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Vitamin A Deficiency in the Mother-Infant Dyad

by Rebecca J. Stoltzfus, PhD., Division of Human Nutrition, School of Hygiene and Public Health, The Johns Hopkins University.

Transfer of Vitamin A from Mother to Infant

Vitamin A is transferred in two ways from mother to offspring: via the placenta during gestation, and via the mammary gland (breastmilk) during lactation. Adequate transfer of vitamin A is essential during both of these periods of development. Animal models of severe vitamin A deficiency have shown that maternal vitamin A deficiency during pregnancy results in placental dysfunction, stillbirths, and congenital malformations. Maternal vitamin A deficiency during lactation rapidly disposes the nursling to severe vitamin A deficiency.

Although the fetus requires vitamin A for normal development, it is vulnerable to toxic effects of vitamin A if it receives too much. The placenta is well-adapted for this situation. Unless the mother’s normal metabolism of vitamin A is overwhelmed by a very high intake of vitamin A, the placenta allows only the small amount of vitamin A required by the fetus to pass from mother to fetus. Thus, infants of well-nourished mothers are born with small reserves of vitamin A.

Human lactation is equally well-adapted to protecting the vulnerable neonate from vitamin A deficiency. Colostrum is particularly rich in vitamin A (containing approximately 7 umol/L) and thus provides an excellent dietary source of the vitamin during the infant’s first days of life. The mature milk of well-nourished women contains around 2.3 umol/L vitamin A, ample to meet the infant’s metabolic requirement and to accumulate safe and adequate stores of the vitamin. In addition, Vitamin A in human milk is uniquely well-absorbed, in part because of a lipase present in milk that helps the infant digest vitamin A.

Of these two routes, a far greater quantity of vitamin A is transferred during lactation than during pregnancy. Normal birth weight American infants were found to have liver vitamin A concentrations of 0.038 umol/g. Based on this figure, a 3200g newborn would have liver stores of around 5 umol vitamin A. In contrast, during the first 6 months of life, the breastfed infant consumes approximately 310 umol of vitamin A from mother’s milk. Thus, normally 60 times more vitamin A is transferred from mother to infant in 6 months of lactation than is accumulated by the fetus during the whole period of gestation.

In sum, the mammalian “strategy” for providing vitamin A to the offspring is to ensure that the fetus acquires adequate but small amounts of vitamin A during gestation, and to provide plentiful vitamin A post-natally through breastmilk, so that the infant rapidly builds protective stores of vitamin A. However, maternal vitamin A deficiency can compromise these normal processes.

Vitamin A Deficiency During Pregnancy and Fetal Health

Pregnant laboratory animals with severe vitamin A deficiency are less fertile, tend to resorb their fetuses or abort their pregnancies, and bear malformed offspring. Additionally, vitamin A is essential for the development of vital organ systems, particularly the lung. However there is very little evidence with which to judge the impact on fetal health of maternal vitamin A deficiency as commonly observed in human populations.

Cases have been reported of congenital ocular defects in infants born to mothers who were very vitamin A deficient. It is plausible that these defects were caused by vitamin A deficiency, because of the similarity with animal studies. However, these mothers undoubtedly had many nutritional deficiencies and perhaps other illnesses that might also explain this finding.

A question of greater public health importance is whether maternal vitamin A deficiency compromises the growth and vitamin A stores of the fetus. If maternal vitamin A deficiency contributes to low birth weight, maternal vitamin A deficiency would significantly impact infant mortality. Here again, animal studies modelling severe deficiency suggest the possibility, but there is no direct evidence from human studies. Fetal weight gain and accumulation of vitamin A are strongly associated in animals and humans (that is, smaller fetuses have lower vitamin A stores), but it is not clear that vitamin A is limiting growth. Possibly, low weight gain and vitamin A gain result from general fetal malnutrition, due to inadequate placental size, function, or blood perfusion.

Animal studies also suggest that fetal stores of vitamin A are even lower than normal when the mother is very deficient. However, because the vitamin A stores of newborns are so small, variation in the stores of newborns can have little direct impact on the subsequent vitamin A status of the breastfed infant. A few days intake of vitamin A from breastmilk is equal to the total vitamin A stores of a healthy newborn.

In summary, based on findings primarily from animal studies, there are several ways that maternal vitamin A deficiency might have negative consequences for the fetus, but there is scanty evidence from human studies. Research in progress should begin to provide answers.

Vitamin A Deficiency During Lactation

Breastfeeding is the key to preventing vitamin A deficiency in infants and young children, and this is especially true in vitamin A deficient regions. Even when breastmilk vitamin A content is less than optimal, mother’s milk is the best dietary source of vitamin A for the young infant, and very likely continues to be the best source into the second half of life. In addition, breastmilk protects the infant against infectious disease, which may deplete vitamin A stores and can precipitate xerophthalmia if vitamin A stores are very low. For these reasons, xerophthalmia is practically never observed in fully breastfed infants, and breastfeeding provides significant protection against xerophthalmia throughout and even after weaning.

It is clear, however, that the vitamin A content of human milk is dependent on the mother’s own vitamin A status. In regions where vitamin A deficiency is common, mature human milk typically contains around 1 umol/L vitamin A. The observed means range from 0.4 to 1.8 umol/L. These lower levels are a direct result of maternal vitamin A deficiency, and breastmilk vitamin A will increase if the mother’s vitamin A status is improved. This has been demonstrated in both supplementation trials and food fortification trials.

Overall, the typical breastmilk vitamin A content in vitamin A deficient areas is about one half of the content of milk from well-nourished mothers. Infants of well-nourished mothers increase their vitamin A stores about 20-fold from birth to one year of life. In contrast, it has been estimated that if the mother’s milk contains only 1 umol/L vitamin A, the infant will accumulate no storage vitamin A, a state considered to be subclinical vitamin A deficiency. A bout of anorexia, illness, or a temporary shortage of vitamin A-containing foods may bring about clinical deficiency.

These calculations are in accord with research findings. In Central Java, 24% of breastfeeding mothers at 6 month post-partum had milk concentrations below 1 umol/L (Stoltzfus et al., 1993). At the same time, 23% of their breastfed infants had very low vitamin A stores. Among mothers randomly allocated to be supplemented with vitamin A, 9% had milk concentrations below 1 umol/L, and 10% of their infants had very low vitamin A stores. It is reasonable to consider 1 umol/L to be the minimal breastmilk vitamin A concentration necessary to meet infant requirements, and 1.75 umol/L to be necessary to meet infant requirements, and 1.75 umol/L to be necessary for adequate vitamin A storage in infancy.

What are the public health implications of subclinical vitamin A deficiency in infancy? Improving the vitamin A status of young children through low- or high-dose vitamin A supplementation in countries where vitamin A deficiency is a known public health problem can be expected to reduce mortality by about 23%. Although there is less evidence from infants than from one- to five-year-olds, the data at hand suggest that this mortality reduction is consistent across all age groups studied (from 6 months to 5 years). Ongoing research focusing on infants (including the first half of infancy) will improve our understanding of the role of vitamin A deficiency in infant mortality. Because infants are at higher risk of mortality than older children, improving the vitamin A status of infants could potentially save the greatest number of lives.

Although breastfed infants are largely protected from xerophthalmia, improving vitamin A stores during infancy will help to protect children from xerophthalmia during weaning. The weaning period is typically when young children are at risk of xerophthalmia because breastmilk is replaced by foods that are often low in vitamin A. Furthermore, weaning foods may be contaminated with infectious agents, putting the weanling at risk of infectious diseases that may precipitate xerophthalmia. Vitamin A stores accumulated during breastfeeding provide a margin of safety during this nutritionally vulnerable transition.

Improving the vitamin A status of infants might also improve their growth and iron status, although neither of these benefits has been demonstrated. The impact of vitamin A supplementation on growth of preschool children has been inconsistent among research studies, but as with mortality, the potential for impact is greatest in infancy because growth faltering is usually most marked in the second half of infancy. Improved vitamin A status has been shown to raise hemoglobin levels in children and pregnant women. It may help to prevent anemia in infancy, and this important possibility should be investigated.

Vitamin A Deficiency and the Health of Women

Although the infant has been the focus of most research in this area, it must be clear that we are dealing with a deficiency of the mother-infant dyad-two interconnected individuals. What does vitamin A deficiency mean for women’s health? Unfortunately, we don’t really know.

Several areas deserve attention. First, we need to determine the prevalence of night blindness in women and its impact on their lives. Recent surveys indicate that night blindness is more prevalent among women than previously assumed, and preliminary ethnographic research from the Indian subcontinent indicates that women perceive it to be an important health problem. Second, how great is the role of vitamin A deficiency in the etiology of anemia among women? If improving women’s vitamin A status raises their hemoglobin levels, does this bring about the same benefits in work efficiency achieved by iron supplementation? Third, does vitamin A deficiency in women contribute to infectious morbidity and mortality, as it does in children?

By considering women and infants together as we plan public health research and programmes, we gain the potential for improved health of women, for greater participation of women in the development and implementation of programmes and thus, greater programme effectiveness.

Interventions to Improve Vitamin A Nutrition of Women and Infants

The fundamental means of improving the vitamin A status of women and breastfed infants is to improve dietary intake of vitamin A for women and their families. Achieving this goal will likely require a combination of strategies, such as improving women’s knowledge about vitamin A food sources and their preparation, increasing the availability of vitamin A-containing foods, increasing families’ food purchasing power, and fortifying key food items with vitamin A.

Until dietary goals are fully achieved, supplementation to breastfeeding mothers at delivery or in the first month post-partum is a safe and effective way to improve breastmilk vitamin A content. This intervention also offsets the depleting effect that lactation may have on the mother’s own vitamin A stores.

Where vitamin A deficiency is an urgent public health problem, supplementing lactating mothers may not be sufficient to prevent subclinical vitamin A deficiency in all breastfed infants. In such cases, maternal supplementation could be combined with direct supplementation of infants.

Healthy breastfeeding practices are essential to preventing vitamin A deficiency in infants. Where breastfeeding practices have eroded, breastfeeding promotion activities must be a central part of any plan to prevent vitamin A deficiency. In vitamin A-deficient communities, infants who are not breastfed are at greatest risk of vitamin A deficiency and should receive direct vitamin A supplementation.

In areas where night blindness is experienced by women in pregnancy, this problem should be detected and treated as part of antenatal care programs. Women experiencing night blindness could be treated with a course of daily low doses of vitamin A (e.g. 10,000 IU) or advised to eat vitamin A-rich foods. These women should also be targeted for high-dose vitamin A supplementation post-partum, as they would be expected to have low milk vitamin A concentrations.

The last decade has brought tremendous advances in our understanding of the causes and consequences of vitamin A deficiency in preschool children and interventions to prevent it. With this knowledge and experience, we are well-equipped to make similar progress in the coming decade to improve the vitamin A status of women and infants.

Acknowledgement

I am indebted to B.A. Underwood for the estimation of infant vitamin A storage at different levels of breastmilk vitamin A content, and to P.S. Christian for discussions of her ethnographic research on night blindness in pregnancy.

References

Beaton, G.H., Martorell, R., Aronson, K.J., et al. (1993) Effectiveness of Vitamin A Supplementation in the Control of Young Child Morbidity and Mortality in Developing Countries. University of Toronto.

International Vitamin A Consultative Group (IVACG). (1986) The Safe Use of Vitamin A by Women During the Reproductive Years. Washington, D.C.

Stoltzfus, R.J., Hakimi, M., Millar, K.W., et al. (1993) High Dose Vitamin A Supplementation of Breastfeeding Indonesian Mothers: Effects on the Vitamin A Status of Mother and Infant. J Nutr, 123, 666-675.

Wallingford, J.C., & Underwood, B.A. (1986). Vitamin A Deficiency in Pregnancy, Lactation, and the Nursing Child. In: Vitamin A deficiency and its control. Baurenfiend, JC, ed. Orlando: Academic Press, Inc.


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