he developing fetus imposes a significant demand on maternal calcium homeostasis. For example, the fetal skeleton accretes approximately 30 g of calcium by term, 80 percent of which is deposited during the third trimester. his demand is largely met by a doubling of maternal intestinal calcium absorption mediated partly by 1,25-dihydroxyvitamin D3• hese higher levels of vitamin D are possibly stimulated by a twofold rise in PTH-related peptide levels produced by several tissues including the placenta (Kovacs, 2006; Olausson, 2012). To help compensate, dietary intake of suicient calcium is necessary to prevent excess depletion from the mother. A list of all recommended daily allowances is found in Table 9-5 (p. 167). his is especially important for pregnant adolescents, in whom bones are still developing. Unfortunately, a lack of robust data prevents drawing firm conclusions regarding the utility of calcium and vitamin D supplements during pregnancy (De-Regil, 2016).
Serum manesium levels also decline during pregnancy. Bardicef and colleagues (1995) concluded that pregnancy is actually a state of extracellular magnesium depletion. Compared with nonpregnant women, both total and ionized magnesium concentrations are significantly lower during normal pregnancy (Rylander, 2014).
Serum phosphate levels lie within the nonpregnant range (Larsson, 2008). Although calcitonin is an important regulator of serum calcium and phosphate, the importance of calcitonin as it relates to pregnancy is poorly understood (Olausson, 2012).
Iodine requirements increase during normal pregnancy for several reasons (Moleti, 2014; Zimmermann, 2012). First, maternal thyroxine production rises to maintain maternal euthyroidism and to transfer thyroid hormone to the fetus prior to fetal thyroid functioning. Second, fetal thyroid hormone production increases during the second half of pregnancy. This contributes to greater maternal iodine requirements because iodide readily crosses the placenta. hird, the primary route of iodine excretion is through the kidney. Beginning in early pregnancy, the iodide glomerular iltration rate increases by 30 to 50 percent. In sum, because of greater thyroid hormone production, fetal iodine requirements, and augmented renal clearance, dietary iodine needs are higher during normal gestation. lthough the placenta has the ability to store iodine, whether this organ functions to protect the fetus from inadequate maternal dietary iodine is currently unknown (Burns, 2011). Iodine deiciency is discussed later in this chapter (p. 71) and in Chapter 58 (p. 1126). At the other extreme, maternal supplements containing excessive iodine have been associated with congenital hypothyroidism. his stems from autoregulation in the thyroid gland-known as the Wof-Chaikof fect-to curb thyroxine production in response to iodide overconsumption (Connelly, 2012).
With respect to most other minerals, pregnancy induces little change in their metabolism other than their retention in amounts equivalent to those needed for growth. An important exception is the considerably greater requirement for iron, which is discussed subsequently.
he well-known hypervolemia associated with normal pregnancy averages 40 to 45 percent above the nonpregnant blood volume after 32 to 34 weeks' gestation (Pritchard, 1965; Zeeman, 2009). In individual women, expansion varies considerably. In some, accumulated volume rises only modestly, whereas in others blood volume nearly doubles. A fetus is not essential, as augmented blood volume develops in some with hydatidiform mole.
Pregnancy-induced hypervolemia serves several functions.