The requirement for vitamin E by animals for successful pregnancy is well established. Vitamin E deficiency has been shown to cause foetal resorption in rats and other animals. In fact, the route word for the name of the vitamin E isomers, toco-, is derived from the Greek word, tokos, which means childbirth. Since the establishment of vitamin E as a requirement for successful pregnancy outcomes, other roles in reproduction such as zygote implantation, placental maturation and embryogenesis, have been discovered. Vitamin E is an important fat soluble vitamin, and in this role it protects cell membranes from lipid peroxidation. The ability of vitamin E to protect from cellular damage may explain its role in reproductive function, and associations between the two have been suggested. High levels of oxidative stress may therefore produce poor pregnancy outcomes and increasing the intake of vitamin E to prevent such oxidative stress may improve pregnancy outcomes.
The association between low levels of vitamin E and plasma levels of tocopherols have been studied. For example in one study1, researchers measured the plasma levels of α-tocopherol and γ-tocopherol and the risk of miscarriage in the first trimester of pregnancy in Bangladeshi women. The results showed that high plasma levels of α-tocopherol were associated with a reduced risk of miscarriage whereas high levels of γ-tocopherol were associated with an increased risk of miscarriage. In humans, α-tocopherol is the prefered form of vitamin E and γ-tocopherol is able to interfere with α-tocopherol absorption, transport and tissue distribution. This may explain the reason for the association between high plasma levels of γ-tocopherol and the risk of miscarriage. This data supports other data to show the importance of vitamin E, particularly α-tocopherol, in reproductive function in humans.
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