Department of Psychology, College of Life and Environmental Sciences, University of Exeter, Exeter, UK.
NIHR Bristol BRC Nutrition Theme, University Hospitals Bristol Education & Research Centre, University of Bristol, Bristol, UK.
Int J Epidemiol. 2023 Dec 25;52(6):1926-1938. doi: 10.1093/ije/dyad092.
The mechanisms underlying genetic predisposition to higher body mass index (BMI) remain unclear.
We hypothesized that the relationship between BMI-genetic risk score (BMI-GRS) and BMI was mediated via disinhibition, emotional eating and hunger, and moderated by flexible (but not rigid) restraint within two UK cohorts: the Genetics of Appetite Study (GATE) (n = 2101, 2010-16) and the Avon Longitudinal Study of Parents and Children (ALSPAC) (n = 1679, 2014-18). Eating behaviour was measured by the Adult Eating Behaviour Questionnaire and Three-Factor Eating Questionaire-51.
The association between BMI-GRS and BMI were partially mediated by habitual, emotional and situational disinhibition in the GATE/ALSPAC meta-mediation [standardized betaindirect 0.04, 95% confidence interval (CI) 0.02-0.06; 0.03, 0.01-0.04; 0.03, 0.01-0.04, respectively] external hunger and internal hunger in the GATE study (0.02, 0.01-0.03; 0.01, 0.001-0.02, respectively). There was evidence of mediation by emotional over/undereating and hunger in the ALSPAC study (0.02, 0.01-0.03; 0.01, 0.001-0.02; 0.01, 0.002-0.01, respectively). Rigid or flexible restraint did not moderate the direct association between BMI-GRS and BMI, but high flexible restraint moderated the effect of disinhibition subscales on BMI (reduction of the indirect mediation by -5% to -11% in GATE/ALSPAC) and external hunger (-5%) in GATE. High rigid restraint reduced the mediation via disinhibition subscales in GATE/ALSPAC (-4% to -11%) and external hunger (-3%) in GATE.
Genetic predisposition to a higher BMI was partly explained by disinhibition and hunger in two large cohorts. Flexible/rigid restraint may play an important role in moderating the impact of predisposition to higher BMI.
遗传易感性导致更高体重指数(BMI)的机制仍不清楚。
我们假设 BMI-遗传风险评分(BMI-GRS)与 BMI 之间的关系通过抑制、情绪化进食和饥饿来介导,并在两个英国队列中得到调节:食欲研究的遗传学(GATE)(n=2101,2010-16)和雅芳纵向父母和儿童研究(ALSPAC)(n=1679,2014-18)。饮食行为通过成人饮食行为问卷和三因素饮食问卷-51 进行测量。
在 GATE/ALSPAC 元中介分析中,BMI-GRS 与 BMI 之间的关联部分通过习惯性、情绪性和情境性抑制来介导[标准化贝塔间接 0.04,95%置信区间(CI)0.02-0.06;0.03,0.01-0.04;0.03,0.01-0.04,分别]在 GATE 研究中,外部饥饿和内部饥饿(0.02,0.01-0.03;0.01,0.001-0.02,分别)。在 ALSPAC 研究中,有情绪过度/不足进食和饥饿的中介证据(0.02,0.01-0.03;0.01,0.001-0.02;0.01,0.002-0.01,分别)。刚性或柔性约束并没有调节 BMI-GRS 与 BMI 之间的直接关联,但高柔性约束调节了抑制亚量表对 BMI(在 GATE/ALSPAC 中减少间接中介作用-5%至-11%)和外部饥饿(-5%)的影响。高刚性约束减少了 GATE/ALSPAC 中抑制亚量表的中介作用(-4%至-11%)和 GATE 中的外部饥饿(-3%)。
在两个大型队列中,遗传易感性导致更高的 BMI 部分是由抑制和饥饿引起的。灵活/刚性约束可能在调节较高 BMI 易感性的影响方面发挥重要作用。