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Objective: Hypocalcemia is common in infants of diabetic mothers (IDMs) and may be caused by secondary hypoparathyroidism related to hypomagnesemia. This study was designed to test the hypothesis that prophylactic magnesium sulfate (MgSO4) administration at birth in IDMs with low cord magnesium concentrations will prevent neonatal hypocalcemia., Study Design: In this randomized trial conducted in IDMs with a cord magnesium concentration of <0.74 mM (1.8 mg/dl), 26 subjects received 6 mg/kg elemental magnesium and 23 subjects received no treatment. Serum concentrations of total and ionized calcium, phosphorus, and magnesium were recorded at birth, by measuring the concentrations within the umbilical cord, and at 24 and 72 hours of age., Results: The incidence of hypocalcemia at 72 hours was 0% (0 of 23) in the magnesium-treated group and 12.5% (2 of 16) in the group with no treatment (p = 0.16). There was no difference in mean serum calcium concentration at 72 hours between infants in the treated group and the group with no treatment (2.28 +/- 0.04 vs 2.22 +/- 0.05 mM; p = 0.39). The drop in serum calcium concentration from birth to 72 hours of age was less for the treated group (0.30 +/- 0.05 mM [1.23 +/- 0.18 mg/dl]) than the group with no treatment (0.45 +/- 0.05 mM [1.81 +/- 0.21 mg/dl]; p = 0.04)., Conclusion: Administration of intramuscular MgSO4 to IDMs with cord magnesium <0.74 mM (1.8 mg/dl) does not reduce the incidence of hypocalcemia in infants of well-controlled diabetic mothers.

Calcium has been shown to inhibit iron absorption. The consequences of chronic calcium supplementation on iron status are unclear, however. As part of a randomized calcium-supplementation trial in lactating and nonlactating women in the postpartum period, we determined whether long-term calcium supplementation and lactation status affected iron stores as measured by serum ferritin concentrations. Subjects (95 lactating and 92 nonlactating) were enrolled at approximately 6 mo postpartum and then randomly assigned to receive either 500 mg Ca as calcium carbonate or a placebo twice daily with meals for 6 mo. Lactating women weaned their infants approximately 2 mo after enrollment (ie, approximately 8 mo postpartum). Calcium supplementation had no effect on serum ferritin concentrations. At the end of the study, geometric mean serum ferritin concentrations were 28.4 microg/L in the calcium-supplemented group and 27.5 microg/L in the placebo group (P > 0.5). Lactation status was significantly related to serum ferritin concentrations. At baseline, serum ferritin concentrations were higher in lactating women than in nonlactating women (47.7 compared with 31.5 microg/L, P < 0.001). In lactating women, serum ferritin concentrations decreased by a mean of 17 microg/L after weaning. By 12 mo postpartum, mean serum ferritin concentrations in women who were previously lactating were not significantly higher than those of nonlactating women (30.5 compared with 25.5 microg/L). These findings provide reassurance that long-term calcium supplementation does not impair iron stores. Furthermore, lactation status should be considered when assessing iron nutriture of women and determinants of iron status in populations.

Background: Women may lose bone during lactation because of calcium lost in breast milk. We studied whether calcium supplementation prevents bone loss during lactation or augments bone gain after weaning., Methods: We conducted two randomized, placebo-controlled trials of calcium supplementation (1 g per day) in postpartum women. In one trial (the study of lactation), 97 lactating and 99 nonlactating women were enrolled a mean (+/-SD) of 16+/-2 days post partum. In the second trial (the study of weaning), 95 lactating women who weaned their infants in the 2 months after enrollment and 92 nonlactating women were enrolled 5.6+/-0.8 months post partum. The bone density of the total body, lumbar spine, and forearm was measured at enrollment and after three and six months., Results: The bone density of the lumbar spine decreased by 4.2 percent in the lactating women receiving calcium and by 4.9 percent in those receiving placebo and increased by 2.2 and 0.4 percent, respectively, in the nonlactating women (P<0.001 for the effect of lactation; P= 0.01 for the effect of calcium). After weaning, the bone density of the lumbar spine increased by 5.9 percent in the lactating women receiving calcium and by 4.4 percent in those receiving placebo; it increased by 2.5 and 1.6 percent, respectively, in the nonlactating women (P<0.001 for the effects of lactation and calcium). There was no effect of either lactation or calcium supplementation on bone density in the forearm, and there was no effect of calcium supplementation on the calcium concentration in breast milk., Conclusions: Calcium supplementation does not prevent bone loss during lactation and only slightly enhances the gain in bone density after weaning.

Objective: The effect of varying mineral intakes on total body bone mass accretion during the first year of life in healthy full-term infants is unknown. The purpose of this study was to determine whether total body bone mass accretion during the first year of life was influenced by the calcium and phosphorus intake of an infant and whether early differences in bone accretion persist through 1 year of age., Design: This prospective, randomized trial was conducted in two phases. In phase I, 67 infants were randomized within the first 2 weeks of life into either a low (439 mg of calcium per liter and 240 mg of phosphorus per liter) or moderate (510 mg of calcium per liter and 390 mg of phosphorus per liter) mineral-containing formula feeding group. An additional group of 34 human milk-fed (low mineral) infants also was enrolled. Phase II involved an additional randomization of all infants at 6 months of age into moderate-mineral formula (see above), high-mineral formula (1350 mg of calcium per liter and 900 mg of phosphorus per liter), or cow milk (1230 mg of calcium per liter and 960 mg of phosphorus per liter) feeding group. Anthropometric measurements, nutrient intake, and total body bone mineral content (BMC) by dual-energy x-ray absorptiometry were measured at 1, 3, 6, 9, and 12 months., Results: During the first 6 months, the moderate-mineral group had a greater increase in weight (3.42 +/- 0.62 kg) compared with the human milk group (2.93 +/- 0.56 kg); the low-mineral group (3.19 +/- 0.62 kg) was intermediate. Bone mass accretion differed in a similar direction, with the moderate-mineral feeding group having a greater increase than the human milk group and the low-mineral group being intermediate of the two. Including weight, length, and bone area as covariates, both the low-mineral formula- and human milk-fed groups had similar BMC, which was lower than that of the moderate-mineral group at 3 and 6 months of age. Adjusted mean BMC values for the moderate-mineral formula-fed group compared with the low-mineral formula- and human milk-fed groups were 127.8 +/- 1.5 (SEM) g vs 119. 2 +/- 1.5 and 122.1 +/- 1.4 g, respectively, at 3 months of age and 168.7 +/- 2.5 g vs 157.6 +/- 2.5 and 158.7 +/- 2.4 g, respectively, at 6 months of age. The BMC at 6 months of age among the formula-fed infants was correlated with both average dietary phosphorus intake (r = .592) and average daily calcium intake (r = .620) during the first 6 months. The relationships between BMC and these minerals remained significant even after controlling for caloric intake. It was not possible to determine the independent effects of dietary calcium and phosphorus on BMC because of the strong correlation of these minerals with each other. Despite significant differences in both calcium and phosphorus intakes during the second 6 months of life, there were no differences in growth parameters or bone mass accretion. Means for BMC, adjusted for body weight, length, and bone area, were not significantly different among feeding groups at either 9 or 12 months of age. Adjusted means were 199 +/- 2 (SEM) and 237 +/- 3 g at 9 and 12 months of age for infants receiving moderate-mineral formula; 198 +/- 2 and 236 +/- 3 g at 9 and 12 months of age for infants receiving the high-mineral formulas and 202 +/- 5 and 233 +/- 5 g at 9 and 12 months of age for infants receiving cow milk. The gain in bone mass during the second 6 months differed by the first 6-month feeding group; mean changes in BMC between 6 and 12 months, adjusted for changes in weight, length, and bone area, were greater in human milk-fed infants than in either the low- or moderate-mineral-containing formula groups: 81 +/- 16 g in human milk-fed infants and 73 +/- 15 and 71 +/- 15 g in the low- and moderate-mineral formula groups, respectively. Infants fed whole cow milk during the second 6 months were excluded from this analysis because of the small number of infants completing the study. By 12 months of age t

Measurement of milk intake by breast-fed infants is difficult and a simple measure would be helpful for research and clinical practice. Maternal urinary lactose excretion has been proposed as a simple measure of lactation performance. The objectives of this study were to describe the pattern of urinary lactose excretion postpartum, and to determine whether lactose excretion could predict breast milk output. Lactose excretion was determined in 50 lactating and 49 nonlactating women at 0.5, 3, and 6 mo postpartum, and in 29 weaning women and 30 nonlactating women at 5, 8, and 11 mo postpartum. Lactose excretion was 4- to 17-fold higher in lactating than in nonlactating women, depending on the time point studied, and was highest in both groups 0.5 mo postpartum. Lactose excretion decreased after weaning but remained higher than in nonlactating women 1.3 mo after weaning was completed. Sixty-two additional women between 1.5 and 12 mo postpartum were studied to determine the ability of urinary lactose to predict milk output. There was a positive association between milk output and urinary lactose excretion, with correlation coefficients ranging from 0.17 to 0.30 depending on the measurement interval for lactose excretion. Lactose excretion could explain 2-9% of the variance in milk output, and could correctly classify 29-40% of individuals into tertiles of milk output. Although urinary lactose excretion reflects changes in biological activity of the mammary gland and gross changes in milk production, it is not a precise predictor of milk output.

We investigated whether intestinal calcium absorption and serum 1,25-dihydroxycholecalciferol (calcitriol) concentrations are higher in women during lactation and after weaning to compensate for calcium lost in breast milk. Measurements were obtained at 4.6 mo postpartum in 24 lactating women and 24 nonlactating women, at 9.6 mo postpartum in 24 lactating women (2.6 mo after complete weaning) and 24 nonlactating women. One-half of the women in each group were randomly assigned to receive 1 g supplemental Ca/d as calcium carbonate. Fractional calcium absorption was measured by using stable isotopic tracers 42Ca and 44Ca. Fractional absorption was 0.32+/-0.02 (+/-SEM) in both lactating and nonlactating women, but was higher in lactating women after weaning (0.37+/-0.02) compared with nonlactating postpartum control subjects (0.31+/-0.02). These effects were independent of calcium intake. Changes in serum calcitriol paralleled changes in fractional absorption. There were no differences in calcitriol concentrations between lactating and nonlactating women, but calcitriol was greater in women after weaning compared with postpartum control subjects. Lactating women who had resumed menses had higher fractional absorption and serum calcitriol than did lactating women who had not. Serum calcium and phosphorus concentrations were greater in lactating compared with nonlactating women; there were no differences between groups after weaning. We conclude that lactation stimulates increases in fractional calcium absorption and serum calcitriol, but the responses are only apparent after weaning or the resumption of menses.

The effects of exercise training on riboflavin requirements and of riboflavin intake on endurance were examined in 14 women, 50-67 y of age, who participated in a 10-wk, two-period crossover exercise study at two riboflavin intakes, 0.15 micrograms/kJ (0.6 micrograms/kcal) and 0.22 micrograms/kJ (0.9 micrograms/kcal). Subjects exercised 20-25 min/d, 6 d/wk, for 4-wk periods on a cycle ergometer at 75-85% of their maximal heart rate. Riboflavin status was assessed by measuring the erythrocyte glutathione reductase activity coefficient (EGRAC) and urinary riboflavin excretion. Physical performance was evaluated by using a walking treadmill test to determine maximal oxygen capacity (VO2max) and anaerobic threshold by gas exchange (ATGE). Exercise significantly affected riboflavin status as EGRAC increased (P less than 0.001) and riboflavin excretion decreased (P less than 0.01) in both groups. VO2max increased significantly with exercise (P less than 0.01). However, changes in VO2max (L/min) and ATGE with exercise training were not different in the two groups. Riboflavin requirements of older women increased with exercise training, but increased riboflavin intake did not enhance improvements in endurance.

To determine whether dl-fenfluramine increased metabolic rate in humans, hourly indirect calorimetry measurements were made on 16 nonobese males over a 5 h period under each of four conditions: placebo/no meal, placebo/meal, 60 mg dl-fenfluramine/no meal, and 60 mg dl-fenfluramine/meal. Drug administration was double-blind and a Latin square design was used with treatments separated by 7 days. To confirm that active drug was administered when assigned, subjective sensations were measured by questionnaires administered three times during each treatment. Metabolic rate (kcal/min) during the four treatments was compared by analysis of variance over the entire 5 h and at the end of the measurement period. The 750 kcal (3140 kJ) meal increased metabolic rate over the fasting conditions (0.160 +/- 0.035 kcal/min, P less than 0.0005) and the combination of fenfluramine and meal caused a further significant increase beyond that found with placebo and meal (0.072 +/- 0.035 kcal/min, P less than 0.025). At the end of the measurement period, metabolic rate during the placebo/meal treatment had returned to the level of the fasting treatments. In contrast, during the fenfluramine/meal condition, metabolic rate was still elevated (0.173 +/- 0.04 kcal/min, P less than 0.003). The results of this study suggested that fenfluramine increased metabolic rate by potentiating the thermic effect of food.

The effect of dietary fiber from wheat bran and psyllium gum on the apparent absorption of riboflavin was studied in 12 healthy women. The test fiber was consumed in crackers that contained approximately 7.5 gm fiber from psyllium gum, wheat bran, or a combination of the two sources. Each subject was given a riboflavin load test after consuming one of the three different fiber supplements or a control supplement that contained 1.3 gm fiber. Fractional urine collections were made for 24 hours, and riboflavin was measured by fluorometric techniques. The psyllium gum and combination supplements reduced the 24-hour apparent absorption of riboflavin from 31.8% to 25.4% and 26.1%, respectively (p less than .01). No effect of the wheat bran supplement on riboflavin was detected.

The riboflavin requirement of young women during periods of sedentary living and exercise was determined during a 12-wk metabolic study. The study was divided into a 6-wk no exercise period followed by a 6-wk exercise period in which subjects jogged around a track for 20 to 50 min/day. Twelve subjects, aged 19 to 27 yr, were fed a basic diet containing 0.6 mg riboflavin/1000 kcal of intake. Riboflavin intake was increased by 0.2 mg/1000 kcal increments by provision of riboflavin in a glucose polymer mixture. Linear regression analysis was used to estimate the riboflavin intake required for an erythrocyte glutathione reductase activity coefficient of 1.25 during both the no exercise and exercise periods. Individual riboflavin requirements ranged from 0.62 to 1.21 mg/1000 kcal before exercise and 0.63 to 1.4 mg/1000 kcal during the exercise periods. Riboflavin requirement could not be related to the kilocalorie intake or lean body mass of the subjects. It is concluded that healthy young women require more riboflavin to achieve biochemical normality than the 1980 Recommended Dietary Allowances and that exercise increases riboflavin requirements.

The effects of ultraviolet (UV) irradiation on plasma levels of carotenoids and vitamin A in human subjects were investigated in two crossover trials. UV exposures were given on 11 r 12 days of a 2-wk period. The 12 female and 12 male subjects received mean cumulative UV-A (320-400 nm) doses of 17.8 +/- 1.9 J/cm2 and 21.0 +/- 3.3 J/cm2 to the anterior and posterior sides of the body, respectively. UV-B (280-320 nm) doses were equivalent to 10% of UV-A doses given. Significant reductions in plasma total carotenoid levels were observed in both female (p less than 0.004) and male (p less than 0.05) subjects after repeated irradiation. There was no significant effect on plasma vitamin A levels. It was concluded that UV treatment can reduce plasma carotenoid levels in vivo.