Department of Public Health, California State University Fullerton, Fullerton.
Department of Obstetrics and Gynecology, Loma Linda University School of Medicine, Loma Linda, CA.
Ann Epidemiol. 2021 Jan;53:50-55.e1. doi: 10.1016/j.annepidem.2020.08.009. Epub 2020 Sep 9.
Maternal obesity has been consistently associated with offspring risk for ASD, as well as lipid metabolism derangements. However, few ASD studies have examined maternal lipids in conjunction with maternal prepregnancy body mass index (BMI).
This nested case-control study was based on the Boston Birth Cohort, a prospective cohort study of mother-child dyads recruited at the Boston Medical Center. Maternal blood samples were collected shortly after delivery and analyzed for total plasma cholesterol, HDL, and triglyceride (TG) concentrations. Low-density lipoprotein (LDL) was subsequently calculated by the Friedewald equation. Cases were identified using ASD diagnoses in children's medical records. The odds of ASD were estimated with continuous lipid levels for a linear relationship, and we further explored the nonlinear relationship using the tertile of each lipid analyte with the highest tertile as the reference group. Logistic regression was used to estimate the risk of ASD adjusting for potential confounders. The analyses were performed separately for mothers with normal weight and overweight/obese based on maternal prepregnancy BMI.
One standard deviation decrease in postpartum maternal LDL was associated with increased odds of ASD aOR 1.35 [1.04-1.75]. There was no association between postpartum maternal HDL and TG levels and ASD risk. Decreasing levels of LDL were not associated with ASD risk in normal-weight mothers (aOR 1.2 [0.83-1.75]), but the ASD risk was more pronounced in overweight and obese mothers (aOR 1.54 [1.03-2.27]). Follow-up analysis of nonlinear association models showed that, when compared to the highest tertile, lower maternal LDL concentrations were associated with approximately two times increased risk of ASD (first tertile: aOR 2.49 [1.27-4.87] and second tertile: aOR 2.79 [1.42-5.48]). A similar pattern was observed with overweight/obese mothers but not in normal-weight mothers.
Lower maternal postpartum plasma LDL concentration was associated with increased odds of ASD in offspring among children born to overweight and obese mothers. Our findings suggest that both maternal BMI and lipids should be considered in assessing their role in offspring ASD risk, and additional longitudinal studies are needed to better understand maternal lipid dynamics during pregnancy among normal-weight and overweight/obese mothers.
母体肥胖与后代患自闭症谱系障碍(ASD)的风险以及脂质代谢紊乱密切相关。然而,很少有 ASD 研究同时检查了母体脂质和母体孕前体重指数(BMI)。
本巢式病例对照研究基于波士顿出生队列,这是一项在波士顿医疗中心招募母婴对子的前瞻性队列研究。在分娩后不久采集母体血液样本,分析总血浆胆固醇、高密度脂蛋白(HDL)和甘油三酯(TG)浓度。随后通过 Friedewald 方程计算低密度脂蛋白(LDL)。通过儿童病历中的 ASD 诊断确定病例。使用连续的脂质水平来估计 ASD 的可能性,以线性关系表示,并进一步使用每个脂质分析物的最高三分位数作为参考组来探索非线性关系。使用逻辑回归来估计 ASD 的风险,同时调整潜在的混杂因素。分析根据母体孕前 BMI 分别在正常体重和超重/肥胖的母亲中进行。
产后母体 LDL 每降低一个标准差,ASD 的患病几率就会增加 aOR 1.35 [1.04-1.75]。产后母体 HDL 和 TG 水平与 ASD 风险无关。在正常体重母亲中,LDL 水平降低与 ASD 风险无关(aOR 1.2 [0.83-1.75]),但在超重和肥胖母亲中,ASD 风险更为明显(aOR 1.54 [1.03-2.27])。对非线性关联模型的随访分析表明,与最高三分位相比,母体 LDL 浓度较低与 ASD 风险增加约两倍相关(第一三分位:aOR 2.49 [1.27-4.87]和第二三分位:aOR 2.79 [1.42-5.48])。在超重/肥胖母亲中观察到类似的模式,但在正常体重母亲中没有观察到。
在超重和肥胖母亲所生的子女中,产后母体血浆 LDL 浓度较低与后代患 ASD 的几率增加有关。我们的研究结果表明,在评估母体 BMI 和脂质在后代 ASD 风险中的作用时,两者都应考虑在内,还需要进行更多的纵向研究,以更好地了解正常体重和超重/肥胖母亲在怀孕期间的母体脂质动态。