Pilot Study of the Effect of Methyl B12 Treatment on Behavioral and Biomarker Measures in Children with Autism

Bertoglio, Kiah; James, S. Jill; Deprey, Lesley; Brule, Norman; Hendren, Robert L.

doi:10.1089/acm.2009.0177

Cited by 83 publications

(75 citation statements)

References 18 publications

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“…One prior small randomized, placebo-controlled trial of methyl B12 in 30 children with ASD did not find statistically significant improvements in the overall Clinical Global Impressions (CGI) score; however, a subset of children (9/30) showed clinically significant improvements in the CGI and improvements in glutathione levels, again suggesting that improvements in the antioxidant defense might lead to improvements in symptoms (Bertoglio et al 2010). …”

Section: Introductionmentioning

confidence: 99%

Randomized, Placebo-Controlled Trial of Methyl B12 for Children with Autism

Widjaja

et al. 2016

Journal of Child and Adolescent Psychopharmacology

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Objective: Children with autism spectrum disorder (ASD) have been reported to have reduced ability to methylate DNA and elevated markers of oxidative stress. We sought to determine if methyl B12, a key metabolic cofactor for cellular methylation reactions and antioxidant defense, could improve symptoms of ASD. Methods: A total of 57 children with ASD were randomly assigned to 8 weeks of treatment with methyl B12 (75 lg/kg) or saline placebo every 3 days in a subcutaneous injection. The primary outcome measure was overall improvement in symptoms of ASD as measured by the Clinical Global Impressions-Improvement (CGI-I) score. Secondary outcome measures included changes in the Aberrant Behavior Checklist (ABC) and the Social Responsiveness Scale (SRS). Laboratory measures of methionine methylation and antioxidant glutathione metabolism were assessed at baseline and 8 weeks.Results: A total of 50 children (mean age 5.3 years, 79% male) completed the study. The primary outcome measure -the clinician rated CGI-I score -was statistically significantly better (lower) in the methyl B12 group (2.4) than in the placebo group (3.1) (0.7 greater improvement in the methyl B12 group, 95% CI 1.2-0.2, p = 0.005). Clinical improvement among children treated with methyl B12 was positively correlated with increases in plasma methionine ( p = 0.05), decreases in S-adenosyl-lhomocysteine (SAH) ( p = 0.007) and improvements in the ratio of S-adenosylmethionine (SAM) to SAH ( p = 0.007), indicating an improvement in cellular methylation capacity. No improvements were observed in the parent-rated ABC or SRS. Conclusions: Methyl B12 treatment improved clinician-rated symptoms of ASD that were correlated with improvements in measures of methionine metabolism and cellular methylation capacity. Clinical Trial Registry: Efficacy Study of Subcutaneous Methyl B12 in Children with Autism: NCT01039792 (clinical trials.gov1).

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Section: Introductionmentioning

confidence: 99%

Randomized, Placebo-Controlled Trial of Methyl B12 for Children with Autism

Widjaja

et al. 2016

Journal of Child and Adolescent Psychopharmacology

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“…In the B12 randomised controlled trial by Bertoglio et al (2010) reported side effects were increased hyperactivity and increased mouthing of objects. No serious adverse events were reported.…”

Section: Vitamin B12mentioning

confidence: 99%

Complementary Medicine Products Used in Autism - Evidence for Efficacy and Safety

Semple¹,

Hewton²,

Paterson³

et al. 2011

Autism Spectrum Disorders - From Genes to Environment

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“…As a result, caregivers may elect to implement CAM interventions to treat or prevent nutritional deficiencies. Oxidative stress (Villagonzalo et al 2010) Deficiency (Clark et al 1993;Steinemann &Christiansen 1998;Ming et al 2005) Reconnect retinoid receptor pathways (Megson 2000) Immunomodulation (Megson 2000) Antioxidant ( Gut dysbiosis and inflammation results in decreased GI synthesis of B12 and/or absorption (Kidd 2002b;Erickson et al 2005) Trans-methylation and trans-sulphation pathway abnormalities Bertoglio et al 2010) causing oxidative stress (Villagonzalo et al 2010) Normalise B12 levels Correct folate/methionine metabolite profile and other indexes of oxidative stress James et al 2009;Bertoglio et al 2010) www.intechopen.com Trans-methylation pathway abnormalities Bertoglio et al 2010) causing oxidative stress (Villagonzalo et al 2010) Neurotransmitter level abnormalities (Lam et al 2006) Correct folate/methionine metabolite profile and other indexes of oxidative stress James et al 2009 Neurotransmitter level abnormalities (Lam et al 2006) Folate/methionine pathway abnormalities Bertoglio et al 2010) Oxidative stress (Villagonzalo, et al 2010) Immunoadjuvant (Graber et al 1981) Modulate neurotransmitters (Kern et al 2001) Methyl donor (Kern et al 2001) Antioxidant (Kern et al 2001) General autistic behaviours Vitamin C Neurotransmitter level abnormalities (Lam et al 2006) Oxidative stress (Villagonzalo et al 2010) Immune system dysfunction (Goines&Van de Water 2010)…”

Section: Nutritional Deficienciesmentioning

confidence: 99%