The epidemic of overweight and obesity presents a major challenge to chronic disease prevention and health across the life course around the world. Fueled by economic growth, industrialization, mechanized transport, urbanization, an increasingly sedentary lifestyle, and a nutritional transition to processed foods and high calorie diets over the last 30 years, many countries have witnessed the prevalence of obesity in its citizens double, and even quadruple. Rising prevalence of childhood obesity, in particular, forebodes a staggering burden of disease in individuals and healthcare systems in the decades to come. A complex, multifactorial disease, with genetic, behavioral, socioeconomic, and environmental origins, obesity raises risk of debilitating morbidity and mortality. Relying primarily on epidemiologic evidence published within the last decade, this non-exhaustive review discusses the extent of the obesity epidemic, its risk factors—known and novel—, sequelae, and economic impact across the globe.

OBJECTIVETo conduct a systematic review of cross-sectional and prospective human studies evaluating metabolite markers identified using high-throughput metabolomics techniques on prediabetes and type 2 diabetes.RESEARCH DESIGN AND METHODSWe searched MEDLINE and EMBASE databases through August 2015. We conducted a qualitative review of cross-sectional and prospective studies. Additionally, meta-analyses of metabolite markers, with data estimates from at least three prospective studies, and type 2 diabetes risk were conducted, and multivariable-adjusted relative risks of type 2 diabetes were calculated per study-specific SD difference in a given metabolite.RESULTSWe identified 27 cross-sectional and 19 prospective publications reporting associations of metabolites and prediabetes and/or type 2 diabetes. Carbohydrate (glucose and fructose), lipid (phospholipids, sphingomyelins, and triglycerides), and amino acid (branched-chain amino acids, aromatic amino acids, glycine, and glutamine) metabolites were higher in individuals with type 2 diabetes compared with control subjects. Prospective studies provided evidence that blood concentrations of several metabolites, including hexoses, branched-chain amino acids, aromatic amino acids, phospholipids, and triglycerides, were associated with the incidence of prediabetes and type 2 diabetes. We meta-analyzed results from eight prospective studies that reported risk estimates for metabolites and type 2 diabetes, including 8,000 individuals of whom 1,940 had type 2 diabetes. We found 36% higher risk of type 2 diabetes per study-specific SD difference for isoleucine (pooled relative risk 1.36 [1.24–1.48]; I2 = 9.5%), 36% for leucine (1.36 [1.17–1.58]; I2 = 37.4%), 35% for valine (1.35 [1.19–1.53]; I2 = 45.8%), 36% for tyrosine (1.36 [1.19–1.55]; I2 = 51.6%), and 26% for phenylalanine (1.26 [1.10–1.44]; I2 = 56%). Glycine and glutamine were inversely associated with type 2 diabetes risk (0.89 [0.81–0.96] and 0.85 [0.82–0.89], respectively; both I2 = 0.0%).CONCLUSIONSIn studies using high-throughput metabolomics, several blood amino acids appear to be consistently associated with the risk of developing type 2 diabetes.

The NHS cohorts have contributed to our understanding of the risk factors for and consequences of obesity and made a lasting impact on clinical and public health guidelines on obesity prevention.

Background The associations between dietary saturated fat and risk of coronary heart disease (CHD) remain controversial, but few studies have compared saturated with unsaturated fats and sources of carbohydrates in relation to CHD risk. Objective This study sought to investigate associations of saturated fats as compared with unsaturated fats and different sources of carbohydrates in relation to CHD risk. Methods We followed 84,628 women (Nurses’ Health Study, 1980 to 2010), and 42,908 men (Health Professionals Follow-up Study, 1986 to 2010) who were free of diabetes, cardiovascular disease, and cancer at baseline. Diet was assessed by semiquantitative food frequency questionnaire every 4 years. Results During 24 to 30 years of follow-up, we documented 7,667 incident cases of CHD. Higher intakes of polyunsaturated fatty acids (PUFAs) and carbohydrates from whole grains were significantly associated with lower risk of CHD (hazard ratios [HR] (95% confidence intervals [CI]) comparing the highest to the lowest quintile for PUFA: 0.80 [0.73 to 0.88], p trend <0.0001; and for carbohydrates from whole grains: 0.90 [0.83 to 0.98], p trend = 0.003). In contrast, carbohydrates from refined starches/added sugars were positively associated with risk of CHD (1.10 [1.00 to 1.21], p trend = 0.04). Replacing 5% of energy intake from saturated fats with equivalent energy intake from either PUFAs, monounsaturated fats (MUFAs), or carbohydrates from whole grains was associated with 25%, 15%, and 9% lower risk of CHD, respectively (PUFAs: 0.75 [0.67 to 0.84]; p < 0.0001; MUFAs: 0.85 [0.74 to 0.97]; p = 0.02; carbohydrates from whole grains (0.91 [0.85 to 0.98]; p = 0.01). Replacing saturated fat with carbohydrates from refined starches/added sugars was not significantly associated with CHD risk (p > 0.10). Conclusions Our findings indicate that unsaturated fats, especially PUFAs, and/or high-quality carbohydrates should replace dietary saturated fats to reduce CHD risk.