If you read my book, “Eating for Autism”, the information regarding Vitamin B12 has changed since the book was first published. Now research reports improvements in autistic children taking methyl-B12. Below in a update on the current research related to Vitamin B12 and autism.
Update to Page 143 in book; “Eating for Autism”.
Vitamin B12 in the form of methylcobalamin, also known as methyl B12, has become a very popular nutraceutical treatment for Autism Spectrum Disorder (ASD). It is imperative to fully understand the functions of methyl B12, especially related to methylation and detoxification, and its potential role in treating ASD. Vitamin B12 is a water-soluble B complex vitamin found in foods from animal origin (ie, meats, liver, poultry, and fish). Vitamin B12 is also produced by gastrointestinal flora mainly in the colon, but the majority is excreted in the feces and does not significantly contribute to the body’s stores of vitamin B12. The coenzyme forms of vitamin B12, adenosylcobalamin and methylcobalamin (methyl B12), are naturally found in foods. Cyanocobalamin and hydroxocobalamin are the synthetic forms of vitamin B12 used in supplements. Absorption of vitamin B12 requires both intrinsic factor and a normal gastric pH. Under ideal conditions vitamin B12 is cleaved from proteins in food and absorbed in the terminal ileum. Vitamin B12 is required for methylation, myelin synthesis, cell reproduction, erythropoiesis, and folate utilization.1
Deficiency of vitamin B12 results from inadequate dietary intake, malabsorption from food, and other medical conditions such as gastritis or use of acid-suppressing drugs. A deficiency of vitamin B12 may result in neurologic damage beginning with an inability to produce myelin and progressing to degeneration of the axon and nerve head. Neurologic symptoms of vitamin B12 deficiency include depression, paresthesias, ataxia, memory loss, and personality and mood changes. Vitamin B12 deficiency has also been associated with impaired cognitive performance in 10- to 16-year-old adolescents who were fed a strict vegetarian diet from infancy to age 6.1
Methyl B12 has gained a lot of attention in the autism community due to its role in glutathione metabolism, the transmethylation cycle, and the transsulfuration pathway. Functions of these methyl B12-dependent pathways are essential for error-free methylation (ie, DNA, RNA, protein, phospholipids, and neurotransmitters) and also for detoxification and stress response. The role methyl B12 has on increasing glutathione in the body is critical considering the major functions of glutathione. Glutathione is called the master antioxidant playing a key role in protecting all cells including brain cells against oxidative stress. Glutathione also has a key role in detoxifying heavy metals.
It is theorized that some children with ASD have reduced detoxification capacity and may be experiencing chronic oxidative stress. A research study published in Free Radicals in Biology & Medicine in 2012 examined the role of oxidative damage, transmethylation, and the transsulfuration pathway connections to the pathogenesis of ASD.2 The study indicated that patients with ASD had decreased blood levels of glutathione, glutathione peroxidase, methionine, and cysteine, and increased concentrations of oxidized (inactive) glutathione compared to controls. In 2010, the Journal of Alternative and Complementary Medicine published a placebo-controlled study on the effect of injectable methyl B12 on behavior and biomarkers in children with ASD.3 The dosage of methyl B12 was 64.5 mcg/kg every three days for six weeks. The study found that the positive responders exhibited significantly increased plasma concentrations of glutathione and an increased glutathione redox ratio. Glutathione redox ratio is reduced (active) glutathione to oxidized (inactive) glutathione. Researchers concluded that methyl B12 may alleviate symptoms of autism in a subgroup of children by reducing oxidative stress.
Another study published in 2009 in The American Journal of Clinical Nutrition looked at the effect of both methyl B12 and folinic acid.4 The dosage of methyl B12 was 75 mcg/kg twice per week, and 400 mcg folinic acid twice per day for three months. The results indicated a significant increase in cysteine, cysteinylglycine, and glutathione, as well as an increased glutathione redox ratio. Researchers concluded that there were significant improvements in transmethylation metabolites and glutathione redox status after the methyl B12 and folinic acid treatment. It appears that a subgroup of children with ASD may have significant deficits in methylation and detoxification capacity; methyl B12 may be a promising treatment for these children.4
1. Vitamin B12. Natural Medicines Comprehensive Database website. http://naturaldatabase.therapeuticresearch.com/nd/Search.aspx?cs=&s=ND&pt=100&id=926&fs=ND&searchid=54051639. Accessed September 2014.
2. Frustaci A, Neri M, Cesario A, et al. Oxidative stress-related biomarkers in autism: systematic review and meta-analyses. Free Radic Biol Med. 2012;52(10):2128-2141.
3. Bertoglio K, Jill James S, Deprey L, Brule N, Hendren RL. Pilot study of the effect of methyl B12 treatment on behavioral and biomarker measures in children with autism. J Altern Complement Med. 2010;16(5):555-560. 4. James SJ, Melnyk S, Fuchs G, et al. Efficacy of methylcobalamin and folinic acid treatment on glutathione redox status in children with autism. Am J Clin Nutr. 2009;89(1):425-430.