THIAMINE

Fetal Risk Summary

Thiamine (vitamin B1), a water-soluble B complex vitamin, is an essential nutrient required for carbohydrate metabolism (1). The National Academy of Sciences' recommended dietary allowance (RDA) for thiamine in pregnancy is 1.5 mg (1).

Thiamine is actively transported to the fetus (2,3,4 and 5). Like other B complex vitamins, concentrations of thiamine in the fetus and newborn are higher than in the mother (4,5,6,7,8,9,10 and 11).

Maternal thiamine deficiency is common during pregnancy (11 and 12). Supplementation with multivitamin products reduces the thiamine hypovitaminemia only slightly (9). Since 1938, several authors have attempted to link this deficiency to toxemia of pregnancy (13,14,15 and 16). A 1945 paper summarized the early work published in this area (14). All of the reported cases, however, involved patients with poor nutrition and pregnancy care in general. More recent investigations have failed to find any relationship between maternal thiamine deficiency and toxemia, fetal defects, or other outcome of pregnancy (8,17).

No association was found between low birth weight and thiamine levels in a 1977 report (7). One group has shown experimentally, though, that the characteristic intrauterine growth retardation of the fetal alcohol syndrome may be caused by ethanol-induced thiamine deficiency (18).

Thiamine has been used to treat hyperemesis gravidarum, although pyridoxine (vitamin B6) was found to be more effective (see Pyridoxine) (19,20 and 21). In one early report, thiamine was effective in reversing severe neurologic complications associated with hyperemesis (19). A mother treated with frequent injections of thiamine and pyridoxine, 50 mg each/dose, for hyperemesis during the first half of two pregnancies delivered two infants with severe convulsions, one of whom died within 30 hours of birth (21). The convulsions in the mentally retarded second infant were eventually controlled with pyridoxine. Pyridoxine dependency-induced convulsions are rare. The authors speculated that the defect was caused by in utero exposure to high circulating levels of the vitamin. Thiamine was not thought to be involved (see Pyridoxine).

An isolated case report described an anencephalic fetus whose mother was under psychiatric care (22). She had been treated with very high doses of vitamins B1, B6, C, and folic acid. The relationship between the vitamins and the defect is unknown. Also unproven is the speculation by one researcher that an association exists between thiamine deficiency and Down's syndrome (trisomy 21) or preleukemic bone marrow changes (23).

[* Risk Factor C if used in doses above the RDA.]

Breast Feeding Summary

Thiamine (vitamin B1) is excreted into breast milk (24,25,26 and 27). One group of investigators supplemented well-nourished lactating women with a multivitamin preparation containing 1.7 mg of thiamine (24). At 6 months postpartum, milk concentrations of thiamine did not differ significantly from those of control patients not receiving supplements. In a study of lactating women with low nutritional status, supplementation with thiamine, 0.2–20.0 mg/day, resulted in mean milk concentrations of 125–268 ng/mL (25). Milk concentrations were directly proportional to dietary intake. A 1983 English study measured thiamine levels in pooled human milk obtained from preterm (26 mothers: 29–34 weeks) and term (35 mothers: 39 weeks or longer) patients (26). Milk obtained from preterm mothers rose from 23.7 ng/mL (colostrum) to 89.3 ng/mL (16–196 days) while milk from term mothers increased during the same period from a level of 28.4 to 183 ng/mL.

In Asian mothers with severe thiamine deficiency, including some with beriberi, infants have become acutely ill after breast feeding, leading in some cases to convulsions and sudden death (28,29,30 and 31). Pneumonia was usually a characteristic finding. One author thought the condition was related to toxic intermediary metabolites, such as methylglyoxal, passing to the infant via the milk (28). Although a cause-and-effect relationship has not been proven, one report suggested that thiamine deficiency may aggravate the condition (29). Indian investigators measured very low thiamine milk levels in mothers of children with convulsions of unknown cause (32). Mean milk thiamine concentrations in mothers of healthy children were 111 ng/mL, whereas those in mothers of children with convulsions were 29 ng/mL. The authors were unable to establish an association between the low thiamine content in milk and infantile convulsions (see Pyridoxine for correlation between low levels of vitamin B6 and convulsions).

A 1992 case described the features of “Shoshin beriberi” in a 3-month-old breast-fed infant (33). Both the infant and the mother had biochemical evidence of thiamine deficiency. Clinical features in the infant included cardiac failure with vasoconstriction, hypotension, severe metabolic acidosis, and atypical grand-mal seizures. He responded quickly to thiamine and made an unremarkable recovery.

The National Academy of Sciences' RDA for thiamine during lactation is 1.6 mg (1). If the diet of the lactating woman adequately supplies this amount, maternal supplementation with thiamine is not needed (27). Supplementation with the RDA for thiamine is recommended for those women with inadequate nutritional intake. The American Academy of Pediatrics considers the maternal consumption of thiamine to be compatible with breast feeding (34).

References

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