Socioeconomic position and intergenerational associations of ideal health behaviors

Background: Promoting ideal cardiovascular health behaviors is an objective of the American Heart Association 2020 goals. We hypothesized that ideal health behaviors of parents are associated with health behaviors of their adult offspring, and that higher socioeconomic position in either generation enhances intergenerational associations of ideal health behaviors.Design: Prospective cohort study.Methods: We included 1856 Young Finns Study participants who had repeated measurements of socioeconomic position (education, income, occupation), smoking status, body mass index, physical activity and diet from 2001, 2007 and 2011, and data on parental socioeconomic position and health behaviors from 1980. We calculated the total number of ideal behaviors in both generations using American Heart Association definitions. Intergenerational associations were examined using ordinal and linear multilevel regression with random intercepts, in which each participant contributed one, two or three measurements of adult health behaviors (2001, 2007, 2011). All analyses were adjusted for offspring sex, birth year, age, parental education and single parenthood.Results: Overall, parental ideal health behaviors were associated with ideal behaviors among offspring (odds ratio (OR) 1.28, 95% confidence interval 1.17, 1.39). Furthermore, ORs for these intergenerational associations were greater among offspring whose parents or who themselves had higher educational attainment (OR 1.56 for high vs. OR 1.19 for low parental education; P = 0.01 for interaction, OR 1.32 for high vs. OR 1.04 for low offspring education; P = 0.02 for interaction). Similar trends were seen with parental income and offspring occupation. Results from linear regression analyses were similar.Conclusions: These prospective data suggest higher socioeconomic position in parents or in their adult offspring strengthens the intergenerational continuum of ideal cardiovascular health behaviors.</p

Genome-wide association identifies nine common variants associated with fasting proinsulin levels and provides new insights into the pathophysiology of type 2 diabetes

OBJECTIVE - Proinsulin is a precursor of mature insulin and C-peptide. Higher circulating proinsulin levels are associated with impaired b-cell function, raised glucose levels, insulin resistance, and type 2 diabetes (T2D). Studies of the insulin processing pathway could provide new insights about T2D pathophysiology. RESEARCH DESIGN AND METHODS - We have conducted a meta-analysis of genome-wide association tests of ;2.5 million genotyped or imputed single nucleotide polymorphisms (SNPs) and fasting proinsulin levels in 10,701 nondiabetic adults of European ancestry, with follow-up of 23 loci in up to 16,378 individuals, using additive genetic models adjusted for age, sex, fasting insulin, and study-specific covariates. RESULTS - Nine SNPs at eight loci were associated with proinsulin levels (P < 5 × 10-8). Two loci (LARP6 and SGSM2) have not been previously related to metabolic traits, one (MADD) has been associated with fasting glucose, one (PCSK1) has been implicated in obesity, and four (TCF7L2, SLC30A8, VPS13C/ C2CD4A/B, and ARAP1, formerly CENTD2) increase T2D risk. The proinsulin-raising allele of ARAP1 was associated with a lower fasting glucose (P = 1.7 3 10-4), improved b-cell function (P = 1.1 × 10-5), and lower risk of T2D (odds ratio 0.88; P = 7.8 × 10-6). Notably, PCSK1 encodes the protein prohormone convertase 1/3, the first enzyme in the insulin processing pathway. A genotype score composed of the nine proinsulin-raising alleles was not associated with coronary disease in two large case-control datasets. CONCLUSIONS - We have identified nine genetic variants associated with fasting proinsulin. Our findings illuminate the biology underlying glucose homeostasis and T2D development in humans and argue against a direct role of proinsulin in coronary artery disease pathogenesis