Increased energy intake in pregnant smokers does not prevent human fetal growth retardation.
Increased energy intake in pregnant smokers does not prevent human fetal growth retardation.
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怀孕吸烟者增加能量摄入并不能防止人类胎儿生长迟缓。
DOI：
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发表时间：
1996
期刊：
影响因子：
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通讯作者：
K. Gray‐donald
中科院分区：
文献类型：
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作者：
S. K. Muscati;Kristine G. Koski;K. Gray‐donald
对参加爱德华王子岛产前营养咨询计划（1979-1989）的729名吸烟和610名不吸烟孕妇进行了回顾性队列研究，以研究吸烟者中较低的能量摄入是否会导致较低的母亲体重增加和/或较高的小于胎龄儿（SGA）率。第二个目的是量化，使用病因学分数，吸烟，孕妇孕前体重不足和低妊娠体重增加的风险SGA的独立贡献。测量孕妇妊娠前体重，身高，妊娠体重增加，吸烟状况，体力活动，整个妊娠期间通过一系列3-d食物记录的能量摄入，以及婴儿出生体重，收集无并发症妊娠导致足月单胎婴儿的妇女。多元线性回归分析预测吸烟对母亲能量摄入、体重增加和婴儿出生体重的影响。采用Logistic回归分析确定吸烟、孕前体重不足和妊娠体重增加少对SGA风险的独立贡献。吸烟与较高的能量摄入[+702 kJ/d（+168 kcal/d）]独立相关，但与较低的母亲体重增加（-2.16 kg）和婴儿出生体重（-205 g）相关。膳食能量摄入仅与出生体重的小幅增加呈正相关[5.9 g/418 kJ（100 kcal）]。SGA的病因部分归因于吸烟是30.8%，孕前体重不足16.7%，低妊娠体重增加15.3%。我们的结论是，吸烟对胎儿生长发育的重要负面影响不能通过简单地增加能量摄入来充分减轻。
A retrospective cohort study of 729 smoking and 610 nonsmoking pregnant women participating in the Prince Edward Island Prenatal Nutritional Counselling Program (1979-1989) was undertaken to study whether lower energy intake results in lower maternal weight gain and/or a higher rate of small-for-gestational-age infants (SGA) among smokers. A second objective was to quantify, using etiological fractions, the independent contributions of cigarette smoking, maternal pregravid underweight and low pregnancy weight gain to the risk of SGA. Measurements of maternal pregravid weight, height, pregnancy weight gain, smoking status, physical activity, energy intake by a series of 3-d food records throughout the duration of pregnancy, and infant birth weight were collected for women with uncomplicated pregnancies resulting in full-term singleton infants. Multiple linear regression analyses were performed to predict the effect of smoking on maternal energy intake, weight gain and infant birth weight. The independent contributions of smoking, pregravid underweight and low pregnancy weight gain to the risk of SGA were determined using logistic regression analysis. Smoking was independently associated with a higher energy intake [+702 kJ/d (+168 kcal/d)] but with lower maternal weight gain (-2.16 kg) and infant birth weight (-205 g). Dietary energy intake was positively associated with only a small increment in birth weight [5.9 g per 418 kJ (100 kcal)]. The etiologic fraction for SGA attributable to smoking was 30.8%, pregravid underweight 16.7%, and low gestational weight gain 15.3%. We conclude that the important negative effect of smoking on retarding fetal growth cannot be adequately mitigated by simply increasing energy intake.