Maternal physiologic adaptations

The gastrointestinal (GI) and hepatic systems during pregnancy are characterized by marked anatomic and physiologic alterations that are essential in supporting maternal and fetal nutrition. These changes are related to mechanical forces such as the pressure of the growing uterus and hormonal influences such as effects of progesterone on GI smooth muscle and effects of estrogen on liver metabolism.

Antepartum period

The antepartum period is characterized by anatomic and physiologic changes in all the organs of the GI system. These changes and their implications are summarized in Table 12-1. Pregnancy is associated with increased appetite; increased consumption of food; and alterations in the types of food desired, including cravings, avoidance of certain foods, and, rarely, pica (craving for nonnutrient substances). Specific changes in food consumption and the types of foods craved or avoided are strongly influenced by cultural and economic factors. Food consumption has been reported to increase 15% to 20% beginning in early pregnancy, peaking at mid-gestation and decreasing near term.²⁰⁷ Alterations in food intake and appetite create a positive energy balance during pregnancy to meet the needs of the pregnant woman and fetus and to prepare for lactation (see Chapter 16).¹²⁸ Changes in maternal caloric intake do not parallel changes in basal metabolism or fetal growth.

Table 12-1

Alterations in the Gastrointestinal System during Pregnancy

ORGAN	ALTERATION	SIGNIFICANCE
Mouth and pharynx	Gingivitis	Friable gum tissue with bleeding and discomfort with chewing Increased periodontal disease

  Epulis formation Bleeding and interference with chewing   Increased saliva production Annoyance Esophagus Decreased lower esophageal sphincter pressure and tone Increased risk of heartburn   Widening of hiatus with decreased tone Increased risk of hiatal hernia Stomach Decreased tone and motility with delayed gastric emptying time

Increased risk of gastroesophageal reflux and vomiting

Increased risk of vomiting and aspiration with use of sedatives or anesthetics

  Incompetence of pyloric sphincter Reflux of alkaline biliary material into stomach   Decreased gastric acidity and histamine output Improvement of peptic ulcer symptoms Small and large intestines Decreased intestinal tone and motility with increased transit time   Increased height of duodenal villi Increased absorption of calcium, amino acids, other substances   Altered enzymatic transport across villi; increased activity of brush border enzymes Increased absorption of specific vitamins and other nutrients; increased sodium and water absorption   Displacement of cecum and appendix by uterus Complicates diagnosis of appendicitis Gallbladder Decreased tone and motility Liver Altered position May mask mild to moderate hepatomegaly   Altered production of liver enzymes, plasma proteins, bilirubin, and serum lipids   Presence of spider angiomata and palmar erythema Discomfort because of itching

Mouth and pharynx

Contrary to the old wives’ tale regarding the loss of a tooth per baby, pregnancy does not result in demineralization of the woman’s teeth. Fetal calcium needs are drawn from maternal body stores, not from the teeth (see Chapter 17). The major component of tooth enamel (hydroxyapatite crystals) is not reduced by the biochemical or hormonal changes of pregnancy.^156,167,214 As a result of gingival alterations, however, the pregnant woman may become more aware of preexisting or newly developed dental caries. Changes in saliva and the nausea and vomiting of pregnancy may increase the risk of caries during pregnancy although this has not been well studied.¹⁶⁷ Dental plaque, calculus, and debris deposits increase during pregnancy and are associated with gingivitis.^21,214 In addition, there may be a transient increase in tooth mobility.²¹⁴ 

Pregnancy may exacerbate existing periodontal disease with an increase in periodontal pocket depth during gestation.¹⁶⁵ Periodontal disease has also been associated with intrauterine infection and an increased risk of preterm birth and low–birth weight risk in some but not all studies.^{2,82,150,191,248,261} The mechanism is unclear but may be due to either alterations in maternal and fetal immune responses or translocation of oral bacteria into the uterus with colonization and inflammation of the placenta.⁹⁵ Increased prostaglandin (PG) synthesis mediated by proinflammatory cytokines from inflamed gingival tissues or via release of bacterial endotoxins could then initiate labor onset (see Chapter 4).^150,261 These studies lack consistent definitions of periodontal disease with lack of control for confounding variables such as socioeconomic status and smoking in some studies.²⁶¹ Several recent meta-analyses concluded that oral prophylaxis and treatment of periodontal disease may reduce preterm and low–birth weight rates and that further evaluation is needed; another analysis did not find an association.^82,191,248

Gingivitis occurs in 30% to 80% of pregnant women, generally beginning around the second month and peaking in the middle of the third trimester.^156,167,214 The anterior region of the mouth is usually the most affected site.²¹ Gingival tissue contains both estrogen and progesterone receptors.²¹ Estrogen increases blood flow to the oral cavity and accelerates turnover of gum epithelial lining cells. The gums become highly vascularized (with proliferation of small blood vessels and connective tissue), hyperplastic, and edematous.^21,62,156 Progesterone and estradiol may stimulate located inflammation via production of PGs and decreased levels of inflammatory inhibitors.²¹ Development of gingivitis may be related to these alterations in the inflammatory process during pregnancy (see Chapter 13), with increased intensity of localized irritation, or to changes in connective tissue metabolism.^21,143 These changes, along with the decreased thickness of the gingival epithelial surface, result in friable gum tissues that may bleed easily or cause discomfort with chewing. Bleeding with brushing occurs more frequently during pregnancy. The incidence of gingivitis is higher with increasing maternal age and parity, preexisting periodontal disease, and poor dentition.^156,208

In up to 5% of pregnant women, a specific angiogranuloma known as an epulis or pregnancy tumor develops.^214,249 Epulis formation generally occurs between the second and third month, but can occur later.^21,167 Epulis may gradually increase in size, but rarely is larger than 2 cm in diameter. The etiology is unknown but is thought to relate to hormonal changes (epulis tissue has estrogen and progesterone receptors) and inflammation.²¹ Epulis formation is characterized by gingivitis that is advanced and severe. There is a hyperplastic outgrowth that is generally found along the maxillary gingiva and often appears between the upper anterior maxillary teeth.²¹ This mass is purplish red to dark purple, very friable, bleeds easily, and often interferes with chewing.²¹ Epulis is usually painless, but may ulcerate and become painful in some women.^21,167 Epulis usually regresses spontaneously after delivery, but may recur in the same locations with subsequent pregnancies. Occasionally these growths may need excising during pregnancy due to bleeding, interference with chewing, or increasing periodontal disease.^156,214

Saliva becomes more acidic during pregnancy, with alterations in electrolyte content and microorganism load, but it usually does not increase in volume.¹⁶⁷ Some women may experience a sense of increased saliva production due to difficulty in swallowing saliva during the period of nausea and vomiting in early pregnancy.¹⁵⁶ A few women do experience excessive salivation (ptyalism). This uncommon disorder begins as early as 2 to 3 weeks and ceases with delivery. The excessive salivation seems to occur primarily during the day.⁶² The pathogenesis of ptyalism is unknown, but it is thought to be due to increased saliva, the inability to swallow due to nausea, or activation of the esophagosalivary reflex during gastroesophageal reflux (GER).²¹⁴

Esophagus

Lower esophageal sphincter (LES) tone decreases. This decrease is thought to be primarily due to the smooth muscle relaxant activity of progesterone.^61,117 The LES is a pressure barrier between the stomach and the esophagus, acting as a protective mechanism to prevent or minimize GER. Resting LES pressure decreases during pregnancy with decreased responsiveness to hormonal and physiological stimuli.^61,62,117 At the beginning of the second trimester, basal LES tone is unchanged, although a marked decrease in the normal rise in LES pressure in response to stimulation with a protein meal has been reported.^62,203 This suggests an inhibitory effect and may signal the loss of an important protective response—that is, the ability to modify LES pressure in response to increased intragastric pressure so that reflux is prevented.⁶² LES pressure gradually falls by 33% to 50%, with most of the decrease occurring in the third trimester and reaching a nadir at about 36 weeks.²⁰³

Changes in the LES in pregnancy are similar to changes seen during the ovarian cycle and in women on oral contraceptives, supporting the theory of a hormonal cause for this alteration. An increased incidence of acid reflux with heartburn, which is associated with decreased LES pressure, is seen in nonpregnant women during the luteal phase of the ovarian cycle, when progesterone levels are highest.^203,249 After delivery or discontinuance of oral contraceptives, LES function returns to normal.^62,76,249 Alterations in LES tone and pressure are etiologic factors in the development of heartburn during pregnancy.

Other changes in the esophagus during pregnancy include an increase in secondary peristalsis and nonpropulsive peristalsis and increased incidence of hiatal hernia. Flattening of the hemidiaphragm causes a loss of the normal acute esophageal-gastric angle, which may also lead to reflux.⁶²

Stomach

The stomach of the pregnant woman tends to be hypotonic with decreased motility due to actions of progesterone. GI motility is decreased, with prolonged small intestinal transit time. Incompetence of the pyloric sphincter may result in alkaline reflux of duodenal contents into the stomach.^62,117 Gastric emptying time is thought to be unchanged.^{61,76,204,214,228,242,259}

The effect of pregnancy on gastric acid secretion is unclear. In several studies, gastric volume was not increased nor was gastric pH decreased during early pregnancy.^117,242 Others have reported a decrease in acidity during the first and second trimesters along with normal gastrin levels, with an increase in acidity to greater than nonpregnant values during the third trimester, accompanied by an increase in gastrin.²¹⁴ In general there seems to be a tendency for decreased gastric acidity in pregnancy, especially during the first and second trimesters, with an increase in the third along with small but statistically significant decreases in both basal and histamine-stimulated acid output.⁶² Women with peptic ulcers tend to have fewer symptoms during pregnancy, partly because of these changes (see Pregnancy in Women with Peptic Ulcer Disease).¹¹⁷

Secretion of pepsin parallels changes in gastric acid output.⁶¹ Decreased gastric acidity is thought to result from hormonal influences (particularly estrogen) and increased levels of placental histaminase.^62,208 Placental histaminase is thought to mediate acid and pepsin secretion by reducing parietal cell responsiveness to endogenous histamine.⁶² Gastrin levels are normal during most of pregnancy, with marked increases late in the third trimester, at delivery, and immediately after delivery. The additional gastrin is probably of placental origin.

Small and large intestines

The action of progesterone on smooth muscles decreases intestinal tone and motility. The decreased motility observed in pregnancy may not necessarily be a direct effect of progesterone however, but rather due to inhibition by plasma motilin.²²⁸ Decreased GI tone leads to prolonged intestinal transit time, especially during the second and third trimesters. Alterations in transit time increase with advancing gestation, paralleling the increase in progesterone.

Intestinal transit times during stages of pregnancy have been compared with phases of the ovarian cycle in nonpregnant women. Intestinal motility is altered and transit time prolonged during late pregnancy and the luteal phase of the ovarian cycle when progesterone secretion is elevated. The prolonged transit time in late pregnancy is due to an increase in small bowel transit secondary to inhibition of smooth muscle contraction and not to delayed gastric emptying time. The woman may experience a sense of “bloating” and abdominal distention secondary to the delay in intestinal transit times.²¹⁴ 

The height of the duodenal villi increases (hypertrophies) during pregnancy, which in turn increases absorptive capacity.¹¹⁷ This change, along with the influences of progesterone on intestinal transit time and increased activity of brush border enzymes, increases the absorptive capacity for substances such as calcium, lysine, valine, glycine, proline, glucose, sodium, chloride, and water.^117,249 Progesterone also increases lactase and maltase activity. Absorption of other nutrients (including niacin, riboflavin, and vitamin B₆) is reduced, perhaps due to the influence of progesterone on enzymatic transport mechanisms.^117,214,249 Duodenal absorption of iron increases nearly twofold by late pregnancy, probably in response to a reduction of maternal circulating iron stores due to uptake by the placenta and fetus.²¹⁴ As a result of the decreased intestinal motility, nutrients and fluids tend to remain in the intestinal lumen for longer periods of time. This may facilitate absorption of nutrients such as iron and calcium. The amount and efficiency of intestinal calcium absorption increase, mediated primarily by increased 1,25-dihydroxyvitamin D (see Chapter 17).

Progesterone may also enhance absorption of calcium, sodium, and water and increase net secretion of potassium.^214,249 The reduced motility and increased transit time in the large intestine increase water and sodium absorption in the colon.¹¹⁷ Stools are smaller with lower water content, which contributes to development of constipation during pregnancy. Increased flatulence may also occur due to decreased motility along with compression of the bowel by the growing uterus. The appendix and cecum are displaced superiorly by the growing uterus, so that by term the appendix tends to be located along the right costal margin.

Pancreas

The pancreas contains estrogen receptors, which in the rich estrogen environment of pregnancy may increase the risk of pancreatitis.²⁴⁹ Serum amylase and lipase decrease during the first trimester. The significance of this change is unclear. Changes in the islet cells and the increased production and secretion of insulin are discussed in Chapter 16.

Gallbladder

Muscle tone and motility of the gallbladder decrease during pregnancy, probably due to the effects of progesterone on smooth muscle. As a result, gallbladder volume is increased and emptying rate decreased, especially in the second and third timesters.^61,214 Most measures of gallbladder function are altered during pregnancy, especially after 14 weeks. Some studies have reported that fasting and residual volumes increase to about 20 weeks’ gestation, then remain high to term, paralleling the increase in progesterone.⁷⁶ The residual gallbladder volume after fasting and emptying is nearly twice as large in the pregnant woman as in nonpregnant women who are not taking oral contraceptives. The increased fasting volume may also be due to decreased water absorption by the mucosa of the gallbladder. This change results from reduced activity of the sodium pump in the mucosal epithelium secondary to estrogens. As a result, bile is more dilute, with a decreased ability to solubilize cholesterol. The sequestered cholesterol may precipitate to form crystals and stones, increasing the tendency to form cholesterol-based gallstones in the second and third trimesters.^61,76,142 In the third trimester, bile is supersaturated with lithogenic cholesterol, which, in conjunction with biliary stasis and sludging, increases the risk of gallstones (see Cholelithiasis and Pregnancy).^76,142 Alterations in gallbladder tone also lead to a tendency to retain bile salts, which can lead to pruritus.

Liver

During pregnancy the enlarging uterus displaces the liver superiorly, posteriorly, and anteriorly. Hepatic blood flow per se is not significantly altered despite marked changes in total blood volume and cardiac output. This is because much of the increased cardiac output is sent to the uteroplacental circulation. As a result, the proportion of cardiac output delivered to the liver remains constant at 25% to 35%.¹²¹ Histologically, only minor nonspecific changes in the liver such as increased fat and glycogen storage and variations in cell size have been reported. The size of the liver does not increase.²⁵⁸

Liver production of plasma proteins, bilirubin, serum enzymes, and serum lipids is altered. These changes arise primarily from estrogen, which increases the rough endoplasmic reticulum and liver protein synthesis, and in some cases from hemodilution.²⁵⁸ Progesterone increases proliferation of the smooth endoplasmic reticulum and cytochrome P450 isoenzymes.²⁵⁸ Changes in liver products during pregnancy and their significance are summarized in Table 12-2.

Although liver function is not impaired during pregnancy, most of the changes in liver function tests are in the same direction as seen in individuals with liver disorders. Some liver function tests are less useful in evaluating liver disorders during pregnancy; other tests such as aspartate aminotransferase (AST, or serum glutamic-oxaloacetic transaminase [SGOT]), alanine aminotransferase (ALT, or serum glutamic-pyruvic transaminase [SGPT]), and bilirubin are only slightly lower than nonpregnant values.^61,110,209 Changes in hepatic metabolism of drugs during pregnancy are discussed in Chapter 7.

Spider angiomas (also called spider nevi) and palmar erythema (common findings in many liver disorders) are thought to be caused by estrogens and are seen in many pregnant women (see Chapter 14). These findings tend to develop between the second and fifth months and disappear or diminish following delivery. Increases in the size of previously existing spider angiomas may also be noted.

Weight gain during pregnancy

Weight gain during pregnancy reflects increased maternal stores as well as those of the developing fetus and placenta (Figure 12-1). Approximately 62% of the gain is water, 30% fat, and 8% protein. About 25% of the total gain is attributable to the fetus, 11% to the placenta and amniotic fluid, and the remainder to the mother.¹⁰¹ Optimal weight gain during pregnancy varies with maternal prepregnancy weight; greater weight gain is generally recommended in women who are underweight, and a lower total weight gain is preferable for women who are obese. Maternal weight gain per se lacks sensitivity and specificity as a predictor of pregnancy outcome, in that many women with good pregnancy outcomes have weight gains outside the recommended range.^37,115 However, higher or lower than usual weight gains do increase the risk of maternal and fetal complications and perinatal mortality rates (Figure 12-2).^1,93,215

Body mass index (BMI) and energy expenditure (see Chapter 16) must also be considered. Prepregnancy BMI and adiposity also affect perinatal outcome. Underweight women have an increased risk of preterm and small-for-gestational-age (SGA) infants with decreased macrosomia, preeclampsia and cesarean birth; overweight women have an increase in spontaneous abortion, congenital anomalies, intrauterine death, gestational diabetes, hypertensive disorders, preeclampsia, thromboembolic complications and cesarean birth, and decreased risk of SGA and growth-restricted infants.²¹⁵

The Institute of Medicine (IOM) guidelines for weight gain and the pattern of gain based on prepregnancy weight for height were published in 1990.¹⁰³ These guidelines generated controversy, particularly in relation to the weight gain range for obese women, and concern that using them would increase the number of large-for-gestational-age (LGA) infants and maternal and fetal complications.^{37,115,202,215} Abrams and colleagues reviewed pregnancy outcomes from studies using the IOM guidelines and found that weight gain within these recommendations was associated with the best maternal and fetal outcome.¹ However, they noted that in most women, weight gain was not within the IOM guidelines.¹ In other studies, only about one third of pregnant women gained weight within the recommended limits, with most gaining more than recommended.^37,38 Chu et al. found that using the 1990 IOM guidelines 30% of normal weight women and 60% of overweight women gained more than recommended; excessive gestational weight gain was correlated with weight retention postpartum and later obesity.⁵² Others have found similar outcomes.¹⁷⁸

In response to concerns of excessive weight gain and later development of obesity, the IOM recently revised these guidelines (see Table 12-3). The revised guidelines also added recommended gain for three subcategories of obesity (class I, II, and III). The current IOM guidelines assume a 1.1- to 4-lb weight gain during the first trimester, followed by a recommended 0.8 to 1 lb (0.36 to 0.45 kg) per week for the second and third trimesters in normal BMI women, with higher gains of 1 to 1.3 lb (0.45 to 0.59 kg) per week in underweight and less per week in overweight women (0.6 to 0.7 lb or 0.23 to 0.32 kg). Obese women are recommended to restrict weight gain during the first trimester to 0.4 to 0.6 lb (0.18 to 0.27 kg).^181,198,199

Weight gain during the first trimester goes primarily toward maternal fat stores (see Figure 12-1). Weight gained during the second half of pregnancy goes toward growth of the fetus and maternal supportive tissues. Marked or persistent deviations from these patterns should be evaluated.^198,199 Women whose weight gain significantly exceeds these limits or deviates from the expected pattern require similar evaluation. For example, if a woman gains 30 lb in the first 20 weeks of pregnancy, she has added approximately 25 lb (11.33 kg) of fat to her stores (and additional fat is often difficult to lose postpartum). This woman will still need to gain approximately 20 lb (9.07 kg) during the second half of pregnancy to ensure adequate growth of the fetus and her own tissues.²⁰⁸ Greater gains are needed in women with multifetal pregnancies.^109,181 These women also have increased nutritional needs, including higher energy, vitamin D, linolenic and linoleic acids, calcium, and other minerals.⁴⁴

Intrapartum period

Gastric motility is further decreased during labor. This decrease is probably influenced by anxiety and pain as well as the effects of opioid administration. The reduced competency of the LES, along with decreased gastric motility and increased gastric acidity, delays gastric emptying time and increases the risk of aspiration with sedatives or anesthesia.

Labor is accompanied by delays in gastric emptying times that differ from both third-trimester and nonpregnant values.^61,259 Opioids may be the main factor in delayed gastric emptying during labor. Opioids also delay gastric emptying and increase the risk of aspiration if used in conjunction with general anesthesia. Reduced use of general anesthesia for delivery has reduced the numbers of women at risk for intrapartum aspiration. However, any use of general anesthesia with a pregnant woman, whether for delivery or nonobstetric surgery, requires careful monitoring and use of interventions to prevent vomiting and aspiration.

During labor, alkaline phosphatase levels, which double during pregnancy, increase further. Serum aminotransferases (AST and ALT), which only change slightly during pregnancy, and lactic dehydrogenase increase up to twice normal values.¹⁸⁵ These enzymes are associated with tissue injury and may reflect the stresses of labor on the mother and placenta.

Postpartum period

During the postpartum period, the anatomic and physiologic changes within the GI and hepatic systems gradually return to their prepregnant state. Delivery results in an average weight loss of 4.5 to 5.8 kg (10 to 13 lb).⁶⁰ Findings regarding postpartum weight loss are inconsistent. Some women have further weight loss during the first week; others have no change or gain weight. The increased adrenocortical hormone and arginine vasopressin activity associated with the stress of labor tends to lead to water and sodium retention that may prevent weight loss or lead to a gain. In general, after 4 days, most women begin to show some additional loss, averaging another 2.3 to 3.6 kg (5 to 8 lb) due to diuresis and 0.9 to 1.4 kg (2 to 3 lb) from involution and lochia by the end of the first week.⁵⁸ Alterations in energy utilization may alter losses in nonlactating women.⁶⁰

Most women lose weight steadily over the first 3 to 6 months postpartum, with the greatest loss in the first 3 months. Weight loss occurs sooner and to a greater degree in women of lower parity, age, and prepregnant weight.⁶⁰ Lactation may facilitate postpartum weight and body fat loss as maternal tissue stores are catabolized to use as energy for milk production.⁶⁰ Most women do not lose all of the pregnancy weight gain, with an average retention of 1 kg (2.2 lb) with each pregnancy; 10% retain more than 15 lb (6.8 kg).⁶⁰ Women who are overweight or normal weight before pregnancy are more likely to retain weight following pregnancy than women who were underweight.⁶⁰ Abrams and colleagues found no evidence that weight gain during pregnancy within the IOM recommendations increased the risk of weight retention following birth.¹ However, weight gain above these recommendations was common and associated with an increased risk of further weight gain during the first postpartum year and perhaps later development of obesity.^180,221 Most studies have small sample sizes and often do not control for activity, diet, and psychosocial factors.

Gingivitis often disappears after delivery but may last for up to 6 months postpartum.²¹⁴ Epulis regresses and also usually disappears postpartum, but a scarred area may remain.²¹⁴ LES pressure and tone return to normal levels by 4 to 8 weeks postpartum.^203,214 Gallbladder volume returns to normal by 2 weeks postpartum.⁷⁶ Gallbladder contractility is enhanced postpartum, enabling the previously atonic gallbladder to empty a larger proportion of its volume and expel microgallstones that developed during pregnancy.²⁴⁹ Expulsion of these stones can lead to a gallstone pancreatitis.

Most of the liver enzymes return to nonpregnant levels within 3 weeks of delivery.²⁰¹ Fatty acids, cholesterol, triglycerides, and lipoproteins tend to reach normal levels by about 10 days.²⁰¹ AST, ALT, and serum γ-glutamyl transferase (GGT) (see Table 12-2), which rose during the intrapartum period, may continue to rise for up to 10 days postpartum, especially following cesarean birth.²⁰¹ These parameters generally reach nonpregnant levels by 2 to 3 weeks. Alkaline phosphatase decreases after delivery and usually returns to nonpregnant levels by 20 days, but may remain elevated for up to 6 weeks.^185,201

The appendix returns to its usual position by 10 days postpartum.²²⁸ GI muscle tone and motility are decreased during the intrapartum and early postpartum periods. Decreased gastric motility along with relaxation of the abdominal musculature can result in gaseous distention 2 to 3 days postpartum. Decreased intestinal motility can lead to postpartum ileus and constipation. Bowel movements usually resume 2 to 3 days after birth, with resumption of normal bowel patterns by 8 to 14 days.

Clinical implications for the pregnant woman and her fetus

The normal alterations in GI function and structure in the pregnant woman are responsible for some of the more common discomforts of pregnancy, including heartburn and constipation. Alterations in the anatomic position of structures such as the appendix and liver and in concentrations of liver enzymes and other substances, as well as concerns about potential hazards with the use of radiographic contrast studies on the fetus, can lead to difficulty in assessing and diagnosing pathologic processes that arise. This section examines the basis for development of these problems and reviews the effect of pregnancy on selected disorders such as peptic ulcer disease (PUD) and cholelithiasis.

Nutritional requirements of pregnancy

The physical and physiologic demands of pregnancy on the mother, along with fetal needs for nutrients, significantly increase nutritional requirements during pregnancy (Table 12-4). Nutrient needs are also altered postpartum and during lactation (see Chapter 5). During pregnancy an additional 300 to 340 kcal per day are needed in the second trimester and up to 450 kcal per day are needed in the third trimester to meet energy and growth demands of the mother and fetus and to conserve protein for cell growth.¹⁸¹ Energy needs vary considerably from woman to woman with adaptations in individual metabolism to spare energy for fetal growth. Thus the diet should be individualized based on maternal age, trimester, BMI and activity.¹¹⁶ The woman meets the energy demands of pregnancy by increasing intake, decreasing activity, or limiting maternal fat storage (see Chapter 16).¹²⁰ The total minimum energy costs of pregnancy average 80,000 kcal, although some women may need up to 120,000 kcal.²¹⁵ Protein requirements increase to 60 g or slightly more to provide nitrogen for maternal, fetal, and placental tissue synthesis and growth.^108,188 Sources of protein should contain all the essential amino acids. Adequate maternal intake of the essential fatty acids, linoleic acid, and α-linolenic acid (an omega-3 fatty acid) is important for fetal growth and development, especially brain and vision development.²¹⁵

Table 12-4

Basis for Increased Nutrient Needs in Pregnancy

NUTRIENT	REASON FOR INCREASED NEED IN PREGNANCY
Protein	Rapid fetal tissue growth Placental growth and development Maternal tissue growth (e.g., uterus, breasts) Increased blood volume (increased hemoglobin, plasma proteins) Maternal storage reserves (for labor, delivery, and lactation)

Calories Increased basal metabolic rate (BMR), energy needs, and protein sparing Calcium

Fetal skeleton and tooth bud formation

Increased maternal calcium metabolism

Phosphorus Fetal skeleton and tooth bud formationIncreased maternal phosphorus metabolism Iron Iodine Increased BMR and thyroxine production Magnesium Vitamin A Vitamin D Vitamin E Vitamin C Folic acid