B12/Methylcobalamin injections

Methylcobalamin stimulates the methylation pathway which is responsible for:

  • Making and repairing RNA and DNA, the genetic material responsible for every function in the body.
  • Regulating parts of the immune system.
  • Controls the detoxification of heavy metals and other harmful substances by making glutathione which is the body’s main detoxification pathway. Glutathione
  • Is a major endogenous antioxidant made by cells to neutralize free radicals and reactive oxygen compounds having the ability to maintain vitamin E and vitamin C in their reduced form (active).
  • Production and function of proteins, through the nitric acid pathway.
  • Regulating iron metabolism.
  • Cell cycle and cell death through controlling changes to nuclear proteins needed to differentiate cells.

Methylcobalamin (methyl B12) injections can enhance function in:

  • Awareness
  • Cognition
  • Appropriateness
  • Eye contact
  • Responsiveness
  • normalized behaviours and interaction
  • Speech and language
  • Spontaneous language
  • More complex sentences
  • Increased vocabulary
  • Socialization with respect to understanding and expressing emotion
  • Initiating plan have having more interactive play
  • Understanding and feeling emotions
  • Affection and tolerance to touch

Methylcobalamin (methyl B12) injections increase:

  • Language, social, cognitive, improved behaviours
  • Decrease hyperactivity
  • Help sleep
  • Increase stimming and sensory aggravation
  • Increase mouthing of objects
  • May stimulate diarrhea, constipation or ashes
  • May initiate a period of aggression and irritability

Undesired effects to are a good sign of treatment success. They are not uncommon and include:

  • Hyperactivity
  • Self-stimulating behaviour
  • Increased mouthing of objects
  • Sleep disturbances which can be managed with other treatments such as melatonin
  • Aggression, hitting and biting

The seemingly negative side effects are caused by frustration when an increased awareness is present. Side effects can be mild to severe and are considered transient which means they will pass as treatment progresses.

Mechanism of Action of Methylcobalamin (methyl B12)

The methylation cycle metabolites and glutathione metabolism have been shown to be low in children on the Autism Spectrum Disorder (ASD). Altered methylation metabolism will result in a depletion of the precursors needed for glutathione production. Glutathione synthesis is connected to methylation metabolism. The methionine cycle involves the regeneration of methionine by the transfer to a methyl group from from 5-methyltetrahydrofolate (MTHF) to homocysteine in the methionine synthase reaction.

This system is methylcobalamin (B12) dependent.

Methionine is activated by methionine adenosyltransferase to form S-adenosylmethionine (SAM), the primary methyl donor for most cellular methytransferase reactions including the methylation of DNA, RNA, proteins, phospholipids, and neurotransmitters (brain chemicals).

Čorejová A. Cessation of Nocturnal Enuresis after Intervention with Methylcobalamin in an 18-Year-Old Patient with Autism. J Child Adolesc Psychopharmacol. 2015 Dec;25(10):821-3. doi: 10.1089/cap.2014.0023. Epub 2014 Oct 17.
JB Adams, T. Audhya, S. McDonough-Means et al. Nutritional and metabolic status of children with autism vs. neurotypical children, and the association with autism severity. Nutrition and Metabolism, vol. 8, article 34, 2011.

RE Frye. Effectiveness of methylcobalamin and folinic Acid treatment on adaptive behavior in children with autistic disorder is related to glutathione redox status. Autism Res Treat. 2013;2013:609705. doi: 10.1155/2013/609705. Epub 2013 Oct 12.


RL, Hendren. Randomized, Placebo-Controlled Trial of Methyl B12 for Children with Autism. J Child Adolesc Psychopharmacol. 2016 Nov;26(9):774-783. Epub 2016 Feb 18.


James S Jill. Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism1,2. The American Journal of Clinical Nutrition. 2004;80:1611-7.


  1. J. James, S. Melnyk, G. Fuchs et al. Efficacy of methylcobalamin and folinic acid treatment on glutathione redox status in children with autism. American Journal of Clinical Nutrition, vol. 89, no. 1, pp. 425–430, 2009.


  1. J. James, P. Cutler, S. Melnyk et al., Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism. American Journal of Clinical Nutrition, vol. 80, no. 6, pp. 1611–1617, 2004.


  1. J. James, S. Rose, S. Melnyk et al. Cellular and mitochondrial glutathione redox imbalance in lymphoblastoid cells derived from children with autism. FASEB Journal, vol. 23, no. 8, pp. 2374–2383, 2009.


Y Zhang. Decreased Brain Levels of Vitamin B12 in Aging, Autism and Schizophrenia. PLoS One. 2016 Jan 22;11(1):e0146797. doi: 10.1371/journal.pone.0146797. eCollection 2016.