Increased consumption of refined carbohydrates and the epidemic of type 2 diabetes in the United States: an ecologic assessment

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Abstract

Type 2 diabetes is an epidemic that is affecting an ever-increasing proportion of the US population. Although consumption of refined carbohydrates has increased and is thought to be related to the increased risk of type 2 diabetes, the ecologic effect of changes in the quality of carbohydrates in the food supply on the risk of type 2 diabetes remains to be quantified. The objective was to examine the correlation between consumption of refined carbohydrates and the prevalence of type 2 diabetes in the United States. In this ecologic correlation study, the per capita nutrient consumption in the United States between 1909 and 1997 obtained from the US Department of Agriculture was compared with the prevalence of type 2 diabetes obtained from the Centers for Disease Control and Prevention. In a univariate analysis, a significant correlation with diabetes prevalence was observed for dietary fat (r = 0.84, P < 0.001), carbohydrate (r = 0.55, P < 0.001), protein (r = 0.71, P < 0.001), fiber (r = 0.16, P = 0.03), corn syrup (r = 0.83, P < 0.001), and total energy (r = 0.75, P < 0.001) intakes. In a multivariate nutrient-density model, in which total energy intake was accounted for, corn syrup was positively associated with the prevalence of type 2 diabetes (beta = 0.0132, P = 0.038). Fiber (beta = -13.86, P < 0.01) was negatively associated with the prevalence of type 2 diabetes. In contrast, protein (P = 0.084) and fat (P = 0.79) were not associated with the prevalence of type 2 diabetes when total energy was controlled for. Increasing intakes of refined carbohydrate (corn syrup) concomitant with decreasing intakes of fiber paralleled the upward trend in the prevalence of type 2 diabetes observed in the United States during the 20th century.

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Prevalence of the Metabolic Syndrome Among US Adults

Earl S. Ford, Wayne Giles, William Dietz (2002)

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Carbohydrates, dietary fiber, and incident type 2 diabetes in older women.

Katie Meyer, Lawrence Kushi, David R Jacobs … (2000)

Dietary carbohydrates may influence the development of type 2 (non-insulin-dependent) diabetes, for example, through effects on blood glucose and insulin concentrations. We examined the relations of baseline intake of carbohydrates, dietary fiber, dietary magnesium, and carbohydrate-rich foods and the glycemic index with incidence of diabetes. This was a prospective cohort study of 35988 older Iowa women initially free of diabetes. During 6 y of follow-up, 1141 incident cases of diabetes were reported. Total grain, whole-grain, total dietary fiber, cereal fiber, and dietary magnesium intakes showed strong inverse associations with incidence of diabetes after adjustment for potential nondietary confounding variables. Multivariate-adjusted relative risks of diabetes were 1.0, 0.99, 0.98, 0.92, and 0.79 (P for trend: 0.0089) across quintiles of whole-grain intake; 1.0, 1.09, 1.00, 0.94, and 0.78 (P for trend: 0.005) across quintiles of total dietary fiber intake; and 1.0, 0.81, 0.82, 0.81, and 0.67 (P for trend: 0.0003) across quintiles of dietary magnesium intake. Intakes of total carbohydrates, refined grains, fruit and vegetables, and soluble fiber and the glycemic index were unrelated to diabetes risk. These data support a protective role for grains (particularly whole grains), cereal fiber, and dietary magnesium in the development of diabetes in older women.

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Fructose, weight gain, and the insulin resistance syndrome.

Sharon S Elliott, Nancy Keim, Judith Stern … (2002)

This review explores whether fructose consumption might be a contributing factor to the development of obesity and the accompanying metabolic abnormalities observed in the insulin resistance syndrome. The per capita disappearance data for fructose from the combined consumption of sucrose and high-fructose corn syrup have increased by 26%, from 64 g/d in 1970 to 81 g/d in 1997. Both plasma insulin and leptin act in the central nervous system in the long-term regulation of energy homeostasis. Because fructose does not stimulate insulin secretion from pancreatic beta cells, the consumption of foods and beverages containing fructose produces smaller postprandial insulin excursions than does consumption of glucose-containing carbohydrate. Because leptin production is regulated by insulin responses to meals, fructose consumption also reduces circulating leptin concentrations. The combined effects of lowered circulating leptin and insulin in individuals who consume diets that are high in dietary fructose could therefore increase the likelihood of weight gain and its associated metabolic sequelae. In addition, fructose, compared with glucose, is preferentially metabolized to lipid in the liver. Fructose consumption induces insulin resistance, impaired glucose tolerance, hyperinsulinemia, hypertriacylglycerolemia, and hypertension in animal models. The data in humans are less clear. Although there are existing data on the metabolic and endocrine effects of dietary fructose that suggest that increased consumption of fructose may be detrimental in terms of body weight and adiposity and the metabolic indexes associated with the insulin resistance syndrome, much more research is needed to fully understand the metabolic effect of dietary fructose in humans.