From the Department of Occupational and Environmental Health Sciences (Wu), School of Public Health, Peking University, Beijing, China; Population Health and Science Policy (Gennings), Mount Sinai Hospital, New York, New York; Department of Pediatrics (R.J. Wright), Kravis Children's Hospital, The Mindich Child Health & Development Institute (R.J. Wright), and Department of Preventive Medicine, Icahn School of Medicine at Mount Sinai (Just, Svensson, R.O. Wright), New York, New York; Department of Statistics (Wilson), Colorado State University, Fort Collins, Colorado; Department of Neonatology and Obstetrics, Gynecology and Reproductive Biology (Burris), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts; Department of Epidemiology (Braun), School of Public Health, Brown University, Providence, Rhode Island; Department of Environmental Health Sciences (Zhong, Brennan, Dereix, Baccarelli), Mailman School of Public Health, Columbia University, New York, New York; Center for Research in Nutrition and Health (Cantoral, Téllez-Rojo), National Institute of Public Health, Cuernavaca, Morelos, Mexico; and Division of Research on Community Interventions (Schnaas), National Institute of Perinatology, Mexico City, Mexico.
Psychosom Med. 2018 Jan;80(1):34-41. doi: 10.1097/PSY.0000000000000517.
Maternal stress during pregnancy may influence childhood growth and adiposity, possibly through immune/inflammatory programming. We investigated whether exposure to prenatal stress and methylation in inflammation-related genes were associated with childhood adiposity in 424 mother-child pairs in Mexico City, Mexico.
A stress index was created based on four prenatally administered stress-related scales (Exposure to Violence, Crisis in Family Systems, State-Trait Anxiety Inventory, and Edinburgh Postnatal Depression Scale). We measured weight, height, body fat mass (BFM), percentage body fat (PBF), and waist circumference in early childhood (age range, 4-6 years). Body mass index (BMI) z scores were calculated according to World Health Organization standards. DNA methylation in gene promoters of tumor necrosis factor α, interleukin 8, and interleukin 6 (IL6) in umbilical cord blood were determined by pyrosequencing.
An interquartile range increase in stress index (27.3) was associated with decreases of 0.14 unit in BMI z score (95% confidence interval [CI] = -0.28 to -0.005), 5.6% in BFM (95% CI = -9.7 to -1.4), 3.5% in PBF (95% CI = -6.3 to -0.5), and 1.2% in waist circumference (95% CI = -2.4 to -0.04) in multivariable-adjusted models. An interquartile range increase in IL6 methylation (3.9%) was associated with increases of 0.23 unit in BMI z score (95% CI = 0.06-0.40), 8.1% (95% CI = 2.3-14.3) in BFM, 5.5% (95% CI = 1.7-9.5) in PBF, and 1.7% (95% CI = 0.2-3.3) in waist circumference.
Prenatal stress was associated with decreased childhood adiposity, whereas cord blood IL6 methylation was associated with increased childhood adiposity in Mexican children.
孕妇在怀孕期间所承受的压力可能会通过免疫/炎症编程影响儿童的生长和肥胖，我们调查了在墨西哥城的 424 对母婴中，产前压力暴露和炎症相关基因的甲基化是否与儿童肥胖有关。
基于四个产前应激相关量表（暴露于暴力、家庭系统危机、状态特质焦虑量表和爱丁堡产后抑郁量表），我们创建了一个压力指数。我们在儿童早期（年龄范围 4-6 岁）测量体重、身高、体脂肪量（BFM）、体脂肪百分比（PBF）和腰围。根据世界卫生组织的标准计算体重指数（BMI）z 评分。通过焦磷酸测序测定脐带血中肿瘤坏死因子 α、白细胞介素 8 和白细胞介素 6（IL6）基因启动子的 DNA 甲基化。
压力指数的四分位间距增加（27.3）与 BMI z 评分降低 0.14 个单位（95%置信区间[CI]：-0.28 至-0.005）、BFM 降低 5.6%（95% CI：-9.7 至-1.4）、PBF 降低 3.5%（95% CI：-6.3 至-0.5）和腰围增加 1.2%（95% CI：-2.4 至-0.04）有关，在多变量调整模型中。IL6 甲基化的四分位间距增加（3.9%）与 BMI z 评分增加 0.23 个单位（95% CI：0.06-0.40）、BFM 增加 8.1%（95% CI：2.3-14.3）、PBF 增加 5.5%（95% CI：1.7-9.5）和腰围增加 1.7%（95% CI：0.2-3.3）有关。
产前压力与儿童肥胖呈负相关，而脐带血中 IL6 甲基化与儿童肥胖呈正相关。
