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ARTICLES: Paul T. Shattuck The Contribution of Diagnostic Substitution to the Growing Administrative Prevalence of Autism in US Special Education Pediatrics 2006; 117: 1028-1037 [Abstract] [Full text] [PDF]

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The obfuscation of the iatrogenic Autism epidemic

Kenneth P Stoller   (5 May 2006)

Diagnostic Substitution and ASD: A Brief Comment on Shattuck

John P. Tuman, Danielle Roth-Johnson (Visiting Assistant Professor, Women's Studies, UNLV), Jennifer L Vecchio (M.A., Ph.D. Candidate, Clinical Psychology, UNLV)   (19 May 2006)

The obfuscation of the iatrogenic Autism epidemic 5 May 2006
Kenneth P Stoller, pediatrician International Hyperbaric Medical Assoc Send letter to journal: Re: The obfuscation of the iatrogenic Autism epidemic info{at}hbotnm.com Kenneth P Stoller	UW-Madison researcher Paul Shattuck concludes that special education figures being used are "faulty and do not substantiate such a claim" (that there is an autism epidemic). Paul Shattuck seems to be saying that all the reported autistic children have always been here, they were just called something else. As a pediatrician, who has been in practice for over two decades, I find it more than a little insulting as well as disturbing to have someone say that these children were always there. As a scientist, I find the current approach to the autism epidemic – “The Emperor’s New Clothes” approach - to be deeply disturbing. For years the vaccine division at the CDC and others have said the reason for the dramatic increase in autism is due to "better diagnosing" and "greater awareness." They have encouraged those like Paul Shattuck to manufacture uncertainty. Nevertheless, with eighty percent of autistic Americans under the age of 18, we will see, clothes and all, a dramatic impact on Social Security in coming years as these children become dependent adults. There are no studies that have found the previously undiagnosed or misdiagnosed autistic individuals among older Americans. They simply aren't there. We need to address the real reason for the alarming autism rate. No more secrets or truth-spinning. This is not a faux epidemiological epidemic, nor an infectious epidemic, nor a genetic epidemic (as there are no genetic epidemics). That leaves an epidemic linked to some sort of exposure. Now, the increase of autism has been linked to the increase in mercury exposure through fish and industrial sources, amalgam and additionally, through increased parenteral exposure to ethylmercurithiosalicate. No controlled, randomized study regarding the safety of amalgam or ethylmercurithiosalicate exists. A recent study, using infant Macaca fascicularis primates exposed to injected ethylmercury or those exposed to equal amounts of ingested methylmercury, showed that ethylmercuy was retained twice as much inorganic mercury in their brains in comparison to the methylmercury exposed primates.(Burbacher T, et al. Comparison of blood and brain mercury levels in infant monkeys exposed to methylmercury or vaccines containing thimerosal. Environmental Health Perspectives, 2005 Aug:113(8):1015-21.)These primates were exposed to mercury levels at a rate equal to what children in the United States received via standard childhood vaccines from 1991- 2003. Cysteine and glutathione synthesis are crucial for mercury detoxification, and are reduced in autistic children, possibly due to epigenetic polymorphisms. (Deth, R.C.: Truth revealed: New scientific discoveries regarding mercury in medicine and autism. Congressional Testimony before the U.S. House of Representatives. Subcommittee on human rights and wellness, Sept. 8. 2004, Waly M et al: Activation of methionine synthase by insulin-like growth factor1 and dopamine: a target for neurodevelopmental toxins and thimerosal. Mol. Psychiatry 9, 358-370 2004). Therefore, autistic children have 20% lower levels of cysteine and 54% lower levels of glutathione, which adversely affect their ability to detoxify and excrete metals like mercury. (James, S.J. et al.: Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism. Am. J. Clin. Nutr. 80, 1611-1617 2004).This leads to a higher concentration of free mercury in blood, which then transfers into tissues and increases the half-life of mercury in the body, as compared to children with normal levels of cysteine and glutathione. As was shown by Bradstreet et al (Bradstreet, J et al.: A case control study of mercury burden in children with autistic spectrum disorders. J. Am. Phys. Surg. 8, 76-79 2003) in a study involving 221 autistic children, vaccinated autistic children showed about 6 fold elevation of urinary mercury than normal controls after appropriate mobilization with the chelating agent DMSA. Delayed detoxification of mercury severely impairs methylation reactions (required for the correct expression of DNA, RNA, and neurotransmitters), which further adversely affects growth factor derived development of the brain and attention abilities. Phospholipid methylation, which is crucial for attention, is impaired in autistic and attention deficit hyperactivity disorders. Ethyl mercury levels, seen ten days after vaccination (Pichichero et al: Mercury concentrations and metabolism in infants receiving vaccines containing thiomersal: a descriptive study. Lancet 360, 1737-1741 2002) with ethylmercurithiosalicate doses lower than what infants received during the 1990s, produced greater than 50% inhibition of methylation. In vitro studies have shown that ethylmercurithiosalicate was more than 100-fold more potent than inorganic mercury in inhibiting such essential methylation reactions. Inorganic mercury was found to be 10 fold more potent than lead in inhibition of neuronal microtubule. (Stoiber, T et al.: Disturbed microtubule function and induction of micronuclei by chelate complexes of mercury(II). Mutat. Res. 563, 97-106 2004; Thier, R et al.: Interaction of metal salts with cytoskeletal motor protein systems. Toxicol. Lett. 140141, 75-81 2003). Inorganic mercury also leads to growth inhibition and denudation of neuronal growth cones. (Leong, C.C. et al: Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury. Neuroreport 12, 733-737) . It was also shown that concentrations of ethylmercurithiosalicate, which can occur after vaccination, induce membrane and DNA damage and initiate apoptosis in human neurons. (Baskin, D.S. et al: Thimerosal induces DNA breaks, caspase3 activation, membrane damage, and cell death in cultured human neurons and fibroblasts. Toxicol. Sci. 74, 361-368 2003). It has been estimated that about 15% of the population may show enhanced susceptibility to mercury exposure. Levels of ethyl mercury found 8 days after vaccination leads to 50% inhibition of methionine synthase (MS). Compounding this toxic sequelae of ethylmercurithiosalicate, neurons are unable to synthesize cysteine, the rate limiting amino acid for glutathione synthesis. Thus, neurons are most sensitive to mercury toxicity since glutathione is the major intracellular agent in mercury and heavy metal detoxification. It is known that ethylmercurithiosalicate and inorganic mercury depletes intracellular glutathione levels, which subsequently leads to oxidative stress, neuronal cytotoxicity and death. In vitro studies suggest that the neurotoxicity of ethylmercurithiosalicate is enhanced through neomycin and aluminium hydroxide (ingredients in vaccines) and testosterone, while estrogen decreases the toxic effects. Estrogen has been shown to decrease the toxicity of inorganic mercury which may explain the 4 to 1 ratio of boys to girls in autism. Lead may play a synergistic pathogenetic role in neurodevelopment disorders and autism. Combination of lead and mercury resulted in an increase of toxicity in vitro. In a first analysis of the VSD datasets, Verstraeten et al had described a 7.6 to 11.4 fold increase of autism risk in children at one month, with the highest mercury exposure levels compared to children with no exposure. In four subsequent separate generations of the analysis, which involve the exclusion of children with no ethylmercurithiosalicate exposure and less than two polio vaccines, the statistical significance disappeared. Ethylmercurithiosalicate was tested only once, by Eli Lilly on 22 adult patients suffering from meningitis. There was no chance for follow- up to observe long-term effects, as all of the patients in this "study" died. Even if follow-up had been possible, damage to the developing brains of very young children would have remained an unknown. Eli Lilly said it was safe and the medical community accepted it. After the creation of the FDA, its use was simply continued. The federal government has never tested the type of mercury in vaccines for toxicity. This is an unconscionable oversight failure at best, at worse it is an example that we have left consensus reality to be created by the liars, thieves, cheats, killers, and the PR junk scientists they employ. So, here we have a real problem, autism affecting 1 in 166 or even more – where is the public funding? Where is the public outcry? Where is the response from academia? There isn’t any! But in the case of bird flu, with no real evidence that the H5N1 virus is a health problem for humans that do not have the most intimate contact with birds combined with a compromised immune system, billions of dollars have been allocated to clothe this “Emperor.” We have troubling glimpses, in the press, of the brand-new bird-flu containment plan the White House is laying out as detailed in an April 16 Washington Post piece by Ceci Connolly, “U.S. Plan For Flu Pandemic Revealed Multi-Agency Proposal Awaits Bush's Approval.” “...Experts project that the next pandemic -- depending on severity and countermeasures -- could kill 210,000 to 1.9 million Americans…National Guard troops could be dispatched to cities facing possible ‘insurrection,’ said Jeffrey W. Runge, chief medical officer at the Department of Homeland Security. ...The federal government -- as well as private businesses -- should expect as much as 40 percent of its workforce to be out during a pandemic, said Bruce Gellin, director of the National Vaccine Program Office at HHS. Some will be sick or dead; others could be depressed or caring for a loved one or staying at home to prevent spread of the virus. ‘The problem is, you never know which 40 percent will be out,’ he said.” Putting down INSURRECTIONS, no more Bills Of Rights for the duration of the "pandemic." Chaos! Madness! Protect government workers first and foremost. All based on ZERO scientific evidence, all this is swinging into gear. April 15, two days before the above Washington Post article, an article in the Tacoma Tribune by M.A. Otto. It reports on a public-health conference in downtown Tacoma, with featured speaker, Julie Gerberding, the head of the CDC. “ ‘There is no evidence it will be the next pandemic,’ Dr. Julie Gerberding, head of the Centers for Disease Control and Prevention in Atlanta, said of avian flu. There is ‘no evidence it is evolving in a direction that is becoming more transmissible to people.’” “Gerberding's comments on bird flu contrast earlier statements from the federal government that tended to emphasize worse-case scenarios.” So, there is no evidence of a pandemic, but thank you for the $7 billion anyway? We are living in a time where an incredible overplay and lies and self-aggrandizing behavior and non-science is the norm. Autism is a real problem, not a potential problem. We have tolerated the junk science that has covered up the true cause of this epidemic at a considerable cost to science, the public, and our very way of life in this country. Is it stretch to realize that by putting our heads in the sand about the autism epidemic we have made it possible for the groundwork to be put in place for Marshal Law? Not something easy to contemplate? Then ask why haven’t pediatricians come forward to demand the end of the use of ethylmercurithiosalicate once and for all, and to advocate for the treatment of these children before it is too late? Conflict of Interest: None declared
Diagnostic Substitution and ASD: A Brief Comment on Shattuck 19 May 2006
John P. Tuman, Associate Professor Department of Political Science, University of Nevada, Las Vegas, Danielle Roth-Johnson (Visiting Assistant Professor, Women's Studies, UNLV), Jennifer L Vecchio (M.A., Ph.D. Candidate, Clinical Psychology, UNLV) Send letter to journal: Re: Diagnostic Substitution and ASD: A Brief Comment on Shattuck john.tuman{at}unlv.edu John P. Tuman, et al.	For several years now, researchers have speculated that “diagnostic substitution” may explain trends in the growth of estimated administrative prevalence of autism spectrum disorders (hereafter, ASD) among children who receive special education services in the U.S. In a widely read report of autism released in 2001, a panel of experts convened by the National Research Council recommended that: “…the Department of Education’s Office of Special Education Programs (OSEP) could support a research study examining the prevalence and incidence of autism, using OSEP data gathered for school-age children since the autism category was first recognized in 1991. This study could investigate in particular whether the dramatic increases in numbers of children served with autism spectrum disorders are offset by commensurate decreases in categories in which children with autism might have previously been misclassified” (National Research Council 2001: 25). Shattuck ‘s (2006) approach is consistent with the research strategy recommended by the NRC and has the potential to contribute to the debate about trends in ASD. Nevertheless, due to limitations in the research design and with the data used in the study, the empirical findings of Shattuck’s paper remain open to question. One issue has to do with Shattuck’s interpretation of the trends in the mental retardation (MR) category. As Shattuck notes, from 1994 to 2003 the rate of change for children in the MR and learning disability (LD) categories exhibited a statistically significant decline. Based upon these trends, he suggests that MR and LD “…are the most likely candidates for a putative process of diagnostic substitution…” (Shattuck 2006: 3). This claim is questionable. In particular, the OSEP data, which are employed by Shattuck, do not permit a more refined analysis that would allow one to rule out other possible influences on trends in the MR category. A brief discussion of how children with Down’s Syndrome (DS) are classified illustrates this point. Pursuant to the U.S. Department of Education, Office of Special Education Program’s (OSEP) reporting system criteria, children with DS who receive special education services are not reported in a separate “DS” category; instead, children with DS are frequently placed in the MR category (1). The estimated prevalence of DS among older mothers has fallen, and this may be responsible for some of the decline in the MR category as opposed to a process of diagnostic substitution to ASD as suggested by Shattuck (2). Indeed, based upon an analysis of data from 18 states for the period of 1983 to 1990, the CDC found that the there was a statistically significant decline in the birth prevalence of children with DS born to women 35 years or older (women 35 years or older account for approximately 25 percent of DS births) (CDC 1994). This trend – which was projected to continue – was attributed to the increasing use of prenatal testing and prenatal diagnosis of DS since the early 1970s. In addition, the statistical findings of the study are potentially biased because the model does not include a covariate to control for the cross-sectional variation in levels of wealth and resources among states in the sample. Shattuck acknowledges this limitation but does not consider in enough detail the seriousness of the issue. Differences in wealth and resources levels among states can and should exhibit an influence on the processes of diagnosis and diagnostic substitution (for evidence, see Lester and Kelly 1997: 604; Palmer et al 2005). First, wealthier states are more likely to have well developed advocacy networks that assist parents in the process of obtaining diagnostic evaluations for children with disabilities, in disputing inaccurate diagnoses, and in determining eligibility for public services. The fragmentary evidence suggests that these networks may be particularly helpful for poor families who are at higher risk for not participating in IEP meetings (see the review of literature in Fiedler and Swanger 2000: 42). Second, school districts in wealthier states, on average, are more likely to have sufficient resources to provide professional training to the education staff involved in diagnostic evaluation (3). During the period in question, 1994 to 2003, such training may have played a role in the diffusion of new criteria for ASD (associated with the DSM-IV) to school staff providing evaluations, with attendant consequences for the timing and rate of any diagnostic substitution for ASD children receiving special education in each state. The design and estimation procedures (e.g., multilevel modeling) used by Shattuck could accommodate use of a covariate to control for cross- sectional differences in wealth and resources. The potential improvement in results from the statistical analysis are not trivial. To illustrate this point, we estimated a simple linear regression model with the natural log of real gross state product (GSP) per capita in 2003 (constant 2000 dollars) as a proxy for wealth. We regressed the natural log of real gross state product (GSP) per capita in 2003 on the pooled administrative prevalence rate for children with autism aged 6-11 (in 2003) across 48 states (4); the states selected were the same as in Shattuck’s sample. In this trial, the coefficient for real GSP per capita was positive and statistically significant (b = 20.83, robust standard error = 8.99, p<.05), which suggests that the pooled ASD administrative prevalence is higher in wealthier states. This model, like Shattuck’s, is limited because it uses aggregate data to make inferences about individual diagnostic processes. Moreover, we have not performed time-series estimation or used multilevel modeling. Nevertheless, the results are suggestive of the potential importance of including a covariate for wealth in diagnostic substitution models. To summarize, due to issues related to the data and the research design, we would suggest that it is premature to accept Shattuck’s conclusions regarding diagnostic substitution. It is our hope that future research will address some of the concerns raised in this brief comment. NOTES 1. For OSEP’s reporting criteria and disability categories, see OSEP, “Part B Data Report Memo, Report of Children Receiving Special Education under Part B of the IDEA Act, as Amended,” December 1, 2005. https://www.ideadata.org/docs/childcountPtB.doc. Staff in the Office of Monitoring and Compliance in the Clark County School District (Las Vegas, NV)– one of the largest in the country – confirmed that children with Down’s Syndrome are frequently reported in the MR category based upon results from diagnostic testing (personal communication with staff, May 17, 2006). Anecdotal evidence suggests there is a similar pattern in other school districts around the country. 2. In the United Kingdom, education authorities have already noted the effect of declining birth prevalence of DS for trends in special education counts. 3. Palmer et al (2005) have already demonstrated the importance of within state variation in levels of revenue and higher proportion of socio -economically disadvantaged students as predictors of the variation in ASD prevalence across school districts in Texas. It is also likely, however, that a poor school district situated in a wealthy state is in a relatively better position to obtain resources to facilitate diagnosis of ASD than a poor district located in a poor state. 4. We constructed the data set for the regression model from IDEA data (U.S. Department of Education, Office of Special Education Programs( n.d.), U.S. Census Bureau, Population Estimates Program, State Population datasets (n.d.), U.S. Department of Commerce, Bureau of Economic Affairs. Gross State Product (n.d.) REFERENCES Centers for Disease Control and Prevention. 1994. “Down Syndrome Prevalence at Birth -- United States, 1983-1990.” http://www.cdc.gov/mmwr/preview/mmwrhtml/00032401.htm (Accessed May 17, 2006). Fiedler, Craig R., and Wayne H. Swanger. 2000. “Empowering Parents to Participate: Advocacy and Education.” In Collaboration with Parents and Families of Children and Youth with Exceptionalities, eds. Marvin J. Fine and Richard L. Simpson. Austin: Pro-Ed. Second edition. Lester, Gillian, and Mark Kellman. 1997. “State Disparities in the Diagnosis of Pupils with Learning Disabilities.” Journal of Learning Disabilities 30, no. 6: 599-607. National Research Council. 2001. Educating Children with Autism Committee on Educational Interventions for Children with Autism. Catherine Lord and James P. McGee, eds. Washington, D.C. National Academy of Sciences. Palmer, Raymond F., Stephen Blanchard, Carlos R. Jean, and David S. Mandell. 2005. “School District Resources and Identification of Children with Autistic Disorder.” American Journal of Public Health 95, no. 1: 125 -131. Shattuck, Paul T. 2006. ‘The Contribution of Diagnostic Substitution to the Growing Administrative Prevalence of Autism in U.S. Special Education.” Pediatrics On-line version: http://www.pediatrics.org/cgi/content/full/117/4/1028 (Accessed April 25, 2006). U.S. Department of Commerce, Bureau of Economic Affairs. Gross State Product. n.d. http://www.bea.gov/bea/regional/gsp.htm (Accessed May 10, 2006). Conflict of Interest: None declared