Dopamine genetic risk is related to food addiction and body mass through reduced reward-related ventral striatum activity

被引:15
|
作者
Romer, Adrienne L. [1 ]
Kang, Min Su [2 ]
Nikolova, Yuliya S. [3 ]
Gearhardt, Ashley N. [4 ]
Hariri, Ahmad R. [1 ]
机构
[1] Duke Univ, Durham, NC USA
[2] Univ Penn, Philadelphia, PA 19104 USA
[3] Ctr Addict & Mental Hlth, Toronto, ON, Canada
[4] Univ Michigan, Ann Arbor, MI 48109 USA
基金
美国国家科学基金会; 美国国家卫生研究院;
关键词
Food addiction; Obesity; Dopamine; Ventral striatum; BMI; OBESITY; ACTIVATION; ASSOCIATION; DISORDERS; SMOKERS; TRAITS; RESPONSIVITY; COMORBIDITY; INDIVIDUALS; PREVALENCE;
D O I
10.1016/j.appet.2018.09.010
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
The prevalence rate of obesity continues to rise in the U.S., but effective treatment options remain elusive resulting in increased emphasis on prevention. One such area of prevention research capitalizes on the relatively novel behavioral construct of food addiction, which has been implicated in obesity. Food addiction reflects an individual's propensity for compulsive eating despite negative consequences, and shares not only symptoms with both eating and substance use disorders but also genetic and neural correlates within neural reward-circuitry modulated by dopamine. Here, we examined associations between food addiction scores, body mass index (BMI), reward-related ventral striatum activity, and a polygenic score approximating dopamine signaling in 115 non Hispanic Caucasian young adult university students. As predicted, polygenic dopamine scores were related to ventral striatum activity, which in turn was associated with higher food addiction scores. In addition, food addiction was related to BMI. An exploratory post-hoc path analysis further indicated that polygenic scores were indirectly related to both food addiction and BMI, in part, through ventral striatum activity. Collectively, our results provide evidence supporting the utility of food addiction in weight gain prevention research by establishing links with known risk-related neural and genetic biomarkers.
引用
收藏
页码:24 / 31
页数:8
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