It is known that deficiencies of some nutrients during pregnancy can adversely affect the foetus. A folic acid deficiency causing neural tube defects is a well know example. It is likely that other vitamin deficiencies affect the growing foetus, due to the essential nature of the compounds for normal metabolic functions. For example, children born to women who were vitamin B12 deficient during early pregnancy, were found (at age 6 to 9 years) to have a 26.7% increase in insulin resistance using the homeostasis model assessment (HOMA-IR) method1. Risk increased in those mothers who has vitamin B12 levels <148pmol/L. However, low vitamin B12 status in late pregnancy was not associated with insulin resistance in the offspring of such mothers. Supplementation of the children had no effects on insulin resistance, suggesting that the insulin resistance was not cause by poor vitamin B12 status in the children.
These results suggest the low vitamin B12 status during early pregnancy causes developmental changes that result in an increased risk of insulin resistance in later life. A genetic cause is suggested because vitamin B12 supplementation was unable to modify insulin resistance following birth. The mechanism for the development of insulin resistance in this way is not understood, but may related to high plasma levels of homocysteine. Vitamin B12 is required as a cofactor for methionine synthesis, and deficiency causes increases in plasma homocysteine levels which are known to damage vascular tissue. In this way epigenetic modification during pregnancy may contribute to the development of insulin resistance in the developing foetus. These results add evidence to the growing literature that suggests that maternal diet during pregnancy is far more important than was previously considered.
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