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A life course approach to diet, nutrition and the prevention of chronic diseases

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Public Health Nutrition

CABI Publishing

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      Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance.

      Type 2 diabetes mellitus is increasingly common, primarily because of increases in the prevalence of a sedentary lifestyle and obesity. Whether type 2 diabetes can be prevented by interventions that affect the lifestyles of subjects at high risk for the disease is not known. We randomly assigned 522 middle-aged, overweight subjects (172 men and 350 women; mean age, 55 years; mean body-mass index [weight in kilograms divided by the square of the height in meters], 31) with impaired glucose tolerance to either the intervention group or the control group. Each subject in the intervention group received individualized counseling aimed at reducing weight, total intake of fat, and intake of saturated fat and increasing intake of fiber and physical activity. An oral glucose-tolerance test was performed annually; the diagnosis of diabetes was confirmed by a second test. The mean duration of follow-up was 3.2 years. The mean (+/-SD) amount of weight lost between base line and the end of year 1 was 4.2+/-5.1 kg in the intervention group and 0.8+/-3.7 kg in the control group; the net loss by the end of year 2 was 3.5+/-5.5 kg in the intervention group and 0.8+/-4.4 kg in the control group (P<0.001 for both comparisons between the groups). The cumulative incidence of diabetes after four years was 11 percent (95 percent confidence interval, 6 to 15 percent) in the intervention group and 23 percent (95 percent confidence interval, 17 to 29 percent) in the control group. During the trial, the risk of diabetes was reduced by 58 percent (P<0.001) in the intervention group. The reduction in the incidence of diabetes was directly associated with changes in lifestyle. Type 2 diabetes can be prevented by changes in the lifestyles of high-risk subjects.
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        Banting lecture 1988. Role of insulin resistance in human disease.

         G M Reaven (1988)
        Resistance to insulin-stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in approximately 25% of nonobese individuals with normal oral glucose tolerance. In these conditions, deterioration of glucose tolerance can only be prevented if the beta-cell is able to increase its insulin secretory response and maintain a state of chronic hyperinsulinemia. When this goal cannot be achieved, gross decompensation of glucose homeostasis occurs. The relationship between insulin resistance, plasma insulin level, and glucose intolerance is mediated to a significant degree by changes in ambient plasma free-fatty acid (FFA) concentration. Patients with NIDDM are also resistant to insulin suppression of plasma FFA concentration, but plasma FFA concentrations can be reduced by relatively small increments in insulin concentration. Consequently, elevations of circulating plasma FFA concentration can be prevented if large amounts of insulin can be secreted. If hyperinsulinemia cannot be maintained, plasma FFA concentration will not be suppressed normally, and the resulting increase in plasma FFA concentration will lead to increased hepatic glucose production. Because these events take place in individuals who are quite resistant to insulin-stimulated glucose uptake, it is apparent that even small increases in hepatic glucose production are likely to lead to significant fasting hyperglycemia under these conditions. Although hyperinsulinemia may prevent frank decompensation of glucose homeostasis in insulin-resistant individuals, this compensatory response of the endocrine pancreas is not without its price. Patients with hypertension, treated or untreated, are insulin resistant, hyperglycemic, and hyperinsulinemic. In addition, a direct relationship between plasma insulin concentration and blood pressure has been noted. Hypertension can also be produced in normal rats when they are fed a fructose-enriched diet, an intervention that also leads to the development of insulin resistance and hyperinsulinemia. The development of hypertension in normal rats by an experimental manipulation known to induce insulin resistance and hyperinsulinemia provides further support for the view that the relationship between the three variables may be a causal one.(ABSTRACT TRUNCATED AT 400 WORDS)
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          Predicting obesity in young adulthood from childhood and parental obesity.

          Childhood obesity increases the risk of obesity in adulthood, but how parental obesity affects the chances of a child's becoming an obese adult is unknown. We investigated the risk of obesity in young adulthood associated with both obesity in childhood and obesity in one or both parents. Height and weight measurements were abstracted from the records of 854 subjects born at a health maintenance organization in Washington State between 1965 and 1971. Their parents' medical records were also reviewed. Childhood obesity was defined as a body-mass index at or above the 85th percentile for age and sex, and obesity in adulthood as a mean body-mass index at or above 27.8 for men and 27.3 for women. In young adulthood (defined as 21 to 29 years of age), 135 subjects (16 percent) were obese. Among those who were obese during childhood, the chance of obesity in adulthood ranged from 8 percent for 1- or 2-year-olds without obese parents to 79 percent for 10-to-14-year-olds with at least one obese parent. After adjustment for parental obesity, the odds ratios for obesity in adulthood associated with childhood obesity ranged from 1.3 (95 percent confidence interval, 0.6 to 3.0) for obesity at 1 or 2 years of age to 17.5 (7.7 to 39.5) for obesity at 15 to 17 years of age. After adjustment for the child's obesity status, the odds ratios for obesity in adulthood associated with having one obese parent ranged from 2.2 (95 percent confidence interval, 1.1 to 4.3) at 15 to 17 years of age to 3.2 (1.8 to 5.7) at 1 or 2 years of age. Obese children under three years of age without obese parents are at low risk for obesity in adulthood, but among older children, obesity is an increasingly important predictor of adult obesity, regardless of whether the parents are obese. Parental obesity more than doubles the risk of adult obesity among both obese and nonobese children under 10 years of age.
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            Author and article information

            Journal
            applab
            Public Health Nutrition
            PHN
            CABI Publishing
            1368-9800
            1475-2727
            February 2004
            January 2 2007
            February 2004
            : 7
            : 1a
            10.1079/PHN2003584
            © 2004

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