To clarify the role of the intestine, kidney, and bone in maintaining calcium homeostasis during pregnancy and lactation and after the resumption of menses, a longitudinal comparison was undertaken of 14 well-nourished women consuming approximately 1200 mg Ca/d. Measurements were made before conception (prepregnancy), once during each trimester of pregnancy (T1, T2, and T3), early in lactation at 2 mo postpartum (EL), and 5 mo after resumption of menses. Intestinal calcium absorption was determined from the enrichment of the first 24-h urine sample collected after administration of stable calcium isotopes. Bone mineral of the total body and lumbar spine was measured by dual-energy X-ray absorptiometry and quantitative computerized tomography, respectively. Twenty-four-hour urine and fasting serum samples were analyzed for calcium, calcitropic hormones, and biochemical markers of bone turnover. Despite an increase in calcium intake during pregnancy, true percentage absorption of calcium increased from 32.9+/-9.1% at prepregnancy to 49.9+/-10.2% at T2 and 53.8+/-11.3% at T3 (P < 0.001). Urinary calcium increased from 4.32+/-2.20 mmol/d at prepregnancy to 6.21+/-3.72 mmol/d at T3 (P < 0.001), but only minor changes in maternal bone mineral were detected. At EL, dietary calcium and calcium absorption were not significantly different from that at prepregnancy, but urinary calcium decreased to 1.87+/-1.22 mmol/d (P < 0.001) and trabecular bone mineral density of the spine decreased to 147.7+/-21.2 mg/cm3 from 162.9+/-25.0 mg/cm3 at prepregnancy (P < 0.001). Calcium absorption postmenses increased nonsignificantly to 36.0+/-8.1% whereas urinary calcium decreased to 2.72+/-1.52 mmol/d (P < 0.001). We concluded that fetal calcium demand was met by increased maternal intestinal absorption; early breast-milk calcium was provided by maternal renal calcium conservation and loss of spinal trabecular bone, a loss that was recovered postmenses.

Zinc is required for multiple metabolic processes as a structural, regulatory, or catalytic ion. Cellular, tissue, and whole-body zinc homeostasis is tightly controlled to sustain metabolic functions over a wide range of zinc intakes, making it difficult to assess zinc insufficiency or excess. The BOND (Biomarkers of Nutrition for Development) Zinc Expert Panel recommends 3 measurements for estimating zinc status: dietary zinc intake, plasma zinc concentration (PZC), and height-for-age of growing infants and children. The amount of dietary zinc potentially available for absorption, which requires an estimate of dietary zinc and phytate, can be used to identify individuals and populations at risk of zinc deficiency. PZCs respond to severe dietary zinc restriction and to zinc supplementation; they also change with shifts in whole-body zinc balance and clinical signs of zinc deficiency. PZC cutoffs are available to identify individuals and populations at risk of zinc deficiency. However, there are limitations in using the PZC to assess zinc status. PZCs respond less to additional zinc provided in food than to a supplement administered between meals, there is considerable interindividual variability in PZCs with changes in dietary zinc, and PZCs are influenced by recent meal consumption, the time of day, inflammation, and certain drugs and hormones. Insufficient data are available on hair, urinary, nail, and blood cell zinc responses to changes in dietary zinc to recommend these biomarkers for assessing zinc status. Of the potential functional indicators of zinc, growth is the only one that is recommended. Because pharmacologic zinc doses are unlikely to enhance growth, a growth response to supplemental zinc is interpreted as indicating pre-existing zinc deficiency. Other functional indicators reviewed but not recommended for assessing zinc nutrition in clinical or field settings because of insufficient information are the activity or amounts of zinc-dependent enzymes and proteins and biomarkers of oxidative stress, inflammation, or DNA damage.

Objective: To estimate the energy requirements of pregnant and lactating women consistent with optimal pregnancy outcome and adequate milk production. Design: Total energy cost of pregnancy was estimated using the factorial approach from pregnancy-induced increments in basal metabolic rate measured by respiratory calorimetry or from increments in total energy expenditure measured by the doubly labelled water method, plus energy deposition attributed to protein and fat accretion during pregnancy. Setting: Database on changes in basal metabolic rate and total energy expenditure during pregnancy, and increments in protein based on measurements of total body potassium, and fat derived from multi-compartment body composition models was compiled. Energy requirements during lactation were derived from rates of milk production, energy density of human milk, and energy mobilisation from tissues. Subjects: Healthy pregnant and lactating women. Results: The estimated total cost of pregnancy for women with a mean gestational weight gain of 12.0 kg, was 321 or 325 MJ, distributed as 375, 1200, 1950 kJ day 21 , for the first, second and third trimesters, respectively. For exclusive breastfeeding, the energy cost of lactation was 2.62 MJ day 21 based on a mean milk production of 749 g day 21, energy density of milk of 2.8 kJ g 21, and energetic efficiency of 0.80. In well-nourished women, this may be subsidised by energy mobilisation from tissues on the order of 0.72 MJ day 21, resulting in a net increment of 1.9 MJ day 21 over nonpregnant, non-lactating energy requirements. Conclusions: Recommendations for energy intake of pregnant and lactating women should be updated based on recently available data.

Maintaining a constant state of cellular zinc nutrition, or homeostasis, is essential for normal function. In animals and humans, adjustments in zinc absorption and endogenous intestinal excretion are the primary means of maintaining zinc homeostasis. The adjustments in gastrointestinal zinc absorption and endogenous excretion are synergistic. Shifts in endogenous excretion appear to occur quickly with changes in intake just above or below optimal intake. The absorption of zinc responds more slowly, but it has the capacity to cope with large fluctuations in intake. With extremely low zinc intakes or with prolonged marginal intakes, secondary homeostatic adjustments may augment the gastrointestinal changes. These secondary adjustments include changes in urinary zinc excretion, a shift in plasma zinc turnover rates and, possibly, an avid retention of zinc released from selected tissues, such as bone, in other tissues to maintain function.

Gestational diabetes and obesity are the common metabolic abnormalities occurring during pregnancy. Decreased maternal pregravid insulin sensitivity (insulin resistance) coupled with an inadequate insulin response are the pathophysiological mechanisms underlying the development of gestational diabetes. Insulin-regulated carbohydrate, lipid and protein metabolism are all affected to a variable degree. Decreased maternal insulin sensitivity in women with gestational diabetes may increase nutrient availability to the fetus, possibly accounting for an increased risk of fetal overgrowth and adiposity. Epidemiological studies from Europe show an increased risk of the insulin resistance syndrome in adults who were low birth weight at delivery. However, in the United States over the past 20 y there has been a significant 33% increase in the incidence of type 2 diabetes, which has been associated with a parallel increase in obesity. All age groups have been affected but the most dramatic increases have occurred in adolescents. The relationship between decreased maternal insulin sensitivity and fetal overgrowth particularly in obese women and women with gestational diabetes may help explain the increased incidence of adolescent obesity and related glucose intolerance in the offspring of these women. In this review, we address 1) the pathophysiology of gestational diabetes, 2) the changes in maternal insulin sensitivity during pregnancy that effect maternal accretion of adipose tissue and energy expenditure, 3) the influence of maternal metabolic environment on fetal growth, 4) the life-long effect of being born at either extreme of the birth weight continuum and 5) micronutrients and decreased insulin sensitivity during pregnancy.

An adequate supply of nutrients is probably the single most important environmental factor affecting pregnancy outcome. Women with early or closely spaced pregnancies are at increased risk of entering a reproductive cycle with reduced reserves. Maternal nutrient depletion may contribute to the increased incidence of preterm births and fetal growth retardation among these women as well as the increased risk of maternal mortality and morbidity. In the past, it was assumed that the fetus functioned as a parasite and withdrew its nutritional needs from maternal tissues. Studies in both animals and humans demonstrate, however, that if the maternal nutrient supply is inadequate, the delicate balance between maternal and fetal needs is disturbed and a state of biological competition exists. Furthermore, maternal nutritional status at conception influences how nutrients are partitioned between the mother and fetal dyad. In severe deficiencies maternal nutrition is given preference; in a marginal state the fetal compartment is favored. Although the studies of nutrient partitioning have focused on energy and protein, the partitioning of micronutrients may also be influenced by the maternal nutritional status. Marginal intakes of iron and folic acid during the reproductive period induce a poor maternal status for these nutrients during the interpregnancy interval. Poor iron and folic acid status has also been linked to preterm births and fetal growth retardation. Supplementation with food and micronutrients during the interpregnancy period may improve pregnancy outcomes and maternal health among women with early or closely spaced pregnancies.

Pregnancy consists of a series of small, continuous physiologic adjustments that affect the metabolism of all nutrients. The adjustments undoubtedly vary widely from woman to woman depending on her prepregnancy nutrition, genetic determinants of fetal size, and maternal lifestyle behavior. Studies of protein and energy metabolism illustrate the potential of adjusting the use of those nutrients to conserve a fetal supply. Adjustments in the metabolism of nitrogenous compounds are in place by the second quarter of pregnancy. During the last quarter of pregnancy, when fetal demands are greatest, those adjustments allow a positive nitrogen retention. The energy requirement of basal metabolism is influenced by maternal prepregnant nutrition and by fetal size. If maternal energy reserves are low at conception, the basal metabolic rate is down-regulated to conserve energy. Also, women having larger babies tend to have greater increases in their basal metabolic rate and lower rates of maternal energy storage. Changes in maternal food and physical activity behaviors during gestation may augment the physiologic adjustments. However, the substantial variability in food intakes and physical activity makes it difficult to show those changes. Thresholds in the capacity to adjust nutrient use to the amount supplied exist for all nutrients. When intakes fall below the threshold, fetal growth and development is affected more than is maternal health. Efforts to achieve good maternal nutritional status preconception as well as throughout gestation best assure a good milieu for fetal growth and development.

Zinc is essential for multiple aspects of metabolism. Physiologic signs of zinc depletion are linked with diverse biochemical functions rather than with a specific function, which makes it difficult to identify biomarkers of zinc nutrition. Nutrients, such as zinc, that are required for general metabolism are called type 2 nutrients. Protein and magnesium are examples of other type 2 nutrients. Type 1 nutrients are required for one or more specific functions: examples include iron, vitamin A, iodine, folate, and copper. When dietary zinc is insufficient, a marked reduction in endogenous zinc loss occurs immediately to conserve the nutrient. If zinc balance is not reestablished, other metabolic adjustments occur to mobilize zinc from small body pools. The location of those pools is not known, but all cells probably have a small zinc reserve that includes zinc bound to metallothionein or zinc stored in the Golgi or in other organelles. Plasma zinc is also part of this small zinc pool that is vulnerable to insufficient intakes. Plasma zinc concentrations decline rapidly with severe deficiencies and more moderately with marginal depletion. Unfortunately, plasma zinc concentrations also decrease with a number of conditions (eg, infection, trauma, stress, steroid use, after a meal) due to a metabolic redistribution of zinc from the plasma to the tissues. This redistribution confounds the interpretation of low plasma zinc concentrations. Biomarkers of metabolic zinc redistribution are needed to determine whether this redistribution is the cause of a low plasma zinc rather than poor nutrition. Measures of metallothionein or cellular zinc transporters may fulfill that role.