THE AUTISM EPIDEMIC

Alex Psihogios

April 22, 2009

The Controversy of Autism

The incidence of autism has steadily increased from1/10,000 during the 1970’s to1/150 as of 2008.

This enormous increase in the diagnosis of autism has sparked obvious questions about causality.

Possible explanations include the changing diagnostic criteria for autism (broadening of the autism spectrum), the ability to diagnose the disorder at an earlier age (and therefore, the ability to reassess those who did not receive the autism diagnosis as a child), and environmental contributions (e.g. from childhood vaccines).

Vaccines and Autism

At the same time that the incidence of autism was growing, the number of childhood vaccines containing Thimerosal (a mercury containing preservative) was growing, increasing the amount of ethylmercury to which infants were exposed threefold.

A growing number of scientists and researchers believe that a relationship between the increase in neurodevelopmental disorders of autism, attention deficit hyperactive disorder, and speech or language delay, and the increased use of thimerosal in vaccines is plausible and deserves more scrutiny.

Toxins in vaccines can have devastating effects on children who are genetically predisposed to retain environmental toxins and metals.

Despite the growing amount of research regarding the links between autism and vaccinations, the Food and Drug Administration (FDA), the Institute of Medicine (IOM), the Center for Disease Control and Prevention (CDC) and other government officials continue to deny any causal link.

Dr. Bernadine Healy

Former director of the National Institutes of Health and member of the Institute of Medicine.

In an 2008 interview with CBS news, Healy discussed the possibility that certain children could be more vulnerable to the adverse side effects of vaccines.

She disagrees with the IOM’s 2004 statement that denied any causal link with vaccines and autism because the susceptibility of certain children to harmful side effects has not been adequately researched.

She does not agree with the decision to abandon research because of the government’s fear that what might be found may deter caregivers from obtaining vaccinations for their children.

Video Clip

2008 CBS Interview with Dr. Bernadine Healy

Outline of Presentation

I. Mercury: Properties and Effects on the BodyII. Thimerosal and VaccinesIII. A 2008 Summary of Evidence Supporting the

Links between Mercury Exposure and ASD Development

IV. Pivotal Past ResearchV. Analyses of Recently Published StudiesVI. A Look at the Hannah Poling 2008 Court CaseVII. Arguments Against Causal LinksVIII. Conclusions

Quick Facts About Mercury Heavy metal Widespread and persistent

in the environment. Coal-burning power plants

are the largest human-caused source of mercury emissions to the air in the United States.

Mercury in the air settles in water or on land. Once deposited, certain microorganisms can change mercury into methylmercury.

Methylmercury is a highly toxic form that builds up in fish, shellfish and animals that eat fish (including humans).

Mercury and the Body

Mercury adversely affects multiple systems of the body including the nervous system, the immune system, the gastrointestinal tract, the cardiovascular system, as well as the kidneys and liver.

Mercury interferes with serotonin release and transport, alters dopamine metabolism, elevates glutamate, elevates norepinephrine and epinephrine, and causes demyelination.

“The fetus is considered much more sensitive than the adult. Prenatal exposures interfere with the growth and migration of neurons and have the potential to cause irreversible damage to the developing central nervous system”. (Toxicological Effects of Methylmercury, 2000).

Major Sources of Infant Exposure to Mercury

Maternal seafood consumption (methylmercury).

Maternal mercury amalgam dental fillings.

Environmental mercury release

Thimerosal in childhood vaccines.

Thimerosal

Thimerosal is a mercury containing preservative used in some vaccines and other products since the 1930’s.

It is 49.6% mercury by weight and is metabolized/degraded into ethylmercury. Studies have suggested that ethylmercury is processed

differently in the body than methylmercury. Since ethylmercury is processed more quickly and excreted more rapidly, skeptics infer that ethylmercury is less likely to cause harm.

The Federal Government has established no safety threshold for ethylmercury.

In 1999, it was discovered that the amount of Thimerosal in childhood vaccines far exceeded FDA guidelines (Adams and Romdalvik, 2007) Federal health officials have conceded that the amount of

thimerosal in vaccines exceeded the EPA threshold of 0.1 micrograms per kilogram of bodyweight. In fact, the amount of mercury in one dose of DTaP or Hepatitis B vaccines (25 micrograms each) exceeded this threshold many times over.

Government Reactions to Thimerosal Concerns

July 1999, U.S. Department of Health and Human Services agencies, The American Academy of Pediatrics; and vaccine manufacturers agreed that thimerosal should be reduced or eliminated in vaccines as a precautionary measure and to reduce exposure to mercury from all sources.

According to the FDA, as of 2001, vaccines manufactured for the U.S. market and routinely recommended for children ≤ 6 years of age have contained no thimerosal or only “trace” amounts (≤ 1 microgram of mercury per dose remaining from the manufacturing process), with the exception of inactivated influenza vaccine.

Vaccines Containing Thimerosal (CDC, 2008)

Vaccines Containing Thimerosal

The Influenza (Flulaval), Influenza (Fluvirin), Japanese Encephalitis, Meningitis (Menomune), and Tetanus and Diphtheria vaccines continue to contain more than trace amounts of thimerosal (CDC, 2008) For some of these vaccines, thimerosal-free options are

available. However, the FDA, the CDC, and the IOM continue to refute that

these vaccines cause harm or have influenced the incidence of autism. This may prevent parents from seeking alternative thimerosal-

free vaccines. In 2008, the US CDC recommended that all pregnant women

should receive an influenza vaccine (without regard to the trimester of pregnancy) and that all infants should receive two doses of influenza vaccine in the first year of life, with one influenza vaccine administered on a yearly basis thereafter until 59 months. In addition, the CDC recommends that children under nine who only received one influenza vaccine initially should be given 2 doses of influenza vaccine, at least two weeks apart.

Summary of evidences supporting that Hg exposure during fetal and/or early childhood periods significantly contributes

to the development of ASDs (Geier et al., 2008)

Category Support

↑Hg body-burden * ↑ Hg in ASD baby teeth.* ↑ Hg-associated urinary porphyrins in ASDs.* ↑ or ↓ Hg in ASD hair samples.* ↑ Hg in urine & fecal samples in ASDs.* ↑ Hg in the brain of ASDs.* ↑ Hg in the blood of ASDs.

Biochemical susceptibility factors * Abnormalities in transsulfuration metabolites among ASDs associated with ↑ Hg toxicity.(e.g. ↓ reduced glutathione, ↑ oxidized glutathione, ↓ cysteine, ↓ sulphate, etc.)* ↓ Abnormalities in antioxidant enzymes associated with ↑ Hg toxicity.

Summary of evidences supporting that Hg exposure during fetal and/or early childhood periods significantly contributes

to the development of ASDs (Geier et al., 2008) Cont’d.

Category Support

Epidemiological studies * Thimerosal-containing vaccines & biologics linked to ASDs.* Environmental Hg linked to ASDs.

Animal models * Low-dose Hg exposure (organic or inorganic) is associated with neuroinflammatory pathology found in ASD brains.* Low-dose thimerosal exposure linked to ASD symptoms & brain pathology in a susceptible(i.e. ↑ autoimmunity & ↓ antioxidant capacity) mouse model.

Male/female ratio * Testosterone co-exposure ↑ Hg poisoning, whereas estradiol co-exposure ↓ Hg poisoning.* More males than females diagnosed with ASDs, and have ↑ testosterone & ↓ estradiol.

Summary of evidences supporting that Hg exposure during fetal and/or early childhood periods significantly contributes

to the development of ASDs (Geier et al., 2008) Cont’d.

Category Support

Cellular susceptibility to Hg toxicity

* Cultured cells of ASDs have show significant dose- and time-dependent greater susceptibility to Hg-induced cellular toxicity than unaffected controls.* Cultured neuronal cells exposed to low-dose Hg have similar pathology as ASD brains.

Similarity of ASD & Hg poisoning * Hg-associated oxidative stress markers among ASDs

Temporal association * Symptoms of ASDs emerge within the first several years of life, Hg exposure(i.e. fetal & early infancy) proceeds development of ASD symptoms.

Pivotal Past Studies on Autism and Toxic Metals

94 children with autism matched to 45 controls

Found that their first baby haircuts had mercury levels that were statistically significantly less than controls and levels of mercury were correlated with the severity of autism.

Collected information about the levels of Hg exposure (maternal fish consumption, vaccines, maternal mercury amalgam dental fillings)

The children with autism had higher levels of exposure than controls. This study suggests that children with autism may not be able to eliminate Hg and thus may accumulate it instead.

Supported the Holmes study, found that compared to children with higher levels of Hg, children with lower levels of Hg in their hair were 2.5-fold significantly more likely to be diagnosed with ASDs.

These researchers stated that the lower level of Hg in the baby hair of children with ASDs indicates an altered metabolism of Hg, and may be due to a decreased ability to excrete Hg.

Holmes et al. (2003) Adams et al. (2008)

Pivotal Past Studies on Autism and Toxic Metals Cont’d.

Researchers from Columbia University reported that an autoimmune diathesis is described in ASD patients.

Major histocompatibility complex (MHC) genes regulate risk of Hg-induced autoimmunity in mice.

Exposed mice of differing autoimmunity backgrounds to thimerosal in doses/timing equivalent to the US pediatric immunization schedule of the 1990s.

Observed behavioral and neuropathological side effects after post-natal thimerosal exposure in mice with autoimmune sensitivity but not in mice strains without autoimmune sensitivity.

Symptoms observed in the treated autoimmune sensitive mice were similar to ASD symptoms, including: growth delay; reduced locomotion; exaggerated response to novelty; and, for the brain structure, densely packed, altered glutamate receptors and transporters.

Hornig M., Chian D., Lipkin WI., 2004

Pivotal Studies on Autism and Toxic Metals Cont’d.

Autism disproportionately affects male children (male: female ratio is about 5:1).

Research suggests that those most vulnerable to Hg toxicity are characterized by high testosterone.

In animal models and in human Hg poisonings, males were found to be significantly more susceptible to Hg toxicity (including neurotoxicity) than females (Sager et al., 1984, Clarkson et al., 1985 and Grandjean et al., 1998)

Additionally, in a series of tissue culture experiments with neurons, testosterone was able to potentiate the neuronal toxicity of Hg, whereas estradiol significantly lessened the neuronal toxicity of Hg (Olivieri et al., 2002 and Haley, 2005)

Hormones and Mercury Toxicity

“Mercury, Lead, Zinc in Baby Teeth of Children with Autism Versus Controls”

(Adams, Romdalvick, 2007)

The purpose of this study was to further investigate the mercury/lead body burden of children with autism versus controls by evaluating the amount of mercury/lead in their baby teeth. Baby teeth are formed in utero and during the first few years of life, so they provide a measure of cumulative exposure during critical periods of development. Previous studies have demonstrated that

mercury can be reliably measured in teeth (Eide et al., 1993; Tvinnereim et al., 2000).

The participants were children with autism in the state of Arizona (n=16) and controls (n=11).

“Mercury, Lead, Zinc in Baby Teeth of Children with Autism Versus Controls” (Adams, Romdalvick,

2007) Cont’d

Found that the teeth of the children with autism had a 2.1-fold higher mean level of mercury, and a 3.1-fold higher median level of mercury. The teeth of the children with autism had levels of lead that

were slightly higher than the controls, but the difference was not statistically significant. The teeth of the children with autism had very similar levels of zinc compared to the control children.

By utilizing a medical history questionnaire, it was found that the autism group had similar levels of maternal seafood consumption, number of maternal dental fillings present during pregnancy, and number of maternal dental fillings placed during pregnancy compared to the control group.

The children with autism had significantly higher levels of antibiotic usage at ages 6–12 mo and at ages 0–6 mo. They also had quantitatively higher levels of oral antibiotic usage at ages 12–24 mo and 24–36 mo (though not quite statistically significant).

“Mercury, Lead, Zinc in Baby Teeth of Children with Autism Versus Controls” (Adams, Romdalvick,

2007) Cont’d

“The two- to threefold higher level of mercury in the baby teeth of children with autism is important because it strongly suggests that they had a higher body burden of mercury during several years of prenatal/infant development” Since mercury is a potent neurodevelopmental toxin

that produces many of the symptoms observed in autism (Bernard et al., 2001), this higher body burden of mercury may have exacerbated or produced the development of autism in some of the children in this study.

“Oxidative stress in autism: elevated cerebellar 3-nitrotyrosine levels” (Sajdel-Sulkowska et al., 2008) Harvard University researchers This study compared the cerebellar levels of the

oxidative stress marker 3-nitrotyrosine (3-NT), Hg and the antioxidant selenium levels between control and ASD subjects Mercury has been found to strongly associate

with oxidative stress (Mutter et al., 2005). Antioxidant deficiency has been implicated in

the pathophysiology of autism (McGinnis, 2004).

Analyzed frozen cerebellum tissue samples

“Oxidative stress in autism: elevated cerebellar 3-nitrotyrosine levels” (Sajdel-Sulkowska et al., 2008)

Cont’d

They found an increase in 3-NT levels (a measure of oxidative stress) in the autistic cerebellum, along with a positive correlation between elevated cerebellar 3-NT and high mercury levels. This suggests that increased oxidative stress in brains of autistic

subjects may be related in part to the increased mercury. It is possible that increased levels of Hg in the autistic brain may be caused by defects in the detoxification mechanisms as suggested by studies of Geier and Geier (2006).

Additionally, observed that levels of the antioxidant Se were lower in autistic individuals compared to controls (similar results were found in Audhya and McGinnis, 2004 study). A function of Se is its ability to counteract the neurotoxicity of

heavy metals, such as Hg.

“Biomarkers of environmental toxicity and susceptibility in autism” (Geier et al., 2009)

Hypothesized that autism may be the result of a genetic susceptibility to a decreased ability to excrete mercury and/or a environmental exposure at key times of development.

Purpose of the study was to evaluate potential biomarkers for evidence of mercury susceptibility and toxicity in the transsulfuration and porphyrin pathways in a cohort of participants diagnosed with autism spectrum disorders (ASDs). Geier et al. conducted a similar study in 2008 and found

a significant abnormalities in the biochemical markers in the transsulfuration pathway among participants diagnosed with ASDs in comparison to neurotypical control.

“Biomarkers of environmental toxicity and susceptibility in autism” (Geier et al., 2009) Cont’d

28 autistic children between the ages 2-16 were recruited from the Dallas/Fort Worth area.

The severity of the children’s autism was measured using the Childhood Autism Rating Scale (CARS) and blood and urine samples were collected and tested for transsulfuration metabolites and urinary porphyrins. Previously demonstrated that the transsulfuration pathway

products of glutathione (Ballatori, Clarkson 1985) and sulfate (Ahearn et al., 2004) were related to mercury excretion rates/mercury intoxification and that urinary porphyrins (Woods, 1996) can provide specific profiles that reflect mercury toxicity.

Concentrations of transsulfuration products and urinary porphyrins were compared to neurotypical control children.

“Biomarkers of environmental toxicity and susceptibility in autism” (Geier et al., 2009) Cont’d

Overall results showed that children with ASDs had decreased transsulfuration metabolites and increased urinary porphyrin metabolites associated with mercury toxicity and susceptibility.

There was a significant correlation in the severity of autism (measured by CARS) and urinary porphyrins associated with mercury toxicity. “…it is apparent that an increased mercury body-

burden and toxicity may contribute overall to the abnormal transsulfuration pathway observed among participants diagnosed with ASDs”

“Proximity to point sources of environmental mercury release as a predictor of autism

prevalence” (Palmer, Blanchard, Wood, 2009)

The objective of the study was to determine if proximity of mercury pollution in 1998 related to autism prevalence in 2002 in Texas. Built on two past studies demonstrating an

association between environmental mercury release and autism rates (Palmer et al., 2006, Windham et al., 2006)

Autism count data retrieved from the Texas Educational Agency and environmental mercury release information retrieved from the Environmental Protection Agency (EPA).

“Proximity to point sources of environmental mercury release as a predictor of autism

prevalence” (Palmer, Blanchard, Wood, 2009) Cont’d.

Found that for every 1000 lbs of industrial mercury release, there was a 2.6% increase in autism rates and a 3.7% increase associated with power plant emissions.

For every 10 miles from industrial or power plant sources, there was an associated decrease in autism incident risk (2.0% from industrial, 1.7% from power plants). Release in pounds from industrial sites were correlated with

accelerated autism risk. Major limitation: Cannot verify exposure at the individual level In agreement with past plant, animal, and human studies, this

study demonstrates that proximity to sources of environmental mercury increases the mercury burden on the body.

Researchers advise that this study should be viewed as “hypothesis generating”

The Hannah Poling Case (2008)

In 2000, when Hannah was 19 months old, she received five shots against nine infectious diseases.

Two days later, she developed a fever, became hysterical and refused to walk. Over the next seven months she spiraled downward, and in 2001 she was given a diagnosis of autism.

In addition, she was diagnosed with a mitochondrial disorder.

The Hannah Poling Case (2008) Cont’d.

On March 6, 2008, government health officials conceded that childhood vaccines worsened a rare, underlying disorder that ultimately led to autism-like symptoms in Hannah, and that she should be paid from a federal vaccine-injury fund. First case in which the government has compensated a family

for vaccine-induced autism. Two theories have been posed to describe what happened to

Hannah. The first is that she had an underlying mitochondrial disorder that vaccinations aggravated. The second is that vaccinations caused this disorder. “The government chose to believe the first theory…we don’t

know that she had an underlying disorder” Terry Poling ''This decision gives people significant reason to be cautious

about vaccinating their children,'' John Gilmore, executive director of the group Autism United.

Arguments Against the Correlation Between Autism and Vaccinations

Argument Response

Thimerosal has been removed from vaccines since 2001 but the rates of autism continue to rise.

As of 2008, the CDC lists several vaccinations that still contain more than trace amounts of Thimerosal. Moreover, the introduction of influenza vaccines has provided a full complement of Thimerosal. When Thimerosal was initially removed from vaccines, rates of autism in California significantly decreased. However, after the introduction of the flu vaccine, numbers began to rise again (Cave, 2008). Moreover, environmental mercury exposure may be linked to autism.

Arguments Against the Correlation Between Autism and Vaccinations Cont’d.

Argument Response

Many studies have found no link between autism incidence and vaccines.

Four frequently-cited studies failed to find a link (Andrews et al., 2004; Hviid et al., 2003; Madsen et al., 2003; Stehr-Green et al., 2003). Three of these studies were in countries with much lower usage of Thimerosal in vaccines than in the United States, and they had much lower rates of autism in those countries. Additionally, many studies that claim no link between vaccinations and autism fall just short of statistical significance (therefore, almost significant). We can’t discount past and emerging studies that are finding a causal link. These studies tell us that more research is necessary to determine the real effects of toxins in vaccines on children who are genetically predisposed to retain heavy metals.

Conclusions

The autism epidemic is real and can not be explained by changing diagnostic criteria or early diagnoses alone.

Emerging evidence supports the theory that some autism spectrum disorders may result from a combination of genetic/biochemical susceptibility, specifically a reduced ability to excrete Hg, and exposure to Hg at critical developmental periods.

Government agencies maintain that there is no link between the development of autism and the toxins in vaccines. Despite the introduction of Thimerosal-free vaccines, the public may

not be swayed to pursue these options because of the government’s efforts to minimize evidence that supports the causal link.

By recognizing that physiological functions are altered by mercury intoxification through vaccines during critical periods of development, more research can be conducted to determine the exact causes of the autism epidemic.

References

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Toxicological Effects of Methylmercury (2008). Committee on the Toxicological Effects of Methylmercury, Board on Environmental Studies and Toxicology, National Research Council.

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Grandjean P, Weihe P, White RF, Debes F (1998). Cognitive performance of children prenatally exposed to “safe” levels of methylmercury. Environ Res, 77, 165-72.

References Cont’d

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