Low carbohydrate intake increases the risk of birth defects

Women who are pregnant or planning to become pregnant may want to avoid diets that reduce or eliminate carbohydrates, as they could increase the risk of having babies with neural tube birth defects, according to a new study from the University of North Carolina at Chapel Hill.

Women with low carbohydrate intake are 30 percent more likely to have babies with neural tube defects, such as spina bifida-malformations of the spine and spinal cord and anencephaly-absence of major portions of the brain and skull, that can lead to lifelong disability and infant death, when compared with women who do not restrict their carbohydrate intake.

Folic acid is an essential nutrient that minimizes the risk of neural tube defects. Dietary intake of folic acid among women with restricted carbohydrate intake was less than half of other women. The Centers for Disease Control and Prevention recommends that all women who may become pregnant take a daily multivitamin with at least 400 micrograms of folic acid every day before and during pregnancy.

However, because some pregnancies are not planned, many women do not initiate folic acid supplementation until later in pregnancy, after a neural tube defect may have occurred. This makes fortified foods an important source of folic acid for women who may become pregnant.
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Brain cells may prevent Parkinson's disease

A Norwegian study shows that impairment in mitochondria may actually protect the brain in Parkinson's disease. Mitochondria are microscopic power stations found inside human cells. They convert foodstuffs into fuel, providing the required energy. Studies in brain tissue from individuals with Parkinson's disease showed that an essential component of the mitochondrial energy generators, called respiratory complex-I, becomes impaired in an area of the brain called the "substantia nigra" .

A new study from the University of Bergen (UiB), in Norway, in collaboration with the University of Cambridge, shows that the function of mitochondria, the microscopic powerhouses of the cell, is altered throughout the entire brain of individuals with Parkinson's disease. This new study shows that complex I deficiency is a global phenomenon in the brain of people with Parkinson's disease, and is found indiscriminately in both affected and healthy brain regions.

 Intriguingly, brain cells (neurons) with decreased complex I levels are significantly less likely to contain Lewy bodies, the abnormal protein-aggregates that characterize Parkinson's disease. These discoveries suggest that, contrary to mainstream theory, mitochondrial complex I deficiency may not be entirely deleterious for the brain in Parkinson's disease. It is possible that complex I deficiency is part of a compensatory regulation attempting to protect the brain in Parkinson's disease.

Parkinson's disease is one of the most common brain disorders. It affects millions of people worldwide. It starts after the age of 50 and causes a combination of debilitating symptoms, including shaking and other abnormal movements, loss of balance, low blood pressure, bladder and intestinal problems, sleeping disorders and dementia. Presently, there is no cure and patients die prematurely due to increasing disability.
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