Abstract:We examined the contributions of genetic factors and the family environment to human fatness in a sample of 540 adult Danish adoptees who were selected from a population of 3580 and divided into four weight classes: thin, median weight, overweight, and obese. There was a strong relation between the weight class of the adoptees and the body-mass index of their biologic parents - for the mothers, P less than 0.0001; for the fathers, P less than 0.02. There was no relation between the weight class of the adoptees… Show more
“…However, it is still believed that an obesity-promoting environment determines whether the obese genotype will result in the obese phenotype (69,70) . Therefore it can be speculated that SNP causing a genotype associated with inflammation will also need inflammatory-promoting environmental factors to result in the obesity-inflammatory phenotype.…”
Section: Discussionmentioning
confidence: 99%
“…This association has been made obvious by studies of adoptees who resemble their biological relatives but not their adoptive relatives and by numerous twin studies, suggesting that genetics accounts for 50-90 % of the variance in BMI (69,70) .…”
AbstractObjectiveDespite extensive research into the biological mechanisms behind obesity-related inflammation, knowledge of environmental and genetic factors triggering such mechanisms is limited. In the present narrative review we present potential determinants of adipose tissue inflammation and suggest ways ahead for future research in the field.DesignWe searched the literature for potential determinants of obesity with inflammation through MEDLINE by applying the MeSH headings ‘obesity’ and ‘inflammation’ in combination with specific terms for a series of environmental and genetic factors.ResultsNumerous articles reported on the association between environmental or genetic factors and respectively obesity and inflammation, whereas only a few studies assessed obesity and inflammation as a combined outcome. Among suggested determinants for obesity with inflammation were Adenovirus-36, the gut microbiota,trans-fatty acids, and the four genesFTO,MC4R,TNF-αandLEPR.ConclusionsWe present a limited number of factors potentially contributing to the development of obesity with inflammation, while concluding that overall the area is indeed sparsely investigated. We present ideas for future studies that can identify relevant aetiological factors. This identification is essential for targeted prevention of obesity with inflammation and the clinical consequences thereof.
“…However, it is still believed that an obesity-promoting environment determines whether the obese genotype will result in the obese phenotype (69,70) . Therefore it can be speculated that SNP causing a genotype associated with inflammation will also need inflammatory-promoting environmental factors to result in the obesity-inflammatory phenotype.…”
Section: Discussionmentioning
confidence: 99%
“…This association has been made obvious by studies of adoptees who resemble their biological relatives but not their adoptive relatives and by numerous twin studies, suggesting that genetics accounts for 50-90 % of the variance in BMI (69,70) .…”
AbstractObjectiveDespite extensive research into the biological mechanisms behind obesity-related inflammation, knowledge of environmental and genetic factors triggering such mechanisms is limited. In the present narrative review we present potential determinants of adipose tissue inflammation and suggest ways ahead for future research in the field.DesignWe searched the literature for potential determinants of obesity with inflammation through MEDLINE by applying the MeSH headings ‘obesity’ and ‘inflammation’ in combination with specific terms for a series of environmental and genetic factors.ResultsNumerous articles reported on the association between environmental or genetic factors and respectively obesity and inflammation, whereas only a few studies assessed obesity and inflammation as a combined outcome. Among suggested determinants for obesity with inflammation were Adenovirus-36, the gut microbiota,trans-fatty acids, and the four genesFTO,MC4R,TNF-αandLEPR.ConclusionsWe present a limited number of factors potentially contributing to the development of obesity with inflammation, while concluding that overall the area is indeed sparsely investigated. We present ideas for future studies that can identify relevant aetiological factors. This identification is essential for targeted prevention of obesity with inflammation and the clinical consequences thereof.
“…Evidence for the high heritability of weight both in adults and children indicates that environmental susceptibility may be genetically determined. [2][3][4] The search for genetic markers associated with higher body weights is making progress, [5][6][7][8] and this raises the issue of the mechanisms through which genetic variations affect weight. Most attention has been paid to energy expenditure and fat storage as mechanisms underlying the genetic effects.…”
Background: The modern environment is ubiquitously 'obesogenic', yet people vary enormously in weight. One factor contributing to weight variation could be genetically determined differences in appetite that modulate susceptibility to the environment. We assessed the relative contribution of genes and environment for two aspects of appetite that have been implicated in obesity. Methods: Parents of a population-based sample of 8-to 11-year-old twins (n ¼ 5435 pairs) completed validated, questionnaire measures of responsiveness to satiety and responsiveness to food cues for both children.Results: Quantitative genetic model fitting gave estimates of 63% (95% confidence interval: 39-81%) for the heritability of satiety responsiveness and 75% (52-85%) for food cue responsiveness. Shared and non-shared environmental influences were 21% (0-51%) and 16% (10-21%) for satiety responsiveness, and 10% (0-38%) and 15% (10-18%) for food cue responsiveness, respectively. Conclusions: The high heritability of appetitive traits that are known to be related to weight suggests that genetic vulnerability to weight gain could operate through behavioural as well as metabolic pathways. Intervention strategies aimed at improving satiety responsiveness and reducing food cue responsiveness in high-risk individuals could help in preventing the development of obesity.
“…Although the environment shared by monozygotic twins is more similar than the environment shared by dizygotic twins, the heritability of BMI is not different in identical twins reared together or apart. A genetic component to obesity has also been confirmed in adoption studies (3). These comparisons indicate that the genetic transmission of obesity is at least as large as the nongenetic transmission.…”
mentioning
confidence: 67%
“…The most convincing evidence for a genetic component to obesity comes from twin and adoption studies (1)(2)(3)(4). In studies (1) in which body fat content was measured (either as body mass index [BMI] or skinfold thickness), the comparison of obesity in monozygotic twins with obesity in dizygotic twins indicated heritability quotients ranging from 0.4 to 0.98 (where 0 = no inheritance and 1.0 = complete inheritance of the trait).…”
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