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      Chemical toxins: a hypothesis to explain the global obesity epidemic.

      Journal of alternative and complementary medicine (New York, N.Y.)

      Socioeconomic Factors, Risk Factors, Prevalence, adverse effects, Pesticides, etiology, epidemiology, chemically induced, Obesity, Life Style, Humans, Global Health, Food Contamination, Environmental Health, Environmental Exposure

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          Abstract

          The number of obese people worldwide has escalated recently, revealing a complex picture of significant variations among nations and different profiles among adults and children, regions, and occupations. The commonly held causes of obesity-overeating and inactivity-do not explain the current obesity epidemic. There is evidence of a general decrease in food consumption by humans and a significant decline in their overall levels of physical activity. There is also more evidence to indicate that the body's natural weight-control mechanisms are not functioning properly in obesity. Because the obesity epidemic occurred relatively quickly, it has been suggested that environmental causes instead of genetic factors maybe largely responsible. What has, up to now, been overlooked is that the earth's environment has changed significantly during the last few decades because of the exponential production and usage of synthetic organic and inorganic chemicals. Many of these chemicals are better known for causing weight loss at high levels of exposure but much lower concentrations of these same chemicals have powerful weight-promoting actions. This property has already been widely exploited commercially to produce growth hormones that fatten livestock and pharmaceuticals that induce weight gain in grossly underweight patients. This paper presents a hypothesis that the current level of human exposure to these chemicals may have damaged many of the body's natural weight-control mechanisms. Furthermore, it is posited here that these effects, together with a wide range of additional, possibly synergistic, factors may play a significant role in the worldwide obesity epidemic.

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          Most cited references 40

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          Obesity in Britain: gluttony or sloth?

           A Prentice,  S. Jebb (1995)
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            Prevalence of overweight and obese children between 1989 and 1998: population based series of cross sectional studies.

            To determine trends in weight, height, and body mass index in children between 1989 and 1998. Retrospective series of cross sectional studies of routinely collected data. Primary care in the Wirral Health Authority. 35 662 infants aged 1-3 months (representing 88% of live births) and 28 768 children aged 2.9-4.0 years. 21 582 infants and children (25.1%) were excluded because of missing or inaccurate data. Weight, height, sex, and age routinely recorded by health visitors. Height, weight, and body mass index standardised for age and sex. SD score >1.04 for body mass index (>85th centile) was defined as overweight and >1.64 (>95th centile) as obese. Body mass index was not calculated in infants as it is difficult to interpret. From 1989 to 1998 there was a highly significant increasing trend in the proportion of overweight children (14.7% to 23.6%; P<0.001) and obese children (5.4% to 9.2%; P<0.001). There was also a highly significant increasing trend in the mean SD score for weight (0.05 to 0.29; P<0.001) and body mass index (-0.15 to 0.31; P<0.001) but not height. Infants showed a small but significantly increasing trend in mean SD score for weight (-0.17 to -0.05; P=0.005). From 1989 to 1998 there was a highly significant increase in weight and body mass index in children under 4 years of age. Routinely collected data are valuable in identifying anthropometric trends in populations.
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              Body weight gain induced by antipsychotic drugs: mechanisms and management.

              Long-term administration of typical and atypical antipsychotic drugs (AP) induces excessive weight gain which afflicts up to 50% of patients, impairs health and interferes with treatment compliance. Basic and clinical research has shown that AP may affect body weight through diverse mechanisms. Increased appetite is probably related to the interaction of AP with neuronal receptors to dopamine, serotonin and histamine. Additional metabolic-endocrine disruption of weight regulation may be related to the effects of AP-induced hyperprolactinaemia on gonadal-adrenal steroids and insulin sensitivity. In humans, programmed physical activity, dietary restriction, anorectic agents, and drugs that counteract hyperprolactinaemia have been shown to be successful in a limited number of studies. Two novel strategies could expand the available therapeutic options. First, in preclinical experiments in female rats the estradiol antagonist/agonist drug tamoxifen or estradiol itself have been shown to completely prevent the obesity provoked by the AP sulpiride, and to induce an endocrine-metabolic milieu that seems to counteract AP-induced obesity. Secondly, it has also been shown that oral antihyperglycaemic agents such as metformin may decrease body weight and counteract insulin resistance and hyperinsulinaemia which is correlated with several metabolic abnormalities in obese subjects. Lastly, estradiol replacement, tamoxifen and/or antihyperglycaemic agents are not devoid of significant side-effects, and these drugs have not been tested in obese psychiatric patients. Therefore, further research is needed before their clinical use may be recommended.
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                Author and article information

                Journal
                10.1089/107555302317371479
                12006126

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