Utah Autism Research Program, 650 Komas Dr, Suite 206, Salt Lake City, UT 84108.
Pediatrics. 2013 Nov;132(5):e1276-83. doi: 10.1542/peds.2013-1188. Epub 2013 Oct 28.
The rising population of individuals identified with an autism spectrum disorder (ASD) calls for further investigation of its underlying etiology. A disturbance in the fetal steroid hormone environment may be a mechanism in which environmental and genetic risk factors interact. The mother, fetus, and placenta collectively create the fetal steroid environment. Prepregnancy BMI and pregnancy weight gain have served as markers for fetal steroid hormone exposure in other disease states. This study's objective is to determine whether prepregnancy BMI and pregnancy weight gain are associated with increased ASD risk across study designs and cohorts while controlling for important confounding variables.
A population-based Utah ASD cohort (n = 128) was ascertained in a 3-county surveillance area and gender- and age-matched to 10,920 control subjects. A second, research-based ASD cohort of Utah children (n = 288) and their unaffected siblings (n = 493) were ascertained through participation in an ASD genetics study. Prenatal variables were obtained from birth certificate records.
ASD risk was significantly associated with pregnancy weight gain (adjusted odds ratio = 1.10, 95% confidence interval: 1.03 to 1.17; adjusted odds ratio = 1.17, 95% confidence interval: 1.01 to 1.35 for each 5 pounds of weight gained), but not prepregnancy BMI, in population and research-based cohorts, respectively. When analyses were restricted to ASD cases with normal IQ, these associations remained significant.
ASD risk associated with a modest yet consistent increase in pregnancy weight gain suggests that pregnancy weight gain may serve as an important marker for autism's underlying gestational etiology. This justifies an investigation into phenomena that link pregnancy weight gain and ASD independent of prepregnancy BMI.
被诊断为自闭症谱系障碍（ASD）的个体人数不断增加，这需要进一步研究其潜在病因。胎儿类固醇激素环境的紊乱可能是环境和遗传风险因素相互作用的一种机制。母亲、胎儿和胎盘共同构成了胎儿的类固醇环境。在其他疾病状态下，孕前 BMI 和孕期体重增加已被用作胎儿类固醇激素暴露的标志物。本研究的目的是确定在控制重要混杂变量的情况下，孕前 BMI 和孕期体重增加是否与 ASD 风险增加有关，无论研究设计和队列如何。
在一个由 3 个县组成的监测区域中，确定了一个基于人群的犹他州 ASD 队列（n = 128），并与 10920 名对照者按性别和年龄匹配。第二个是犹他州儿童 ASD 的基于研究的队列（n = 288）及其未受影响的兄弟姐妹（n = 493），他们通过参与 ASD 遗传学研究而被确定。产前变量从出生证明记录中获得。
在人群和研究队列中，ASD 风险与孕期体重增加显著相关（调整后的优势比分别为 1.10，95%置信区间：1.03 至 1.17；调整后的优势比分别为 1.17，95%置信区间：1.01 至 1.35，每增加 5 磅体重），但与孕前 BMI 无关。当将分析仅限于 IQ 正常的 ASD 病例时，这些关联仍然显著。
与孕期体重适度但一致增加相关的 ASD 风险表明，孕期体重增加可能是自闭症潜在妊娠病因的一个重要标志物。这证明了有必要研究与孕前 BMI 无关的与孕期体重增加和 ASD 相关的现象。
