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      Consequences of smoking for body weight, body fat distribution, and insulin resistance

      1 , 1 , 1 , 1
      The American Journal of Clinical Nutrition
      Oxford University Press (OUP)

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          Abstract

          Our aim was to critically evaluate the relations among smoking, body weight, body fat distribution, and insulin resistance as reported in the literature. In the short term, nicotine increases energy expenditure and could reduce appetite, which may explain why smokers tend to have lower body weight than do nonsmokers and why smoking cessation is frequently followed by weight gain. In contrast, heavy smokers tend to have greater body weight than do light smokers or nonsmokers, which likely reflects a clustering of risky behaviors (eg, low degree of physical activity, poor diet, and smoking) that is conducive to weight gain. Other factors, such as weight cycling, could also be involved. In addition, smoking increases insulin resistance and is associated with central fat accumulation. As a result, smoking increases the risk of metabolic syndrome and diabetes, and these factors increase risk of cardiovascular disease. In the context of the worldwide obesity epidemic and a high prevalence of smoking, the greater risk of (central) obesity and insulin resistance among smokers is a matter of major concern.

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          Most cited references89

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          Active smoking and the risk of type 2 diabetes: a systematic review and meta-analysis.

          Observational studies have suggested an association between active smoking and the incidence of type 2 diabetes. To conduct a systematic review with meta-analysis of studies assessing the association between active smoking and incidence of type 2 diabetes. A search of MEDLINE (1966 to May 2007) and EMBASE (1980 to May 2007) databases was supplemented by manual searches of bibliographies of key retrieved articles, reviews of abstracts from scientific meetings, and contact with experts. Studies were included if they reported risk of impaired fasting glucose, impaired glucose tolerance, or type 2 diabetes in relationship to smoking status at baseline; had a cohort design; and excluded persons with diabetes at baseline. Two authors independently extracted the data, including the presence or absence of active smoking at baseline, the risk of diabetes, methods used to detect diabetes, and key criteria of study quality. Relative risks (RRs) were pooled using a random-effects model. Associations were tested in subgroups representing different patient characteristics and study quality criteria. The search yielded 25 prospective cohort studies (N = 1.2 million participants) that reported 45 844 incident cases of diabetes during a study follow-up period ranging from 5 to 30 years. Of the 25 studies, 24 reported adjusted RRs greater than 1 (range for all studies, 0.82-3.74). The pooled adjusted RR was 1.44 (95% confidence interval [CI], 1.31-1.58). Results were consistent and statistically significant in all subgroups. The risk of diabetes was greater for heavy smokers (> or =20 cigarettes/day; RR, 1.61; 95% CI, 1.43-1.80) than for lighter smokers (RR,1.29; 95% CI, 1.13-1.48) and lower for former smokers (RR, 1.23; 95% CI, 1.14-1.33) compared with active smokers, consistent with a dose-response phenomenon. Active smoking is associated with an increased risk of type 2 diabetes. Future research should attempt to establish whether this association is causal and to clarify its mechanisms.
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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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              Norepinephrine and epinephrine release and adrenergic mediation of smoking-associated hemodynamic and metabolic events.

              We studied the effects of cigarette smoking, sham smoking and smoking during adrenergic blockade in 10 subjects to determine whether smoking released the sympathetic neurotransmitter norepinephrine, as well as the adrenomedullary hormone epinephrine, and whether smoking-associated hemodynamic and metabolic changes were mediated through adrenergic mechanisms. Smoking-associated increments in mean (+/- S.E.M.) plasma norepinephrine (227 +/- 23 to 324 +/- 39 pg per milliliter, P less than 0.01) and epinephrine (44 +/- to 113 +/- 27 pg per milliliter, P less than 0.05) were demonstrated. Smoking-associated increments in pulse rate, blood pressure, blood glycerol and blood lactate/pyruvate ratio were prevented by adrenergic blockade; increments in plasma growth hormone and cortisol were not. Since significant smoking-associated increments, in pulse rate, blood pressure and blood lactate/pyruvate ratio, preceded measurable increments in plasma catecholamine concentrations, but were adrenergically mediated, these changes should be attributed to norepinephrine released locally from adrenergic axon terminals within the tissues rather than to increments in circulating catecholamines.
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                Author and article information

                Journal
                The American Journal of Clinical Nutrition
                Oxford University Press (OUP)
                0002-9165
                1938-3207
                April 2008
                April 01 2008
                April 2008
                April 01 2008
                : 87
                : 4
                : 801-809
                Affiliations
                [1 ] From the Institute of Social and Preventive Medicine, Centre Hospitalier Universitaire Vaudois and the University of Lausanne, Lausanne, Switzerland (AC, DF, FP, and JC), and the Departments of Ambulatory Care and Community Medicine (AC and JC) and of Physiology (DF), University of Lausanne, Lausanne, Switzerland
                Article
                10.1093/ajcn/87.4.801
                18400700
                ffbf58f8-e15d-4ff7-a35c-60d304c9782a
                © 2008
                History

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