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      THE ASSOCIATION BETWEEN WEIGHT FLUCTUATION AND MORTALITY: RESULTS FROM A POPULATION-BASED COHORT STUDY

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      Journal of Community Health
      Springer Science and Business Media LLC

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          Abstract

          Previous studies evaluating the association between weight fluctuation and mortality are limited and have conflicting results. This study will further evaluate the association between weight fluctuation and mortality in a nationally representative cohort by performing survival analysis of NHANES I and NHANES I Epidemiologic Follow-up Study (n = 8479; weighted sample = 68,200,905). This cohort was followed from 1971 to 1992 and categorized using weight change over five time points into stable non-obese, stable obese, weight gain, weight loss and weight fluctuation groups. All-cause mortality (ACM) and cardiovascular mortality (CM) were evaluated. Respondents with weight fluctuation had higher ACM (HR: 1.83, 95% CI: 1.25-2.69) and CM hazards ratios (HR: 1.86, 95% CI: 1.10-3.15) than the stable non-obese group, even after controlling for pre-existing disease, initial BMI and excluding those in poor health or incapacitated. Increased mortality was also seen in the weight loss group (ACM HR: 3.36, 95% CI: 2.47-4.55), (CM HR 4.22, 95% CI: 2.60-6.84). The stable obese group did not have increased ACM, but did have increased CM prior to the exclusion of those in poor health or incapacitated. (HR: 2.17, 95% CI: 1.10-4.28). Weight fluctuation is associated with a higher risk of all-cause and cardiovascular disease mortality in the US population, even after adjustment for pre-existing disease, initial BMI and the exclusion of those in poor health or incapacitated. Thus, health care providers should promote a commitment to maintaining weight loss to avoid weight fluctuation and consider patients' weight histories when assessing their risk status.

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          Most cited references18

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          Variability of body weight and health outcomes in the Framingham population.

          Fluctuation in body weight is a common phenomenon, due in part to the high prevalence of dieting. In this study we examined the associations between variability in body weight and health end points in subjects participating in the Framingham Heart Study, which involves follow-up examinations every two years after entry. The degree of variability of body weight was expressed as the coefficient of variation of each subject's measured body-mass-index values at the first eight biennial examinations during the study and on their recalled weight at 25 years of age. Using the 32-year follow-up data, we analyzed total mortality, mortality from coronary heart disease, and morbidity due to coronary heart disease and cancer in relation to intraindividual variation in body weight, including only end points that occurred after the 10th biennial examination. We used age-adjusted proportional-hazards regression for the data analysis. Subjects with highly variable body weights had increased total mortality (P = 0.005 for men, P = 0.01 for women), mortality from coronary heart disease (P = 0.009 for men, P = 0.009 for women), and morbidity due to coronary heart disease (P = 0.0009 for men, P = 0.006 for women). Using a multivariate analysis that also controlled for obesity, trends in weight over time, and five indicators of cardiovascular risk, we found that the positive associations between fluctuations in body weight and end points related to mortality and coronary heart disease could not be attributed to these potential confounding factors. The relative risks of these end points in subjects whose weight varied substantially, as compared with those whose weight was relatively stable, ranged from 1.27 to 1.93. Fluctuations in body weight may have negative health consequences, independent of obesity and the trend of body weight over time.
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            Prospective study of intentional weight loss and mortality in never-smoking overweight US white women aged 40-64 years.

            Although 40% of US women indicate they are currently trying to lose weight, the association between intentional weight loss and longevity is unknown. The authors analyzed prospective data from 43,457 overweight, never-smoking US white women aged 40-64 years who in 1959-1960 completed a questionnaire that included questions on weight change direction, amount, time interval, and intentionality. Vital status was determined in 1972. Proportional hazards regression was used to estimate mortality rate ratios for women who intentionally lost weight compared with women who had no change in weight. Women who died within the first 3 years of follow-up were excluded. Analyses were stratified by preexisting illness and adjusted for age, beginning body mass index, alcohol intake, education, physical activity, and health conditions. In women with obesity-related health conditions (n = 15,069), intentional weight loss of any amount was associated with a 20% reduction in all-cause mortality, primarily due to a 40-50% reduction in mortality from obesity-related cancers; diabetes-associated mortality was also reduced by 30-40% in those who intentionally lost weight. In women with no preexisting illness (n = 28,388), intentional weight loss of > or = 20 lb (> or = 9.1 kg) that occurred within the previous year was associated with about a 25% reduction in all-cause, cardiovascular, and cancer mortality; however, loss of or = 1 year was generally associated with small to modest increases in mortality. The association between intentional weight loss and longevity in middle-aged overweight women appears to depend on their health status. Intentional weight loss among women with obesity-related conditions is generally associated with decreased premature mortality, whereas among women with no preexisting illness, the association is equivocal.
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              Poststarvation hyperphagia and body fat overshooting in humans: a role for feedback signals from lean and fat tissues.

              An increase in the sensation of hunger and overeating after a period of chronic energy deprivation can be part of an autoregulatory phenomenon attempting to restore body weight. To gain insights into the role of fat and lean tissue depletion as determinants of such a hyperphagic response in humans, we reanalyzed the individual data on food intake and body composition available for the 12 starved and refed men in the classical Minnesota Experiment after a shift from a 12-wk period of restricted refeeding to an ad libitum refeeding period of 8 wk. For each individual, the following were determined: 1) the total hyperphagic response during the ad libitum refeeding period, calculated as the energy intake in excess of that during the prestarvation (control) period; 2) the degree of fat recovery and that of fat-free-mass (FFM) recovery before ad libitum refeeding, calculated as the deviation in fat and FFM from their respective prestarvation values (ie, the amount of fat or FFM before ad libitum refeeding as a percentage of fat or FFM during the control period); and 3) the deficit in energy intake before ad libitum refeeding, calculated as the difference between the energy intake during the period of restricted refeeding and that during the control period. The results indicate that 1) the total hyperphagic response is inversely correlated with the degree of fat recovery (r = -0.6) as well as with that of FFM recovery (r = -0.5), 2) the correlation between hyperphagia and FFM recovery persists after adjustment for fat recovery, and 3) the correlations between hyperphagia and fat recovery or FFM recovery persist after adjustment for the variance in the energy deficit during the preceding period of restricted refeeding. Taken together, these results in humans suggest that poststarvation hyperphagia is determined to a large extent by autoregulatory feedback mechanisms from both fat and lean tissues. These findings, which have implications for both the treatment of obesity and for nutritional rehabilitation after malnutrition and cachexia, have been integrated into a compartmental model of autoregulation of body composition, and can be used to explain the phenomenon of poststarvation overshoot in body fat.
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                Author and article information

                Journal
                Journal of Community Health
                J Community Health
                Springer Science and Business Media LLC
                0094-5145
                1573-3610
                June 2005
                June 2005
                : 30
                : 3
                : 153-165
                Article
                10.1007/s10900-004-1955-1
                15847242
                ecd37cb2-2d51-4d5e-aed3-605e8a88d15d
                © 2005

                http://www.springer.com/tdm

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