INCREASED ENERGY-INTAKE IN PREGNANT SMOKERS DOES NOT PREVENT HUMAN FETAL GROWTH-RETARDATION

A retrospective cohort study of 729 smoking and 610 nonsmoking pregnan t 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 ra te of small-for-gestational-age infants (SGA) among smokers. A second objective was to quantify, using etiological fractions, the independen t contributions of cigarette smoking, maternal pregravid underweight a nd low pregnancy weight gain to the risk of SGA. Measurements of mater nal pregravid weight, height, pregnancy weight gain, smoking status, p hysical activity, energy intake by a series of 3-d food records throug hout the duration of pregnancy, and infant birth weight were collected for women with uncomplicated pregnancies resulting in full-term singl eton infants. Multiple linear regression analyses were performed to pr edict the effect of smoking on maternal energy intake, weight gain and infant birth weight. The independent contributions of smoking, pregra vid underweight and low pregnancy weight gain to the risk of SGA were determined using logistic regression analysis. Smoking was independent ly associated with a higher energy intake [+702 kJ/d (+168 kcal/d)] bu t with lower maternal weight gain (-2.16 kg) and infant birth weight ( -205 g). Dietary energy intake was positively associated with only a s mall increment in birth weight [5.9 g per 418 kJ (100 kcal)]. The etio logic fraction for SGA attributable to smoking was 30.8%, pregravid un derweight 16.7%, and low gestational weight gain 15.3%. We conclude th at the important negative effect of smoking on retarding fetal growth cannot be adequately mitigated by simply increasing energy intake.