Since the increase in body mass appears to affect only a part of the society, preventive measures should be targeted at the persons at risk. How can these be identified? Identification of risk factors is domain for epidemiologic research. For overweight and obesity many genetic and behavioral risk factors have been discussed. Obesity of the parents is a major risk factor for childhood obesity [61]. This can be transmitted either by genetic or by tradigenetic inheritance. The latter means adopting habits from parents by imitation.
Genetic versus Environmental Risk Factors
Twin, adoption, and family studies suggested a heritability of fat mass of about 40–70%. Stunkard et al. [62] studied the values for BMI of identical twins reared apart and found intrapair correlation coefficients of 0.70 for men and 0.66 for women. These values were only slightly lower than those for twins reared together. This finding reflects the importance of genetic influences (heritability) on the body-mass index. About 30 Mendelian disorders associated with obesity have been reported like the syndromes of Prader-Willi-Labhart, Bardet-Biedl, Alstrom or Simpson- Golabi-Behmel. Single gene defects leading to obesity have been discovered like
congenital leptin deficiency or leptin receptor deficiency. Further gene defects in the melanocortin system have been described (proopiomelanocortin, proconvertase 1, MC4R) [63]. These genes involved in weight gain do not directly cause obesity but they disrupt the normal controls of ingestive behavior (hyperphagia) leading to increased susceptibility to fat gain when exposed to a specific environment. Genetically defined conditions, however, do only explain obesity in few cases, mainly those with excessive obesity. The twin studies suggest, however, that there may be more genes involved in the etiology of overweight and obesity. Since the genetic pool is unlikely to have changed within one generation, environmental factors are more likely to account for the adiposity epidemic. The so called ‘toxic environment’ is characterized by a sedentary life style (television, computers, etc.), limited physical activity (absence of safe playgrounds or parks in the cities), and an increase of high energy, poor quality processed foods and soft drinks, for which the consumption is aggressively promoted by the fast food industry. At the same time serving sizes rise and large meals are disproportionately cheap. Children consume less fruits, non-starchy vegetables, fiber, and micronutrients, because they are less readily available, certainly more expensive, and often less palatable [10].
Twin, adoption, and family studies suggested a heritability of fat mass of about 40–70%. Stunkard et al. [62] studied the values for BMI of identical twins reared apart and found intrapair correlation coefficients of 0.70 for men and 0.66 for women. These values were only slightly lower than those for twins reared together. This finding reflects the importance of genetic influences (heritability) on the body-mass index. About 30 Mendelian disorders associated with obesity have been reported like the syndromes of Prader-Willi-Labhart, Bardet-Biedl, Alstrom or Simpson- Golabi-Behmel. Single gene defects leading to obesity have been discovered like
congenital leptin deficiency or leptin receptor deficiency. Further gene defects in the melanocortin system have been described (proopiomelanocortin, proconvertase 1, MC4R) [63]. These genes involved in weight gain do not directly cause obesity but they disrupt the normal controls of ingestive behavior (hyperphagia) leading to increased susceptibility to fat gain when exposed to a specific environment. Genetically defined conditions, however, do only explain obesity in few cases, mainly those with excessive obesity. The twin studies suggest, however, that there may be more genes involved in the etiology of overweight and obesity. Since the genetic pool is unlikely to have changed within one generation, environmental factors are more likely to account for the adiposity epidemic. The so called ‘toxic environment’ is characterized by a sedentary life style (television, computers, etc.), limited physical activity (absence of safe playgrounds or parks in the cities), and an increase of high energy, poor quality processed foods and soft drinks, for which the consumption is aggressively promoted by the fast food industry. At the same time serving sizes rise and large meals are disproportionately cheap. Children consume less fruits, non-starchy vegetables, fiber, and micronutrients, because they are less readily available, certainly more expensive, and often less palatable [10].
Environment: Nutrition and Physical Activity
A cohort study in the USA revealed a higher increase in BMI for preadolescents who reported higher caloric intakes and less physical activity. Although the estimated effects were small, their cumulative effects over years could produce substantial gain in body weight [64]. A French cross-sectional study on 10-year-old children [65] revealed that active ingested significantly more energy than less active children, which was accounted for by increased consumption of carbohydrates. The amounts of fat and protein consumed were similar in both groups. In spite of a higher energy intake in the active group, active and less active children had similar BMIs. However, their body composition differed significantly: less active children had a lower proportion of fat-free mass and a higher proportion of fat mass. The assumption that overweight is caused by an imbalance of energy uptake and expenditure is obvious. Therefore it is reasonable to suspect that the epidemic of overweight is related to a change in caloric intake and physical activity
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