Genetic and environmental influences on cardiometabolic disease components, adiposity and eating behavior

The relative impact of genetic and environmental influences on factors associated with cardiovascular disease (CVD) risk and adiposity remains unclear. This research aimed to quantify genetic, common environmental and unique environmental variance components of three phenotypic categories: (1) cardiometabolic disease (CMD) components---waist circumference, blood pressure, fasting plasma glucose and insulin, homeostatic model assessment of insulin resistance (HOMA-IR), fasting plasma lipids; (2) adiposity assessed by six methods---body mass index (BMI), dual energy x-ray absorptiometry (DXA), underwater weighing (UWW), total body water (TBW), bioelectric impedance (BIA), skinfold thickness; and (3) eating behavior assessed by the Eating Inventory. Additionally, this dissertation investigated whether adiposity expression and measurement method affects adiposity heritability estimation. Model-fitting analyses were performed with data from adult male and female monozygotic twins reared apart or together.;Plasma lipid concentrations were highly heritable (56-77%). Waist circumference, HOMA-IR, plasma glucose and insulin, and blood pressure were moderately heritable (43-57%). Unique environmental factors contributed 20-38% of variance of all CMD components. Common environmental factors contributed 23-42% of variance of waist circumference, systolic blood pressure, and plasma glucose. Adiposity expression and measurement method both affected adiposity heritability estimation. Expression as % body fat produced higher heritability estimates compared to expression as fat mass/height2. For fat mass/height 2, UWW gave the highest estimate (69%) and BIA gave the lowest estimate (47%). DXA and TBW produced the least biased heritability estimates, based on the small contribution from specific genetic factors to total genetic variance. A model combining DXA and TBW resulted in a fat mass/height2 heritability estimate of 60%. Variance of most Eating Inventory variables was primarily explained by unique environmental factors (45-71%). However, genetic factors influenced restraint, emotional and situational susceptibility to disinhibition, and internal locus for hunger (heritabilities of 38-55%).;These results suggest that genetic variance has a dominant influence on total variance of CMD components and adiposity, while unique environmental variance has a dominant influence on total variance of eating behavior. These estimates provide insight into the etiology of these factors associated with CVD risk and could help identify successful targets for therapies aimed at lowering CVD risk.