Increased energy intake in pregnant smokers does not prevent human fetal growth retardation.

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.