Micronutrients Vitamins

The B-complex vitamins—folate, pyridoxine (B6), and cobalamin (B12)—are of special concern in pregnant women with AN or BN. The metabolic needs for these vitamins do not appear to be greater in pregnant women with AN or BN compared with pregnant women without these eating disorders. However, due to past and present eating behaviors, women with AN or BN may have subclinical deficiencies prior to pregnancy and poor dietary intakes of these nutrients during pregnancy.

Folic acid supplementation prior to and in early pregnancy has been shown to reduce the risk and incidence of neural tube defect (NTD) in the infant (see Chap. 17, "Folate: a Key to Optimal Pregnancy Outcome"). The risk for NTD incidence was 1.7 times greater in women with eating disorders compared with controls [29]. Moreover, NTD incidence was 2.7 times higher in women who used diuretics compared with control women [29]. Folate intake is generally suboptimal in women with active AN and BN [30].

Pyridoxine and B12 intakes are of concern in women with AN and BN as eating pattern data show limited intakes of meat and whole-grain foods [25, 30], the primary sources of these two nutrients. Vitamin B6 is required for serotonin synthesis. Serotonin is a neurotransmitter that controls satiety and mood, and serotonin deficiency has been implicated in AN, BN, and depression. A lack of dietary B6 limits the conversion of the amino acid tryptophan to serotonin, leading to poor functioning of the serotonergic transmitter system. Moreover, in niacin deficiency, dietary tryptophan is competitively converted to niacin. Thus, in certain phenotypes, inadequate dietary B6 intake may precipitate or exacerbate AN or BN and associated mood disorders.

Because a vegetarian pattern of eating is relatively common in AN and BN, consumption of meat, chicken, fish, milk products, and eggs varies widely. Cobalamin deficiency may result in pernicious anemia for the mother and may impair deoxyribonucleic acid (DNA) synthesis and nerve function in the offspring. Inadequate B12 intake has been reported in women with AN [30].

Hypercarotenemia is common in AN [31] and results in the yellowish skin tone sometimes observed clinically. Elevated blood carotene is due to catabolism of lipid stores and not excessive intake. During pregnancy, vitamin A needs, inclusive of carotenoids and retinoids, increase slightly to support cellular differentiation and tissue and organ formation. Excessive consumption should be avoided (see Chap. 14, "Dietary Supplements during Pregnancy: Need, Efficacy, and Safety").

9.5.2.2 Minerals

Notably in the last trimester of pregnancy, maternal skeletal calcium is mobilized and calcium absorption is upregulated to meet the calcium demands of the fetus [32]. An adequate supply of calcium is necessary to support mineralization of the fetal skeleton (see Chap. 14). Osteoporosis risk is significantly greater in women who have experienced amenorrhea due to low estrogen concentration, as in AN. Therefore, women with AN may begin their pregnancies with poor skeletal calcium reserves [33]. At least 1,000 mg of dietary calcium per day are needed during pregnancy for adult women; however, this requirement may be higher in the woman with AN who also has osteopenia or osteoporosis. Dietary calcium intake in those with BN is generally adequate, with the exception of vegan or fruitarian diets (see Chap. 15, "Vegetarian Diets in Pregnancy").

The physiologic need for iron decreases in a woman with AN in relation to the duration of amenorrhea and degree of catabolism. However, during pregnancy, the iron requirement increases by 50%. A woman with AN may have difficulty meeting this requirement during pregnancy. Moreover, in those women with AN who also present with iron-deficiency anemia prior to or during pregnancy, supplemental iron may be necessary to meet the increased need.

Zinc intake is poor in women with AN and BN [30, 34], particularly in vegetarians. This mineral is required for DNA and ribonucleic acid (RNA) synthesis, protein production, and as a cofactor for enzymatic activity.

Electrolyte balance may be moderately to severely disturbed in those who engage in purging, laxative and diuretic use, and excessive exercise. Self-induced vomiting can lead to hypokalemia and hypochloremic alkalosis. Laxative and diuretic abuse is associated with hypokalemia. Excessive exercise may result in hyponatremia and hypokalemia. These compensatory behaviors lead to dehydration, elevation in blood urea nitrogen (BUN), and retardation of glomerular filtration rate. Alterations in maternal kidney function due to AN or BN may impair the efficiency with which fetal waste products are excreted during pregnancy.

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