When information on both environmental exposures lifestyle and dietary intake and genotyping is collected, the gene-environment interactions can be tested by the observational studies. Cross-sectional and retrospective case-control designs are most often used for studying gene-environment interactions in relation to continuous differences in obesity-related traits and dichotomous obesity status. A case-only design has also been employed for examining multiplicative gene-environment interactions, assuming the environment factors and genotypes are independent.
Although such studies are relatively easy to conduct, they are susceptible to the influence of selection, recall e. Prospective cohort studies collect information on environmental exposure before the occurrence of disease and hold an advantage in minimizing these biases. Among environmental factors, physical inactivity, total energy intake, and consumption of various dietary fats total fat, saturated fat acid [SFA], polyunsaturated fat acid [PUFA] and CHOs including fibers have attracted a great deal of attention.
Due to statistical and computational difficulty, the test on gene-environment interaction has not yet been practical on a whole-genome scale. Several studies specifically examined the interactions between energy intake and genes involved in the regulation of energy balance and adipose tissue metabolism. In a recent study of healthy Japanese men, Song et al. Because of their high energy intensity, dietary fats have been a focus of attention relative to their interactions with genetic components in determining obesity risk. In a cross-sectional study of men, Robitaille et al. A few studies tested the interaction between genetic variants and intake of CHOs Table 1.
Among women with the wild-type homozygotes, CHO intake was associated with reduced obesity risk, although the association was not statistically significant. The opposite association In addition to the dietary components, several studies have documented potential interaction between physical activity and genetic variants Table 1. The Gln homozygotes had significantly higher adiposity measures than the Glu-allele carriers only in men who did not engage in physical activity; the gene-physical activity interaction was not observed in women.
Another study, 69 however, reported a significant interaction between this genetic variant and physical activity in women. Among those who were physically active, Glu-allele carriers had higher BMI than non-carriers. In a cross-sectional study with teen-aged Greeks, Moran et al. This association was strongest in women who participated in no extra exercise and accounted for 6. In a population-based study of women and men aged 30 and 75 years, Ridderstrale et al. Some other studies suggested that the genetic variants in UCP2 and UCP3 genes might also modulate the effects of physical activity on obesity risk 72 , 73 Recently, Andreasen et al.
The results suggest that higher physical activity may attenuate the adverse effects of the FTO variant on obesity. Although observational studies are relatively easy to conduct, the results obtained from them are at most suggestive, as various sources of bias selection, survival, and recall bias may lead to spurious results and statistical significance does not necessarily imply causality. In contrast to observational studies, the study conditions in randomized clinical trials are controlled directly by the investigators, including the specifically defined dietary intakes and physical activity.
This control minimizes the possibility of bias and increases the level of causality. However, this is not an efficient approach considering the increasingly expanding list of susceptibility genes to be tested. Many studies have examined the modification effects of the key genes regulating energy balance on weight loss intervention.
Similar genetic modification effects on dietary intervention were also observed in children. The increases in weight and BMI were significantly lower in obese children without the variant than in the control group. Changes in weight and BMI in obese children with the variant were similar to the results in the controls.
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Some other genetic variants were also found to modulate the effects of dietary intervention on weight loss. In one analysis including obese patients 79 women and 38 men; mean age 42 years; mean BMI Patient compliance was supervised by means of a nutritional diary that was reviewed at follow-up visits at 6 weeks and 3 months.
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Recent changes in the availability and cost of palatable energy-dense food and the reduction in physical activity during work and recreation on the background of evolutionarily engraved response patterns genetic predisposition have undoubtedly contributed to the current obesity epidemic. Evidence from association studies and intervention trials continues to mount, indicating that genetic components may modify lifestyle effects on the development of obesity. However, these findings are at most preliminary. Various sources of bias may lead to spurious interactions in observational studies, especially cross-sectional and retrospective studies.
A randomized clinical trial is an excellent model for testing gene-lifestyle interactions. However, since most interventions combine changes in diet, weight loss, and physical activity, it is difficult to tease out the interactive effect attributable to any specific component. In addition, most intervention trials are small and short-term, thus limiting the statistical power and the ability to identify moderate interactions and long-term genetic effects. Therefore, a large-scale, prospective study with detailed information for lifestyle and dietary intake would be an ideal model for identifying gene-environment interactions.
DNA sequencing alone does not provide enough information to determine the molecular pathways of an organism in healthy and diseased states.
This understanding has helped spawn numerous multidisciplinary approaches to the study of complexity in human health. Increasing research effort is now invested in post-genomic science, particularly in the related disciplines of transcriptomics, proteomics, and metabolomics. Population-wide prevention and treatment efforts aimed at reducing obesity are usually costly and difficult to conduct.
Therefore, efforts to prevent obesity at the public health level can be focused on identification and counseling of susceptible individuals. Attempts to integrate the emerging knowledge into personalized health practices are still in the very early stages. National Center for Biotechnology Information , U.
Author manuscript; available in PMC Jun Lu Qi and Young Ae Cho. Find articles by Lu Qi. Find articles by Young Ae Cho. Author information Copyright and License information Disclaimer. The publisher's final edited version of this article is available at Nutr Rev. See other articles in PMC that cite the published article.
Abstract The epidemic of obesity has become a major public health problem. Table 1 Selected observational studies of gene-lifestyle interactions on obesity. No interaction was observed in women Luan et al. S ratio was low, and the opposite was seen when P: Open in a separate window. Table 2 Selected intervention studies of gene-lifestyle interactions on weight change. The epidemiology of obesity. Prevalence and trends in overweight among US children and adolescents, — Evidence for multiple determinants of the body mass index: Overweight as an avoidable cause of cancer.
Eur Int J Cancer. Genetic and environmental factors in relative body weight and human adiposity. The body-mass index of twins who have been reared apart. N Engl J Med.
Genetic and environmental influences on obesity assessed by the adoption method. Rev Epidemiol Sante Publique. Common variants near MC4R are associated with fat mass, weight and risk of obesity. A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity.
FTO gene variant is associated with obesity: Genome-wide association scan shows genetic variants in the FTO gene are associated with obesity-related traits. Genetic epidemiology of obesity. S my favourite actor.
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