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This study evaulated the effects of diet, weight gain (low = LWG, less than or equal to 15 lb; adequate greater than 15 lb), smoking, and stress on the pregnancy outcomes of 60 women. LWG mothers, compared to adequate weight gain, had lower calorie intakes, shorter gestations (0.5 wk, Dubowitz) smaller placentas (345 +/- 65 versus 373 +/- 75 g), and infants with lower birth weight 2640 +/- 329 versus 3192 +/- 307 g), ponderal indices (2.37 versus 2.62), and growth rates. Mothers who smoked had increased calorie intake, but showed no alterations in gestational age of infants or placenta weights. Infants of smokers weighed less than those of nonsmokers (2875 +/- 522 versus 309 +/- 511 g), but had a normal ponderal index. LWG or smoking were associated with impaired motor performance, visual habituation and orientation, and reflexes. Smoking adversely affected auditory habituation and orientation, and autonomic regulation. LWG and smoking have significant, but separate, detrimental effects on pregnancy outcome.

This study examined the roles of diet, cigarette smoking, and psychological stress in pregnancy weight gain. The 60 were selected by defined criteria to minimize variation in anthropometric, socioeconomic, and medical variables which also affect weight gain. To maximize variation in weight gain, subjects were also selected on the basis of low weight gain (less than or equal to 15 lb) and adequate weight gain (greater than 15 lb). Each weight gain group contained smokers and nonsmokers. Smokers consumed more calories than nonsmokers (2119 versus 1810 kcal/day, p less than 0.01). for nonsmokers, differences between the intakes of low weight gain (1617 kcal/day) and adequate weight gain (1905 kcal/day) women were significant (p less than 0.02) and calorie intake was correlated with weight gain (r=0.44 p, less than 0.02). Psychological stress negatively correlated with weight gain (r=0.37, p less than 0.01) but not with calorie intake. We conclude that low weight gain is associated with a lower food intake. In contrast, smoking and stress may cause low weight gain by reducing the utilization of calories for weight gain.

A B S T R A a . A mild ketosis is known to prevail in the mother, fetus, and newborn infant during the 3rd trimester and in the early neonatal period. It has been shown that during an equivalent period in the rat ketone bodies are readily oxidized and serve a s key substrates for lipogenesis in brain. Since medium-chain triglycerides are known to be ketogenic, preterm infants may benefit from dietary medium-chain triglycerides beyond the point of enhanced fat absorption. Our objective was to determine the ketogenic response in preterm infants (gestational age: 33 + 0.8 wk)fed three different isocaloric formulas by measuring the concentrations of 3-hydroxybutyrate and acetoacetate in the plasma of these infants. At the time of entrance to the study the infants were receiving 110 kcallkg124 h. Study I (1 1 infants): the infants were fed sequentially in the order; P M 60140 (PM), Special Care Formula (SCF), and Similac 20 (SIM). In S C F greater than 50% of the fat consists of medium-chain length fatty acids while P M and S I M contain about 25%. The concentration of 3-hydroxybutyrate in plasma was significantly higher when infants were fed S C F than P M and S I M [0.14 2 0.03, 0.06 f 0.01, and 0.05 f: 0.01 mM, respectively ( p < 0.01)j. Study I1 (12 infants); the infants were fed SCF, then SIM, or the reverse. The concentration of acetoacetate in plasma was 0.05 f 0.01 and 0.03 f 0.01 m M when infants were fed S C F and SIM, respectively (0.1 > p > 0.05). The concentrations of 3-hydroxybutyrate in plasma were similar to those measured in study I for the respective formulas. The increased plasma levels of 3-hydroxybutyrate and total ketone bodies when S C F was fed indicate that S C F promotes a mild ketosis in preterm infants similar to that reported in breast-fed term infants. The past decade has witnessed a major change in our concept of ketone bodies from a limited role as alternative oxidative substrates in muscle and brain to a role as key substrates for tissue respiration and lipid synthesis. Recent studies with animal models (1-4) and in human infants (5-9) suggest that the ketone bodies, AcAc and 3HB, may be particularly important in the developing infant. Several investigators have demonstrated that AcAc and 3HB, in addition to serving as general oxidative substrates, are preferentially incorporated into sterols and fatty acids in the neonatal rat brain (1, 2, 10). This occurs during the "brain growth spurt" when cell proliferation and myelination are major developmental events. In the human myelination is most active during the 3rd trimester and throughout the 1st yr of life (1 1, 12). It has also been demonstrated in both the rat (1 3-1 5) and human (6,8,16) that the uptake of ketone bodies into brain is linearly related to the arterial concentration.The concentrations of the ketone bodies in blood are elevated above typical adult levels both in the fetus during the later half of gestation (8,17) and in the breast-fed term infant (18). These data warrant considering that metabolically stable preterm in...

Amino acid concentrations were measured in the cord blood serum from neonates following 23-41 weeks gestation. These values were then correlated with the gestational age of the newborns. A significant (p less than 0.05) correlation was observed with the concentrations of six amino acids, and five of these correlations were negative. The significance of these normative data are discussed and compared with currently available cord blood aminogram data.

The paper we recently published in JPEN' and discussions about it since its publication raised our interest in the determination of cord blood tryptophan concentrations and total cysteine concentrations. Our initial attempts to analyze samples for these amino acids using standard techniques were unsuccessful. The modifications we have used are described below.Plasma samples were analyzed for total tryptophan by the fluorometric procedure of Denckla and Dewey' as modified by Bloxam and Warren' with further modifications for improved accuracy and precision by our phys-FIG. 1. Regression analysis of gestational age (weeks) at the time of sample and plasma tryptophan concentrations (~mole/dl).iological amino acid analysis laboratory. The major modifications include heating samples in closed vials and extending the heating period to 75 min in boiling water for maximum conversion of tryptophan to norharmon. The accuracy of our plasma tryptophan method was evaluated by comparing data from our method with data generated from a reverse-phase high performance liquid chromatography (HPLC) method. A paired t-test analysis showed no significant difference (p = 0.50) between pairs of tryptophan values obtained by the two analytical methods.Total plasma cyst(e)ine was determined by reverse phase HPLC with electrochemical detection. Dithiothreitol was added to plasma samples and thiols were detected TABLE I Age, tryptophan, and cysteine data FIG. 2. Regression analysis of gestational age (weeks) at the time of sample plasma total cyst{e)ine concentrations (~mole/dl).

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