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. MethodsWe investigated the association between education and lifetime smoking patterns in a birth cohort established in 1959 and followed through adulthood (n ¼ 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

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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.

Childhood adversity, characterized by abuse, neglect, and household dysfunction, is a problem that exerts a significant impact on individuals, families, and society. Growing evidence suggests that adverse childhood experiences (ACEs) are associated with health decline in adulthood, including cardiovascular disease (CVD). In the current review, we first provide an overview of the association between ACEs and CVD risk, with updates on the latest epidemiological evidence. Second, we briefly review plausible pathways by which ACEs could influence CVD risk, including traditional risk factors and novel mechanisms. Finally, we highlight the potential implications of ACEs in clinical and public health. Information gleaned from this review should help physicians and researchers in better understanding potential long-term consequences of ACEs and considering adapting current strategies in treatment or intervention for patients with ACEs.

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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.

This randomized controlled trial evaluated the effect of a mindfulness-based mobile health (mHealth) intervention, tailored to the pandemic context, among young adult students (N = 114) with elevated anxiety and/or depressive symptoms during quarantine in China, compared to a time-and attention-matched social support-based mHealth control. At baseline, postintervention (1 month), and 2-month follow-up, participants completed self-reports of primary outcomes (anxiety and depression), secondary outcomes (mindfulness and social support), and emotional suppression as a culturally relevant mechanism of change. Feasibility and acceptability were also evaluated. Using intent-to-treat (ITT) analysis, linear mixed effects models showed that compared to social support mHealth, mindfulness mHealth had a superior effect on anxiety ( p = .024, between-group d = 0.72). Both conditions improved on depression (baseline-to-FU ds > 1.10, between-group difference not significant, d = 0.36 favoring mindfulness). There was an interaction of Emotional suppression reduction × Condition in the improvement of anxiety and depression.

Background 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 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 inflammation. Methods We studied n=379 adult offspring (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 one standard deviation increase in reappraisal was associated with significantly lower CRP (b = −0.18, se=0.06, p<0.01) controlling for demographics. This relation was somewhat attenuated in life course models, with adulthood body mass index partially explaining the association. A one standard deviation increase in suppression was associated with significantly higher CRP (b=0.21, se=0.05, p<0.001) 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.