Eric B. Loucks

Educational attainment and cigarette smoking: a causal association?

BACKGROUND Despite abundant evidence that lower education is associated with a higher risk of smoking, whether the association is causal has not been convincingly established. METHODS We investigated the association between education and lifetime smoking patterns in a birth cohort established in 1959 and followed through adulthood (n = 1311). We controlled for a wide range of potential confounders that were measured prior to school entry, and also estimated sibling fixed effects models to control for unmeasured familial vulnerability to smoking. RESULTS In the full sample of participants, regression analyses adjusting for multiple childhood factors (including socioeconomic status, IQ, behavioural problems, and medical conditions) indicated that the number of pack-years smoked was higher among individuals with less than high school education [rate ratio (RR) = 1.58, confidence interval (CI) = 1.31, 1.91]. However, in the sibling fixed effects analysis the RR was 1.23 (CI = 0.80, 1.93). Similarly, adjusted models estimated in the full sample showed that individuals with less than high school education had fewer short-term (RR = 0.40; CI = 0.23, 0.69) and long-term (RR = 0.59; CI = 0.42, 0.83) quit attempts, and were less likely to quit smoking (odds ratio = 0.34; CI = 0.19, 0.62). The effects of education on quitting smoking were attenuated in the sibling fixed effects models that controlled for familial vulnerability to smoking. CONCLUSIONS A substantial portion of the education differential in smoking that has been repeatedly observed is attributable to factors shared by siblings that contribute to shortened educational careers and to lifetime smoking trajectories. Reducing disparities in cigarette smoking, including educational disparities, may therefore require approaches that focus on factors early in life that influence smoking risk over the adult life span.

Associations Between Childhood Socioeconomic Position and Adulthood Obesity

Childhood socioeconomic position (SEP) is inversely associated with cardiovascular disease and all-cause mortality. Obesity in adulthood may be a biologic mechanism. Objectives were to systematically review literature published between 1998 and 2008 that examined associations of childhood SEP with adulthood obesity. Five databases (Cochrane Library, MEDLINE, EMBASE, PsycINFO, Web of Science) were searched for studies from any country, in any language. Forty-eight publications based on 30 studies were identified. In age-adjusted analyses, inverse associations were found between childhood SEP and adulthood obesity in 70% (14 of 20) of studies in females and 27% (4 of 15) in males. In studies of females showing inverse associations between childhood SEP and adulthood obesity, typical effect sizes in age-adjusted analyses for the difference in body mass index between the highest and lowest SEP were 1.0-2.0 kg/m(2); for males, effect sizes were typically 0.2-0.5 kg/m(2). Analyses adjusted for age and adult SEP showed inverse associations in 47% (8 of 17) of studies in females and 14% (2 of 14) of studies in males. When other covariates were additionally adjusted for, inverse associations were found in 4 of 12 studies in females and 2 of 8 studies in males; effect sizes were typically reduced compared with analyses adjusted for age only. In summary, the findings suggest that childhood SEP is inversely related to adulthood obesity in females and not associated in males after adjustment for age. Adulthood SEP and other obesity risk factors may be the mechanisms responsible for the observed associations between childhood SEP and adulthood obesity.

Life-Course Socioeconomic Position and Incidence of Coronary Heart Disease The Framingham Offspring Study

Cumulative exposure to socioeconomic disadvantage across the life course may be inversely associated with coronary heart disease (CHD); the mechanisms are not fully clear. An objective of this study was to determine whether cumulative life-course socioeconomic position (SEP) is associated with CHD incidence in a well-characterized US cohort that had directly assessed childhood and adulthood measures of SEP and prospectively measured CHD incidence. Furthermore, analyses aimed to evaluate whether adjustment for CHD risk factors reduces the association between cumulative life-course SEP and CHD. The authors examined 1,835 subjects who participated in the Framingham Heart Study Offspring Cohort from 1971 through 2003 (mean age, 35.0 years; 52.4% women). Childhood SEP was measured as fathers education; adulthood SEP was assessed as own education and occupation. CHD incidence included myocardial infarction, coronary insufficiency, and coronary death. Cox proportional hazards analyses indicated that cumulative SEP was associated with incident CHD after adjustment for age and sex (hazard ratio = 1.82, 95% confidence interval: 1.17, 2.85 for low vs. high cumulative SEP score). Adjustment for CHD risk factors reduced that magnitude of association (hazard ratio = 1.29, 95% confidence interval: 0.78, 2.13). These findings underscore the potential importance of CHD prevention and treatment efforts for those whose backgrounds include low SEP throughout life.

SOCIAL NETWORKS AND INFLAMMATORY MARKERS IN THE FRAMINGHAM HEART STUDY

Lack of social integration predicts coronary heart disease mortality in prospective studies; however, the biological pathways that may be responsible are poorly understood. The specific aims of this study were to examine whether social networks are associated with serum concentrations of the inflammatory markers interleukin-6 (IL-6), C-reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1) and monocyte chemoattractant protein-1 (MCP-1). Participants in the Framingham Study attending examinations from 1998 to 2001 (n=3267) were eligible for inclusion in the study. Social networks were assessed using the Berkman-Syme Social Network Index (SNI). Concentrations of IL-6, CRP, sICAM-1 and MCP-1 were measured in fasting serum samples. Multivariable linear regression analyses were used to assess the association of social networks with inflammatory markers adjusting for potential confounders including age, smoking, blood pressure, total:HDL cholesterol ratio, body mass index, lipid-lowering and antihypertensive medication, diabetes, cardiovascular disease, depression and socioeconomic status. Results found that the SNI was significantly inversely associated with IL-6 in men (p=0.03) after adjusting for potential confounders. In age-adjusted analyses, social networks also were significantly inversely associated with IL-6 for women (p=0.03) and were marginally to modestly associated with CRP and sICAM-1 for men (p=0.08 and 0.02, respectively), but these associations were not significant in the multivariate analyses. In conclusion, social networks were found to be inversely associated with interleukin-6 levels in men. The possibility that inflammatory markers may be potential mediators between social integration and coronary heart disease merits further investigation.

Individual-level socioeconomic status is associated with worse asthma morbidity in patients with asthma.

BackgroundLow socioeconomic status (SES) has been linked to higher morbidity in patients with chronic diseases, but may be particularly relevant to asthma, as asthmatics of lower SES may have higher exposures to indoor (e.g., cockroaches, tobacco smoke) and outdoor (e.g., urban pollution) allergens, thus increasing risk for exacerbations.MethodsThis study assessed associations between adult SES (measured according to educational level) and asthma morbidity, including asthma control; asthma-related emergency health service use; asthma self-efficacy, and asthma-related quality of life, in a Canadian cohort of 781 adult asthmatics. All patients underwent a sociodemographic and medical history interview and pulmonary function testing on the day of their asthma clinic visit, and completed a battery of questionnaires (Asthma Control Questionnaire, Asthma Quality of Life Questionnaire, and Asthma Self-Efficacy Scale). General Linear Models assessed associations between SES and each morbidity measure.ResultsLower SES was associated with worse asthma control (F = 11.63, p < .001), greater emergency health service use (F = 5.09, p = .024), and worse asthma self-efficacy (F = 12.04, p < .01), independent of covariates. Logistic regression analyses revealed that patients with <12 years of education were 55% more likely to report an asthma-related emergency health service visit in the last year (OR = 1.55, 95%CI = 1.05-2.27). Lower SES was not related to worse asthma-related quality of life.ConclusionsResults suggest that lower SES (measured according to education level), is associated with several indices of worse asthma morbidity, particularly worse asthma control, in adult asthmatics independent of disease severity. Results are consistent with previous studies linking lower SES to worse asthma in children, and add asthma to the list of chronic diseases affected by individual-level SES.

Sleep Duration, Insomnia, and Coronary Heart Disease Among Postmenopausal Women in the Women's Health Initiative

BACKGROUND Long and short sleep duration are associated with increased risk for coronary heart disease (CHD) and cardiovascular disease (CVD); however, evidence is inconsistent. We sought to identify whether self-reported sleep duration and insomnia, based on a validated questionnaire, are associated with increased incident CHD and CVD among postmenopausal women. METHODS Womens Health Initiative Observational Study Participants (N=86,329; 50-79 years) who reported on sleep at baseline were followed for incident CVD events. Associations of sleep duration and insomnia with incident CHD and CVD were evaluated using Cox proportional hazards models over 10.3 years. RESULTS Women with high insomnia scores had elevated risk of CHD (38%) and CVD (27%) after adjustment for age and race, and in fully adjusted models (hazard ratio [HR]=1.19, 95% confidence interval [CI] 1.09-1.30; 1.11 95% CI 1.03-2.00). Shorter (≤5 hours) and longer (≥10 hours) sleep duration demonstrated significantly higher incident CHD (25%) and CVD (19%) in age- and race-adjusted models, but this was not significant in fully adjusted models. Formal tests for interaction indicated significant interactions between sleep duration and insomnia for risk of CHD (p<0.01) and CVD (p=0.02). Women with high insomnia scores and long sleep demonstrated the greatest risk of incident CHD compared to midrange sleep duration (HR=1.93, 95% CI 1.06-3.51) in fully adjusted models. CONCLUSIONS Sleep duration and insomnia are associated with CHD and CVD risk, and may interact to cause almost double the risk of CHD and CVD. Additional research is needed to understand how sleep quality modifies the association between prolonged sleep and cardiovascular outcomes.

Divergent associations of adaptive and maladaptive emotion regulation strategies with inflammation.

OBJECTIVE Recent work suggests effective emotion regulation may protect against risk of developing coronary heart disease (CHD), but the mechanisms remain unknown. Strategies for regulating emotions vary in how effectively they mitigate potentially toxic effects of stressful life experiences, and therefore may be differentially associated with CHD risk. In this study, we examined the emotion regulation strategies of reappraisal and suppression in relation to inflammation, a biological state associated with both stress and CHD. We hypothesized that suppression would be associated with elevated inflammation and reappraisal would be associated with lower levels of inflammation. METHODS We studied adult offspring (n = 379; mean age = 42.2 years) of Collaborative Perinatal Project participants, a national cohort of pregnant women enrolled in 1959-1966. Validated measures of two emotion regulation strategies were examined: reappraisal and suppression. Inflammation was measured as plasma C-reactive protein (CRP) levels. We fit multiple linear regression models predicting CRP while controlling for demographic, socioeconomic, and health factors, including depressive symptoms, measured across the life course. RESULTS A 1 standard deviation increase in reappraisal was associated with significantly lower CRP (b = -0.18, SE = 0.06, p < .01) controlling for demographics. This relation was somewhat attenuated in life course models, with adulthood body mass index partially explaining the association. A 1 standard deviation increase in suppression was associated with significantly higher CRP (b = 0.21, SE = 0.05, p < .001), and this association was not substantively attenuated with further covariate adjustment. CONCLUSION Adaptive emotion regulation was associated with lower levels of inflammation and maladaptive emotion regulation was associated with higher levels of inflammation. If these associations are confirmed by prospective and experimental studies, such evidence may provide insight into novel targets for interventions to promote health and reduce cardiovascular risk.

Adiposity is associated with DNA methylation profile in adipose tissue

BACKGROUND Adiposity is a risk factor for type 2 diabetes and cardiovascular disease, suggesting an important role for adipose tissue in the development of these conditions. The epigenetic underpinnings of adiposity are not well understood, and studies of DNA methylation in relation to adiposity have rarely focused on target adipose tissue. Objectives were to evaluate whether genome-wide DNA methylation profiles in subcutaneous adipose tissue and peripheral blood leukocytes are associated with measures of adiposity, including central fat mass, body fat distribution and body mass index. METHODS Participants were 106 men and women (mean age 47 years) from the New England Family Study. DNA methylation was evaluated using the Infinium HumanMethylation450K BeadChip. Adiposity phenotypes included dual-energy X-ray absorptiometry-assessed android fat mass, android:gynoid fat ratio and trunk:limb fat ratio, as well as body mass index. RESULTS Adipose tissue genome-wide DNA methylation profiles were associated with all four adiposity phenotypes, after adjusting for race, sex and current smoking (omnibus p-values <0.001). After further adjustment for adipose cell-mixture effects, associations with android fat mass, android:gynoid fat ratio, and trunk:limb fat ratio remained. In gene-specific analyses, adiposity phenotypes were associated with adipose tissue DNA methylation in several genes that are biologically relevant to the development of adiposity, such as AOC3, LIPE, SOD3, AQP7 and CETP. Blood DNA methylation profiles were not associated with adiposity, before or after adjustment for blood leukocyte cell mixture effects. CONCLUSION Findings show that DNA methylation patterns in adipose tissue are associated with adiposity.

Associations of education with 30 year life course blood pressure trajectories: Framingham Offspring Study

BackgroundEducation is inversely associated with cardiovascular disease incidence in developed countries. Blood pressure may be an explanatory biological mechanism. However few studies have investigated educational gradients in longitudinal blood pressure trajectories, particularly over substantial proportions of the life course. Study objectives were to determine whether low education was associated with increased blood pressure from multiple longitudinal assessments over 30 years. Furthermore, we aimed to separate antecedent effects of education, and other related factors, that might have caused baseline differences in blood pressure, from potential long-term effects of education on post-baseline blood pressure changes.MethodsThe study examined 3890 participants of the Framingham Offspring Study (mean age 36.7 years, 52.0% females at baseline) from 1971 through 2001 at up to 7 separate examinations using multivariable mixed linear models.ResultsMixed linear models demonstrated that mean systolic blood pressure (SBP) over 30 years was higher for participants with ≤12 vs. ≥17 years education after adjusting for age (3.26 mmHg, 95% CI: 1.46, 5.05 in females, 2.26 mmHg, 95% CI: 0.87, 3.66 in males). Further adjustment for conventional covariates (antihypertensive medication, smoking, body mass index and alcohol) reduced differences in females and males (2.86, 95% CI: 1.13, 4.59, and 1.25, 95% CI: -0.16, 2.66 mmHg, respectively). Additional analyses adjusted for baseline SBP, to evaluate if there may be educational contributions to post-baseline SBP. In analyses adjusted for age and baseline SBP, females with ≤12 years education had 2.69 (95% CI: 1.09, 4.30) mmHg higher SBP over follow-up compared with ≥17 years education. Further adjustment for aforementioned covariates slightly reduced effect strength (2.53 mmHg, 95% CI: 0.93, 4.14). Associations were weaker in males, where those with ≤12 years education had 1.20 (95% CI: -0.07, 2.46) mmHg higher SBP over follow-up compared to males with ≥17 years of education, after adjustment for age and baseline blood pressure; effects were substantially reduced after adjusting for aforementioned covariates (0.34 mmHg, 95% CI: -0.90, 1.68). Sex-by-education interaction was marginally significant (p = 0.046).ConclusionEducation was inversely associated with higher systolic blood pressure throughout a 30-year life course span, and associations may be stronger in females than males.

Social integration is associated with fibrinogen concentration in elderly men.

Objective: The objective of this study was to determine whether social integration is associated with plasma concentrations of fibrinogen in an elderly population. Methods: Participants (ages 70–79; n = 375 men and 425 women) were part of the MacArthur Successful Aging Study, a longitudinal study from three community-based cohorts in the United States, who have relatively high physical and cognitive functioning. Social integration was measured using a social integration score, which assessed marital status, number of contacts with family and friends, frequency of religious service attendance, and participation in voluntary organizations. Fibrinogen concentrations were measured in plasma using an automated clot-rate assay. Cross-sectional multivariate logistic regression analyses were performed. Results: Social integration was significantly associated with elevated concentrations of fibrinogen (>336 mg/dL) in men after adjusting for smoking, alcohol consumption, physical activity, body mass index, comorbidity, physical functioning, depression, age, race, and education (odds ratio [OR] = 2.29, 95% confidence interval [CI] = 1.07–4.89, p = .03 for having elevated fibrinogen in the least integrated quartile versus the most integrated quartile). There was no significant association between social integration and fibrinogen in women (multivariate-adjusted OR = 0.57, 95% CI = 0.27–1.21, p = .15). Conclusions: Social integration is associated with fibrinogen concentrations in elderly men. This provides evidence of a biologic mechanism that may help explain the observed associations between social integration and mortality in men. There may be gender differences in the physiological pathways by which social integration influences health. OR = odds ratio; CI = confidence interval.