Broadney M M, Chahal N, Michels K A, McLain A C, Ghassabian A, Lawrence D A, Yeung E H
Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA.
Section on Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA.
Int J Obes (Lond). 2017 Jan;41(1):30-37. doi: 10.1038/ijo.2016.187. Epub 2016 Oct 26.
BACKGROUND/OBJECTIVES: Maternal obesity may influence neonatal and childhood morbidities through increased inflammation and/or altered immune response. Less is known about paternal obesity. We hypothesized that excessive parental weight contributes to elevated inflammation and altered immunoglobulin (Ig) profiles in neonates.
SUBJECTS/METHODS: In the Upstate KIDS Study maternal pre-pregnancy body mass index (BMI) was obtained from vital records and paternal BMI from maternal report. Biomarkers were measured from newborn dried blood spots (DBS) among neonates whose parents provided consent. Inflammatory scores were calculated by assigning one point for each of five pro-inflammatory biomarkers above the median and one point for an anti-inflammatory cytokine below the median. Linear regression models and generalized estimating equations were used to estimate mean differences (β) and 95% confidence intervals (CI) in the inflammatory score and Ig levels by parental overweight/obesity status compared with normal weight.
Among 2974 pregnancies, 51% were complicated by excessive maternal weight (BMI>25), 73% by excessive paternal weight and 28% by excessive gestational weight gain. Maternal BMI categories of overweight (BMI 25.0-29.9) and obese class II/III (BMI≥35) were associated with increased neonatal inflammation scores (β=0.12, 95% CI: 0.02, 0.21; P=0.02 and β=0.13, CI: -0.002, 0.26; P=0.05, respectively) but no increase was observed in the obese class I group (BMI 30-34.9). Mothers with class I and class II/III obesity had newborns with increased IgM levels (β=0.11, CI: 0.04, 0.17; P=0.001 and β=0.12, CI: 0.05, 0.19); P<0.001, respectively). Paternal groups of overweight, obese class I and obese class II/III had decreased neonatal IgM levels (β=-0.08, CI: -0.13,-0.03, P=0.001; β=-0.07, CI: -0.13, -0.01, P=0.029 and β=-0.11, CI:-0.19,-0.04, P=0.003, respectively).
Excessive maternal weight was generally associated with increased inflammation and IgM supporting previous observations of maternal obesity and immune dysregulation in offspring. The role of paternal obesity requires further study.
背景/目的：母亲肥胖可能通过增加炎症反应和/或改变免疫反应来影响新生儿和儿童的发病率。关于父亲肥胖的影响知之甚少。我们推测父母体重超标会导致新生儿炎症反应增强和免疫球蛋白（Ig）谱改变。
对象/方法：在纽约州北部儿童研究中，孕前母亲体重指数（BMI）从出生记录中获取，父亲BMI通过母亲报告获得。在父母同意的新生儿中，从新生儿干血斑（DBS）中测量生物标志物。通过为高于中位数的五种促炎生物标志物各计一分，为低于中位数的一种抗炎细胞因子计一分来计算炎症评分。使用线性回归模型和广义估计方程来估计与正常体重相比，父母超重/肥胖状态下炎症评分和Ig水平的平均差异（β）和95%置信区间（CI）。
在2974例妊娠中，51%的妊娠母亲体重超标（BMI>25），73%的妊娠父亲体重超标，28%的妊娠孕期体重增加过多。母亲超重（BMI 25.0 - 29.9）和肥胖II/III级（BMI≥35）与新生儿炎症评分增加相关（β = 0.12，95% CI：0.02，0.21；P = 0.02和β = 0.13，CI： - 0.002，0.26；P = 0.05），但肥胖I级组（BMI 30 - 34.9）未观察到增加。I级和II/III级肥胖的母亲所生新生儿IgM水平升高（β = 0.11，CI：0.04，0.17；P = 0.001和β = 0.12，CI：0.05，0.19；P < 0.001）。父亲超重、肥胖I级和肥胖II/III级组的新生儿IgM水平降低（β = - 0.08，CI： - 0.13， - 0.03，P = 0.001；β = - 0.07，CI： - 0.13， - 0.01，P = 0.029和β = - 0.11，CI： - 0.19， - 0.04，P = 0.003）。
母亲体重超标通常与炎症反应增加和IgM升高相关，支持了先前关于母亲肥胖与后代免疫失调的观察结果。父亲肥胖的作用需要进一步研究。
