Sanderson S C, Persky S, Michie S
Mount Sinai School of Medicine, Department of Genetics and Genomic Sciences, New York, N.Y. 10029, USA.
Public Health Genomics. 2010;13(1):34-47. doi: 10.1159/000217794. Epub 2009 May 4.
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.
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.
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.
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.
常见的肥胖相关基因变异可能通过增加进食或降低新陈代谢来发挥作用。这些差异可能会影响个体对肥胖基因检测结果的反应。
这是一项实验模拟研究:191名参与者被要求想象他们收到了一份基因检测结果,表明基于进食的肥胖风险高(n = 37)或基于新陈代谢的肥胖风险高(n = 41),一份酶检测结果表明基于进食的肥胖风险高(n = 35)或基于新陈代谢的肥胖风险高(n = 41),或者没有风险信息(n = 37)。结果包括感知风险、自我效能感(对健康饮食能力的信心)、反应效能感(对健康饮食将降低风险的信心)以及健康饮食的意愿。
与无风险信息组相比,收到增加肥胖风险信息的组报告的感知风险和健康饮食意愿更高(均p < 0.01)。检测类型对感知风险有主要影响(基因检测与酶检测:3.91对3.55,p = 0.031),因果途径对担忧有主要影响(进食与新陈代谢:3.33对2.86,p = 0.049),但两种操作对任何其他结果均无影响。
表明肥胖风险增加的个人风险信息可能会增加健康饮食的动机,无论风险被描述为基因风险还是非基因风险,或者是通过基于进食的还是基于新陈代谢的因果途径起作用。