 1.12, 1.72), while the corresponding relative risk in the 7 case-control studies was 2.43 (95% CI: 1.81, 3.26). Little evidence of publication bias but relatively large heterogeneity was observed. Studies varied in size, design, measurement of exposure and outcome, and adjustments. In conclusion, results from prospective observational studies suggest an approximately 40% excess risk of CHD in employees working long hours.
cardiovascular diseases; coronary disease; employment; meta-analysis; myocardial infarction; review; work
Both anaemia and cardiovascular disease (CVD) are common in people with diabetes. While individually both characteristics are known to raise mortality risk, their combined influence has yet to be quantified. In this pooling project, we examined the combined impact of baseline haemoglobin levels and existing CVD on all-cause and CVD mortality in people with diabetes. We draw comparison of these effects with those apparent in diabetes-free individuals.
A combined analyses of 7 UK population-based cohorts resulted in 26,480 study members. There were 946 participants with physician-diagnosed diabetes, 2227 with anaemia [haemoglobin<13 g/dl (men) or <12 (women)], 2592 with existing CVD (stroke, ischaemic heart disease), and 21,396 with none of the conditions. Across diabetes and anaemia subgroups, and using diabetes-free, non-anaemic participants as the referent group, the adjusted hazard ratios (HR) were 1.46 (95% CI: 1.30–1.63) for anaemia, 1.67 (1.45–1.92) for diabetes, and 2.10 (1.55–2.85) for diabetes and anaemia combined. Across combined diabetes, anaemia and CVD subgroups, and compared with non-anaemic, diabetes-free and CVD-free participants, HR (95% CI) for all-cause mortality were 1.49 (1.32–1.69) anaemia, 1.60 (1.46–1.76) for existing CVD, and 1.66 (1.39–1.97) for diabetes alone. Equivalents were 2.13 (1.48–3.07) for anaemia and diabetes, 2.68 (2.14–3.36) for diabetes and existing CVD, and 3.25 (1.88–5.62) for the three combined. Patterns were similar for CVD mortality.
Individually, anaemia and CVD confer similar mortality risks in people with diabetes, and are excessively fatal in combination. Screening for anaemia would identify vulnerable diabetic patients whose outcomes can potentially be improved.
Objective To quantify the link between lower, subclinically symptomatic, levels of psychological distress and cause-specific mortality in a large scale, population based study.
Design Individual participant meta-analysis of 10 large prospective cohort studies from the Health Survey for England. Baseline psychological distress measured by the 12 item General Health Questionnaire score, and mortality from death certification.
Participants 68 222 people from general population samples of adults aged 35 years and over, free of cardiovascular disease and cancer, and living in private households in England at study baseline.
Main outcome measures Death from all causes (n=8365), cardiovascular disease including cerebrovascular disease (n=3382), all cancers (n=2552), and deaths from external causes (n=386). Mean follow-up was 8.2 years (standard deviation 3.5).
Results We found a dose-response association between psychological distress across the full range of severity and an increased risk of mortality (age and sex adjusted hazard ratio for General Health Questionnaire scores of 1-3 v score 0: 1.20, 95% confidence interval 1.13 to 1.27; scores 4-6: 1.43, 1.31 to 1.56; and scores 7-12: 1.94, 1.66 to 2.26; P<0.001 for trend). This association remained after adjustment for somatic comorbidity plus behavioural and socioeconomic factors. A similar association was found for cardiovascular disease deaths and deaths from external causes. Cancer death was only associated with psychological distress at higher levels.
Conclusions Psychological distress is associated with increased risk of mortality from several major causes in a dose-response pattern. Risk of mortality was raised even at lower levels of distress.
Dietary fats are routinely considered key determinants of cardiovascular risk, yet the scientific basis of this association has never been demonstrated using objective measures of fat intakes in a large prospective study in a general population.
Methods and results
Adipose tissue was taken from 3944 participants, predominantly aged 40–59 years, in Scotland, 1984–87. Percentages of individual fatty acids were measured using gas chromatography. Over a median of 19.5 years, 870 incident cardiovascular disease (CVD) events occurred. Hazard ratios (HRs) were obtained from Cox models and the additional prognostic value, accounting for variables in the Framingham and ASSIGN CVD risk scores, were assessed using discrimination indices. Adjusting for age, sex, total and HDL-cholesterol, systolic blood pressure, smoking, hypertensive medication use, diabetes, socio-economic status and family history, the percentage of monounsaturated adipose tissue fatty acids had a positive log-linear relationship with incident CVD: the HR comparing risk between the fourth and first quartiles was 1.29 (95% confidence interval: 1.05, 1.59). n-3 polyunsaturated fat showed the reverse trend, the corresponding result being 0.77 (0.63, 0.94). These two composite variables improved the classification of incident CVD events by 1.0 and 6.4%, respectively, with only the latter being significant at the 5% level.
A diet which is proportionately rich in polyunsaturated fat, as opposed to other fats, is expected to decrease the risk of CVD independently of the effects of common CVD risk factors, including social deprivation. Taking account of such diets improves the classification of future CVD events.
Fatty acids; Myocardial infarction; Stroke; Risk score
Background A number of prospective cohort studies have examined the association between intelligence in childhood or youth and life expectancy in adulthood; however, the effect size of this association is yet to be quantified and previous reviews require updating.
Methods The systematic review included an electronic search of EMBASE, MEDLINE and PSYCHINFO databases. This yielded 16 unrelated studies that met inclusion criteria, comprising 22 453 deaths among 1 107 022 participants. Heterogeneity was assessed, and fixed effects models were applied to the aggregate data. Publication bias was evaluated, and sensitivity analyses were conducted.
Results A 1-standard deviation (SD) advantage in cognitive test scores was associated with a 24% (95% confidence interval 23–25) lower risk of death, during a 17- to 69-year follow-up. There was little evidence of publication bias (Egger’s intercept = 0.10, P = 0.81), and the intelligence–mortality association was similar for men and women. Adjustment for childhood socio-economic status (SES) in the nine studies containing these data had almost no impact on this relationship, suggesting that this is not a confounder of the intelligence–mortality association. Controlling for adult SES in five studies and for education in six studies attenuated the intelligence–mortality hazard ratios by 34 and 54%, respectively.
Conclusions Future investigations should address the extent to which attenuation of the intelligence–mortality link by adult SES indicators is due to mediation, over-adjustment and/or confounding. The explanation(s) for association between higher early-life intelligence and lower risk of adult mortality require further elucidation.
Intelligence; mortality; meta-analysis; socio-economic factors; systematic review
To examine the relation of scores on tests of mental ability across childhood with established risk factors for premature mortality at the age of 30 years.
A prospective cohort study based on members of the British Cohort Study born in Great Britain in 1970 who had complete data on IQ scores at five (N = 8203) or 10 (N = 8171) years of age and risk factors at age 30 years.
In sex‐adjusted analyses, higher IQ score at age 10 years was associated with a reduced prevalence of current smoking (ORper 1 SD advantage in IQ 0.84; 95% CI 0.80, 0.88), overweight (0.88; 0.84, 0.92), obesity (0.84; 0.79, 0.92), and hypertension (0.90; 0.83, 0.98), and an increased likelihood of having given up smoking by the age of 30 years (1.25; 1.18, 1.24). These gradients were attenuated after adjustment for markers of socioeconomic circumstances across the life course, particularly education. There was no apparent relationship between IQ and diabetes. Essentially the same pattern of association was evident when the predictive value of IQ scores at five years of age was examined.
The mental ability–risk factor gradients reported in the present study may offer some insights into the apparent link between low pre‐adult mental ability and premature mortality.
mental ability; risk factors; mortality
While several plausible biological mechanisms have been advanced for the association between greater physical stature and lower coronary heart disease (CHD) risk in prospective cohort studies, the importance of one of the principal artifactua explanations – reverse causality due to shrinkage – remains unresolved. To explore this issue, studies with repeat measurements of height are required, however, to date, such data have been lacking.
We analysed data from the Whitehall II prospective cohort study of 3802 men and 1615 women who participated in a physical examination in 1985/88, had their height re-measured in 1997/99, and were then followed for fatal and non-fatal CHD.
A mean follow-up of 7.4 years after the second height measurement gave rise to 69 CHD events in men (18 in women). After adjustment for baseline CHD risk factors, greater loss of physical stature between survey and resurvey was associated with an increased risk of CHD in men (hazard ratio; 95% CI for a one SD increase: 1.24; 1.00, 1.53) but not women (0.93; 0.58, 1.50).
It is possible that reverse causality due to shrinkage may contribute to the inverse association between a single measurement of height and later CHD in other studies.
To examine the association between objectively measured second–hand-smoke (SHS) exposure and incident CVD death, and assess the extent to which this association can be explained through novel circulating markers of inflammation and haemostasis.
Existing evidence suggests there is an association between SHS and cardiovascular disease (CVD) risk, although the mechanisms remain poorly understood.
In a prospective study of 13,443 participants living in England and Scotland [aged 53.5, (SD 12.6 yrs), 52.3% women] we measured salivary cotinine (an objective marker of SHS exposure) and novel CVD biomarkers (C-reactive protein, fibrinogen) at baseline.
20.8% of the sample had high SHS exposure based on elevated levels of salivary cotinine (0.71 – 14.99 ng/mL). During a mean follow-up of 8 years, there were 1221 all-cause deaths and 364 CVD deaths. High SHS was associated with all-cause (age adjusted HR= 1.25, 95% CI, 1.02 – 1.53) and CVD death (age adjusted HR= 1.21, 95% CI, 0.85 – 1.73). High SHS was also associated with elevated CRP, which explained 48% of the association between SHS and CVD death. The excess risk of CVD associated with active smoking was exaggerated in relation to self report (age adjusted HR= 3.27, 95% CI, 2.48 – 4.31) compared with objective assessment (age adjusted HR= 2.44, 95% CI, 1.75 – 3.40).
Among a large representative sample of British adults we observed elevated levels of low grade inflammation in otherwise healthy participants exposed to high SHS, and this partly explained their elevated risk of CVD death.
cotinine; inflammation; nicotine; passive smoke; mortality; epidemiology
There is conflicting evidence regarding the association of hypertension with psychological distress, such as anxiety and depressive symptoms. The association may be due to a direct effect of the raised blood pressure; side effects of treatment; or the consequences of labelling. In a representative study of 33,105 adults (aged 51.7 ±12.1 yrs, 45.8% men) we measured levels of psychological distress using the 12-item General Health Questionnaire and collected blood pressure, data on history of hypertension diagnosis, and medication usage. Awareness of hypertension was confirmed through a physician’s diagnosis or the use of anti-hypertensive medication and unaware hypertension was defined by elevated clinic blood pressure (systolic/diastolic ≥140/90 mm Hg) without prior treatment or diagnosis. In comparison with normotensive participants, an elevated risk of distress (General Health Questionnaire score ≥4) was observed in aware hypertensive participants (multivariable adjusted odds ratio [OR]=1.57, 95% CI, 1.41 – 1.74), although not in unaware hypertensives (OR = 0.91, 95% CI, 0.78 – 1.07). Anti-hypertensive medication and co-morbidity was also associated with psychological distress although this did not explain the greater risk of distress in aware hypertensives. We observed a weak curvilinear association between systolic blood pressure and distress which suggested that distressed participants were more likely to have low or highly elevated blood pressure. These findings suggest that labelling individuals as hypertensive, rather than elevated blood pressure per se, may partially explain the greater levels of distress in patients treated for hypertension.
depression; anxiety; blood pressure; medication; cardiovascular risk; labelling
A series of studies have shown an association between high childhood IQ scores and reduced rates of total mortality in adulthood. Several mechanisms have been advanced to explain these relationships, including mediation via established risk factors. This study examines the association between childhood IQ and a range of established physiological and behavioural risk factors for premature mortality in adulthood.
Design, setting and participants
In 1962, 12 150 children took part in a school‐based survey when their IQ scores were extracted from educational records. When re‐surveyed forty years later (n = 7183; 63.7% response), they self‐reported information on risk factors for premature mortality (smoking, heavy alcohol consumption, obesity, height, hypertension and diabetes).
In sex‐adjusted analyses based on an analytical sample of 5340 (2687 women), higher childhood IQ scores were associated with a decreased prevalence of ever having smoked regularly in adulthood (ORper SD increase in IQ (95% CI): 0.77 (0.73 to 0.81)), heavy alcohol consumption (0.89 (0.84 to 0.94)), obesity (0.78 (0.72 to 0.83)) and overweight (0.86 (0.81 to 0.91)). Higher IQ scores were similarly related to a reduced prevalence of short stature and higher rates of smoking cessation in smokers; effects that were stronger in women (p value for interaction: ⩽0.04). Adjusting for indicators of early and, particularly, later‐life socioeconomic circumstances led to heavy attenuation of these gradients with statistical significance at conventional levels lost in most analyses.
The IQ–risk factor gradients reported may offer some insights into the apparent link between high pre‐adult IQ and reduced mortality rates.