Sulfate is a vital nutrient required for foetal development, and for this reason, normally flows in abundant supply from the mother to the foetus. The developing foetus receives sulfate from the mother through the placenta and later through colostrum, the mother's first milk. Neonatal development depends heavily upon sulfate for myelination in the brain, and for modulation of neurotransmitters. For instance, a reduced supply of sulphate can impair the action of the neurotransmitter, serotonin. Increased levels of serotonin have been identified in up to 48 percent of children diagnosed with autism. It is important to realise that increased levels of serotonin can affect day to day brain functioning. Interestingly, increased serotonin during prenatal brain development has been found to cause autistic symptoms in animal models.
Several sulfate-dependent neurodevelopmental processes have been shown to be defective in association with autism. For example, it has been recently shown that children with autism (specifically children aged 5-16, diagnosed PDD-NOS and Asperger's) have significantly lower levels of plasma sulfate, including both free and total sulfate. The energy producing compound adenosine triphosphate (ATP) is required in the kidney to reabsorb sulphate (recycling of sulphate is important because sulphate is poorly absorbed from the gastrointestinal tract, and conversion from the amino acid, cysteine, is low. Significant correlations between ATP availability and free and total plasma sulfate has given rise to the theory that decreased ATP is a significant contributor to decreased sulphate levels in children diagnosed with autism. The most recent research paper on this topic has indicated that 56 percent of participants (PDD-NOS and Asperger's) presented with sulfate levels below the neurotypical reference range.
Moreover, it is acknowledged that low plasma sulfate can impair a process known as methylation, in children diagnosed with PDD-NOS and Asperger's. Children diagnosed with the foregoing forms of autism have been shown to present with low levels of the methyl donor, S-adenosyl methionine (SAMe). SAMe is formed from the amino acid, methionine, by the enzyme, methionine adenosyl transferase, which requires ATP. It is suggested that low levels of ATP may not only compromise plasma sulphate, but decrease levels of SAMe. Methionine in the body comes partially from the diet (essential amino acid) and partially from the recycling of homocysteine (plasma amino acid) to methionine. The synthesis of methionine requires methyl B12 and 5-methyl-tetrhydrofolate, a derivative of folic acid. Impairment in the re-methylation of methionine has also been associated with a genetic mutation for MTHFR.
Beyond methylation, children with PDD-NOS and Asperger's have, recently, been shown to present with low levels of biotin (B7), and trends towards lower levels of vitamin B5, vitamin E and total carotenoids. Please note, however, that the previous nutrients are also likely to be below reference range in children with no diagnosis of PDD-NOS or Asperger's. There is also evidence of compromised choline, B6 (P-5-P) and vitamin D conversion in children diagnosed with PDD-NOS and Asperger's. Before implementing a regime of supplementation, I strongly advise that you discuss nutrient deficits with a qualified health care provider.
If you have any questions regarding this post please contact:
Mark Hinchey, Naturopath: Autism; 601 Glebe Road Adamstown, Newcastle, Australia.
Contact: (02) 40235959 or 0432234822 or firstname.lastname@example.org