Vitamin B12 Deficiency

Vitamin B12 deficiency and autism

There is increasing evidence to suggest that a combined deficiency of vitamin D and Vitamin B12 of the foetus is responsible for the development of autism in the neonate. It is already well established that vitamin B12 is necessary for development of the foetus and neonate. Developmental delay is a known consequence of vitamin B12 deficiency in addition, babies of mothers who are deficient in vitamin B12 may have lower cognitive scores one year after birth, even if the deficiency is detected, and low serum levels of vitamin B12 in the neonate have been linked to negative impacts on cognitive function, as well as motor and growth outcomes in the developing neonate. Further there is evidence of decreased levels of vitamin B12 seen in the brains of children with Autism (1), and also the association of vitamin B12 deficiency and developmental delay and adverse neurological outcomes in the neonate (2-6).

Critically, loading of the brain of the child occurs primarily in the foetus and up to 17% of vitamin B12 that crosses the placenta goes to the brain of the developing foetus. Brain loading with vitamin B12 (and selenium) is maximal in the final stages of development and as such babies that are born prematurely (commonly seen in children who develop autism) would have lower brain levels of vitamin B12.

Studies have shown that during pregnancy there is a significant drop in the level of vitamin B12 in the serum of the mothers, which progressively drops further during the course of the pregnancy and while the mothers are breast-feeding. Overt vitamin B12 deficiency may occur in pregnant women who have lower levels of vitamin B12 at the start of their pregnancy, or who are vegetarian or vegan, have Crohn of coeliac disease, who are on Metformin™ for diabetes, or who have undergone gastric bypass surgery. More recently it has been shown that functional vitamin B12 deficiency may also be present in women who are obese. Children born to mothers who have had weight loss bariatric surgery are more likely to be premature, a co-contributing factor to giving birth to a child who develops autism.

Studies on the metabolism of over 250 children with autism showed that they were all functionally deficient in vitamin B12. Accompanying the deficiency in vitamin B12, the children were all functionally deficient in vitamin B2. Hair metals analysis showed them to also be deficient in Iodine (~50%), Selenium (~80%) and Molybdenum (~50%). Deficiency in any of Iodine, Selenium and/or Molybdenum can all result in functional vitamin B2 deficiency, which in turn gives rise to functional B12 deficiency. Given that functional vitamin B2 deficiency is also associated with the development of obesity and subsequent gestational diabetes, there is good reason to believe that the mothers of the children with autism were more likely to be functionally deficient in vitamin B2 at time of pregnancy. Such deficiency would in turn result in functional vitamin B12 deficiency.

Other signs of vitamin B12 deficiency in the neonate include megalobastic anaemia, feeding difficulties (difficulties in suckling), developmental delay, microcephaly, hyptonia, lethargy, irritability, involuntary movements, seizures and cerebral atrophy" (Benbir etal, 2007).

Further Information on the role of vitamin B12 deficiency in autism

Further information on the biochemistry of autism can be found at http://wipeoutautism.org/

References