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Solving the Autism Puzzle: The Science They Don’t Want You To Know About Print E-mail
Written by Brendan McBride   
Sunday, 21 August 2005
Brendan McBride is a co-founder of Dads Against Mercury ( and the father of a two-year old child diagnosed with autism. A Texas-based appellate attorney, Brendan specializes in the use and interpretation of scientific evidence in the courtroom. Brendan recently accepted an invitation to join the Science Committee of Safeminds ( Dads Against Mercury asked Brendan to prepare this brief essay looking at the most up-to-date science regarding the Autism/Mercury debate.

Mercury advocates, those in the vaccine industry, and some hired guns in the media continue to defend the use of neurotoxic ethylmercury in infant vaccines, hoping the public will ignore the growing body of research demonstrating that thousands of cases of autism and other neurological disorders are probably related to mercury exposure.   Having no alternative explanation for the sudden surge in autism cases, which happened to coincide with a nearly three-fold increase in the amount of ethylmercury injected into American children on the CDC’s recommended vaccine schedule, the vaccine industry and its spokesmen want the American public to be satisfied with the vague assertion that it’s "just genetics."

While genetics definitely plays a role in autism, there is also no doubt that an environmental factor has also played a crucial role in the sudden explosion in rates of autism over the past 15 years - from 1 in 2,500 children in the eighties to 1 in 166 by 2004 (1 in 80 boys). Despite the position taken by the Centers for Disease Control (CDC) and the Institute of Medicine (IOM) that mercury has nothing to do with autism, the most current research is beginning to show that autism may in fact be caused by an inherited (i.e. genetic) mercury "efflux disorder."

An "efflux disorder" has to do with a body's reduced ability to handle a toxin. Under normal circumstances, a body would rid itself or flush out— literally, efflux— a toxin so that it would pose no harm. But in some instances this efflux process does not work properly or adequately. We know of several efflux disorders already. Wilson's Disease, for example, results from a body’s inability to properly excrete (or efflux) copper. Rather than flushing the excess copper out of the body, those who suffer from Wilson’s Disease experience a build-up of copper in the liver and brain tissue. Wilson’s Disease can be a fatal efflux disorder if not diagnosed properly. It now effects roughly 1 in 30,000 people.

A growing body of research indicates that a similar phenomenon is occurring with regard to mercury and autism. Specifically, studies continue to support the theory that autism may be caused by a genetically inherited mercury efflux disorder which leads to excessive accumulation of inorganic mercury in brain tissue.

Inorganic mercury, white matter and Thimerosal

There is a critical distinction that must be understood.  The likely environmental trigger in question is not vaccines nor is it mercury in vaccines.  It is the accumulation of "inorganic mercury" in brain tissues. 

A recent study by Harvard Pediatric Neurologist Dr. Martha Herbert conducted at Massachusetts General Hospital demonstrated that people diagnosed as autistic have excess and asymmetrical amounts of microglial tissue ("white matter") in their brains compared to non-autistic people - creating a "big brain" phenomenon in people diagnosed with autism (Herbert 2004, 2005).  Interestingly, an earlier biological study published in Neurotoxicology in 1996 demonstrated that the accumulation of inorganic mercury in brain tissue resulted in just such a build-up of microglial tissue (Charleston 1996).  In other words, research has proven that the build-up of inorganic mercury in the brain leads to increased white matter— and people diagnosed with autism have been shown to have greater levels of white matter in their brain tissue.

Inorganic mercury can find its way into brain tissue from several sources. For example, it can come from mercury-based dental fillings (amalgams) (Nylander 1987; Godfrey 2003). But a major source of exposure appears to be to the mercury-containing organic compounds methylmercury (ingested by eating mercury-tainted fish) and ethylmercury (injected in Thimerosal, a preservative used in vaccines, Rhogam shots and other medicinal products).  These organic compounds are broken down in the body releasing inorganic mercury, which is ordinarily bound by certain proteins so that the inorganic mercury can be safely effluxed.  However, exposure to high levels of methylmercury and ethylmercury result in the excess inorganic mercury finding its way into the tissues of the brain, liver, and kidneys.  (Burbacher 2005)  We know now that injected ethylmercury breaks down faster in the body and as such releases inorganic mercury much faster than the ingested methylmercury increasing the danger that ethylmercury poses to brain tissues (Burbacher 2005). 

Representatives of the IOM have argued to the contrary— concluding that ethylmercury (in Thimerosal) poses less of a threat than methylmercury (in fish). They based their conclusion on the fact that studies show that ethylmercury "clears the blood" faster than methylmercury. IOM assumed that because ethylmercury disappears from the bloodstream faster, then it must be headed out of the body faster and is therefore less dangerous. The IOM misinterpreted the data.

The IOM did not appreciate that the culprit was not mercury blood levels, but rather inorganic mercury in brain tissue. Further study has shown that while injected ethylmercury may clear from the blood faster, its rapid breakdown and more sudden release of inorganic mercury poses a much more dire threat to health. Injected ethylmercury may result in the accumulation of twice as much inorganic mercury in brain tissues compared to ingested methylmercury (Burbacher 2005). 

The study's authors specifically criticized reliance on "blood clearance levels" (as the IOM had done when it purported to "clear" Thimerosal in its 2004 report), because such an approach misses the crucial fact that this faster clearance rate greatly increases the likelihood of inorganic mercury finding its way into the brain where it stays for a much longer period of time. Thus, the IOM made a crucial mistake in understanding the biological evidence in its report. 

Dr. Herbert's recent work revealed the presence of elevated white matter in autistic brains. The Charleston study linked increased white matter to inorganic mercury in brain tissue. And there is good reason to believe that Burbacher's study demonstrates precisely why the ethylmercury-laced Thimerosal is likely the trigger that cause autistic symptoms. Remember, the injection of ethylmercury into children (via Thimerosal in vaccines) increased to dangerous levels between 1989 and 1992. Over the next ten years the rate of autism in America increased on average 1000%.

Glutathione & Efflux: Key Pieces of the Autism Puzzle

There is one important question still to answer. If ethylmercury is so dangerous, why didn’t every child get autism? Why did the body’s natural defense against the toxin— the efflux system— appear to work very well in some children and not in others? The research current being conducted to answer these questions is very compelling and complements the studies discussed above.

In studies of hair samples from autistic children, mercury levels were shown to contain on average less than 50% of the mercury contained in hair samples from non-autistic children (Holmes 2001). In other words, children diagnosed with autism were excreting much less mercury from their bodies than children that didn’t have autism. 

A recent study by toxicologists at Arizona State University in conjunction with MIT duplicated Holmes’ results.  That second study also found autistic hair samples to be significantly lower in mercury (43% on average) (Adams 2005). One thing is clear: these studies show an anomaly related to mercury in autistic children. Children with autism do not process or efflux mercury in the same way that other children do. 

This is where the genetic link comes in. Some children inherit a reduced ability to naturally bind and excrete mercury— what scientists would call a "mercury efflux disorder."  For children with such a mercury efflux disorder, even low doses of mercury (that most other children might be able to flush out quite easily) would cause an accumulation of inorganic mercury in their brains. This mercury poisoning or build-up of inorganic mercury in the body would then cause the symptoms of mercury poisoning, which are strikingly similar to the symptoms of autism (Bernard 2001).

The mercury efflux disorder theory is further corroborated by research showing that autistic children have substantially reduced levels of the key protein essential to safely binding and excreting toxic heavy metals: glutathione (James 2004).  The James study shows that children with regressive autism have consistently elevated levels of oxidative stress compared to other children. Individuals with reduced glutathione suffer chronic oxidative stress and are more vulnerable to toxins like mercury (James 2004). Dr. James also found that glutathione protects brain cells from oxidative damage and cell death caused by thimerosal exposure (James 2005).

Glutathione binds with cadmium, lead, mercury, nickel and other heavy metals (Stohs 1995). The resulting, water-soluble chemical is more easily filtered out of the body. Consequently, children deficient in 'active glutathione' will not be able to excrete metals as quickly. For example, cells treated with chemicals to inhibit glutathione recycling are much more sensitive to manganese toxicity (Desole 1997). People chronically exposed to arsenic in drinking water have increased oxidative damage and decreased antioxidant potential (Wu 2001).

As a result, excessive exposure to mercury essentially opens the door to environmental insult by a whole host of toxic heavy metals, including lead, cobalt, antimony and chromium, against which the body’s primary defense is a ready supply of active glutathione. Several studies confirm the toxicity of metals to brain cells at doses similar to those experienced by vaccinated children (Makani 2002, Shanker 2003, Baskin 2003, Waly 2004, Ueha-Ishibashi 2004).

For children born with a diminished efflux system, the results of injecting ethylmercury are sadly predictable. Children begin life already with a background level of in utero mercury exposure that could be exacerbated by further exposure to ethylmercury in vaccines. For children who have inherited this efflux disorder, they lack sufficient defenses against toxic heavy metals so that when the surge of "inorganic mercury" is released after a thimerosal injection, there is more free inorganic mercury to enter brain tissue and cause neurological damage because there are reduced amounts of glutathione present to bind and protect against the neurotoxic mercury.

According to Dr. H. Vasken Aposhian, Professor of Pharmacology at the University of Arizona, since children are exposed to mercury in the womb through their mother's blood, later exposure in infancy and early childhood through vaccines may simply add to the mercury burden in autistic children or may be enough to trigger the efflux disorder in those children genetically predisposed to mercury poisoning (Aposhian 2004).

Numerous studies link Thimerosal with neurological damage at concentrations similar to those that were experienced by children vaccinated in the 1990s. Researchers found mercury concentrations between 10 and 30 nanomoles per liter (nM) in premature infants given a single Hepatitis B shot at birth (Stajich 2000). Mercury concentrations ranging from 4 to 21 nM are reported in young children when measurements were collected 3 to 20 days after vaccination (Pichichero 2002). Four recent studies of thimerosal toxicity to human brain cells report oxidative damage, interruption of methylation, and decreased cell energy resulting from Thimerosal exposure (Waly 2004, Baskin 2003, Ueha-Ishibashi 2004, Makani 2002). Several studies documented the protective benefits of antioxidants, especially glutathione, which attenuate the damages caused by Thimerosal (Makani 2004, James 2005, Shanker 2003).

Putting The Pieces Together

Once it is understood that a genetic disorder affecting glutathione levels may be a key factor in causing autism, many other important pieces of the autism puzzle then fall into place.

For example, it has long been known that boys are substantially more susceptible to autism than girls. Seventy to eighty percent of autistic children are boys. Studies of tissue samples from newborn infants showed significantly higher glutathione levels, glutathione production, and cell survival in response to oxidative stress in cells from girls compared to boys (Lavoie 1997). Studies of brain injury in newborns have found that inherently stronger glutathione capacity in females protects their brain cells from damage after a traumatic injury. Glutathione concentrations remain constant in females but they drop by as much as 80 percent in males after a brain injury (Du 2004). A boy born with a genetic predisposition for reduced glutathione levels (the genetic factor) has a substantially reduced defense system to protect his brain against the release of neurotoxic inorganic mercury produced when Thimerosal is broken down in the body (the environmental trigger).

The common coincidence of gastrointestinal disorders in autism also supports the mercury efflux theory. Glutathione is vital to proper intestinal function. Deficits in glutathione cause degeneration of the jejunum and colon (Martensson 1990). Research suggests that oral administration of glutathione protects intestines against toxicity associated with inflammatory diseases, oxidative damage, and other toxins (Martensson 1990). Rodent studies highlight the role of glutathione in preventing positively charged substances—like metals—from passing through the gut (Samiec 2000).

Autistic children commonly suffer from intestinal disorders (Bernhard 2001). In these 'leaky gut' disorders, undigested proteins pass through the gut and cause oxidative damage to the brain and nervous system (White 2003). This is similar to PKU, a metabolic disorder in which the toxic accumulation of undigested phenylalanine causes oxidative damage leading to autistic-like symptoms. PKU can be averted in laboratory animals by antioxidant supplementation (Martinez-Cruz 2002).

Reports from thousands of parents regarding the use of "mercury chelation" therapy (the same type of medical intervention used to treat lead and copper poisoning), further confirm that the culprit in causing autistic symptoms is mercury. Many parents who have treated their autistic children with heavy metal chelators (such as DMSA and DMPS) report substantial reversal of autistic symptoms including the re-emergence of language and social interaction. Admittedly, evidence for the effectiveness of chelation in reversing autism is largely anecdotal at this time. However, parents have consistently been ahead of the science on this issue and large numbers of anecdotal reports from parents should not be dismissed. Rather, this type of evidence should be considered sufficient to require further inquiry such as large-scale clinical studies.

For many years parents of autistic children reported that their children suffered from an autistic "regression" – that their children’s mental, social and language development seemed normal for the first year or two of life and then suddenly regressed (often coinciding with vaccines). Such concerns were dismissed outright by most pediatricians. Despite significant doubt by the scientific community that these children were regressing, recent research from the University of Washington now confirms that the parents were right all along. Many autistic children develop normally and then suffer a sudden regression into autism (Dawson 2005).

Other large scale studies are linking mercury exposure to increased incidents of autism in America. A recent study by the University of Texas at San Antonio comparing rates of environmental release of mercury from coal-burning plants in Texas counties to reported rates of autism from local special education programs, demonstrated a correlation between mercury exposure and autism. For every 1000 lbs. of environmentally released mercury, reported autism cases increased by 61% (Palmer 2005).

Although the symptoms of mercury poisoning can vary greatly, and may depend on a number of factors related to the nature of the exposure and the individual exposed, the symptoms of autism are all common and recognized symptoms of mercury poisoning (Blaxill 2003). Research confirms, for example, a dose-response correlation between prenatal methylmercury exposure and deficits in attention, memory and language (Weihe 2003).

Where do we go from here?

All of this is to say that there is very real, peer-reviewed and published science, performed by very real scientists to support a possible link between autism and mercury exposure. The mere fact that a genetic component is also at work does not exclude the possibility that autism is related to environmental exposure to mercury generally, or to Thimerosal in particular - especially given the heightened risk that Thimerosal injections can cause accumulation of inorganic mercury in brain tissue.  Moreover, epidemiological studies of foreign populations with different Thimerosal exposure levels, and where no effort has been made to account for alternative mercury exposures, neurological disorders less severe than autism, or the genetic frequency of the efflux disorder, are meaningless. 

Simply put, more research needs to be done into the established connection between mercury exposure and autism.  For example, a study of brain tissue from autistic persons to confirm whether autistic brains do indeed have elevated inorganic mercury levels is a logical next step and should be a top priority. 

Full-scale clinical research on mercury chelation and other possible treatments should be performed. And objective, independent epidemiological research of American children - with a full understanding of the biological research - should eventually be performed to assess the extent of the damage.

But the scientific debate is far from settled. And despite what the CDC would have the public believe, it is not between "parents" and "science." If anything, the debate is between toxicologists - who specialize in toxicity and efflux disorders - and pediatricians – who don’t.

Ideally, a double blind study of the side effects of injecting Thimerosal into human infants is what current medical science requires before declaring a substance "safe" for human use.  Given the obvious dangers of injecting ethylmercury into human infants, such a study would never be approved.  Yet, Thimerosal proponents continue to insist ethylmercury injections are "harmless" despite decades of research showing that it is very harmful even in trace amounts. 

In fact, research published in Pediatrics demonstrates a pregnant woman's body flushes large amounts of mercury into the unborn fetus (Ramirez 2000), which caused the FDA to issue very public warnings to pregnant women about eating fish.  At the same time, physicians continued injecting Thimerosal-containing Rhogam and Microgam shots into pregnant women for at least three more years after it was well known where that mercury would end up: in the tissues of the defenseless fetus.  And based on recent research comparing the two types of mercury exposure, we now know those injections were probably much more dangerous than eating tuna (Burbacher 2005).

It is false, or dangerously ignorant, to suggest that there is no scientific evidence to support a possible connection between mercury exposure and autism.  The public needs to know that there is much more to this issue than has been reported by the CDC, IOM and the American Academy of Pediatricians. There is very real science— but it’s science they don’t want you to know about.


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