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Is information on genetic determinants of obesity helpful or harmful for obese people?--A randomized clinical trial.

ABSTRACT: BACKGROUND AND OBJECTIVES: Although more and more genetic information is available, it is unclear whether this information is helpful for patients. Therefore, we assessed the positive and negative effects of informing obese people about the genetic etiology of being overweight. DESIGN, PARTICIPANTS: Two hundred ninety-four obese people were randomized to 2 interventions (a 1-session consultation for obese people on how to manage obesity either including genetic information or not); their results were compared to a control group (116). Subjects were assessed before and after consultation and 6 months later. MEASUREMENTS: Weight, scales on feeling guilty for being overweight, self-control, negative mood (primary endpoint), body acceptance, restraint eating. RESULTS: Both types of consultations were considered helpful by the participants, and had comparable effects on body weight. The consultation with genetic information was rated superior in terms of leading to new insights (advantage for consultation with genetic information, even 6 months later; p = 0.046). No negative effects (e.g., loss of self-efficacy/self-control, increase of body weight; all p > 0.20 for interaction consultation x time) were observed for informing obese people about the genetic etiology of being overweight. The consultation resulted in long-term improvement of negative mood if it included genetic information in the case of participants with a family history of obesity and if it included no genetic information in the case of obese people without a family history of obesity (p = 0.03 for interaction of group, intervention, and time). CONCLUSIONS: Consultations in obesity can be helpful in general. These consultations should include genetic information if people have a family history of obesity.

SUBMITTER: Rief W

PROVIDER: S-EPMC2219810 | biostudies-other | 2007 Nov

REPOSITORIES: biostudies-other

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Project description:Obesity represents a major health burden to both developed and developing countries. Furthermore, the incidence of obesity is increasing in children. Obesity contributes substantially to mortality in the United States by increasing the risk for type 2 diabetes, cardiovascular-related diseases, and other comorbidities. Despite environmental changes over past decades, including increases in high-calorie foods and sedentary lifestyles, there is very clear evidence of a genetic predisposition to obesity risk. Childhood obesity cases can be categorized in one of two ways: syndromic or non-syndromic. Syndromic obesity includes disorders such as Prader-Willi syndrome, Bardet-Biedl syndrome, and Alström syndrome. Non-syndromic cases of obesity can be further separated into rarer instances of monogenic obesity and much more common forms of polygenic obesity. The advent of genome-wide association studies (GWAS) and next-generation sequencing has driven significant advances in our understanding of the genetic contribution to childhood obesity. Many rare and common genetic variants have been shown to contribute to the heritability in obesity, although the molecular mechanisms underlying most of these variants remain unclear. An important caveat of GWAS efforts is that they do not strictly represent gene target discoveries, rather simply the uncovering of robust genetic signals. One clear example of this is with progress in understanding the key obesity signal harbored within an intronic region of the FTO gene. It has been shown that the non-coding region in which the variant actually resides in fact influences the expression of genes distal to FTO instead, specifically IRX3 and IRX5. Such discoveries suggest that associated non-coding variants can be embedded within or next to one gene, but commonly influence the expression of other, more distal effector genes. Advances in genetics and genomics are therefore contributing to a deeper understanding of childhood obesity, allowing for development of clinical tools and therapeutic agents.

Project description:As obesity, circulating lipids and other vascular/metabolic factors influence the risk of stroke, we examined if genetic variants associated with these conditions are related to risk of stroke using a case-control study in Galicia, Spain. A selection of 200 single-nucleotide polymorphisms previously found to be related to obesity, body mass index, circulating lipids, type 2 diabetes, heart failure, obesity-related cancer and cerebral infarction were genotyped in 465 patients diagnosed with stroke and 480 population-based controls. An unsupervised Lasso regression procedure was carried out for single-nucleotide polymorphism selection based on their potential effect on stroke according to obesity. Selected genotypes were further analysed through multivariate logistic regression to study their association with risk of stroke. Using unsupervised selection procedures, nine single-nucleotide polymorphisms were found to be related to risk of stroke overall and after stratification by obesity. From these, rs10761731, rs2479409 and rs6511720 in obese subjects [odds ratio (95% confidence interval) = 0.61 (0.39-0.95) (P = 0.027); 0.54 (0.35-0.84) (P = 0.006) and 0.42 (0.22-0.80) (P = 0.0075), respectively], and rs865686 in non-obese subjects [odds ratio (95% confidence interval) = 0.67 (0.48-0.94) (P = 0.019)], were independently associated with risk of stroke after multivariate logistic regression procedures. The associations between the three single-nucleotide polymorphisms found to be associated with stroke risk in obese subjects were more pronounced among females; for rs10761731, odds ratios among obese males and females were 1.07 (0.58-1.97) (P = 0.84), and 0.31 (0.14-0.69) (P = 0.0018), respectively; for rs2479409, odd ratios were 0.66 (0.34-1.27) (P = 0.21), and 0.49 (0.24-0.99) (P = 0.04), for obese males and females, respectively; the stroke-rs6511720 association was also slightly more pronounced among obese females, odds ratios were 0.33 (0.13-0.87) (P = 0.022), and 0.28 (0.09-0.85) (P = 0.02) for obese males and females, respectively. The rs865686-stroke association was more pronounced among non-obese males [odds ratios = 0.61 (0.39-0.96) (P = 0.029) and 0.72 (0.42-1.22) (P = 0.21), for non-obese males and females, respectively]. A combined genetic score of variants rs10761731, rs2479409 and rs6511720 was highly predictive of stroke risk among obese subjects (P = 2.04 × 10-5), particularly among females (P = 4.28 × 10-6). In summary, single-nucleotide polymorphisms rs1076173, rs2479409 and rs6511720 were found to independently increase the risk of stroke in obese subjects after adjustment for established risk factors. A combined score with the three genomic variants was an independent predictor of risk of stroke among obese subjects in our population.

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Is information on genetic determinants of obesity helpful or harmful for obese people?--A randomized clinical trial.

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