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Purpose To examine racial differences in gestational weight gain (GWG) and pregnancy-related hypertension. Methods Logistic regression models tested racial differences in adequacy of GWG and pregnancy-induced hypertension in all singleton live births from the South Carolina 2004-2006 birth certificates. Results Compared to white women, black and Hispanic women had 16%-46% lower odds of gaining weight above the recommendations. However, the odds of inadequate GWG was ~50% higher in black and Hispanic women with a pregnancy body mass index (BMI) <25kg/m2. Furthermore, compared to women with adequate GWG, women with excessive GWG had higher odds of pregnancy-related hypertension (underweight: 2.35, 95% CI(1.66, 3.32); normal: 2.05, 95% CI(1.84, 2.27); overweight: 1.93, 95% CI(1.64, 2.27); obese: 1.46, 95% CI(1.30, 1.63)). Among women with a BMI <25 kg/m2, black women had higher odds of pregnancy-related hypertension than white women (underweight: 1.64, 95% CI(1.14, 2.36); normal weight: 1.28, 95% CI(1.15, 1.42)), while among women with a BMI ≥25 kg/m2, Hispanic women had 40% lower odds. Conclusion Programs are needed to curb excessive GWG in all racial groups and to help some sub-groups ensure adequate GWG. Maternal obesity and GWG are two factors that should be used in combination to reduce racial differences in pregnancy-related hypertension.

Research Method and Procedures:A retrospective observational design using medical records first identified patients with mental retardation (MR) and age-matched controls without disabilities. Data on BMI collected during each primary care visit allowed exploration of obesity at three levels. Moving out of obesity was defined as having a BMI Ͻ25 kg/m 2 . We also abstracted data on age, sex, race, and other medical conditions. Results: For adults 20 to 29 years of age, 33.1% of patients without disability and 21% of patients with MR had a BMI Ͼ30 kg/m 2 . Between the ages of 50 and 59 years, 40.5% of the patients without disability and 35.2% of the patients with MR had a BMI Ͼ30 kg/m 2 . Patients with mild MR had similar prevalence rates of obesity and patients with severe MR had significantly lower prevalence of obesity compared with the patients without disability through 50 years of age. Throughout the period from 20 to 60 years of age, between 15% and 40% of individuals with and without MR, who were previously obese, were not currently obese.Discussion: Throughout the adult years, an increasing proportion of individuals with and without MR are obese. However, obesity is not a chronic state; many people transition back to a normal body weight.

Weight-loss interventions generally improve lipid profiles and reduce cardiovascular disease risk, but effects are variable and may depend on genetic factors. We performed a genetic association analysis of data from 2,993 participants in the Diabetes Prevention Program to test the hypotheses that a genetic risk score (GRS) based on deleterious alleles at 32 lipid-associated single-nucleotide polymorphisms modifies the effects of lifestyle and/or metformin interventions on lipid levels and nuclear magnetic resonance (NMR) lipoprotein subfraction size and number. Twenty-three loci previously associated with fasting LDL-C, HDL-C, or triglycerides replicated (P = 0.04–1×10−17). Except for total HDL particles (r = −0.03, P = 0.26), all components of the lipid profile correlated with the GRS (partial |r| = 0.07–0.17, P = 5×10−5–1×10−19). The GRS was associated with higher baseline-adjusted 1-year LDL cholesterol levels (β = +0.87, SEE±0.22 mg/dl/allele, P = 8×10−5, P interaction = 0.02) in the lifestyle intervention group, but not in the placebo (β = +0.20, SEE±0.22 mg/dl/allele, P = 0.35) or metformin (β = −0.03, SEE±0.22 mg/dl/allele, P = 0.90; P interaction = 0.64) groups. Similarly, a higher GRS predicted a greater number of baseline-adjusted small LDL particles at 1 year in the lifestyle intervention arm (β = +0.30, SEE±0.012 ln nmol/L/allele, P = 0.01, P interaction = 0.01) but not in the placebo (β = −0.002, SEE±0.008 ln nmol/L/allele, P = 0.74) or metformin (β = +0.013, SEE±0.008 nmol/L/allele, P = 0.12; P interaction = 0.24) groups. Our findings suggest that a high genetic burden confers an adverse lipid profile and predicts attenuated response in LDL-C levels and small LDL particle number to dietary and physical activity interventions aimed at weight loss.

The primary finding is a high RQ is predictive of gains in body weight and fat mass over a 12-month period among young adults, with changes occurring as soon as 3 months. In addition, a low RMR was not associated with gains in body weight or fat mass over the same period.