Low Vitamin B12 in Brain Linked to Schizophrenia, Autism

Patients with schizophrenia and autism exhibit low levels of vitamin B₁₂ in the brain, suggesting that these disorders could be related to poor B₁₂ uptake from the blood into the brain.

Richard C. Deth, PhD, a pharmacist and professor in the Department of Pharmaceutical Sciences at Nova Southeastern University, told Pharmacy Times that pharmacists are an important resource for patients when it comes to supplementation education.

“Indeed, I think that there is an unmet need for such expertise and, to the extent they are able to do so, pharmacists can fill this role,” Dr. Deth said.

He noted that several studies have touted the benefits of methylcobalamin (methyl B₁₂) in autism, so pharmacists may want to consider recommending these supplements.

“It is important to recognize that methyl B₁₂ is the active form of B₁₂ for supporting methylation, while the more commonly available cyanocobalamin is inactive until it is converted to methyl B₁₂, and impaired conversion can be a problem,” Dr. Deth explained. “Therefore, methyl B₁₂ would be the preferred form.”

In a recent study published in PLOS One, Dr. Deth and his fellow researchers also found that supplemental vitamin B₁₂ could be useful in treating brain disorders like autism, though it is possible that the required dosage would significantly exceed the recommended daily allowance of 2.4 μg.

“Adequate absorption from the gastrointestinal tract is essential for oral dosage, and transport across the choroid plexus is critical for raising brain levels,” the researchers stated, adding that nasal administration could be potentially be used as an alternate method.

Beyond supplementation, pharmacists can tell patients that they can absorb vitamin B₁₂ through meat, dairy, eggs, and fish.

Pharmacists should also know that vitamin B₁₂ exists in several forms, including methylcobalamin (MeCbl) and adenosylcobalamin (AdoCbl). In the study, the researchers measured both forms in the brains of deceased patients.

They examined the frontal cortex of 43 individuals who ranged in age from 19 weeks to 80 years and served as control subjects. They also examined 12 patients with autism and 9 patients with schizophrenia.

The study authors found that those with autism and schizophrenia had MeCbl and AdoCbl levels more than 3-fold lower than the age-matched control subjects’ levels.

In addition, subjects aged 60 years or older had significantly lower vitamin B₁₂ levels, which may mean that older patients begin to see a decline in their ability to send the vitamin to the brain.

Patients aged 61 to 80 years had 12.4-fold lower MeCbl levels than patients who were 0 to 20 years old and 6.7-fold lower MeCbl levels than those aged 41 to 60 years.

The researchers also found that the level of MeCbl was 65% higher in fetal samples than in patients younger than 20 years, which may relate to prenatal vitamin B₁₂ use.

“Although the number of brain samples analyzed was limited, our findings highlight a possible role for vitamin B₁₂-dependent methylation reactions in brain function and in the etiology of neurological disorders,” the researchers concluded.

Dr. Deth also pointed to another recent study that was published in the Journal of Child and Adolescent Psychopharmacology and suggested methyl B₁₂ could improve autism spectrum disorder symptoms.

In that study, researchers examined 57 children with autism who were randomly assigned to placebo or methyl B₁₂ every 3 days via subcutaneous injection. After 8 weeks, the researchers found that the children who received methyl B₁₂ achieved better scores on the Clinical Global Impressions-Improvement scale.

The children who received the intervention treatment also saw increases in plasma methionine, decreases in S-adenosyl-l-homocysteine (SAH), and improvements in the ratio of improvements in the ratio of S-adenosylmethionine to SAH. This indicated that the children who received methyl B₁₂ saw improvements in cellular methylation capacity.