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close this bookMaternal Diet, Breast-Feeding Capacity, and Lactational Infertility (UNU/WHO, 1983, 107 pages)
close this folder3. Effect of diet on maternal health and lactational performance
View the document(introductory text...)
View the documentBody size and composition
View the documentProtein status of the mother
View the documentMaternal vitamin status
View the documentDiet and breast-milk composition
View the documentDiet and the quantity of milk produced
View the documentThe effect of maternal dietary supplementation on milk output and composition
View the documentGeneral conclusion
View the documentReferences

Maternal vitamin status

3.4. All available evidence shows that both the mother's own vitamin status and that of the milk she produces (see 3.12, 3.13) are very sensitive to dietary intake. Table 6 shows the percentage incidence of clinical symptoms and abnormal blood vitamin biochemistry among poor indian women living in Baroda, as reported by Rajalakshmi (3). Similarly, in the Gambia (7) there are marked biochemical signs of vitamin deficiency reflecting the poor maternal diet. The mean erythrocyte glutathione reductase activation coefficient in lactating mothers is 1.6 throughout lactation, with some values over 2.0. The upper limit of acceptability is 1.3 and thus these data must be interpreted as being indicative of widespread deficiency. It needs to emphasized, however, that signs of abnormality were even more marked during the late stages of pregnancy, with mean activation coefficients approaching 2.0. Again, this could mean that pregnancy produces a greater metabolic strain on the mother than lactation, even though the recommended dietary allowance is more during lactation.

TABLE 6. Nutritional Status of Poor Indian Women during Pregnancy and Lactation


Percentage incidence

No. of cases










Clinical symptoms 33 66 39      
xerosis of conjunctive       48 23 18
pigmentation of conjunctiva       55 38 33
xerosis of cornea       33 3 5
pale tongue       73 67 62
fissured tongue       39 38 21
adipose tissue deficientc       36 11 26
oedema on dependent parts       3 2 0
anorexia       24 2 0
diarrhoea       9 2 0
Values per 100 ml            
blood haemoglobin<10m g 63 34 24 41 12 4
serum protein<6m g 63 34 24 45 9 8
serum b -carotene <15m g 41 30 11 30 3 18
serum vitamin A < 10m g 41 30 11 28 10 18
Radiological evidence of coarse trabeculae            
pelvis 0 27 5 - 26 50
wrist 0 27 5 - 7 20
Cortical thickness (cm) of bone            
second metacarpal 0 13 4 - 0.44±0.02 0.42±0.03
femur 0 34 4 - 1.30±0.03 1.50±0.02

a Close to term.
b. In established lactation.
c. As judged by mid-arm skinfold.

Source: ref. 3.

3.5. The vitamin C status of the mother is also very sensitive to dietary intake. Figure 7 (see

FIG. 7. Plasma Ascorbic Acid Concentrations in the Gambia by Season (Source: ref. 8)) shows plasma vitamin C levels in lactating women in the Gambia (8). These swing from a high level suggesting tissue saturation during the mango season down to almost unmeasurable levels in the rainy season, when intakes are extremely low. In contrast to riboflavin, plasma vitamin C levels were lower during lactation than in pregnancy. For example, during January 1979 mean lactating maternal values were around 0.2 mg per 100 ml, while in pregnant mothers the values were about 0.5 mg. A similar effect has been reported from Baroda (3), where the corresponding values were 0.58-0.75 mg per 100 ml during pregnancy but only 0.36-0.50 mg in lactation. The extra 40 mg/d of dietary vitamin C during lactation recommended by the NRC, but only an extra 20 mg/d in pregnancy, would therefore not seem unreasonable.

3.6. Vitamin A status can also be affected in lactation, although pregnancy again seems to be the time when the mother is most at risk. Rajalakshmi, for example (3), has found that among poor Indian women, serum levels fall during pregnancy but rise again after parturition, with an associated increase and decrease, respectively, in the prevalence of clinical symptoms of vitamin A deficiency. It was suggested that this could parallel the situation that has been observed in cattle, in which for some reason not completely understood, pregnancy can be associated with an increase in liver stores and the vitamin seems not so generally available to the other tissues.

In the Gambia, in spite of very low intakes, no gross clinical signs of vitamin A deficiency, such as keratomalacia or Bitot spots, have been observed even though plasma carotene levels vary in concentration closely following the seasonal variations in dietary intake, and plasma vitamin A concentrations are consistently lower than those observed in the United Kingdom (C.J. Bates, personal communication). The Gambian data would suggest that, at least within that country, the current RDA is unnecessarily high both for pregnancy and lactation. This could be because carotene rather than vitamin A is the major dietary source of retinol, and estimates of requirements are based on the assumption that six molecules of ,ß-carotene yield approximately only one molecule of retinol in vivo. It is known, however that this conversion varies in different foodstuffs and, more importantly, it may also vary with physiological status. Metabolic efficiency is believed to increase during pregnancy and lactation with energy (see 3.2) and other nutrients, and it is not unreasonable to postulate that this could be the same with ß-carotene and vitamin A. There is clearly a need for the 6:1 conversion factor to be reinvestigated under differing prevailing conditions during pregnancy and lactation in relation to the types of carotene-containing foods customarily consumed.

There is another possible explanation. Clinical vitamin A deficiency may not occur only as a result of exhausted body stores. Interaction with other nutrient deficiencies would also appear to be of crucial importance. Very recent evidence suggests that the classical signs develop from the combined effects of vitamin A deficiency plus protein and zinc deficiency (5, 10). This could well explain variability between countries in the relationship between vitamin A intake and the appearance of signs of clinical deficiency. There is clearly a need for these interactions to be studied on an objective basis to determine their relevance for practical nutritional and dietary planning.

3.7. The amount of folic acid required during lactation understandably depends on the status of the mother at the end of pregnancy. In the Gambia preliminary evidence shows that red-cell concentrations fall steadily during lactation, and some very low values have been obtained towards the end of the second year (Bates, personal communication). The women studied had been given a therapeutic iron-folate preparation during pregnancy as part of a standard clinical routine, but not during lactation. The extent to which it is the strain of pregnancy or the process of milk production that has been the cause of the megaloblastic anaemia observed in other countries early in lactation is uncertain. Chanarin, for example(11), found that 52 per cent of his cases were diagnosed postpartum, mostly in the first few weeks after delivery.

The problem of relating food folate intake to physiological performance has already been discussed (section 1.14). It is readily apparent that more work needs to be carried out, and such studies will have to take account of the effects of intercurrent infection. It is known in children that diseases such as malaria or hookworm can exacerbate poor folate status both in terms of FIGLU excretion and in the incidence of megaloblastic anaemia (12). There is also a close association between folate status and the prevalence of diarrhoeal disease (13).