Evidence for gene-environment correlation in child feeding: Links between common genetic variation for BMI in children and parental feeding practices.
Evidence for gene-environment correlation in child feeding: Links between common genetic variation for BMI in children and parental feeding practices.
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DOI：
10.1371/journal.pgen.1007757
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发表时间：
2018-11
期刊：
影响因子：
4.5
通讯作者：
Llewellyn CH
中科院分区：
文献类型：
--
作者：
Selzam S;McAdams TA;Coleman JRI;Carnell S;O'Reilly PF;Plomin R;Llewellyn CH
父母过度限制食物摄入量的喂养做法(“限制”)和增加食物摄入量的压力(“压力”)被认为对儿童体重的影响是相反的(高限制导致超重；高压力导致体重不足)。然而，儿童体重也会“引发”PFP。一种新的方法是调查儿童遗传对BMI和PFP的影响之间的基因-环境相关性。来自双胞胎早期发育研究的10,346名儿童(包括3,320对DZ双胞胎)使用独立的全基因组关联研究荟萃分析的结果，创建了结合BMI相关变异的全基因组多基因评分(GPS)。父母的“限制”和“压力”使用儿童喂养问卷进行评估。根据儿童10岁时的身高和体重计算儿童BMI标准差得分(BMI-SDS)。采用线性回归和固定家庭效应模型检验GPS和PFP之间的关联(n=4,445人)和家庭内关联(n=2,164 DZ对)。此外，我们还进行了多变量双胞胎分析(n=4,375对双胞胎)，以估计PFP的遗传力以及BMI-SDS和PFP之间的遗传相关性。全球定位指数与体重指数抑郁自评量表呈正相关(β=0.2，p=2.41×10-38)。与基因-环境相关假说一致，儿童体重指数与“限制”呈正相关(β=0.0 5，p=4.19×10-4)，与“压力”呈负相关(β=-0.0 8，p=2.70×10-7)。在控制父母BMI和控制总体家庭贡献(家庭内部分析)后，这些结果仍然是一致的。“限制”(43%[40-47%])和‘压力’(54%[50-59%])的遗传力为中到高。BMI-SDS与“限制”呈中等正相关(Ra=0.28[0.23-0.32])，与“压力”呈显著负相关(Ra=-0.48[-0.52-0.44])。结果表明，父母限制或鼓励孩子摄入食物的程度在一定程度上受到孩子对较高或较低BMI的遗传倾向的影响。这些发现指出了一种唤起的基因-环境相关性，在这种相关性中，儿童的遗传特征引发了父母的喂养行为。人们普遍认为，父母通过某些喂养方式影响孩子的体重指数。例如，严格的限制会导致超重，强迫饮食会导致体重不足。然而，最近的纵向研究并不支持这一模型。另一种假设是，儿童BMI有很强的遗传基础，会引发父母的喂养做法(基因-环境相关性)。为了验证这一点，我们在双胞胎早期发展研究的10岁儿童的大样本中应用了两种遗传方法：多基因得分分析(基因组范围的荟萃分析中与BMI相关的常见遗传变异的基于DNA的得分)和双胞胎分析(比较同卵和异卵双胞胎之间的相似性)。多基因得分与父母限制进食呈正相关(β=0.0 5，p=4.19×10-4)，与父母增加进食压力呈负相关(‘压力’；β=-0.0 8，p=2.70×10-7)。在控制了家庭内部共有的所有遗传和环境影响后，关联性没有变化。双胞胎分析的结果是一致的。“限制”(43%)和“压力”(54%)基本上是可遗传的，儿童BMI与“限制”呈正遗传相关(Ra=0.28)，与“压力”呈负遗传相关(Ra=-0.48)。这些发现支持了另一种假设，即儿童BMI也会导致父母的喂养行为，从而挑战了主流观点，即父母的行为是儿童BMI的唯一原因。
The parental feeding practices (PFPs) of excessive restriction of food intake (‘restriction’) and pressure to increase food consumption (‘pressure’) have been argued to causally influence child weight in opposite directions (high restriction causing overweight; high pressure causing underweight). However child weight could also ‘elicit’ PFPs. A novel approach is to investigate gene-environment correlation between child genetic influences on BMI and PFPs. Genome-wide polygenic scores (GPS) combining BMI-associated variants were created for 10,346 children (including 3,320 DZ twin pairs) from the Twins Early Development Study using results from an independent genome-wide association study meta-analysis. Parental ‘restriction’ and ‘pressure’ were assessed using the Child Feeding Questionnaire. Child BMI standard deviation scores (BMI-SDS) were calculated from children’s height and weight at age 10. Linear regression and fixed family effect models were used to test between- (n = 4,445 individuals) and within-family (n = 2,164 DZ pairs) associations between the GPS and PFPs. In addition, we performed multivariate twin analyses (n = 4,375 twin pairs) to estimate the heritabilities of PFPs and the genetic correlations between BMI-SDS and PFPs. The GPS was correlated with BMI-SDS (β = 0.20, p = 2.41x10-38). Consistent with the gene-environment correlation hypothesis, child BMI GPS was positively associated with ‘restriction’ (β = 0.05, p = 4.19x10-4), and negatively associated with ‘pressure’ (β = -0.08, p = 2.70x10-7). These results remained consistent after controlling for parental BMI, and after controlling for overall family contributions (within-family analyses). Heritabilities for ‘restriction’ (43% [40–47%]) and ‘pressure’ (54% [50–59%]) were moderate-to-high. Twin-based genetic correlations were moderate and positive between BMI-SDS and ‘restriction’ (rA = 0.28 [0.23–0.32]), and substantial and negative between BMI-SDS and ‘pressure’ (rA = -0.48 [-0.52 - -0.44]. Results suggest that the degree to which parents limit or encourage children’s food intake is partly influenced by children’s genetic predispositions to higher or lower BMI. These findings point to an evocative gene-environment correlation in which heritable characteristics in the child elicit parental feeding behaviour. It is widely believed that parents influence their child’s BMI via certain feeding practices. For example, rigid restriction has been argued to cause overweight, and pressuring to eat to cause underweight. However, recent longitudinal research has not supported this model. An alternative hypothesis is that child BMI, which has a strong genetic basis, evokes parental feeding practices (‘gene-environment correlation’). To test this, we applied two genetic methods in a large sample of 10-year-old children from the Twins Early Development Study: a polygenic score analysis (DNA-based score of common genetic variants associated with BMI in genome-wide meta-analyses), and a twin analysis (comparing resemblance between identical and non-identical twin pairs). Polygenic scores correlated positively with parental restriction of food intake (‘restriction’; β = 0.05, p = 4.19x10-4), and negatively with parental pressure to increase food intake (‘pressure’; β = -0.08, p = 2.70x10-7). Associations were unchanged after controlling for all genetic and environmental effects shared within families. Results from twin analyses were consistent. ‘Restriction’ (43%) and ‘pressure’ (54%) were substantially heritable, and a positive genetic correlation between child BMI and ‘restriction’ (rA = 0.28), and negative genetic correlation between child BMI and ‘pressure’ (rA = -0.48) emerged. These findings challenge the prevailing view that parental behaviours are the sole cause of child BMI by supporting an alternate hypothesis that child BMI also causes parental feeding behaviour.
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影响因子：
4.5
作者：
Daniels LA;Magarey A;Battistutta D;Nicholson JM;Farrell A;Davidson G;Cleghorn G
通讯作者：
Cleghorn G
DOI：
10.1093/bioinformatics/btu848
发表时间：
2015-05-01
期刊：
Bioinformatics (Oxford, England)
影响因子：
--
作者：
Euesden J;Lewis CM;O'Reilly PF
通讯作者：
O'Reilly PF
影响因子：
3
作者：
Boker S;Neale M;Maes H;Wilde M;Spiegel M;Brick T;Spies J;Estabrook R;Kenny S;Bates T;Mehta P;Fox J
通讯作者：
Fox J
影响因子：
7.1
作者：
Llewellyn, Clare H.;van Jaarsveld, Cornelia H. M.;Wardle, Jane
通讯作者：
Wardle, Jane
影响因子：
7.1
作者：
Afonso, Lisa;Lopes, Carla;Oliveira, Andreia
通讯作者：
Oliveira, Andreia