Tag Archives: autism

An Exploration of Thimerosal Toxicity and the Autistic Brain: Part I

In their paper, “Thimerosal Exposure and the Role of Sulfation Chemistry and Thiol Availability with Thimerosal,” Janet Kern, Boyd Haley, David Geier, Lisa Sykes, Paul King and Mark Geier explore recent studies that suggest children with the autism spectrum disorder(ASD) have physical biomarkers for the disorder:  abnormal levels of sulfation chemistry, limited thiol ability, and lower levels of glutathione (GSH—a type of thiol) that lead to weaker oxidation capacities and detoxification. Specifically, Kern et al. discuss the extent to which the hypothesis that GSH and sulfation chemistry impact how the body reacts to Thimerosal, a mercury-containing compound that was used as a preservative in many standard childhood vaccines in the United States and around the world. Kern wondered: could a combination of abnormal sulfation chemistry, lower GSH, and limited thiol ability make an individual’s susceptibility to the toxic effects of Thimerosal greater?


While many characterize autism as a psychological/behavioral disorder, some researchers, including Mark and David Geier, have shown that ASD individuals also demonstrate physical abnormalities. These physical symptoms include seizures, sleep disorders, gastrointestinal issues, and incontinence, among others. The presence of physical symptoms suggests that there should be metabolic biomarkers for ASD, given that it is in fact a disorder with symptoms beyond abnormal neurodevelopment.

We also know that autism can be a regressive disorder, in which individuals aren’t born as autistic, but rather only begin to display symptoms of ASD after 15-24 months of age. Research offers widely varying rates for the frequency of autistic regression, but the lowest frequency reported among populations of ASD sample studies has been 15% to more than half of all cases. To determine how a potential environmental factor like Thimerosal could affect ASD, Kern et al. looked specifically at ASD individuals with regressive autism.

A Word on Thimerosal

Even though Thimerosal began to be phased out of some common childhood vaccines around 2000, at the same time, the CDC began to encourage pregnant women in their 2nd and 3rd trimesters, and infants as early as 6 months, to receive flu vaccines, vaccines which were still preserved with Thimerosal. Today, more than half of all flu vaccines are preserved in Thimerosal.  Thimerosal is not found in nature, and its toxicity has been proven in many studies; in fact, it’s the most toxic non-radioactive metal to fetal and neuronal cells.

GSH, Thiols and Sulfation

Let’s return to Thimerosal’s connection to thiols and GSH. Thiols are known to mitigate the toxicity of Hg, and in turn, the toxicity of Thimerosal; studies have shown that the extent of Thimerosal’s toxicity to the body is largely dependent upon the cellular content of the GSH thiol. The degree of cell damage after Thimerosal exposure is highly dependent upon the availability of these thiols; yet paradoxically, Thimerosal decreases their production and effectiveness when introduced. Studies have shown that GSH levels in mice not only decreased after exposure to Thimerosal, but persisted at low levels for weeks after exposure. Exposure to mercury (the toxic element of Thimerosal) has also been shown to hinder the development of the brain’s GSH antioxidant system, which can cause oxidative damage.

It’s also been demonstrated that individuals with ASD have unusual sulfation chemistry, to the extent that researchers believe it’s the result of either faulty sulfate production or use that exceeds the body’s rate of replenishment.  Specifically, ASD individuals maintain approximately 50 times the sulfite levels of control children. It’s important to note here that sulfite is an extremely toxic compound that, in a properly functioning body, is converted to the non-toxic compound sulfate. As Kern et al. point out, studies have shown that Hg has the potential to interrupt this conversion process, and thus result in higher levels of toxic sulfite in the body. In fact, children with abnormal transulfuration (a term used to describe this conversion process) also are found to have lower levels of accompanying transulfuration metabolites. Interestingly, the majority of children with these levels developed autism after 15 months of age, suggesting their autism is regressive.

Researchers have also discovered that the lower an individual’s sulfate levels, the more severe the nature of their autism; this was also found to be the case with GSH levels. In other words, these biomarkers play a role in the manifestation of autistic symptoms. Should they be limited, by something like Hg, which is known to affect both GSH and sulfation, research suggests the severity of autistic symptoms increases.  All of the relationships Kern et al. have analyzed between Thimerosal and GSH/sulfation lay the framework, as detailed in the second half of the blog, for a compelling argument for Thimerosal’s ability to affect some ASD children more severely than others.


Is Autism a Neurodegenerative Disorder?

How does autism affect the brain? This is a question that’s motivated researchers in pursuit of understanding the autism spectrum disorder (ASD) for years. We already know that ASD is a neurodevelopmental disorder that impairs an individual’s ability to communicate, interact socially, comprehend, and behave the way neurotypical individuals do. However, pinpointing ASD’s root cause may be aided by an exploration into the neurodegeneration hypothesis. This hypothesis, which suggests that ASD can be regressive, stems from reports that some autistic children acquired neurological impairments after certain skills were developed. In other words, rather than being born with the inability to communicate, interact, and comprehend in a typical fashion, children can acquire these skills and then lose them. This regression suggests that development is somehow interrupted, rather than impaired from birth. ASD regression is said to affect anywhere between 15% and 65% of individuals on the autism spectrum. Whether autism can be officially considered a neurodegenerative disorder has remained under debate.

Recent research from David Geier, Mark Geier, Janet Kern, and Lisa Sykes probes deeper into the neurodegeneration hypothesis in their 2013 paper, “Evidence of Neurodegeneration in the Autism Spectrum Disorder.” According to the researchers, when synthesizing an array of related research, it can be determined that there is enough credible evidence to conclude ASD can be a neurodegenerative disorder.

To start, widespread post-mortem evaluations of individuals with ASD demonstrate that these individuals experienced a loss of neuron cells (a defining characteristic of neurodegeneration). It’s also been found that individuals with ASD have fewer neuron cells and pyramidal cells in their amygdala than control subjects. Further, the role of microglia, non-neuron cells that maintain homeostasis in the body and can contribute to the development of other neurological disorders, may also point to neurodegeneration in ASD individuals. Studies have found that these microglia can be responsible for the dissolution of neurons, and can also produce toxic cytokines that can damage neurons and lead to neurodegeneration.  Findings from a number of recent studies support the hypothesis that microglia activation could be evidence of degeneration, given that many regions of the brain with activated microglia, most prominently the cerebellum, were found to be inflamed in those with ASD.

The toxins that can be released by microglia activation, which include nitric oxide, reactive oxygen species, and a number of proinflammatory cytokines, also point to neurodegeneration. These inflammatory cytokines have been found to be present in other neurodegenerative disorders, including Alzheimer’s disease, Parkinson’s disease and Multiple Sclerosis, yet have in appeared in the spinal cords and brains of those with ASD, too. An increase in the production of ROS (reactive oxygen species), is also prominent in neurodegenerative diseases like ALS, Parkinson’s disease and Alzheimer’s disease, as ROS ultimately results in the loss of neuron cells. As with individuals of these neurodegenerative disorders, those with ASD also maintain high levels of cell death as a result of oxidative stress.

Studies have also revealed that an oxidative stress damage marker that appears in the brains of those with neurodegenerative disorders, 8oHdG, appears at 63% higher levels in those with ASD than in control subjects.

While “Evidence of Neurodegeneration in Autism Spectrum Disorder” presents compelling evidence that ASD can in fact be considered a neurodegenerative disorder, as the researchers assert, its link to toxic exposures must also become more widely studied and accepted. Prolific research has suggested toxins can trigger the onset of ASD, yet this research has been largely dismissed by institutions like the World Health Organization because ASD is not currently classified as a neurodegenerative disorder. With additional research and awareness, this may soon change.