Autism: A Result of Toxic Environmental Exposures?
Recently, I came across an interesting article written by Jill Neimark for the magazine Discover (April 2007) reporting on the devastating derangements of autism being shown up in the gut and in the immune system that are possibly caused by toxic environmental exposures. This is not something new and such reports have appeared every now and then, creating some form of sensational news for the general public consumption.
Neimark (2007) has listed three revolutionary insights on autism spectrum disorder (ASD). First, ASD may not be rigidly determined. Instead, it may be related to common gene variants, known as polymorphisms, which may be derailed by environmental triggers. Second, according to her, affected genes may disturb fundamental pathways in the body and lead to chronic inflammation across the brain, immune system, and digestive system. Lastly, she said that inflammation is treatable. Certainly, this gives parents with autistic children some hope that autism is treatable and perhaps, preventable.
According to Prof Martha Herbert (cited in Neimark, 2007), a Harvard pediatric neurologist, autism should no longer to be seen as a disorder of the brain but as a disorder that affects the brain. It also affects the immune system and the gut. Many reported cases of autistic children placed on special diets have shown that they improved over a short time frame simply by avoiding certain foods (especially gluten and casein). This suggests that some subtype of autism probably comes from a kind of metablic encephalopathy - according to Prof Herbert, a systemwide process that affects the brain.
In another study on ASD conducted by a John Hopkins neurologist, Dr Carlos Pardo et al (2005), reported in the Annals of Neurology, inflammation in immune-responsive brain cells (known as neuroglia) have been found in autistic individuals between 5 and 45 years old. According to Pardo et al (2005), the inflammatory reaction appears to occur early and/or late in the course of the ASD. If it happens early, the brain development would be dramatically affected. One potential treatment approach is to downregulate the cortical immune response. Currently, Pardo and his team are conducting a test using minocycline (an anti-inflammatory antibiotic drug) to treat autistic children, and their findings are yet to be made known to the general public. The drug is already used to treat multiple sclerosis and Parkinson’s disease.
In yet another provocative study reported by Neimark (2007), a team led by Prof Jill James, director of the Autism Metablic Genomics Laboratory (Arkansas Children’s Hospital Research Institute) found that many autistic children do not manufacture as much of glutathione in their body as neurotypical children do. Glutathione is the cellular anti-oxidant that is crucial for removing toxins. If cells lack sufficient anti-oxidants, they experience oxidative stress (often found with chronic inflammation). Prof James et al (2006) reported their findings in the American Journal of Medical Genetics that common gene variants supporting the glutathione pathway could be associated with ASD risk. This pathway is linked metabolically to the methylation pathway. According to James et al (2006), methylation is the basic biochemical process that regulates which genes are expressed, and hence, abnormality in methylation could result in some form of a disease. Since the methylation pathway provides the precursors to glutathione, impairments in this pathway can lead to oxidative stress. However, such a problem is treatable with targeted nutritional intervention. According to James et al (2006), autistic children who have taken supplements that include the key nutrients (folic acid, trimethylglycine, and methyl-B12) essential for the methylation pathway showed a significant increase in important markers of methylation and glutathione synthesis.
Prof James (cited in Neimark, 2007) has hypothesized that mitochondrial dysfunction could be one possible trigger of ASD since mitochondria are where most free radicals (they play a role in oxidative stress) are produced. Faulty mitochondria will reduce the production of ATP and this in turn increase the free radicals in our body and, in turn, deplete the glutathione. Hypothetically speaking, if that is correct, then nutrients such as coenzyme CoQ10, magnesium and acetyl-L-carnitine that help to stablize the mitochondria will be useful in treating the dysfunctional condition.
Finally, to quote Prof Issac Pessah (Chairman, Molecular Biosciences, University of California at Davis) (cited in Neimark, 2007): “… glutathione balance in the kids is potentially very important in terms of toxic environmental exposures.” In an article reported in The Lancet (December 2006), it is summarily reported that industrial chemicals may be impairing the brain development of children around the world, resulting in the many reported autism cases we see today - a new frightening disorder of the present generation.
Copyright © 2007 Dr Noel K.H. Chia. All rights reserved. see Disclaimer