Selenium is an important trace mineral required as a cofactor for the cellular enzyme glutathione peroxidase. This enzyme is pivotal to cellular health because it inhibits the free radical chain reactions that damage cell components. Increasingly, the Western diet is becoming deficient in selenium due to a combination of an over-processing of foods and extensive farming techniques that remove, but do not replace, the selenium content of the soil. Following the pivotal paper by Clark et al in 1996 (here; please read this paper it is important), it is increasingly being realised that selenium deficiency is implicated in the development of a number of types of cancer, possibly because deficiency is associated with increased oxidative stress in the cellular milieu. Because the growing infant is reliant on the maternal milk for its nutrition, the selenium status of breastfeeding women is paramount in determining the selenium status of the infant. Regarding this, researchers have investigated the effects of breastfeeding on maternal selenium status.
For example1, in one study researchers investigated the association between the selenium content of the milk and maternal indices of selenium status. The milk from the mothers was collected at weeks 4, 8, 12 and 16 postpartum and blood samples were taken from the breastfeeding women and from non-lactating female controls. The first interesting finding was that the lactating women had a significantly lower selenium status compared to non-lactating females. In fact the glutathione peroxidase activity was 22 % lower, and the erythrocyte selenium concentration 40 % lower in the lactating women. There was also a correlation between the plasma selenium and plasma glutathione peroxidase activity, and this correlation was linear for the lactating women, but not for the control subjects. Further the milk selenium concentration was associated positively with the glutathione peroxidase activity of the milk. Therefore plasma selenium has a clear association with concentrations of selenium in milk.
These results support other studies regarding the association between plasma selenium concentrations and glutathione peroxidase activity. Low intakes of selenium result in a depletion of plasma selenium, which then causes low cellular concentrations of glutathione peroxidase. Evidence for this comes from clinical trials involving supplementation of depleted subjects with selenium. In such studies, plasma levels of selenium rise with supplementation, and with them glutathione peroxidase. That maternal plasma selenium is associated with milk selenium suggests that the diet of the mother is paramount in supplying adequate nutrition for the growing infant. The low selenium status of the breast feeding mothers suggests that supplying the growing infant may deplete the mother of her own selenium stores. Therefore it is important to ensure adequate selenium status during breast feeding to maintain the selenium supply to the infant, and also following breastfeeding to replete the selenium stores of the mother.
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