Weight Gain Recommendations
In 2009, the Institute of Medicine and National Research Council revised guidelines for weight gain in pregnancy and continued to stratify suggested weight gain ranges based on prepregnancy body mass index (BMI) (Table 9-4). The new guidelines included a specific, relatively narrow range of recommended weight gains for obese women. Also, the same recommendations apply to adolescents, short women, and women of all racial and ethnic groups. The American College of Obstetricians and Gynecologists (2016i) has endorsed these measures.
TABLE 9-4Recommendations for Total and Rate of Weight Gain During Pregnancy ||Download (.pdf) TABLE 9-4 Recommendations for Total and Rate of Weight Gain During Pregnancy
|Category (BMI) ||Total Weight Gain Range (lb)a ||Weight Gain in 2nd and 3rd Trimesters Mean in lb/wk (range) |
|Underweight (<18.5) ||28–40 ||1 (1–1.3) |
|Normal weight (18.5–24.9) ||25–35 ||1 (0.8–1) |
|Overweight (25.0–29.9) ||15–25 ||0.6 (0.5–0.7) |
|Obese (≥30.0) ||11–20 ||0.5 (0.4–0.6) |
When the Institute of Medicine guidelines were formulated, concern focused on low-birthweight newborns, however, current emphasis is directed to the obesity epidemic (Catalano, 2007). This explains renewed interest in lower weight gains during pregnancy. Obesity is associated with significantly greater risks for gestational hypertension, preeclampsia, gestational diabetes, macrosomia, cesarean delivery, and other complications (Chap. 48, Maternal Morbidity). The risk appears “dose related” to prenatal weight gain. In a population-based cohort of more than 120,000 obese pregnant women, those who gained <15 lb had the lowest rates of preeclampsia, large-for-gestational age neonates, and cesarean delivery (Kiel, 2007). Among 100,000 women with normal prepregnancy BMI, DeVader and colleagues (2007) found that those who gained <25 lb during pregnancy had a lower risk for preeclampsia, failed induction, cephalopelvic disproportion, cesarean delivery, and large-for-gestational age neonates. This cohort, however, had an increased risk for small-for-gestational age newborns. Lifestyle intervention during pregnancy can result in less weight gain (Sagedal, 2017).
There is irrefutable evidence that maternal weight gain during pregnancy influences birthweight. Martin and coworkers (2009) studied this using birth certificate data for 2006. Approximately 60 percent of women gained 26 lb or more during pregnancy, and maternal weight gain positively correlated with birthweight. Moreover, women with the greatest risk— 14 percent—for delivering a newborn weighing <2500 g were those with weight gain <16 lb. Nearly 20 percent of births to women with such low weight gains were preterm.
Meaningful studies of nutrition in human pregnancy are exceedingly difficult to design because experimental dietary deficiency is not ethical. In those instances in which severe nutritional deficiencies have been induced as a consequence of social, economic, or political disaster, coincidental events have often created many variables, the effects of which are not amenable to quantification. Some past experiences suggest, however, that in otherwise healthy women, a state of near starvation is required to establish clear differences in pregnancy outcome.
During the severe European winter of 1944 to 1945, nutritional deprivation of known intensity prevailed in a well-circumscribed area of The Netherlands occupied by the German military (Kyle, 2006). At the lowest point during this Dutch Hunger Winter, rations reached 450 kcal/d, with generalized rather than selective malnutrition. Smith (1947) analyzed the outcomes of pregnancies that were in progress during this 6-month famine. Median neonatal birthweights declined approximately 250 g and rose again after food became available. This indicated that birthweight can be influenced significantly by starvation during later pregnancy. The perinatal mortality rate, however, was not altered. Moreover, the incidence of fetal malformations or preeclampsia did not rise significantly. Parenthetically, weight loss in obese women during pregnancy is also associated with an increased risk for low-birthweight neonates (Cox Bauer, 2016).
Evidence of impaired brain development has been obtained in some animal fetuses whose mothers had been subjected to intense dietary deprivation. Subsequent intellectual development was studied by Stein and associates (1972) in young male adults whose mothers had been starved during pregnancy in the aforementioned Hunger Winter. The comprehensive study was made possible because all males at age 19 underwent compulsory examination for military service. It was concluded that severe dietary deprivation during pregnancy caused no detectable effects on subsequent mental performance.
Several studies of the long-term consequences to this cohort of children born to nutritionally deprived women have been performed and have been reviewed by Kyle and Pichard (2006). Progeny deprived in mid to late pregnancy were lighter, shorter, and thinner at birth, and they had a higher incidences of subsequent hypertension, reactive airway disease, dyslipidemia, diminished glucose tolerance, and coronary artery disease. Early pregnancy deprivation was associated with greater obesity rates in adult women but not men. Early starvation was also linked to higher rates of central nervous system anomalies, schizophrenia, and schizophrenia-spectrum personality disorders.
These observations and others have led to the concept of fetal programming by which adult morbidity and mortality are related to fetal health. Known widely as the Barker hypothesis, as promulgated by Barker and colleagues (1989), this concept is discussed in Chapter 44 (Placental Abnormalities).
Weight Retention after Pregnancy
Not all the weight gained during pregnancy is lost during and immediately after delivery. Schauberger and coworkers (1992) studied prenatal and postpartum weights in 795 women. Their average weight gain was 28.6 lb or 12.9 kg. As shown in Figure 9-4, most maternal weight loss was at delivery—approximately 12 lb or 5.4 kg—and in the ensuing 2 weeks—approximately 9 lb or 4 kg. An additional 5.5 lb or 2.5 kg was lost between 2 weeks and 6 months postpartum. Thus, average retained pregnancy weight was 2.1 lb or 1 kg. Excessive weight gain is manifest by accrual of fat and may be partially retained as long-term fat (Berggren, 2016; Widen, 2015). Overall, the more weight that was gained during pregnancy, the more that was lost postpartum. Interestingly, there is no relationship between prepregnancy BMI or prenatal weight gain and weight retention.
Cumulative weight loss from last antepartum visit to 6 months postpartum. *Significantly different from 2-week weight loss; **Significantly different from 6-week weight loss. (Redrawn from Schauberger CW, Rooney BL, Brimer LM: Factors that influence weight loss in the puerperium. Obstet Gynecol 79:424, 1992.)
Dietary Reference Intakes—Recommended Allowances
Periodically, the Institute of Medicine (2006, 2011) publishes recommended dietary allowances, including those for pregnant or lactating women. The latest recommendations are summarized in Table 9-5. Certain prenatal vitamin–mineral supplements may lead to intakes well in excess of the recommended allowances. Moreover, the use of excessive supplements, which often are self-prescribed, has led to concern regarding nutrient toxicities during pregnancy. Those with potentially toxic effects include iron, zinc, selenium, and vitamins A, B6, C, and D.
TABLE 9-5Recommended Daily Dietary Allowances for Pregnant and Lactating Women ||Download (.pdf) TABLE 9-5 Recommended Daily Dietary Allowances for Pregnant and Lactating Women
| ||Pregnant ||Lactating |
|Fat-Soluble Vitamins |
| Vitamin A ||770 μg ||1300 μg |
| Vitamin Da ||15 μg ||15 μg |
| Vitamin E ||15 mg ||19 mg |
| Vitamin Ka ||90 μg ||90 μg |
|Water-Soluble Vitamins |
| Vitamin C ||85 mg ||120 mg |
| Thiamine ||1.4 mg ||1.4 mg |
| Riboflavin ||1.4 mg ||1.6 mg |
| Niacin ||18 mg ||17 mg |
| Vitamin B6 ||1.9 mg ||2 mg |
| Folate ||600 μg ||500 μg |
| Vitamin B12 ||2.6 μg ||2.8 μg |
| Calciuma ||1000 mg ||1000 mg |
| Sodiuma ||1.5 g ||1.5 g |
| Potassiuma ||4.7 g ||5.1 g |
| Iron ||27 mg ||9 mg |
| Zinc ||11 mg ||12 mg |
| Iodine ||220 μg ||290 μg |
| Selenium ||60 μg ||70 μg |
|Other || || |
| Protein ||71 g ||71 g |
| Carbohydrate ||175 g ||210 g |
| Fibera ||28 g ||29 g |
As shown in Figure 9-5, pregnancy requires an additional 80,000 kcal, mostly during the last 20 weeks. To meet this demand, a caloric increase of 100 to 300 kcal/d is recommended during pregnancy (American Academy of Pediatrics and the American College of Obstetricians and Gynecologists, 2017). This greater intake, however, should not be divided equally during the course of pregnancy. The Institute of Medicine (2006) recommends adding 0, 340, and 452 kcal/d to the estimated nonpregnant energy requirements in the first, second, and third trimesters, respectively. The addition of 1000 kcal/d or more results in fat accrual (Jebeile, 2015).
Cumulative kilocalories required for pregnancy. (Redrawn from Chamberlain G, Broughton-Pipkin F (eds): Clinical Physiology in Obstetrics, 3rd ed. Oxford, Blackwell Science, 1998.)
Calories are necessary for energy. Whenever caloric intake is inadequate, protein is metabolized rather than being spared for its vital role in fetal growth and development. Total physiological requirements during pregnancy are not necessarily the sum of ordinary nonpregnant requirements plus those specific to pregnancy. For example, the additional energy required during pregnancy may be compensated in whole or in part by reduced physical activity (Hytten, 1991).
Protein requirements rise to meet the demands for growth and remodeling of the fetus, placenta, uterus, and breasts, and for increased maternal blood volume (Chap. 4, Protein Metabolism). During the second half of pregnancy, approximately 1000 g of protein are deposited, amounting to 5 to 6 g/d (Hytten, 1971). To accomplish this, protein intake that approximates 1 g/kg/d is recommended (see Table 9-5). Data suggest this should be doubled in late gestation (Stephens, 2015). Most amino-acid levels in maternal plasma fall markedly, including ornithine, glycine, taurine, and proline (Hytten, 1991). Exceptions during pregnancy are glutamic acid and alanine, the concentrations of which rise.
Preferably, most protein is supplied from animal sources, such as meat, milk, eggs, cheese, poultry, and fish. These furnish amino acids in optimal combinations. Milk and dairy products are considered nearly ideal sources of nutrients, especially protein and calcium, for pregnant or lactating women. Ingestion of specific fish and potential methylmercury toxicity are discussed in Common Concerns.
The intakes recommended by the Institute of Medicine (2006) for various minerals are listed in Table 9-5. With the exception of iron and iodine, practically all diets that supply sufficient calories for appropriate weight gain will contain enough minerals to prevent deficiency.
Iron requirements are greatly increased during pregnancy, and reasons for this are discussed in Chapter 4 (Iron Metabolism). Of the approximately 300 mg of iron transferred to the fetus and placenta and the 500 mg incorporated into the expanding maternal hemoglobin mass, nearly all is used after midpregnancy. During that time, iron requirements imposed by pregnancy and maternal excretion total approximately 7 mg/d (Pritchard, 1970). Few women have sufficient iron stores or dietary intake to supply this amount. Thus, the American Academy of Pediatrics and the American College of Obstetricians and Gynecologists (2017) endorse the recommendation by the National Academy of Sciences that at least 27 mg of elemental iron be supplemented daily to pregnant women. This amount is contained in most prenatal vitamins.
Scott and coworkers (1970) established that as little as 30 mg of elemental iron, supplied as ferrous gluconate, sulfate, or fumarate and taken daily throughout the latter half of pregnancy, provides sufficient iron to meet pregnancy requirements and protect preexisting iron stores. This amount will also provide for iron requirements of lactation. The pregnant woman may benefit from 60 to 100 mg of elemental iron per day if she is large, has a multifetal gestation, begins supplementation late in pregnancy, takes iron irregularly, or has a somewhat depressed hemoglobin level. The woman who is overtly anemic from iron deficiency responds well to oral supplementation with iron salts. In response, serum ferritin levels rise more than the hemoglobin concentration (Daru, 2016).
Iodine is also needed, and the recommended iodine allowance is 220 μg/d (see Table 9-5). The use of iodized salt and bread products is recommended during pregnancy to offset the increased fetal requirements and maternal renal losses of iodine. Despite this, iodine intake has declined substantially in the past 15 years, and in some areas it is probably inadequate (Casey, 2017). Severe maternal iodine deficiency predisposes offspring to endemic cretinism, which is characterized by multiple severe neurological defects. In parts of China and Africa where this condition is common, iodide supplementation very early in pregnancy prevents some cretinism cases (Cao, 1994). To obviate this, many prenatal supplements now contain various quantities of iodine.
Calcium is retained by the pregnant woman during gestation and approximates 30 g. Most of this is deposited in the fetus late in pregnancy (Pitkin, 1985). This amount of calcium represents only approximately 2.5 percent of total maternal calcium, most of which is in bone and can readily be mobilized for fetal growth. As another potential use, routine calcium supplementation to prevent preeclampsia has not proved effective (Chap. 40, Antihypertensive Drugs).
Zinc deficiency if severe may lead to poor appetite, suboptimal growth, and impaired wound healing. During pregnancy, the recommended daily intake approximates 12 mg. But, the safe level of zinc supplementation for pregnant women has not been clearly established. Vegetarians have lower zinc intakes (Foster, 2015). The bulk of studies support zinc supplementation only in zinc-deficient women in poor-resource countries (Nossier, 2015; Ota, 2015).
Magnesium deficiency as a consequence of pregnancy has not been recognized. Undoubtedly, during prolonged illness with no magnesium intake, the plasma level might become critically low, as it would in the absence of pregnancy. We have observed magnesium deficiency during pregnancies in some with previous intestinal bypass surgery. As a preventive agent, Sibai and coworkers (1989) randomly assigned 400 normotensive primigravid women to 365-mg elemental magnesium supplementation or placebo tablets from 13 to 24 weeks’ gestation. Supplementation did not improve any measures of pregnancy outcome.
Trace metals include copper, selenium, chromium, and manganese, which all have important roles in certain enzyme functions. In general, most are provided by an average diet. Selenium deficiency is manifested by a frequently fatal cardiomyopathy in young children and reproductive-aged women. Conversely, selenium toxicity resulting from oversupplementation also has been observed. Selenium supplementation is not needed in American women.
Potassium concentrations in maternal plasma decline by approximately 0.5 mEq/L by midpregnancy (Brown, 1986). Potassium deficiency develops in the same circumstances as in nonpregnant individuals—a common example is hyperemesis gravidarum.
Fluoride metabolism is not altered appreciably during pregnancy (Maheshwari, 1983). Horowitz and Heifetz (1967) concluded that no additional offspring benefits accrued from maternal ingestion of fluoridated water if the newborn ingested such water from birth. Sa Roriz Fonteles and associates (2005) studied microdrill biopsies of deciduous teeth and concluded that antenatal fluoride provided no additional fluoride uptake compared with postnatal fluoride alone. Finally, supplemental fluoride ingested by lactating women does not raise the fluoride concentration in breast milk (Ekstrand, 1981).
The increased requirements for most vitamins during pregnancy shown in Table 9-5 usually are supplied by any general diet that provides adequate calories and protein. The exception is folic acid during times of unusual requirements, such as pregnancy complicated by protracted vomiting, hemolytic anemia, or multiple fetuses. That said, in impoverished countries, routine multivitamin supplementation reduced the incidence of low-birthweight and growth-restricted fetuses, but did not alter preterm delivery or perinatal mortality rates (Fawzi, 2007).
Folic acid supplementation in early pregnancy can lower neural-tube defect risks (Chap. 13, Genetic Tests). Namely, the CDC (2004) estimated that the number of affected pregnancies had decreased from 4000 pregnancies per year to approximately 3000 per year after mandatory fortification of cereal products with folic acid in 1998. Perhaps more than half of all neural-tube defects can be prevented with daily intake of 400 μg of folic acid throughout the periconceptional period. Evidence also suggests that folate insufficiency has a global effect on brain development (Ars, 2016). Putting 140 μg of folic acid into each 100 g of grain products may increase the folic acid intake of the average American woman of childbearing age by 100 μg/d. Because nutritional sources alone are insufficient, however, folic acid supplementation is still recommended (American College of Obstetricians and Gynecologists, 2016e). Likewise, the U.S. Preventive Services Task Force (2009) recommends that all women planning or capable of pregnancy take a daily supplement containing 400 to 800 μg of folic acid.
A woman with a prior child with a neural-tube defect can reduce the 2- to 5-percent recurrence risk by more than 70 percent with a daily 4-mg folic acid supplement taken during the month before conception and during the first trimester. As emphasized by the American Academy of Pediatrics and the American College of Obstetricians and Gynecologists (2017), this dose should be consumed as a separate supplement and not as multivitamin tablets. This practice avoids excessive intake of fat-soluble vitamins.
Vitamin A, although essential, has been associated with congenital malformations when taken in high doses (>10,000 IU/d) during pregnancy. These malformations are similar to those produced by the vitamin A derivative isotretinoin (Accutane), which is a potent teratogen (Chap. 12, Retinoids). Beta-carotene, the precursor of vitamin A found in fruits and vegetables, has not been shown to produce vitamin A toxicity. Most prenatal vitamins contain vitamin A in doses considerably below the teratogenic threshold. Dietary intake of vitamin A in the United States appears to be adequate, and additional supplementation is not routinely recommended. In contrast, vitamin A deficiency is an endemic nutritional problem in the developing world (McCauley, 2015). Vitamin A deficiency, whether overt or subclinical, is associated with night blindness and with an increased risk of maternal anemia and spontaneous preterm birth (West, 2003).
Vitamin B12 plasma levels drop in normal pregnancy, mostly as a result of reduced plasma levels of their carrier proteins—transcobalamins. Vitamin B12 occurs naturally only in foods of animal origin, and strict vegetarians may give birth to neonates whose B12 stores are low. Likewise, because breast milk of a vegetarian mother contains little vitamin B12, the deficiency may become profound in the breastfed infant (Higginbottom, 1978). Excessive ingestion of vitamin C also can lead to a functional deficiency of vitamin B12. Although its role is still controversial, vitamin B12 deficiency preconceptionally, similar to folate, may elevate the risk of neural-tube defects (Molloy, 2009).
Vitamin B6, which is pyridoxine, does not require supplementation in most gravidas (Salam, 2015). For women at high risk for inadequate nutrition, a daily 2-mg supplement is recommended. As discussed in Caffeine, vitamin B6, when combined with the antihistamine doxylamine, is helpful in many cases of nausea and vomiting of pregnancy.
Vitamin C allowances during pregnancy are 80 to 85 mg/d—approximately 20 percent more than when nonpregnant (see Table 9-5). A reasonable diet should readily provide this amount, and supplementation is not necessary (Rumbold, 2015). Maternal plasma levels decline during pregnancy, whereas cord-blood levels are higher, a phenomenon observed with most water-soluble vitamins.
Vitamin D is a fat-soluble vitamin. After being metabolized to its active form, it boosts the efficiency of intestinal calcium absorption and promotes bone mineralization and growth. Unlike most vitamins that are obtained exclusively from dietary intake, vitamin D is also synthesized endogenously with exposure to sunlight. Vitamin D deficiency is common during pregnancy. This is especially true in high-risk groups such as women with limited sun exposure, vegetarians, and ethnic minorities—particularly those with darker skin (Bodnar, 2007). Maternal deficiency can cause disordered skeletal homeostasis, congenital rickets, and fractures in the newborn (American College of Obstetricians and Gynecologists, 2017k). Vitamin D supplementation to women with asthma may decrease the likelihood of childhood asthma in their fetuses (Litonjua, 2016). The Food and Nutrition Board of the Institute of Medicine (2011) established that an adequate intake of vitamin D during pregnancy and lactation was 15 μg/d (600 IU/d). In women suspected of having vitamin D deficiency, serum levels of 25-hydroxyvitamin D can be obtained. Even then, the optimal levels in pregnancy have not been established (De-Regil, 2016).
Pragmatic Nutritional Surveillance
Although researchers continue to study the ideal nutritional regimen for the pregnant woman and her fetus, basic tenets for the clinician include:
Advise the pregnant woman to eat food types she wants in reasonable amounts and salted to taste.
Ensure that food is amply available for socioeconomically deprived women.
Monitor weight gain, with a goal of approximately 25 to 35 lb in women with a normal BMI.
Explore food intake by dietary recall periodically to discover the occasional nutritionally errant diet.
Give tablets of simple iron salts that provide at least 27 mg of elemental iron daily. Give folate supplementation before and in the early weeks of pregnancy. Provide iodine supplementation in areas of known dietary insufficiency.
Recheck the hematocrit or hemoglobin concentration at 28 to 32 weeks’ gestation to detect significant anemia.