| ASA's 36th National Conference on Autism Spectrum Disorders (July 13-16, 2005) |
ASA Homepage |
| Friday, July 15, 2005: 3:30 PM-5:00 PM | |||
| 206 | |||
| #1224- Responding to Metabolic and Genomic Abnormalities: Improving Outcomes through Nutritional Biochemistry | |||
| New research in genomics will be discussed. It has enabled a more detailed understanding of the neuroscience and metabolism of autism. Since genes code for proteins and control metabolism through enzymes, supplementing the child’s metabolism in these areas would be expected to influence behavior and function. Interventions will be discussed. | |||
| Presenter: | - Jeff Bradstreet MD, FAAFP, is a professor of nutritional neuroscience and child development at ICDRC and Southwest College of Naturopathic Medicine. He received his medical degree from the University of South Florida and his residency at Wilford Hall, USAF Medical Center. He has published landmark studies in the role of mercury and measles virus in ASD. | ||
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Advances in genomic profiling has allowed us to focus our attention at specific areas of metabolic dysfunction. Straight forward assessment of biochemical markers can be used with genomic studies to determine best treatment interventions. We have looked at single nucleotide polymorphisms (SNP) in the methylation, sulfation and glutathione pathways in several hundred children with ASD. SNP are point mutations on the DNA which may interfere with critical enzymatic function or neurochemistry. We have addressed these with detailed metabolic studies and used specific nutritional biochemistry. Approximately 60% of children with ASD symptoms have a mutation in methionine synthase gene, compared to only 10% of controls (6.1 OR with p< 0.0001). This is a new and unique finding. Waly and colleagues observed mercury and thimerosal potently inhibits methionine synthase, and they have discussed the consequences of this impairment. Given the high prevalence of the mutation in methionine synthase, it appears likely this is critical defect influences susceptibility to environmental neurodevelopmental toxins. A nearly equal number of children have a homozygous deletion of the glutathione S-transferase (GST M-1) loci. A significant increase in polymorphisms in the catecholamine methyltransferase (COMT) system are also over-represented in ASD. This combination appears to interfere with normal methylation prior to catecholamine regulation, upregulation of catecholamines and increases in oxidative stress through peroxides which cannot be removed via glutathione reduction. Anecdotal observations of successful interventions with methylcobalomin (active B12) and other methyl-donors (folinic acid and trimethylglycine) have demonstrated significant interest and active prospective research is underway through two multicentered trials. Results of these research studies may be available by the time of the conference. Further, we have published increased total body burden of mercury in children with autism. Again anecdotal observations demonstrate a variety of mercury removal (chelation) protocols may have applications to autism treatment. These are under active investigation and findings, as available will be discussed at the conference as well. The attendee will understand the specific genomic and metabolic disorders present in autism. Available nutritional interventions will be clearly described and protocols discussed.
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