Psychological and Behavioral Responses to Genetic Test Results Indicating Increased Risk of Obesity: Does the Causal Pathway from Gene to Obesity Matter?

被引:39
作者
Sanderson, S. C. [1 ]
Persky, S. [2 ]
Michie, S. [3 ]
机构
[1] Mt Sinai Sch Med, Dept Genet & Genom Sci, Icahn Med Inst, New York, NY 10029 USA
[2] NHGRI, Bethesda, MD 20892 USA
[3] UCL, Dept Psychol, London, England
关键词
Genetics and prevention; Genetic testing; Health behavior; Obesity; Prevention of common complex diseases; Psychological impact; Risk; Translational research; FTO GENE; HEART-DISEASE; FAT MASS; PERCEPTION QUESTIONNAIRE; PARENTAL OBESITY; ADULT OBESITY; WEIGHT; HEALTH; ANALOG; CONSEQUENCES;
D O I
10.1159/000217794
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Background: Common obesity-associated genetic variants may exert their effects through increasing eating or decreasing metabolism. Such differences might influence individual responses to obesity genetic test results. Methods: This was an experimental analogue study: 191 participants were asked to imagine they had received a genetic test result indicating high eating-based (n = 37) or high metabolism-based (n = 41) risk of obesity, an enzyme test result indicating high eating-based (n = 35) or high metabolism-based (n = 41) risk of obesity, or no risk information (n = 37). Outcomes included perceived risk, self-efficacy (confidence in ability to eat healthily), response-efficacy (confidence that eating healthily will reduce risk), and intention to eat healthily. Results: The groups receiving increased obesity risk information reported greater perceived risk and intention to eat healthily than the no risk information group (both p < 0.01). There were main effects of test type on perceived risk (genetic vs. enzyme: 3.91 vs. 3.55, p = 0.031) and of causal pathway on worry (eating vs. metabolism: 3.33 vs. 2.86, p = 0.049), but no effects of either manipulation on any other outcomes. Conclusion: Personal risk information indicating increased obesity risk may increase motivation to eat healthily, regardless of whether the risk is described as genetic or non-genetic or as acting through an eating-based or metabolism-based causal pathway. Copyright (C) 2009 S. Karger AG, Basel
引用
收藏
页码:34 / 47
页数:14
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