Substantial intergenerational increases in body mass index are not explained by the fetal overnutrition hypothesis:: the Cardiovascular Risk in Young Finns Study
Substantial intergenerational increases in body mass index are not explained by the fetal overnutrition hypothesis:: the Cardiovascular Risk in Young Finns Study
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DOI：
10.1093/ajcn/86.5.1509
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发表时间：
2007-11-01
影响因子：
7.1
通讯作者：
Raitakari, Olli T.
中科院分区：
文献类型：
--
作者：
Kivimaeki, Mika;Lawlor, Debbie A.;Raitakari, Olli T.
背景资料：根据胎儿营养过剩假说，母体肥胖的宫内影响增加了后代终身肥胖的风险。如果这个假设成立，那么母亲的体重指数（BMI;单位为kg/m2）和后代的BMI之间的联系应该比父亲的BMI和后代的BMI之间的联系更强，因为只有母亲直接影响胎儿的环境。目的：我们前瞻性地研究了BMI的代际变化，并检验了胎儿营养过剩假说。设计：后代体重的数据来自母亲。从2980个完整的父母-子女三人组中评估了3至18岁子女的BMI。21年后，在24-39岁时重复评估后代BMI。结果如下：后代的成年BMI比同龄父母的BMI高1.21个单位，这表明肥胖水平在几代人之间增加（P < 0.0001）。母亲BMI与后代出生体重的相关性比父亲BMI更强（P = 0.0009）。而在3-39岁年龄段，亲子间BMI相关性无显著性差异（P > 0.35）。在1%至15%非亲子关系的敏感性分析中，结果没有实质性变化。结论：由于后代与父母共享所有基因，因此观察到的后代的成年BMI明显高于父母的成年BMI可能是由环境影响解释的。没有发现任何支持胎儿环境对成年肥胖代际增加的具体影响。这些发现仅在与出生体重有关方面与胎儿营养过剩假说一致。
Background: According to the fetal overnutrition hypothesis, intrauterine influences of maternal obesity increased lifelong obesity risk in the offspring. If the hypothesis is true, then the association between maternal body mass index (BMI; in kg/m(2)) and offspring BMI should be stronger than the association between paternal BMI and offspring BMI, because only the mother directly influences the fetal environment. Objectives: We prospectively examined intergenerational change in BMI and tested the fetal overnutrition hypothesis. Design: Data on offspring weight were obtained from mothers. BMI was assessed from 2980 complete parent-offspring trios when the offspring were 3 to 18 y of age. The assessment of offspring BMI was repeated 21 y later at age 24-39 y. Results: Adult BMI of the offspring was 1.21 units higher than the BMI of their parents at the same age, which indicates an increase in obesity levels across generations (P < 0.0001). Maternal BMI was more strongly associated with offspring birth weight than was paternal BMI (P = 0.0009). However, there were no such differences in parent-offspring associations for BMI at later developmental stages when offspring were aged 3-39 y (P > 0.35). The results did not materially change in a sensitivity analysis for 1% to 15% nonpaternity. Conclusions: Because offspring share all genes with their parents, the observed substantially higher adult BMI for offspring than for parents is likely explained by environmental influences. No support was found for any specific influence from fetal environment on this intergenerational increase in adult obesity. The findings were consistent with the fetal overnutrition hypothesis only in relation to birth weight.