Improbable Causes & Extravagant Claims (Excerpts from Dwyer v. HHS) · 4 days ago

The following excerpts are drawn from Special Master Denise Vowell’s 310-page decision in Dwyer v. Secretary of HHS (Case No. 03-1202V), one of the three “thimerosal theory” test cases presented in the Omnibus Autism Proceeding. The claim was dismissed on March 12, 2010, for failure to prove that thimerosal-containing vaccines can cause autism, or that they did so in this instance.

For links to case filings, rulings, expert witness biographies, and other autism and vaccine injury litigation resources, see Neurodiversity Weblog’s newly-updated Omnibus Autism Proceeding: Resources & Documents directory.


Introduction (p. 3)

Colin’s case was heard as part of the largest omnibus proceeding in the history of the Vaccine Act. It was one of three test cases on the second of two theories of causation [“Theory 2”] advanced by petitioners in the Omnibus Autism Proceeding [“OAP”]. Theory 2 is that the mercury in TCVs can cause at least some forms of ASD, and that it did so in the three Theory 2 test cases, including Colin’s. After considering the record as a whole, I find that petitioners have failed to establish by preponderant evidence that Colin’s condition was caused or significantly aggravated by TCVs. They failed to demonstrate either that the mercury component of TCVs can cause ASD or that it did so in Colin’s case. None of the causation hypotheses advanced were reliable as medical or scientific theories. In essence, petitioners propose effects from mercury in TCVs that do not resemble mercury’s known effects on the brain, either behaviorally or at the cellular level. To prevail, they must show that the exquisitely small amounts of mercury in TCVs that reach the brain can produce devastating effects that far larger amounts experienced prenatally or postnatally from other sources do not. In order to account for this dichotomy, they posit a group of children hypersensitive to mercury’s effects, but the only evidence that these children are unusually sensitive is the fact of their ASD itself. In an effort to render irrelevant the numerous epidemiological studies of ASD and TCVs that show no connection between the two, they contend that their children have a form of ASD involving regression that differs from all other forms biologically and behaviorally. World-class experts in the field testified that the distinctions they drew between forms of ASD were artificial, and that they had never heard of the “clearly regressive” form of autism about which petitioners’ epidemiologist testified. Finally, the causal mechanism petitioners proposed would produce, not ASD, but neuronal death, and eventually patient death as well. The witnesses setting forth this improbable sequence of cause and effect were outclassed in every respect by the impressive assembly of true experts in their respective fields who testified on behalf of respondent. Therefore, I hold that petitioners have failed to establish their entitlement to compensation, and their petition is denied.


On the qualifications of expert witnesses (p. 13-15, 44)

Witness qualifications are an important, and a largely objective, basis upon which to assess and weigh expert opinions. In virtually every area of specialization in science and medicine about which testimony was offered, respondent’s experts were far more qualified to opine than those of petitioners. Speaking generally, the qualifications of the experts proffered by respondent, the relationship of those qualifications to the subject matter of their testimony, and the quality of their testimony far exceeded those of petitioners’ experts.

In terms of research, clinical experience, and publications in the subject matter of the testimony proffered, respondent’s witnesses were truly experts, and some were world-class experts, in their fields. In contrast, most of petitioners’ experts had few publications relating to the subject matter of their testimony and far less experience in the subject matter of their proffered opinions. Respondent’s experts were practicing physicians or research scientists (and sometimes both) who have taught and written extensively on the specific subject matter about which they testified. Although most of petitioners’ witnesses had adequate, and occasionally excellent, qualifications as physicians and scientists, most were either not engaged in research and treatment, or were engaged in research that was, at best, tangential to the subject matter of their testimony. One of petitioners’ expert witnesses had testified very frequently in Vaccine Act cases, and thus appeared to derive substantial income from expert witness fees.

In terms of clinical experience in diagnosing and treating children with ASD, every one of respondent’s experts who treated children with ASD had more academic training and clinical and research experience than petitioners’ experts. None of Colin’s own treating physicians testified in this case, and to the extent that any of his medical records reflect any opinions on causation, they focused on a temporal connection between onset of his symptoms and a purported second MMR vaccination. Thus, there are no opinions of treating physicians to be considered on the causation issue. Of the three witnesses who specifically opined on the cause of Colin’s condition, two were engaged in treating children with ASD, but respondent’s expert had far more years of experience in such treatment, more advanced training, and a record of research and publication in the field not possessed by petitioners’ expert. The third expert filed a very generic expert report, and did not testify.

The responses of witnesses to questions, whether from opposing counsel or from the special masters themselves, was also a factor in weighing and evaluating testimony. In general, respondent’s experts provided more responsive answers to such questions. Respondent’s experts were generally more careful and nuanced in their expert reports and testimony. In contrast, petitioners’ experts were more likely to offer opinions that exceeded their areas of expertise, to “cherry-pick” data from articles that were otherwise unsupportive of their position, or to draw conclusions unsupported by the data cited. When an expert relied on a specific medical or scientific journal article in testimony or referenced it in his or her report, I carefully compared the testimony or report to the article cited. Drs. [Marcel] Kinsbourne and [H. Vasken] Aposhian, in particular, on several occasions cited articles for propositions not contained in the publication. Several of these instances are set forth in greater detail in the sections dealing with their testimony.

…Two of petitioners’ experts, Drs. Kinsbourne and [Elizabeth] Mumper, had qualifications that warranted consideration of their testimony about autism’s symptoms, diagnosis, treatments, and causes, but their testimony was not particularly helpful in providing the background information in this section. Although qualified to testify about autism by virtue of his general training and experience in pediatric neurology, Dr. Kinsbourne’s practice never focused on children with ASDs. He no longer sees or treats patients and has conducted no research into autism’s causes, diagnosis, or treatment, other than a review of medical literature. In many cases, his expert report lacked citations for the statements he made and, in some cases, his citations were simply incorrect.

Dr. [Elizabeth] Mumper is a pediatrician, not a neurologist, psychiatrist, or psychologist, and has had only the standard training provided to pediatricians in these disciplines. Although she has considerable experience in treating children with autism, her testimony was largely anecdotal, rather than based on systematic research, and was thus less helpful in terms of input to this section.


On “regressive autism,” “clearly regressive autism,” and the relationship between regression and genetics (pp. 86-87, 95, 98-99)

I conclude that the preponderance of the evidence demonstrates that regressive autism is not a distinct phenotype, and overwhelmingly demonstrates that “clearly regressive autism” is, at best, only a hypothetical construct, unsupported by any credible evidence. I likewise conclude that opinions, such as Dr. [Sander] Greenland’s, that are based on the existence of this subtype lack the factual underpinnings to be considered reliable evidence. Thus, I conclude that the impressive body of epidemiological evidence that TCVs are not causally associated with ASD is relevant and should be considered in determining whether TCVs do indeed cause or substantially contribute to ASDs…

Not surprisingly, respondent’s experts had sharp disagreements with the assertions of Drs. Kinsbourne and Greenland. Those assertions and the criticisms thereof are set forth below.

With respect to Dr. Kinsbourne, respondent’s experts noted that some of his assertions were made without any reference to supportive medical literature, were based on “cherry-picked” data, and conflicted with the weight of scientific and medical authority. Other aspects of Dr. Kinsbourne’s testimony made analysis of his assertions difficult. For example, he declined to define regressive autism. In view of the numerous definitions discussed, Dr. Kinsbourne’s reluctance to specify what he considered to be regressive autism was troublesome. He could not state whether regressive autism was considered a separate diagnostic category by either the DSM-IVTR or the ICD-10.

…The evidence was overwhelming that genetics alone can account for regression, as regression is present in a number of entirely genetic conditions, some with striking similarities to autism. A postnatal environmental cause for regression is highly unlikely, but not impossible. The lack of 100% concordance in identical twins indicates that something other than genetics alone affects who develops ASD, but the “something else” is more likely epigenetic influences, rather than a postnatal toxic insult.

…The evidence for regressive autism constituting a separate phenotype was singularly unpersuasive. The evidence for an even smaller subtype of regression, “clearly regressive autism,” was non-existent. Dr. Greenland lacked the professional qualifications to opine that autism has distinct “clinically recognizable subtypes with distinct development[al] trajectories and possibly different etiologies.” Unlike Drs. [Eric] Fombonne, [Michael] Rutter, and [Steven] Goodman, Dr. Greenland is not a medical doctor and his CV does not reflect any education, training, or experience in diagnosing or treating autism. Dr. Greenland is thus not qualified to opine on subtypes of autism or whether subtypes of autism have distinct causes. He acknowledged this lack of expertise himself.

Other than Dr. Greenland’s assertions, petitioners offered absolutely no evidence that “clearly regressive autism” is considered a separate diagnostic category by anyone with expertise in diagnosing autism. The medical literature does not use the term. Dr. Greenland was unable to present any evidence indicating that regressive autism is biologically distinct from nonregressive autism.

Most of Dr. Kinsbourne’s assertions about regressive autism were simply wrong. He failed to demonstrate that regression is a separate phenotype. In Dr. [Robert] Rust’s words, his assertion that regressive and classic autism are different conditions is an artificial one. There are a very small number of children with apparently normal development who suffer “sudden and even shocking” regression in their second year of life. Aside from this regression, which is not unique to autism, there is nothing else that sets them apart from children whose regression manifests more slowly or who have sudden regression after some slow or abnormal development.

His assertion that regression is caused by a disease process rather than genetics does not follow logically from what is known about regression in other conditions. Brain development in human infants occurs in phases. At each phase of brain development, genetic signals turn on processes that result in elaborations, development, and eliminations of brain structures. These changes in the brain result in behavioral changes as well. The evidence establishes that whatever sets the development of the brain of an autistic child apart from a typically developing peer likely occurs early in gestation. On a theoretical basis, some changes might be postnatally influenced, but the evidence for such postnatal events is scant. Even when disease processes such as herpes encephalitis postnatally induce autistic-like symptoms, the behaviors induced are similar to, but qualitatively different from, those seen in most children with autism.

Regressive autism cannot be distinguished biologically from other forms of ASD. There is no evidence of any brain abnormality that sets those with regression apart from those with classic or early onset ASD. With regard to “clearly regressive autism,” it was petitioners’ burden to demonstrate its existence as a separate phenotype. I find that petitioners failed to do so. Because the facts that formed the basis for his opinion were not satisfactorily established, Dr. Greenland’s opinion that the existing studies cannot rule out a substantial causal role for TCVs in one form of autism is not relevant or persuasive.


Conclusions regarding epidemiology (p. 120)

Epidemiological evidence has limitations. It cannot speak to causation in an individual case. It can, however, sufficiently undermine a hypothesis or theory regarding causation, making reliance on such a theory unreasonable under all the facts and circumstances of an individual case.

To use Althen’s terms, epidemiological studies point out possible logical connections between two events; further scientific effort must ensue to establish whether the connections are biologically plausible and therefore truly logical. After studying the evidence available, the IOM concluded that the evidence favored rejection of the TCV-ASD hypothesis. Since that 2004 conclusion, all of the reliable epidemiological studies have buttressed the finding of no relationship.

Each epidemiological study filed has limitations that affect the data acquired and may affect the conclusions drawn. However, when numerous well-designed studies have looked at a particular issue and arrived at the same or similar conclusions, the likelihood that the studies’ limitations have caused the negative results becomes vanishingly small. Epidemiology can never be direct proof that vaccines do not cause ASD, but it can be strong circumstantial evidence that causation is improbable. In this case, the epidemiological studies furnish powerful evidence refuting a causal association between TCVs and ASD.


On Dr. H. Vasken Aposhian’s testimony (p. 121)

Some aspects of Dr. Aposhian’s testimony were troubling. He occasionally cited studies in support of his testimony, that, when examined, did not support that testimony. In spite of his acknowledgment that the various species of mercury had different toxicokinetics, he often attributed the effects of one species to another. Much of his direct testimony appeared scripted, consisting of reading his slides verbatim. On cross-examination, he provided wandering, anecdotal, and nonresponsive answers. He avoided responding to cross-examination questions with comments such as “it depends on how you define…” or “this is a court of law and I must tell the truth.”


Factual conclusions regarding mercury and “hypersusceptibility” (p. 172)

Dr. Brent referred to a scientific methodology for determining if a given substance was responsible for a particular toxic effect, in which four questions must be answered: (1) to what chemical was the patient exposed; (2) how much of the substance was involved; (3) what conditions is the chemical known to cause; and (4) did this exposure cause the condition from which the patient suffers? Essentially, this methodology asks: what, how much, can it, and did it?

Applying Dr. [Jeffrey] Brent’s methodology, I conclude that it is undisputed that human beings are born with some amount of mercury present in their brains. Throughout the first year of life, U.S. children have additional mercury exposure from diet, environment (air and water), and, prior to the removal of most TCVs from the U.S. market, TCVs. Mercury exposure continues throughout life, and some portion of the mercury to which human beings are exposed adds to brain mercury levels.

Petitioners have contended that inorganic mercury in the brain is responsible for at least some cases of ASD. However, the amount of inorganic mercury produced in the brains of infants who received TCVs is extremely low. Dr. Aposhian’s calculations of the contribution of TCVs to brain inorganic mercury levels were incorrect, but even if I use his figures, TCVs produced far less than the amount of inorganic mercury in the brain that produced inflammatory responses in adult primates. The actual TCV contribution was undoubtedly much smaller than Dr. Aposhian postulated. The evidence is clear that ethylmercury, in sufficient doses, is neurotoxic. The brain levels at which toxic effects have been observed are not well-established for ethylmercury, but total brain mercury levels associated with toxic effects are thousands of times higher than the levels produced by TCVs, and hundreds of times higher than baseline measurements in autopsies of human neonates.

Through a series of accidental poisonings, toxicologists have determined the neurotoxic effects from prenatal and early postnatal mercury exposure. Those effects are not ASDs. Through sophisticated tests administered to children in populations exposed pre- and postnatally to levels insufficient to produce toxicity, but sufficient to produce measurable cognitive effects, effects of lower dose exposure have been described. Once again, those effects are not ASDs.

The levels of inorganic and total brain mercury at which widespread evidence of neuroinflammation was observed in the adult monkeys were far higher than the levels found in human neonates (baseline exposure) plus any amount attributable to vaccines. Even in the adult primates, the cellular changes in the brain produced no observable neurological effects after months of daily exposure. Every two days, the adult primates received approximately as much mercury as is contained in all the mercury in the first six months of TCVs, calculated at a dose per kilogram.

Methylmercury has an affinity for certain areas of the brain. The brain areas most affected by mercury are not the areas affected in ASD patients. The brain cells most vulnerable to mercury’s effects are largely unaffected in ASD patients. Conversely, the loss of Purkinje cells is the most consistent pathological finding in the ASD autopsy studies, but mercury exposure spares Purkinje cells while damaging others. The neurological symptoms caused by mercury exposure do not resemble ASD’s symptoms and behaviors.

The evidence that some individuals are hypersusceptible to mercury’s effects is singularly unconvincing. There is no reliable evidence that mercury levels in children with ASD, with or without regression, differ from those in the general population. There is no reliable evidence that children with ASD respond differently to mercury than neurotypical children do. The studies upon which Dr. Aposhian relied were, in general, poorly performed, and in all cases, their results either had not been or could not be duplicated.

Through Dr. Aposhian, petitioners attempted to demonstrate mercury’s probable causal role in ASD. Similarly, through Dr. Aposhian, petitioners attempted to demonstrate that vaccine levels of TCVs, alone or in combination with other sources of mercury exposure, would produce brain levels of mercury sufficient to provoke oxidative stress, oxidative injury, and neuroinflammation. The evidence presented by Dr. Aposhian failed to do either.


On Dr. Richard Deth’s testimony regarding mercury, oxidative stress and sulfur metabolism (pp. 176, 185, 192, 208, 224)

Summarizing Dr. Deth’s opinions on the causal role of mercury in autism is difficult. Not only were the biochemical processes allegedly affected very complex, his explanations of those processes lacked coherence. He opined that very small amounts of mercury had a scattershot effect on a number of biochemical processes, inducing systemic metabolic abnormalities and oxidative stress. He also opined that these metabolic abnormalities resulted in interference with neuronal functioning in attention and cognition, causing the major symptoms of autism. His entire hypothesis rested on a speculative “genetic susceptibility” to environmental toxins, such as heavy metals in general, and mercury in particular. He asserted that children with autism have polymorphisms – variations in genes that are not considered mutations—that render them more sensitive to mercury’s effects by impairing their ability to eliminate ethylmercury, maintain normal oxidative and methylation balance, and maintain synchronization in neuronal signaling. The scientific studies upon which he relied provided, at best, only tangential support for his hypothesis. His own research, most of which was unpublished, unduplicated, or mentioned for the first time during the Theory 2 general causation hearing, was poorly performed and scientifically implausible. Based on in vitro effects of mercury on “neuronal cells,” he claimed that mercury had the same effects on human brain cells.

In addition to his own unpublished research, Dr. Deth relied heavily on his one article on mercury, the Waly study. He relied on two studies conducted by Dr. S. Jill James, calling them the strongest evidence in support of his hypothesis. He also claimed that the “strongest evidence” in favor of his hypothesis derived from his own unpublished work on post-mortem brain samples from individuals with ASD.

Perhaps his most extravagant claim involved the quantity of mercury required to induce the claimed effects. He claimed the ability to detect the effects of mercury on cells at levels 100-1000 times lower than levels used by other researchers. He testified that mercury, in amounts at or well below the amounts contained in TCVs, could induce some individuals to enter into and remain in a state of oxidative stress.

In the course of the hearing, nearly every premise of his causation theory, other than that of the ubiquity of mercury exposure in children (with or without autism), was seriously undermined, where not completely demolished. Mercury, and a number of other heavy metals, can affect cellular metabolism, but Dr. Deth’s assertions that mercury does so in the manner and at the levels of exposure postulated and with the effects claimed were not scientifically supported. His assertion that oxidative stress in children with autism is causal of their autism was pure speculation.

…Although Dr. Deth’s testimony was superficially coherent, the defects pointed out by true experts revealed the critical flaws in Dr. Deth’s presentation, and, ultimately established that his hypothesis of causation was not reliable.

…The discovery of an extracellular methylation cycle, when all other methylation cycles take place inside cells, is so highly unusual that it warrants independent confirmation. That confirmation is lacking. The assertion in the Waly study that the D4 receptor was the site of the methylation activity was based on gel electrophoresis, but a critical failure in that process was noted by Dr. [Richard] Mailman. In view of Dr. Mailman’s many publications on dopamine receptors, his testimony regarding them carries exceptional weight.

As Dr. Deth had not conducted studies on human brain cells, other than his unpublished work discussed below, his testimony that human neurons lack the ability to use SAM to reactivate methionine synthase lacks scientific support. He based his findings on experiments conducted on cells with a known methionine synthase mutation. In summary, Dr. Deth and his colleagues designed an experiment around two faulty premises: the existence of the only extracellular methylation cycle, and a purported defect in human neuronal cells. In view of these problems, and the other issues noted by Drs. Jones and Mailman, any conclusions drawn from the first part of the Waly study are so unreliable as to render its evidentiary value virtually nil.

…Dr. Deth’s late-in-the-game switch from mercury’s impact on glutathione to its binding to otherwise unidentified “regulatory proteins” was unpersuasive. After considerable testimony about mercury’s effects on transsulfuration and the methionine methylation cycle and his many experiments that purported to measure these effects, Dr. Deth’s new focus on “regulatory proteins” was disingenuous at best. Given the ubiquity of thiols and sulfur in the brain and elsewhere in the body, the tiny amounts of mercury administered through TCVs, and the even smaller amounts that will reach and remain in the brain, are unlikely to deplete the thiols available. Most mercury in the brain is already bound, and only the small amount not already bound to thiols would be available to react with these “regulatory proteins.”

…Initially, to someone unacquainted with mercury’s toxicology, ASD, or biochemistry, Dr. Deth’s opinions on mercury, oxidative stress, and sulfur metabolism might appear to be solidly based and plausible. After all, mercury can be toxic to cells and is known to produce neurological injuries. Mercury does bind to glutathione, the body’s primary antioxidant molecule, and thus might be expected to affect adversely the body’s oxidative status. Mercury is known to bind to cysteine transporters, and thus might be expected to affect cysteine levels in cells, and thus adversely affect cells that cannot manufacture their own cysteine, such as neurons. There is evidence to indicate that mercury can cause proliferation of microglia and reductions in astrocyte numbers in at least some areas of the brain, which Dr. Deth equated to the neuroinflammation found in the brains of individuals with ASD. There is some evidence that children with ASD display biomarkers of oxidative stress in peripheral blood, and may even have some polymorphisms associated with higher levels of oxidative stress.

However, when critically examined, Dr. Deth’s causal assertions fall apart. Mercury, at sufficient doses, is toxic to cells, but humans are born with mercury in their brains, blood, and hair as a result of maternal exposures. Humans continue to be exposed to mercury throughout their lives, and methods for detoxifying and eliminating mercury have evolved to account for this exposure. In populations with high mercury exposure, there is no increased incidence of ASD, and thus the low levels once found in vaccines are unlikely to be a cause or a substantial contributor to the condition. Mercury, at sufficient doses, can produce neurological injuries, but not at the levels of mercury found in vaccines. The neurological injuries it produces are well established and do not resemble ASD. A comparison of autopsy findings in mercury’s victims and autopsy findings from individuals with ASD do not show the same patterns of damage or injury.

Dr. Deth attempted to demonstrate that vaccine levels of mercury could adversely affect sulfur metabolism and produce oxidative injury in the human brain through a series of experiments on cells in culture. He represented the cells as “neuronal,” although they were not neurons and had defects affecting the processes he attempted to measure. His laboratory experiments, funded largely by contributions from groups associated with the belief that vaccines cause ASD (ARI [Autism Research Institute] and SafeMinds), found adverse effects from doses of mercury between 100-10,000 times lower than those used by other researchers. Assuming, arguendo, that these experiments were properly performed and produced correct results (both points about which I am unconvinced), the experiments contribute little to nothing to the causation hypothesis. In vitro experiments on cells in culture may suggest likely avenues for further research, but the complexity of sulfur metabolism presented in Dr. Deth’s testimony and report demonstrates the robust systems in place in human beings to handle oxidative stress and produce the methylated products needed for cellular functioning, including DNA expression. I note that Dr. Deth heavily relied on mercury’s effects on glutathione, but the evidence overwhelmingly illustrated that glutathione levels in the body would be unaffected by vaccine level doses.

Dr. Deth also relied heavily on evidence indicating that children with ASD display peripheral markers of oxidative stress, and that brains of those with ASD have evidence of neuroinflammation, which he equated to oxidative damage. He failed to mention that oxidative stress in the periphery is associated with many different diseases, but that peripheral levels do not represent brain redox status. He likewise failed to point out that neuroinflammation is found in many brain disorders and injuries, including those produced by trauma. Thus, a finding of oxidative stress or even oxidative injury says little about mercury as a probable cause of the stress or injury because there are so many other possible causes, including neuroinflammation as a response to the other pathophysiological findings in the brains of those with ASD. Since ASD is a highly genetic disorder, it is unsurprising that preliminary studies have found some polymorphisms exist in children with ASD in higher numbers than in neurotypical individuals. It is equally unsurprising that some of these polymorphisms are associated with problems in oxidation or sulfur metabolism. Children with Down syndrome, an entirely genetic disorder involving mental retardation, also have oxidative stress levels higher than neurotypical children. Children with Rett’s disorder, another entirely genetic condition, have impairments in DNA methylation, a sulfur metabolism problem. The preliminary findings in children with ASD say nothing about a genetic susceptibility to mercury or even that the oxidative stress levels found actually affect mercury detoxification.

Dr. Deth’s own experiments were based on faulty premises regarding methylation of the D4 receptor and defects in methionine synthase activity in human neurons. His experiments detecting effects of nanomolar levels of mercury on glutathione, cysteine, methylcobalamin, and methionine synthase had so many flaws that they cannot be considered reliable as evidence. Respondent’s experts in oxidative stress, sulfur metabolism, neurodegenerative disorders, and mercury pointed out the serious deficiencies in Dr. Deth’s hypothesis, experiments, and conclusions. Their criticisms, coupled with the flaws in Dr. Deth’s logic, his own acknowledgment that eliminating TCVs has not produced any decline in ASD rates, and the conflicts between his testimony and what is well established about mercury’s toxicology, all convince me that Dr. Deth’s hypothesis is not reliable, and cause me to accord his testimony and report little weight.


On Dr. Richard Deth’s and Dr. Marcel Kinsbourne’s neuroinflammation hypothesis (p. 226)

Drs. Deth and Kinsbourne presented hypotheses that involved persistent inorganic mercury in the brain causing neuroinflammation, leading to autism. The majority of Dr. Deth’s testimony focused on the effects of mercury on sulfur metabolism, leading to a state of oxidative stress in the brain, manifesting with the neuroinflammatory findings reported by the Vargas study. His neuroinflammation hypothesis was similar, but not identical, to that of Dr. Kinsbourne, and he was less clear about how the neuroinflammation resulted in ASD. Dr. Kinsbourne’s hypothesis attempted to fill that gap. Dr. Kinsbourne asserted that mercury-induced neuroinflammation caused excitotoxicity, which manifested as overarousal of individuals with ASD, causing autistic behaviors. Dr. Kinsbourne made it clear that his opinion did not depend on that of Dr. Deth, who “was studying at the molecular level a particular component of the broader process that I was invoking.” However, Dr. Kinsbourne did not tie his neuroinflammation process specifically to Dr. Deth’s oxidative stress model. For purposes of his hypothesis, it did not matter how the neuroinflammation was produced. However, Dr. Kinsbourne’s hypothesis was based on Dr. Aposhian’s opinions about the amount of mercury required to cause the excitotoxic process he proposed. As indicated in Section VI, I did not find Dr. Aposhian’s calculations regarding the amount of mercury in the brain generated from vaccines to be correct. I did not credit Dr. Aposhian’s testimony that TCVs could produce enough mercury to cause the widespread glial activation necessary to Dr. Kinsbourne’s hypothesis. Nevertheless, because of the role of Dr. Kinsbourne’s testimony in the general causation test case, I evaluate his general causation hypothesis as if these evidentiary prerequisites had been met. I conclude that there are other fatal flaws in his hypothesis. The method of injury he proposed would lead to neuronal death, and eventually patient death, not ASD. The brain cell interactions he proposed are not consistent with the complex interactions that actually occur in human brains. Mercury’s effects on the brain and the symptoms it produces do not resemble those of ASD. Dr. Kinsbourne’s overarousal model of ASD is not new, but it has never been widely accepted because there is no evidence linking the behaviors Dr. Kinsbourne attributed to overarousal to physiological measurements of hyperexcitability.


On Dr. Marcel Kinsbourne’s methodology (pp. 235-238, 248, 253-255)

… Although Dr. Kinsbourne cited a number of studies as supporting his model of autism as a consequence of an excitatory-inhibitory imbalance, many either do not support the points for which he cited them or the points he made were taken out of context. Dr. Rust generally characterized Dr. Kinsbourne as overstating the support found in these studies. What emerges when these studies are critically examined is validation for Dr. Rust’s characterization. The data Dr. Kinsbourne cited are not representative of the studies’ findings, and much of the data contained in the studies do not support Dr. Kinsbourne’s hypothesis. As Dr. Rust further observed: “Prominent countervailing data and theories are not considered.” An occasional misstatement of a study might be expected in any expert’s analysis of such complex issues. However, the pattern that emerges in Dr. Kinsbourne’s citations is not that of an occasional misstatement. A scientist might well pick data from many different sources to serve as circumstantial evidence for a particular hypothesis, but a reliable expert would not ignore contrary data, misstate the findings of others, make sweeping statements without support, and cite papers that do not provide the support asserted.

When confronted with evidence that one of the studies upon which he relied stated that Purkinje cells were not damaged by methylmercury exposure, Dr. Kinsbourne’s response was more than a little illogical. He testified that he was not attributing the loss of Purkinje cells directly to mercury poisoning, but rather to the excitotoxic effects of mercury. That is, he was saying that high doses of methylmercury (which converts to inorganic mercury) will spare Purkinje cells, but low-dose exposure will kill them through excitotoxicity caused by inorganic mercury. The evidence established that doses of mercury sufficient to cause harm spared Purkinje cells, while damaging other cell types… Dr. Kinsbourne could not explain why high-dose exposure would spare cells, but low-dose mercury exposure would damage them or impair their function.

A careful examination of his cited references reflected Dr. Kinsbourne’s penchant for extracting data and out-of-context references to support his position, while ignoring contrary data or remarks in the same study or article. Although some studies contained support for specific aspects of his hypothesis, the studies Dr. Kinsbourne cited were not supportive of glutamate excess as a cause of ASD.

Dr. Kinsbourne’s proposed mechanisms of injury from TCVs (or mercury in general) do not account for any of the development anomalies Dr. [Thomas] Kemper and others have found in autistic brains. Dr. Kemper provided a list of clinical features and neuropathological findings in autism compared to those of mercury toxicity. The clinical features and neuropathology of the two conditions do not overlap; in many cases, the findings in autistic brains are the opposite of those caused by mercury.

Dr. Rust commented that if inorganic mercury causes overexcitation, and the amount of mercury increases over time, patients with autism would get progressively worse over time. Because human beings are continually exposed to various sources of mercury, brain inorganic mercury levels increase over time, even in the absence of TCV exposure. Dr. Kinsbourne’s report indicated both that autistic symptoms plateau, but may also become more severe if epilepsy ensues. Although he distinguished ASD from metabolic brain degeneration, the implication of a steadily increasing toxic element causing a reaction is that there would be a steady deterioration in function. That is not what is seen in autism; individuals with autism improve over time. This is inconsistent with Dr. Kinbourne’s hypothesis.

…In his Theory 2 general causation hypothesis, Dr. Kinsbourne added a new coat of paint to an old building, but failed to shore up the building’s basic structural failings. As Dr. Rust characterized it, Dr. Kinsbourne’s hypothesis has “lethal problems in terms of scientific support.” Rather than producing ASD, the excitotoxic state Dr. Kinsbourne’s hypothesis envisioned would produce neuronal death, followed by patient death. That is not descriptive of the natural history of ASD. His whole hypothesis relied on “a toxicologist” (presumably Dr. Aposhian) to establish that exposure to TCVs could produce enough mercury in the brain, either alone or in conjunction with other environmental mercury exposure, to cause neuroinflammation. For reasons detailed at length in Section VI, Dr. Aposhian’s opinion that TCVs would produce enough mercury to cause the effects postulated was not reliable.

Even if, arguendo, sufficient brain mercury is produced by TCVs, Dr. Kinsbourne’s hypothesis cannot explain why most children with ASD improve over time, while the mercury levels in their brains are likely increasing over the same time frame from diet and other sources. His assertion that brain protective measures kick in at some point to ameliorate the effects of additional mercury was sheer speculation. Dr. Kinsbourne opined that neuroinflammation produces ASD through a glutamate excess. None of the studies he cited measured glutamate levels in the brains of those with ASD. The evidence of neuroinflammation does not establish a cause for neuroinflammation, and there was ample evidence that it is a nonspecific finding with many possible causes, including a response to injury.

Witnesses with far better qualifications in research into neurodegenerative diseases and oxidative stress established that the cellular processes Dr. Kinsbourne described do not work the way he asserted. Dr. Kinsbourne’s testimony about what happened to astrocytes in his model was inconsistent. He relied on the Lopez-Hurtado study’s findings of gliosis, which he erroneously equated to astrocytic death. He relied on damage to astrocytes as an essential component of his theory of a glutamate imbalance, and indicated that astrocytic death was not required. Then, he postulated an increase in astrocyte numbers as responsible for causing ASD. He was not only inconsistent, he was wrong.

Although, on a theoretical level, other physicians and scientists have considered Dr. Kinsbourne’s overarousal model as an explanation for autism’s behavior, a mercury-produced glutamate excess is not a probable explanation for overarousal. As Dr. Kinsbourne conceded, glutamate has never been identified as a cause of ASD. What mercury does in the brain is well-known. In sufficient doses, it is a potent neurotoxin, but not one that has ever been shown to cause autism or autistic symptoms. To properly place a factor on a list of differential causes for a disease or disorder requires some evidence that it is capable of causing that disease or disorder. To prevail, petitioners must establish by preponderant evidence that TCV exposure belongs “on the differential” as a cause for ASD. Even by this standard, which is much lower than that of “scientific certainty,” petitioners’ case falls well short.


Conclusion regarding general causation (pp. 256-263)

A. Conclusions in General

A diagnosis of ASD can be heartbreaking. Although most children improve, few ever lose the diagnosis. Most children with ASD will never live independently as adults. The true cost of ASD is borne by those who live daily with the condition and contend with its financial and emotional tolls. In the caring and compassionate words of Dr. Rust during the general causation hearing, those of us on the outside looking in “do not understand.”

When petitions for compensation alleging that ASD was the result of childhood vaccinations were filed in mounting numbers, the OAP was created to help resolve the factual and legal questions the petitions presented. The Vaccine Program exists to compensate victims of vaccine injuries easily, quickly, and with generosity, but entitlement to compensation requires more than a sincere and honest belief that a vaccine is responsible for causing ASD. In these cases, as in all other off-Table cases, petitioners must establish by preponderant evidence that a vaccine can cause ASD, and that it did so in their children’s cases. The evidence produced in the Theory 2 cases alone was voluminous and highly technical, and the hypotheses presented were very complex. This illustrates not only the difficulty of making factual conclusions regarding that evidence, but also the utility of an omnibus hearing to produce and evaluate it. However, nearly a decade after the OAP was created, all of the evidence produced to date is inadequate to demonstrate any causal connection between vaccines and ASD.

The TCV causation hypothesis emerged from a combination of mercury’s long-established role as a neurotoxin, ASD’s status as a neurological disorder, and the ubiquity of exposure to TCVs prior to the perceived emergence of ASD’s symptoms. The Faroe Islands studies suggested that maternal methylmercury exposure during gestation was a statistically significant predictor of poorer performance on some neurological tests. Although the Seychelles Island studies did not make the same findings, the Faroe Islands studies were some evidence that smaller doses of methylmercury than previously thought could cause neurological harm. The Internet likely played a role as well, according to at least one commentator.

The focus on TCV causation of regressive ASD emerged in the Theory 2 cases as a consequence of what Dr. Kinsbourne called the “striking” and “shocking” presentation in some cases of regression, in which apparently normal toddlers lost skills and sociability. Without an understanding of how behavior at age two could be caused by some brain systems coming on line while others were disconnected, it made sense for parents and others to look for a more recent triggering event. Most children with ASD had received vaccines containing “a known neurotoxin” and, equating the reference dose for methylmercury to ethylmercury, parents voiced concerns about the amount of mercury children received in vaccines. Even the prestigious IOM called the mercury hypothesis “biologically plausible” in 2001, although what the IOM meant by that term was not what the parents perceived.

However, over the following three years, more scientific studies were published. The toxicokinetics of ethylmercury were studied in primates and human infants, and every reputable study confirmed that methylmercury studies were not a good predictor of ethylmercury’s effects. Well-conducted epidemiological studies found no connection between TCVs and ASD. In 2004, the IOM reexamined the TCV-ASD hypothesis and concluded, in the strongest terms available to it, that the evidence favored rejection of any causal connection. Since 2004, every epidemiological study except one has continued to find no connection between TCVs and ASD. The one study that found a connection was funded by the Petitioners’ Steering Committee representing the OAP petitioners in this omnibus proceeding.

The Theory 2 cases may have continued to press the TCV-ASD hypothesis because some of the factual predicates for the hypothesis are well established. The strong beliefs of many parents (and a small group of physicians and scientists) that vaccines are causal undoubtedly played a role as well. Vaccines received by most U.S. children in the 1990s through the 2001-2003 time frame contained more than trace amounts of thimerosal. When injected, thimerosal is metabolized into ethylmercury. A small portion of this ethylmercury reaches the brain, where an even smaller amount is converted to inorganic (mercuric) mercury. Once converted to inorganic mercury in the brain, it is virtually immobile. At certain brain levels in primates, organic mercury has been shown to cause fairly widespread activation of microglial cells and some reduction in astrocytic cells. Activated microglia have been found in autopsies of the brains of patients with ASD in greater numbers than in the brains of neurotypical individuals.

In spite of these widely-accepted factual predicates, the TCV-ASD causation hypothesis has been rejected by the general scientific community for many cogent reasons. However, it continues to be pressed by a small group of physicians and scientists associated with groups such as SafeMinds, DAN [Defeat Autism Now!], and ARI. Most of petitioners’ experts were drawn from this group. Dr. Deth’s research has been funded by them; Dr. Mumper is the medical director of ARI, and Dr. Aposhian has participated in ARI’s “think tanks.” Many of the published studies relied upon by the testifying experts, including nearly all of those relied upon by Dr. Aposhian in his “six pillars,” were written by individuals associated with ARI and other similar groups. As discussed in Sections VI-VIII above, the conclusions of this group are not grounded on reputable and reliable scientific foundations.

The view that ASD is caused by mercury may have persisted because it provides some hope that ASD can be treated, and even cured. The general scientific consensus is that ASD is the result of prenatal developmental problems shaped largely by genetic and epigenetic contributions. This consensus provides little hope for parents of children with ASD. Mainstream science does not, at present, offer many effective therapies, much less offer hope of a cure. Mainstream science tells us that some manifestations of autistic behavior can be treated with drugs, behavioral therapy, and speech and language therapy, but that few children will lose the diagnosis or live independently in adulthood. Understandably, many parents have looked to practitioners who offer hope of improvement, and even a cure.

After extensively reviewing the testimony, expert reports, and other evidence, I have concluded that petitioners have failed in the general causation case to demonstrate that TCVs cause or substantially contribute to ASD. Their experts proffered hypotheses that were illogical, contrary to the weight of the evidence, and, ultimately, unpersuasive.

B. Qualifications of the Experts

The quality of the expert opinions proffered in this case was heavily influenced by the expertise of the scientists and physicians offering them. Respondent produced an impressive group of physicians and scientists who were truly experts in the fields about which they testified. They had garnered awards from both peers and autism advocacy groups. Many had published hundreds of peer reviewed articles and book chapters pertaining to the subjects about which they testified. Dr. Rutter has been researching ASD for more than four decades, and Drs. Lord, Kemper, Rodier, Leventhal, and Rust have been involved in such research for nearly as long. Doctors [Jeff] Johnson, Mailman, [Dean] Jones, and [L. Jackson] Roberts each had extraordinarily impressive qualifications in the highly technical subject matter about which they testified. Dr. Brent brought both a treating physician’s perspective and a toxicologist’s background to the discussion of mercury’s effects on human beings, and clearly and carefully explained the significance of the science about which he testified. Only in epidemiology did the qualifications of petitioners’ expert even approach those of respondent’s, and even there, Drs. Fombonne and Rutter brought the additional expertise from their own research and publications in the epidemiology of ASDs. Dr. Goodman offered much-needed insight into the IOM reports on TCVs and expertise on the issues of “subgroups” and biological plausibility.

In contrast, petitioners produced a very well-qualified epidemiologist, Dr. Greenland, whose opinion was so limited as to be essentially useless as part of a causation hypothesis. Because the factual predicates for his opinion on “clearly regressive autism” were not established, Dr. Greenland’s primary contribution was pointing out the generally acknowledged weaknesses in the epidemiological studies of ASD and TCVs. Dr. Aposhian was qualified to opine on mercury, but lacked the qualifications in medical toxicology that Dr. Brent possessed. Dr. Deth’s experience in mercury, sulfur metabolism, oxidative stress, and ASD was minimal and recently acquired, and paled in comparison to that of respondent’s experts in academic background, teaching experience, research focus, publications, and awards and recognitions. Dr. Kinsbourne has not had a clinical practice in nearly two decades, and, in comparison to respondent’s experts, relatively little experience before that in diagnosing and treating children with ASD.

I emphasize that the qualifications of the experts were not, standing alone, determinative in my conclusion that petitioners have failed to make a prima facie case for mercury’s causal role in ASD. Not only were respondent’s experts far better qualified to opine, the evidentiary quality of their opinions exceeded that of petitioners’ witnesses. With very few exceptions, when one of respondent’s witnesses cited a medical or scientific study for a point, the study fully supported that point. Their opinions were well supported by other evidence, and, when contrary studies existed, they were careful to explain why they found them unpersuasive or unreliable. In contrast, on many occasions when I read a study that one of petitioners’ experts cited, I found that it did not provide substantial support for the point for which it was cited, or did so only in part, with the study as a whole being unsupportive of the proposition advanced by the expert. The studies that were supportive often had problems of their own in that they could not be duplicated by other researchers. Many of Dr. Aposhian’s conclusions were drawn from studies that could not be duplicated. Most of Dr. Deth’s opinions were based on his own unpublished work, certain aspects of which were, according to experts in the field, poorly performed and unlikely to be correct. Although peer review and publication are not necessary conditions for consideration in Vaccine Act cases, the problems with Dr. Deth’s own work cast substantial doubt on the conclusions he drew from it. As respondent’s experts correctly noted, Dr. Kinsbourne sometimes cited studies for unsupported propositions, misstated the degree of support found, and “cherry-picked” data from studies, while ignoring contrary data in the same study.

C. A Failure of Proof

As Dr. Rust stated, a hypothesis that is so broad that anything from measles virus to an environmental toxin could cause ASD is unlikely to be correct. Where the evidence was in conflict, the great weight of the evidence favored respondent. Thus, I have resolved most of the factual disputes against petitioners. With regard to ASD itself, I concluded that there is no reliable evidence that regressive autism is a disorder distinct from that of classic or early onset ASD. The evidence for any postnatal causal factors, including environmental toxins, is very weak. The weight of the evidence is that ASD originates prenatally, with genetics playing a very strong role in its origin and manifestations.

1. TCVs Do Not Substantially Contribute to Brain Mercury Levels.

Humans are born with some mercury present in their brain as the result of maternal exposure to various sources of mercury. Inorganic mercury continues to accumulate in the brain over a lifetime from sources ranging from food products and dental amalgams to air and water. Mercury is considered a neurotoxin, and its neurotoxic effects are more pronounced when the exposure occurs in utero. Harmful effects are a function of dose and other factors, including the method of administration, the species of mercury involved, and the time period over which exposure occurs.

However, there is no reliable evidence that TCVs produced anything more than minuscule levels of inorganic mercury in the brain of infant monkeys exposed to approximately 2.5 times as much mercury as human infants received in TCVs. In contrast, autopsy studies of U.S. infants who died within a few days of birth demonstrated mercury levels much higher than those of the infant monkeys, likely a result of prenatal exposure. A number of studies established that at birth, human infants have blood mercury levels strikingly similar to those of their mothers.

Dr. Aposhian’s contrary testimony and calculations were based on faulty premises. Although the widespread use of TCVs contributed some amount to the level of inorganic mercury in the brain, the amount contributed was very small in comparison to amounts that accrue from environmental exposures over time. The levels of mercury that have produced toxic symptoms, including the subtle neurodevelopmental testing abnormalities observed in children from areas with high levels of dietary exposure, have all been much higher than those produced by TCVs.

2. Evidence that TCVs Produce Neuroinflammation is Lacking.

Although exposure to far higher doses of methylmercury has been observed to produce neuroinflammatory responses in the brains of adult primates, there is no direct evidence that the ethylmercury from TCVs produces the same effects. The circumstantial evidence that vaccine level doses can do so, even in conjunction with other mercury exposure, is likewise lacking. Microglial activation is not specific to mercury, other heavy metals, or ASD; it occurs in many brain disorders, and may represent a response to injury, rather than its cause. An author of the Vargas study, one of the papers on which petitioners primarily relied, wrote that the neuroinflammatory responses observed in the brains of autism patients were not consistent with a response to a toxic exposure.

3. Mercury’s Known Biological Effects in the Brain Do Not Resemble Those of ASD.

What mercury exposure does to the brain is well established, and neither the structures nor the cell types principally injured by mercury exposure are those that are malpositioned, damaged, missing, or destroyed in ASD. Petitioners’ hypothesis requires that high level doses of mercury spare Purkinje cells, while low level doses damage them. The pathophysiological changes in the brain in ASD largely occur prenatally; prenatal exposure to high enough doses of mercury to cause observable neurological symptoms produces cerebral palsy and developmental delays, but has not been observed to produce anything resembling ASD’s core symptoms. Mercury causes damage to discrete anatomical regions of the brain associated with motor coordination; motor skills are largely unaffected in ASD.

4. The Symptoms of ASD Do Not Resemble Symptoms Produced by Mercury Exposure.

Dr. Rodier, the one witness with considerable expertise in both mercury exposure and ASD, testified that there are no similarities between ASD and either ethylmercury poisoning or mercury poisoning in general. If ASD results from a hypersusceptibility to mercury in a small group of children, one would expect the symptoms of this group to resemble closely those of mercury poisoning victims, with a lower dose producing similar effects in those genetically hypersusceptible. It does not. Sensory and motor disturbances are the first effects observed in mercury poisoning; language, communication, and social skills losses are among the first symptoms observed in ASD.

5. There is No Evidence of Hypersusceptibility to Mercury in Individuals with ASD.

Although both Drs. Aposhian and Deth testified about a hypersusceptibility to mercury, or mercury efflux disorder, there is no reliable evidence that one exists. The studies on which Dr. Aposhian relied could not be duplicated by other researchers. At best, preliminary evidence that children with ASD have higher biomarkers of oxidative stress suggests that they may be more affected by administration of substances that produce oxidative stress, but there is no evidence that they respond differently to vaccine level doses of thimerosal. To point to the existence of ASD as validation of that aberrant response is simply circular reasoning.

6. Postnatal Causes for ASD Are Unlikely.

The pathophysiological findings from the autopsy studies strongly point to a prenatal origin for nearly all the abnormal findings observed. The co-occurrence of dysmorphology in substantial numbers of those with ASD, and the dating of the origin of the dysmorphology to points in early gestation, buttresses the autopsy studies. ASD is strongly genetic, and although there is not a 100% concordance rate for ASD diagnoses in monozygotic twins, epigenetics may account for the discordance. Dr. Rutter explained that the development of human beings is designed to work in a particular way, but genes do not tell each cell what to do. Genetics specifies a pattern, but the pattern may be altered by many factors.

Injuries early in the prenatal period produce, as Dr. [Patricia] Rodier remarked, a cascade of further injuries in the nervous system. As the authors of the Connors study, relied upon by Dr. Aposhian, noted: “The neurobiologic mechanisms underlying autism are in place before birth.”

7. There is Insufficient Evidence that Regression or “Clear Regression” in ASD has a Separate Biological Basis.

Dr. Kinsbourne was unpersuasive in his attempts to establish that regression in ASD has a separate biological basis or even that it should be considered a separate type of ASD. His opinions were contradicted by several witnesses, each of whom had far more experience in diagnosis of ASD and research into how ASD presents. They described some loss of skills occurring in many, if not most, children with ASD, and rarely constituting the first sign or symptom of the disorder. Loss of skills is something apparent to parents; failure to meet milestones may or may not be. ASD may present in any number of subtle ways not readily apparent to untrained observers. Regression occurs in several genetically-caused disorders, clearly indicating that it need not be the result of a triggering postnatal event.

8. Neither Excitotoxicity nor Oxidative Injury is Likely as a Cause of ASD.

Glutamate may well play a role in ASD’s symptomology, but a general level of excitotoxicity caused by mercury damage is unlikely as a cause for ASD. Dr. Kinsbourne hypothesized that mercury causes neuroinflammation, which causes damage to astrocytes, leading to overexcited neurons firing too frequently. This scenario, in the opinion of several of respondent’s experts who have researched brain disorders, would lead to neurodegeneration and neuronal death. There is little evidence of neuronal death in ASD; neurons are frequently smaller and more numerous in ASD patients. Neuronal death progresses to patient death in other neurological disorders, most of which occur later in life. There is no evidence of progressive neurological injury in ASD.

9. Epidemiology Has Failed to Detect Any Connection Between TCV Exposure and ASD.

The epidemiological evidence presented was strong, but not dispositive, on the issue of general causation. These studies indicated that a causal connection between TCVs and ASD is unlikely, but not impossible. Because I have concluded that there is no evidence to show that “clearly regressive” autism exists as a separate phenotype of the disorder, and have likewise concluded that there is virtually no evidence suggesting that regression in general constitutes a separate phenotype with a distinct etiology, I consider the epidemiology relevant to my ultimate conclusion on general causation. Strong epidemiological evidence indicates that TCVs are unlikely to play a causal role. Although most U.S. vaccines manufactured after 2001 contained no more than trace amounts of thimerosal, its removal had no effect on the prevalence of ASD rates, even considering that stockpiles of TCVs may have been used for a year or two after manufacturing ceased.

D. Conclusion

The Theory 2 hypotheses have fared no better than the Theory 1 hypotheses. The evidence in favor of TCV causation of ASD is weak and singularly unpersuasive. Two processes that are not pathognomonic of any disorder, neuroinflammation and oxidative stress, were assigned a causal role in the development of ASD, but the presence of either or both in ASD patients says little to nothing about ASD’s potential causes. If ASD can be caused by neuroinflammation and/or oxidative stress, then anything that can cause either of those conditions belongs, according to Dr. Kinsbourne’s reasoning, “on the differential” for ASD causation. Petitioners have failed to demonstrate why TCVs – among all the possible causes of neuroinflammation and oxidative stress – are a probable cause of, or a substantial contributor to, ASD.


On Dr. Mumper’s clinical judgment (pp. 303-304)

Dr. Mumper’s willingness to rely on testing she considered of dubious reliability gave me pause, in addition to her willingness to make causal determinations based on laboratory testing not specific for ASD. Many of the test results she relied upon could be attributed to nutritional problems in a child with an extremely restricted diet. Others focused on peripheral markers that could not reflect what was happening in the brain. She proffered opinions on Colin’s mercury levels based on tests showing an absence of mercury in the presence of chelation, and opined that the one positive test result was extremely elevated without any reliable basis to do so.

…Having conducted little to no research herself, Dr. Mumper relied on the opinion of Dr. Aposhian regarding mercury efflux disorders in ASD. I rejected that opinion in Section VI. She relied on Dr. Deth’s opinions regarding sulfur metabolism and oxidative stress. However, even if the test results upon which she based her opinion regarding Colin’s sulfur metabolism and level of oxidative stress are accurate and reliable, they say little about mercury as a causal factor. Children with many diseases and disorders display markers of oxidative stress. Diet alone is a significant confounder of plasma levels of the oxidative biomarkers upon which Dr. Mumper relied, and she acknowledged that diet could skew these results. She relied on Dr. Kinsbourne’s opinion about neuroinflammation in ASD, and tried to tie Colin’s neurofilament test results to that opinion, but those results were performed by an unreliable laboratory. Furthermore, Dr. Kinsbourne did not suggest that neurofilament testing would be helpful or useful in detecting neuroinflammation. Most significantly, even if Colin had some degree of neuroinflammation, which the Vargas study would suggest is likely in those with ASD, neuroinflammation is so nonspecific that it would be of little evidentiary value to establish that mercury was its cause.

Dr. Mumper’s willingness to rely on Colin’s mercury test results as evidence of high levels of mercury in his body was particularly troubling. She admitted that his results were not typical of those she saw in other autistic children. She admitted that she knew of no research into normal mercury excretion levels after chelation against which Colin’s one positive mercury test could be measured. It appeared that regardless of the results for mercury levels, Dr. Mumper was willing to opine that they reflected mercury’s role in ASD. If levels were low, it was because the child had excretion difficulties even in response to chelation or was hypersusceptible to the low level of mercury present. If the levels were high, then the child was retaining mercury, demonstrating excretion difficulties, and thus had more mercury available to cause neuroinflammation. Thus, either the presence or the absence of mercury in test results in a child with ASD could be interpreted as “proof” of a mercury excretion problem. Finally, because Colin did not appear to be exposed to mercury on any continuing basis from diet and was not breast fed, he likely had a lower level of mercury in his system than other children. Thus, his TCV exposure would not be likely to “tip him over the edge.”


On the standard of proof in Vaccine Court: Applying Althen (pp. 304-310)

The burden on the petitioners in Colin’s specific case is to demonstrate by preponderant evidence that Colin’s ASD was caused by his vaccines. They asserted that the thimerosal component of those vaccines either caused or substantially contributed to his ASD. To meet their burden under Althen, petitioners must demonstrate by preponderant evidence “(1) a medical theory causally connecting the vaccination and the injury; (2) a logical sequence of cause and effect showing that the vaccination was the reason for the injury; and (3) a showing of a proximate temporal relationship between vaccination and injury.” Althen v. Sec’y, HHS, 418 F.3d 1274, 1278 (Fed. Cir. 2005).

In their post-hearing brief, petitioners acknowledged their burden to establish each of Althen’s three factors by a preponderance of the evidence. Petitioners correctly noted that scientific certainty regarding causation is not required by the Vaccine Act, and that circumstantial evidence showing that a vaccine was a preponderant cause is sufficient. Petitioners framed Althen’s first prong as requiring them to demonstrate that the immunizations in question can cause the type of injury at issue, and the second prong as “addressing the question of whether the particular vaccines did cause the particular condition at issue.”

1. Medical Theory

Evaluating petitioners’ medical theory is complicated by the many links in the chain of causation hypothesized. Some of the links are not reasonably subject to dispute, others are partially correct, and still others are just plain wrong. Concisely stated, their hypothesis is that Colin’s “neurodevelopmental injuries are the result of a neuroinflammatory process triggered by inorganic mercury…deposited in [his] brain[] as a byproduct of exposure to TCVs in the first two years months [sic] of life.” The inorganic mercury triggered neuroinflammation, characterized by the activation of the brain’s innate immune system. This neuroinflammation produced two interrelated effects. First, it created an environment of oxidative stress in the brain, “with a complex cycle of impaired and disrupted biochemical processes that interfered with brain function.” Second, it produced an excess of glutamate, the primary excitatory neurotransmitter in the brain, leading to a persistent state of overexcitation or overarousal.

Petitioners asserted that exposure to vaccines leads to an accumulation of “toxic” mercury in the brain. They asserted that inorganic mercury can cause neuroinflammation, which can disrupt neuronal functioning, leading to an excitatory-inhibitory imbalance, which is amplified by mercury-induced oxidative stress. This imbalance manifested in the development of other symptoms of ASD in a genetically susceptible child.

As the recitation and discussion of the evidence in Sections VI-VIII above demonstrate, petitioners failed to establish that their medical theory was probable, plausible, or reliable. They failed to produce sufficient reliable evidence to show that TCVs, either alone or in combination with other environmental mercury exposure, were a cause of ASD in children susceptible or vulnerable to such exposure. They failed to produce sufficient reliable evidence to demonstrate that TCVs, either alone or in combination with other environmental mercury exposure, can produce mercury levels capable of causing neuroinflammation. Thus, they failed to show that TCVs belong on the list of potential causes of ASD.

They framed the general causation question in terms of regression. “Can TCVs in general be a substantial factor in causing autistic regression in some susceptible or vulnerable number of children?” Petitioners relied on the general causation evidence “to establish by a preponderance of the evidence that TCVs could have been substantial contributing causes of [the] autistic regression[]” in Colin’s case. In making this argument, they appeared to distinguish Colin from other autistic children without loss of skills. Although they claimed that they were not seeking to show that regression is a separate diagnostic category or syndrome, they relied on Colin’s regression as a evidence of an environmental trigger or “second hit” demonstrating the effect of TCVs on a genetically susceptible child. Although petitioners argued that “none of the epidemiology addresses autistic regression of the sort these three boys experienced,” they did not explicitly state that Colin experienced the “clearly regressive autism” about which Dr. Greenland testified.

Petitioners correctly asserted that they have no burden to present epidemiologic evidence demonstrating an association between ASD and TCVs, calling such evidence “scant, at best.” The testimony of their own epidemiologist was even stronger. Dr. Greenland testified that he did not find the only studies purporting to show an increased risk of autism associated with TCVs – studies by Dr. [Mark Geier] and Mr. [David] Geier – to be of evidentiary value.

While certain subpoints of their causation hypothesis – their medical theory – were clearly established or uncontested, most were not. Although they called their evidence “robust and reliable” and claimed that a prima facie case for causation in general had been established, I have concluded otherwise.

Althen requires more than merely asserting a medical theory. Petitioners must offer a reputable medical theory, and inherent in that standard is a requirement that the theory be biologically plausible. See Walther, 485 F.3d at 1148 and Pafford, 451 F.3d at 1355-56 (petitioner’s theory must be reputable). The theory of TCV causation is simply not reliable, and can no longer be considered “biologically plausible,” in view of all that is known about mercury in the brain.

2. Logical Sequence of Cause and Effect

Petitioners equated Althen’s second prong to establishing whether causation had been shown in Colin’s specific case. They argued that “ample indirect and circumstantial evidence” established that Colin’s TCVs caused neuroinflammation that caused his ASD. Even if Dr. [Bennett] Leventhal applied a heightened evidentiary standard to determining causation in Colin’s specific case, I have not. At best, the evidence established that Colin received vaccines that probably contained thimerosal and that he had a diagnosis of ASD. No sequence of cause and effect between the two can be logical, in view of the conclusion that petitioners have failed to establish a causal connection in general between ASD and TCVs.

Furthermore, Dr. Mumper’s causal opinion is based, in large part if not in its entirety, on the opinions of Drs. Kinsbourne, Deth, and Aposhian, whose opinions I have rejected as scientifically implausible and unsound. Notwithstanding this defect, the specific factors she cited as important in Colin’s case largely concerned testing performed by laboratories with questionable reliability. Many of the laboratory tests upon which she relied are not tests appearing in standard laboratory manuals or tests that would even be ordered by most practitioners, and the data they provide are not diagnostic of ASD. Treatments designed to target the “problems” noted in Colin’s test results were not efficacious, either in the view of Colin’s parents or in the view of Colin’s subsequent treating physician.

In their post-hearing brief, petitioners appear to acknowledge the problematic nature of Colin’s test results. Although Dr. Mumper testified about a number of test results that contributed to her opinion that Colin’s ASD was caused by his TCVs, in their post-hearing brief they only mentioned a “latent, genetic inabilit[y] to properly metabolize and excrete mercury.” Colin’s only positive mercury test occurred after chelation, and its results were not measured against any standardized normal values. In spite of numerous other rounds of chelation with a variety of chemical and “natural” chelators, no detectible levels of mercury were ever again excreted. This result is not compatible with a child with problems metabolizing and excreting mercury.

Petitioners’ causation claim is unaffected by Dr. Greenland’s opinion that the existing epidemiological studies of ASD cannot detect a causal connection with TCVs on a small subgroup. The hypothetical subgroup he described involved regression after previously normal development. Contrary to petitioners’ assertions, Colin was not developmentally normal at the time he received his last TCV. Colin’s ASD had already begun to manifest by the time he was 20 months of age. Thus, Dr. Greenland’s opinion that the epidemiological studies of ASD cannot rule out an effect on a small subgroup of children is irrelevant to Colin’s case.

Ruling out known causes of ASD, as Dr. Mumper did in her report and testimony, is not sufficient to put TCVs on the list of possible causes. “Although probative… a simplistic elimination of other potential causes” is insufficient to show actual causation. Moberly 592 F.3d at 1323 (citing Althen, 418 F.3d at 1278); see also Ruggiero v. Warner-Lambert Co., 424 F.3d 249, 254 (2d Cir. 2005) (using differential diagnosis to eliminate other causes is insufficient to demonstrate causation). Thus, the process of differential diagnosis cannot be applied to conclude that Colin’s ASD must have been caused by TCVs, once other causes are ruled out. A differential diagnosis is only as good as the list of possible causes.

3. Proximate Temporal Relationship

Onset after vaccination is not enough, standing alone, to satisfy Althen’s third prong. Petitioners have the burden to demonstrate the existence of a “scientific temporal relationship.” Pafford v. Sec’y, HHS, 64 Fed. Cl. 19, 29-30 (2005), aff’d, 451 F.3d 1352 (Fed. Cir. 2006). The time frame must be medically acceptable. De Bazan 539 at 1352.

Petitioners did not address this prong of the Althen standard in their briefs and this omission is a significant flaw. The failure to show that a disease arose in the time expected by the medical community means a petitioner is not entitled to compensation. Pafford, 451 F.3d at 1358-60. It is clear that Colin’s ASD manifested with speech delay at or before 20 months of age, before he received his last round of vaccinations. At that point in his life, he had already received vaccines containing as much as 212.5 μg of ethylmercury. However, none of petitioners’ experts opined on the time frame in which mercury must be received in order to cause autism in a developing brain. The weight of the evidence was that ASD’s origins are largely prenatal, and thus any environmental insult contributing to its largely genetic cause must have occurred prenatally. Respondent’s experts indicated that if post-natal causes played any role in the many neuropathological differences found in individuals with ASD, they must occur very early in the post-natal period, but the experts did not think postnatal causes were likely or probable.

At best, petitioners have demonstrated that Colin’s ASD manifested after most of his vaccinations. That would be true of any child with this condition who had received vaccines, because ASD cannot be reliably diagnosed until at least one year of age, even if subtle indicators may have existed earlier. Most ASD symptoms become apparent to parents at 18-24 months of age, and thus onset will follow vaccinations in almost every child with ASD.

4. No Burden on Respondent to Establish an Alternate Cause

Petitioners have failed to establish any of Althen’s three factors. Thus, they have failed to establish that Colin’s vaccines were a substantial cause of his injury. Because they have failed to establish causation by a preponderance of the evidence, the burden never shifted to respondent to establish an alternative cause for Colin’s condition. De Bazan, 539 F.3d at 1353-54.

5. Summary

In concluding that petitioners have failed to establish that Colin’s TCVs caused his ASD, I emphasize that I have not applied a heightened evidentiary burden. I did not require scientific certainty, nor direct evidence of causation. Daubert requires that an opinion be supported by something more than subjective belief; it must be grounded in “the methods and procedures of science.” 509 U.S. at 590. There is no evidence that mercury has ever caused an ASD, only speculation that it might. At best, there is some evidence of an ongoing inflammatory process in ASD, but no indication that it is caused by mercury, and many indications that it is not. The excitation-inhibition theory is likewise unsupported in the peer reviewed medical literature; at best, there is some speculation that some ASD symptoms may be a reflection of an excitatory-inhibitory imbalance, but no proof of any biological overarousal when the symptoms are observed.

Scientists use the terms “hypothesis” and “theory” with very specific meanings. A hypothesis is an idea proffered to explain an event. A theory is what is developed after a hypothesis has been subjected to many attempts to disprove it, and thus, it is likely correct. This is an important distinction, because in biology, almost anything is possible. The pertinent question is whether something is probable or likely. Petitioners had several hypotheses but nothing that approached a theory. As Dr. Rust commented: “Hypotheses are a dime a dozen.”

A number of governmental and non-governmental scientific agencies have looked at the issue of a relationship between TCVs and ASD. These agencies include the National Academy of Sciences, Institute of Medicine, American College of Medical Toxicology, American Academy of Pediatrics, World Health Organization, U.S. Center for Disease Control and Prevention, the European Medicine Agency, and the American Academy of Family Practice. They have all concluded that there is no causal connection between the two.

Unfortunately, the Dwyers (and uncounted other parents of children with ASD) have relied upon practitioners and researchers who peddled hope, not opinions grounded in science and medicine. My heart goes out to parents like the Dwyers who struggle daily, emotionally and financially, to care for their children, but I must decide cases based on the law and not sentiment. The law in this case requires preponderant evidence that TCVs caused or substantially contributed to Colin’s ASD, and, by that standard, petitioners are not entitled to compensation.

Conclusion

Petitioners have not demonstrated by a preponderance of the evidence that Colin’s condition was either caused or significantly aggravated by his vaccinations. Thus, they have failed to establish entitlement to compensation and the petition for compensation is therefore DENIED. In the absence of a motion for review filed pursuant to RCFC, Appendix B, the clerk is directed to enter judgment accordingly.

IT IS SO ORDERED.

Denise K. Vowell
Special Master

Thimerosal-Autism Test Cases Dismissed · 6 days ago

This afternoon, the issued decisions in King v. Secretary of HHS (Case No. 03-584V), Mead v. Secretary of HHS (Case No. 03-215V), and Dwyer v. Secretary of HHS (No. 03-1202V), the three Vaccine Injury Compensation Program claims chosen by the Omnibus Autism Proceeding Petitioners’ Steering Committee for the presentation of evidence supporting the hypothesis that autism can be caused by the administration of vaccines containing the mercury-based antifungal thimerosal.

All three claims have been dismissed for failure to demonstrate that thimerosal-containing vaccines can cause autism, or that they did cause autism in any individual case.

Arguments in King and Mead were presented at a joint hearing held in Washington, D.C., from May 12 through May 30, 2008, before Special Master George L. Hastings and Special Master Patricia Campbell-Smith. A hearing in Dwyer was held on June 21-22, 2008, before Special Master Denise K. Vowell.

The ruling in King was written by Special Master George L. Hastings; in Mead by Special Master Patricia Campbell-Smith; and in Dwyer by Special Master Denise K. Vowell.

The following passages have been excerpted from the King ruling. Excerpts from Mead and Dwyer, will be published on this weblog over the next few days.


From King v. Secretary of HHS (Case No. 03-584V)

Issued March 12, 2010

Introduction (p. 2)

The petitioners in this case have advanced the theory that thimerosal-containing vaccines can substantially contribute to the causation of autism, and that such vaccines did contribute to the causation of Jordan King’s autism. However, as to each of those issues, I conclude that the evidence is overwhelmingly contrary to the petitioners’ contentions. The expert witnesses presented by the respondent were far better qualified, far more experienced, and far more persuasive than the petitioners’ experts, concerning the key points. The numerous medical studies concerning the issue of whether thimerosal causes autism, performed by medical scientists worldwide, have come down strongly against the petitioners’ contentions. Considering all of the evidence, I find that the petitioners have failed to demonstrate that thimerosal-containing vaccines can contribute to the causation of autism. I further conclude that while Jordan King has tragically suffered from autism, the petitioners have also failed to demonstrate that his vaccinations played any role at all in causing that condition.

The scope of the record (p. 15)

[T]he evidentiary record, based upon which I have decided this case, is massive. This record far exceeds any evidentiary record that I have seen in other Program cases, with the exception of the record in the three test cases concerning the PSC’s first theory of autism causation. A few statistics may give a flavor of the amount of material involved. The parties filed a total of 26 expert reports in this King case and the companion Mead and Dwyer cases. At the evidentiary hearings, expert witnesses testified during the combined King/Mead hearing, and two during the Dwyer hearing. The hearing transcripts totaled more than 3200 pages for the King/Mead hearing, plus more than 300 pages in Dwyer. And the petitioners filed more than 1000 pages of Jordan King’s medical records in this King case alone.

In addition, the amount of medical literature filed into the records of the three cases was staggering. In the three cases, the parties filed more than 1200 medical journal articles, medical textbook excerpts, or other items of medical literature (even after excluding from the count those documents that were filed in more than one case). Some of those items were extremely lengthy. The total number of pages of those documents runs well into the tens of thousands of pages. And most of those documents are densely packed with technical information.

Petitioners’ theory summarized (p. 19)

As noted above, the petitioners’ overall “general causation” theory in this case can be summarized as follows. Petitioners note that the thimerosal in thimerosal-containing vaccines, received by infants during their early months of life, after entering the body breaks down into its component parts, one of which is ethylmercury; some of that ethylmercury then makes its way into the brain and is converted into inorganic mercury. They contend that such inorganic mercury can, in susceptible individuals, trigger a process of “neuroinflammation,” including “oxidative stress,” in the infant’s brain. The neuroinflammation, they contend, can impair and disrupt the infant’s brain function, resulting in autistic symptoms.

The petitioners contend that such an autism causation process has occurred in many children. They do not argue that the thimerosal is the sole cause of the autism in such cases, but that the thimerosal substantially contributes to the causation of autism, in individuals who for genetic reasons are especially susceptible to that causation process. They contend that this causation process occurs in individuals who suffer from a particular subcategory of autism known as “regressive autism.”

Respondent’s argument, and points in dispute, summarized (p. 20)

Respondent’s experts explained that all humans have some amount of mercury in their brains from a number of non-vaccine sources, without harm, and those experts argued that there is no evidence that the extremely small amounts of mercury in thimerosal-containing vaccines would make any significant difference in the overall amount of mercury in a child’s brain, or can cause any harm to the brain.

Respondent’s experts also pointed out what they believe to be many gaps, inaccuracies, and errors in the individual parts of the petitioners’ theories, and in the testimony offered by each of the petitioners’ expert witnesses. For example, respondent’s experts explained that while evidence of neuroinflammation has been found in the brains of some autistic children, medical researchers have as yet not discovered whether such inflammation plays a role in causing autism. Those experts also argued that there is no evidence that inorganic mercury in the brain causes neuroinflammation, and that even if inorganic mercury in the brain could cause autism, the evidence shows that infants have substantially more inorganic mercury in the brain from other sources than from the very small amounts of mercury in thimerosal-containing vaccines.

Respondent’s experts also pointed out that the petitioners’ theory seems unlikely in light of certain basic scientific understandings about the causation of autism, including the facts (1) that autism is very strongly genetic in origin, (2) that the only established non-genetic factors in causing autism are prenatal exposures, and (3) that autopsy studies indicate that the abnormal features of autistic brains are features that of necessity would arise during the early prenatal period.

Respondent’s experts argued further that when, on occasions in the past, mercury exposure (involving much greater amounts of mercury) has been harmful to the human brain, the actual symptoms involved have been nothing like autism.

Respondent’s experts also stressed that the theory that thimerosal-containing vaccines can contribute to the causation of autism has been addressed by many “epidemiologic” studies performed by researchers around the world, and that all of the competent studies have found no association between thimerosal-containing vaccines and autism.

Summary concerning qualifications of experts (p. 31)

I must stress that the weighing of the relative credentials of the respective parties’ experts is not necessarily a determinative factor in any Vaccine Act case. To the contrary, a Vaccine Act factfinder need not automatically adopt the view of the expert or experts with more experience or more striking academic credentials. Sometimes an expert with lesser experience or credentials may offer superior analysis, and may therefore prove to be more persuasive.

In this case, the superiority in expert credentials is certainly not the decisive factor in my analysis. In this case, the testimony of the respondent’s experts, concerning virtually every issue, was simply better explained, more logical, and backed by far greater scientific evidence than that of the petitioners’ experts. Accordingly, the outcome of my analysis would be the same regardless of the credentials of the experts.

Nevertheless, in this case it is simply noteworthy that respondent’s experts, in addition to offering more persuasive testimony, also do possess substantially superior experience and background concerning the causation issues in this case

Summary concerning impact of accepted science on petitioners’ general causation theory (p. 41)

Considering the existing evidence concerning the causation of autism as a whole, I must conclude that such evidence tends to make the petitioners’ theory advanced in this case seem unlikely. That is, as explained above, first we know for certain that genetic factors and prenatal exposures can cause autism, while it is as yet unclear whether postnatal factors play any causal role.

Second, the petitioners’ theory is strongly contradicted by the above-discussed autopsy studies, which indicate that autism is caused by brain malformations occurring prior to birth.

In this regard, however, I must raise three caveats. First, as noted above, the causation of autism is still not well understood, and we also have the evidence discussed above raising the possibility that postnatal factors might play a causal role. Therefore, my point set forth in this section V©(6) of this decision is certainly not the strongest argument against the petitioners’ theory. But this point does add some additional reason to be doubtful of the causation theory advanced by the petitioners in this case.

Second, I want to be clear that, in including this point concerning “accepted” scientific understandings, I do not mean to suggest that a petitioner’s causation theory must automatically be rejected simply because it differs from “generally accepted” medical thinking, or because it goes

Summary concerning “regressive autism” (p. 47)

In sum, another severe problem with Dr. Kinsbourne’s and petitioners’ causation theory is their attempt to offer it as a possible cause only for “regressive autism,” and not for autism in general. Dr. Kinsbourne could offer no explanation
limitation is inconsistent with the phenomenon of sudden regression in some cases. is inconsistent with the extensive evidence that makes it very unlikely that regressive autism is a distinct sub-type of autism that would be likely to have different causes than other forms of autism. This problem, thus, is another factor that casts grave doubt on the petitioners’ causation theory.

Dr. Kinsbourne’s theory is inconsistent with the improvement commonly seen in autism (p. 53)

Another aspect in which Dr. Kinsbourne’s theory is inconsistent with what is known about autism concerns the fact that children with autism often improve at some point. Dr. Lord, the psychologist who has studied autism for about 40 years, including nearly 30 years of studying regression in autism, testified that most children with autism experience improvement to some extent, including children who have experienced regression in autism. Dr. Rust, also with extensive experience in autism, similarly testified that autistic children commonly improve, often at the age of four or five years. Dr. Kinsbourne’s theory, however, involving persistent neuroinflammation by inorganic mercury that accumulates and remains in the brain, is inconsistent with this common phenomenon of improvement of autistic symptoms, as Dr. Rust pointed out. To the contrary, as Dr. Rust also noted, if Dr. Kinsbourne’s theory were true one would expect to see progressive deterioration of such individuals over a lifetime, which is not the case. That would be true because most people would continue to get additional amounts of inorganic mercury into their brains throughout their lifetimes from sources other than thimerosal, especially from methylmercury via food sources such as fish.

Summary concerning “genetic hypersusceptibility” and “mercury efflux disorder” theories (p. 60)

I find that Dr. Brent’s testimony concerning these issues was persuasive, and that the testimony of Dr. Aposhian was not. I conclude that the Holmes, Hu, Adams, and Bradstreet studies are of doubtful reliability, and that the contrary studies cited by Dr. Brent provide better evidence. I conclude that the Woods and Nataf articles also provide no significant support to Dr. Aposhian’s theory. Accordingly, after analysis of all of the evidence in this regard, I conclude that there is no merit to the “genetic hypersusceptibility” and “mercury efflux disorder” theories proposed by Dr. Aposhian and the petitioners.

Summary concerning Dr. Aposhian (p. 69)

For the reasons set forth above, as to each of the specific topics addressed by Dr. Aposhian, I find that the testimony of Dr. Brent, and/or that of another of respondent’s witnesses, was much more persuasive than that of Dr. Aposhian. I find that Dr. Aposhian’s testimony did not supply any credible support to the petitioners’ general causation theory.

Summary concerning Dr. Deth (p. 76)

Each of respondent’s five experts who discussed Dr. Deth’s theory found it to be without merit. Dr. Johnson, the neuropathologist, opined that Dr. Deth’s entire approach to the issue was simply unscientific, and wholly invalid. Dr. Jones, the medical biochemist, explained that the evidence indicates that the small amounts of inorganic mercury from thimerosal-containing vaccines would not have any of the effects proposed by Dr. Deth, so that there is “no plausibility * * * at all” to Dr. Deth’s hypothesis Dr. Mailman, the neuropharmacologist, stated that “the odds of [Dr. Deth’s theory] being correct are literally almost infinitesimal.” Dr. Roberts, the expert with superb experience concerning oxidative stress, summarized that there is no reliable evidence at all that autism is caused by oxidative stress, much less oxidative stress resulting from thimerosal-containing vaccines. And Dr. Brent, the medical toxicologist, stated that there is “absolutely not” any evidence that thimerosal-containing vaccines induce oxidative stress.

Indeed, even Dr. Deth himself admitted that his theory still awaits testing, is only a “useful starting point” for considering the thimerosal/autism causation issue, and could be “revised or discarded.”

Dr. Mumper’s view concerning “general causation” (p. 78)

I acknowledge that Dr. Mumper is a pediatrician of considerable experience, with a creditable academic background, and with very substantial experience in treating autistic children. I find no reason to believe that Dr. Mumper is not sincere in her general view that thimerosal-containing vaccines can contribute to causing autism. And I acknowledge that the mere fact that she holds that general view, given her credentials, is at least some evidence in favor of that general view. However, having already thoroughly considered and rejected the reasoning and evidence upon which Dr. Mumper seems to rely, I conclude that the evidentiary value of her general opinion is far outweighed by the overwhelming evidence to the contrary provided by respondent’s experts and the medical literature supplied by respondent.

Summary concerning epidemiological studies (p. 84)

In sum, following the initiation of public concerns that thimerosal in vaccines might be a contributing factor in causing autism, a number of research groups in several countries devised several different types of studies to test that issue. Each of the studies described and discussed above, however, failed to find any evidence that thimerosal-containing vaccines are associated with autism, as pointed out by all three of respondent’s epidemiologic experts. To be sure, none of those studies is definitive by itself. While each of the study approaches has its strengths, each also has acknowledged limitations and weaknesses. However, when all of the studies are considered together, the study results are highly important. First of all, the studies show that medical researchers have looked extensively for any affirmative evidence that thimerosal-containing vaccines can contribute to the causation of autism, but have failed to find any such evidence. Therefore, when taken together, the studies make it appear extremely unlikely that thimerosal-containing vaccines have played any significant role in the overall causation of autism. Of course, it is true that epidemiologic studies cannot prove definitively that Factor A never causes Condition B; such a study cannot ever completely rule out the possibility that Factor A causes a tiny percentage of the cases of Condition B, a percentage too small for the study to detect. However, when a variety of well-designed studies by different researchers have looked extensively for evidence of an association between Factor A and Condition B, but have found none, not only can one conclude confidently that Factor A does not cause a significant percentage of cases of Condition B, but it is also reasonable to interpret those studies as casting at least some doubt on the proposition that Factor A ever causes Condition B. In this case, the studies described above, taken as a whole, show very clearly that thimerosal-containing vaccines do not cause any substantial portion of the cases of autism in the studied countries. And while those studies cannot completely rule out any possibility that thimerosal-containing vaccines might play some causative role in a tiny fraction of autism cases (a fraction too small to be detected by even the largest studies), it seems to me that the failure of so many studies to find any association between thimerosal-containing vaccines and autism at least casts doubt upon the proposition that thimerosal-containing vaccines ever play a role in causing autism.

Studies by the Geiers (p. 86)

After careful consideration, I conclude that the Geiers’ studies cannot be given any weight. A number of those studies were considered by the Institute of Medicine (IOM) committee that fully studied the entire thimerosal/autism causation issue in 2004. That committee concluded that the studies were so flawed as to be “uninterpretable,” and that the studies contributed nothing meaningful (“noncontributory”) concerning the causation issue. The committee noted that the studies were based on databases that themselves had “significant limitations”, and that the studies had “serious methodological problems” or “serious methodological limitations”. The committee added that the Geiers’ articles describing their analytical methods were “not transparent” and omitted “important details,” so that it was impossible to evaluate the studies. Other specific deficiencies in the studies were also discussed, including the fact that the Geiers incorrectly used several epidemiologic terms and measures.

In addition, Dr. Fombonne agreed with the IOM’s criticisms of the Geier studies, and testified that the Geier studies in general failed to use accepted epidemiologic methods. Dr. Rutter was critical of the Geier studies as well. Further, petitioners’ own expert witness concerning epidemiology, Dr. Greenland, agreed with the criticisms of the Geier articles, acknowledging that those studies are “deficient in methodology.” And none of the expert witnesses for the petitioners vouched for the reliability of the Geier studies.

I have reviewed the published Geier studies discussed in the 2004 IOM report, and I agree with the analysis of those studies set forth in that IOM report. Further, I have reviewed the additional studies published by the Geiers since the 2004 IOM report, and find that those studies suffer from the same type of flaws as the earlier Geier studies. That view includes a study published in 2008 by the Geiers, along with Young as a third author. Two of respondent’s experts, Drs. Fombonne and Rutter, testified that that 2008 study was again deeply flawed, and those experts provided a number of specific examples of deficiencies in the study. And, again, none of the petitioners’ experts testified in support of that 2008 Young, Geier, and Geier study.

In summary, I conclude that all of the Geier epidemiologic studies are not reliable, and cannot be accorded any weight.

There is absolutely no evidence for the proposition that there is an association between thimerosal-containing vaccines and “clearly regressive autism.” (p. 93)

Finally, with respect to Dr. Greenland’s point regarding “clearly regressive autism,” it is important to stress again that there is not a shred of evidence to support the idea that there is an association between thimerosal-containing vaccines and “clearly regressive autism.”

Again, the fact that when confronted by the epidemiologic evidence the petitioners need to alter their causation theory in a fashion inconsistent with the rest of their expert testimony, and to rely on the mathematical possibility of a hypothetical association between thimerosal-containing vaccines and “clearly regressive autism” for which there is zero evidence in the record, is further evidence of the lack of merit to the petitioners’ “general causation” theory.

In addition, there is no good reason to even suspect that there might be an association between thimerosal-containing vaccines and “clearly regressive autism.” As respondent’s epidemiologic expert Dr. Goodman explained, to even seriously consider Dr. Greenland’s hypothetical “clearly regressive autism” theory, there must be some plausible biologic reason to suspect that “clearly regressive autism” might be causally different than other forms of autism. But petitioners’ experts have never even proposed such a biologic reason. As explained in detail above, there is no reason to think that regressive autism might have different causal factors than autism in general. For similar reasons, the record of this case contains no reason to suspect that the theorized category of “clearly

In sum, the petitioners’ “clearly regressive autism” argument is completely devoid of any supporting evidence.

Summary concerning “irrelevancy” argument (pp. 93-94)

[I]t is true, as a statistical matter, that the epidemiologic studies detailed above, while showing clearly that thimerosal-containing vaccines could not be causing any substantial portion of the cases of autism in general, do not completely rule out the possibility that thimerosal-containing vaccines might be associated with some theoretical very small subgroup of autism. Nonetheless, the balance of evidence from those studies weighs substantially against the petitioners’ causation theory. First, it is an exceedingly slight point in the petitioners’ favor for them to claim that these many studies by different researchers in different countries have not completely ruled out the possibility of any merit to their “general causation” claim. The larger point is that none of those many competent studies has yielded the slightest bit of evidence in the petitioners’ favor — and, of course, it is the petitioners’ burden to show that thimerosal-containing vaccines do likely contribute to the causation of some form of autism, not the respondent’s burden to show that there is absolutely no possibility of a causal link.

Second, in my view the failure of so many studies to find any association between thimerosal-containing vaccines and autism, while not completely ruling out a possible causal role with respect to a subset of autism, at least casts doubt upon the proposition that thimerosal-containing vaccines ever play a role in causing any kind of autism, including “regressive autism” or “clearly regressive autism.” This is especially true given the absence of any credible evidence that “regressive autism” or “clearly regressive autism” might constitute a distinctive subtype of autism that might be likely to have different causative factors than other forms of autism.

Summary concerning epidemiology (p. 96)

The numerous epidemiologic studies done over the past ten years, when taken together, make it extremely unlikely that thimerosal-containing vaccines have played any significant role in the overall causation of autism. It is true, as the petitioners argue, that the available epidemiologic studies do not completely rule out the possibility that thimerosal-containing vaccines might be associated with some small subgroup of autism, such as the newly-theorized subgroup of “clearly regressive autism.” However, the epidemiologic evidence still must be said to provide significant evidence against the petitioners’ general causation theory set forth in this case. First, none of the numerous competent studies has yielded the slightest bit of evidence in the petitioners’ favor.

Second, the failure of so many studies to find any association between thimerosal-containing vaccines and autism, while not ruling out a possible causal role with respect to a very small subgroup of autism, at least casts doubt upon the proposition that thimerosal-containing vaccines have ever played a role in causing any kind of autism, including “regressive autism” or “clearly regressive autism.” This is especially true given the absence of any evidence that “regressive autism” or “clearly regressive autism” might constitute a distinctive subtype of autism that might be likely to have different causative factors than other forms of autism.

Accordingly, my conclusion is that the epidemiologic evidence does provide yet another strong reason to reject the petitioners’ general causation theory presented in this case.

Summary concerning “general causation” issue (p. 99)

For all the reasons stated above, I conclude that the petitioners have failed completely to demonstrate that it is “more probable than not” that thimerosal-containing vaccines can be a substantial factor in contributing to the causation of autism, in individuals suffering from regressive autism, “clearly regressive autism,” or any type of autism. To the contrary, the evidence in the record of this case makes it appear extremely unlikely that thimerosal-containing vaccines contribute to the causation of any form of autism.

Dr. Mumper’s reliance on the testing of Jordan was misplaced. (pp. 102-108)

[A] careful analysis of the record demonstrates that there is no valid basis for Dr. Mumper’s view that the results of mercury excretion testing on Jordan King offer support for a conclusion that thimerosal-containing vaccines played a role in causing Jordan’s autism. To the contrary, the evidence supports a conclusion that Dr. Mumper’s reliance on such mercury tests has no basis in science or logic. Indeed, upon cross-examination even Dr. Mumper acknowledged that there is no particular profile or pattern of post-provocation test results that points to a finding that a child has mercury-induced autism. When pressed, Dr. Mumper could not even suggest an example of any type of result on a post-provocation mercury urine test that would not, in her analysis, support a claim of mercury-induced autism. Dr. Mumper’s analysis in this regard was illogical, and completely unpersuasive. (Footnote: There are so many defects in Dr. Mumper’s testimony that it is impossible to list them all. But another major point of illogic in her testimony is that even if Dr. Mumper’s testimony showed that mercury did have some role in causing Jordan King’s autism, she made no case that the inorganic mercury resulting from thimerosal-containing vaccines would be the culprit, rather than the greater amounts of mercury that Jordan likely received from other sources.)

Summary concerning “specific causation” (p. 112)

I conclude that the petitioners have failed completely to demonstrate that it is “more probable than not” that thimerosal-containing vaccines contributed to the causation of Jordan King’s own autism.

Legal arguments raised by petitioners (p. 115-116)

In their initial post-hearing brief filed in this case, the petitioners set forth a brief discussion of the legal considerations in a causation-in-fact case, under the Program statute and the Althen test. Most of their points are correct statements of the applicable law. As the petitioners stress, their burden is to demonstrate causation by a “preponderance of the evidence” — i.e., “more probable than not” — not “scientific certainty.” Althen, 418 F.3d at 1279. They need not demonstrate that Jordan’s thimerosal-containing vaccines were the sole cause or even a predominant cause of Jordan’s autism, but only that thimerosal-containing vaccines were a “substantial factor” in causing his autism, and a “but for” cause. Shyface v. Secretary of HHS, 165 F.3d 1344, 1352 (Fed. Cir. 1999). Petitioners’ causation showing need not necessarily be supported by epidemiologic evidence or other medical literature, but could, in appropriate circumstances, be accomplished by medical opinion and/or circumstantial evidence. Althen, 418 F.3d at 1279-80; Capizzano v. Secretary of HHS, 440 F.3d 1317, 1325 (Fed. Cir. 2006). Petitioners need not demonstrate the exact biological mechanism of causation. Knudsen v. Secretary of HHS, 35 F.3d 543, 549 (Fed. Cir. 1994). And the Federal Circuit has also stated that “close calls regarding causation are resolved in favor of injured claimants.” Althen, 418 F.3d at 1280.

I have kept all of these points in mind in deciding this case. I have not required a level of proof greater than “more probable than not,” which has also been described as “50 percent plus a feather.” I understand fully that petitioners are not claiming that Jordan’s thimerosal-containing vaccines were the sole cause of his autism, but are alleging only that such vaccines contributed to the causation of his autism, allegedly in concert with an underlying genetic vulnerability. I have looked beyond the epidemiologic evidence to determine whether the overall evidence — i.e., medical opinion, circumstantial evidence, and other evidence considered as a whole — tips the balance even slightly in favor of a causation showing as to Jordan’s autism.

This case, however, is not a close case. The overall weight of the evidence is overwhelmingly contrary to the petitioners’ causation theories. The result of this case would be the same even if I totally ignored the epidemiologic evidence. The result would be the same if I restricted my consideration to the evidence originally filed into the record of this King case, disregarding the additional “general causation” evidence imported from the Dwyer case. The petitioners’ evidence has been unpersuasive on many different points, concerning virtually all aspects of their causation theories, with each such deficiency having been discussed in detail above. The petitioners have failed to persuade me that there is validity to any of their general causation arguments, and have also failed to persuade me that there is any likelihood that Jordan’s thimerosal-containing vaccines contributed in any way to the causation of Jordan’s own autism. To the contrary, based upon all the evidence that I have reviewed, I find that it is extremely unlikely that Jordan’s autism was in any way causally connected to his thimerosal-containing vaccines. In short, this is a case in which the evidence is so one-sided that any nuances in the interpretation of the causation case law would make no difference to the outcome of the case.

Conclusion (p. 116)

The record of this case demonstrates plainly that Jordan King and his family have been though a tragic ordeal. I had the opportunity, in the courtroom during the evidentiary hearing, to meet and observe Jordan’s mother. I have also studied the records describing Jordan’s medical history, and the efforts of his family in caring for him. Based upon those experiences, the great dedication of Jordan’s family to his welfare is readily apparent to me.

Nor do I doubt that Jordan’s parents are sincere in their belief that vaccines played a role in causing Jordan’s autism. Jordan’s parents have heard the opinions of physicians who profess to believe in a causal connection between thimerosal-containing vaccines and autism. After studying the extensive evidence in this case for many months, I am convinced that the opinions provided by the petitioners’ experts in this case, advising the King family that there is a causal connection between thimerosal-containing vaccines and Jordan’s autism, have been quite wrong. Nevertheless, I can understand why Jordan’s parents found such opinions to be believable under the circumstances. I conclude that the Kings filed this Program claim in good faith.

Thus, I feel deep sympathy for the King family. Further, I find it unfortunate that my ruling in this case means that the Program will not be able to provide funds to assist this family, in caring for their child who suffers from a serious disorder. It is certainly my hope that our society will find ways to ensure that generous assistance is available to the families of all autistic children, regardless of the cause of their disorders. Such families must cope every day with tremendous challenges in caring for their autistic children, and all are deserving of sympathy and admiration. However, I must decide this case not on sentiment, but by analyzing the evidence. Congress designed the Program to compensate only the families of those individuals whose injuries or deaths can be linked causally, either by a Table Injury presumption or by a preponderance of “causation-in-fact” evidence, to a listed vaccine. In this case, the evidence advanced by the petitioners has fallen far short of demonstrating such a link. Accordingly, I conclude that the petitioners in this case are not entitled to a Program award on Jordan’s behalf.

George L. Hastings, Jr.
Special Master

U.K. General Medical Council Rules Wakefield & Co. "Dishonest," "Irresponsible" · 50 days ago

Today, the General Medical Council (GMC), which registers doctors to practice medicine in the U.K., issued a decision in its inquiry into the professional conduct of Dr. Andrew Wakefield and his colleagues Dr. John Walker-Smith, and Dr. Simon Murch, co-authors of a study which concluded that a causal connection exists between the measles-mumps-rubella vaccine and autism.

The GMC determined that the three doctors failed to act in the best interests of the autistic children under their care, that Dr. Wakefield was dishonest, misleading and irresponsible in his descriptions of research, and that the findings of the investigation “would not be insufficient to support a finding of serious professional misconduct” against all three doctors.

The study at the center of the inquiry was published in The Lancet in 1998. Six years later, ten of its thirteen co-authors retracted their conclusions in that study.

Further background can be found on the website of journalist Brian Deer, whose in-depth investigation of Wakefield and his research alleged numerous irregularities — including his failure to disclose his role in litigation against vaccine manufacturers, failure to disclose pending vaccine patents, performance of needless, invasive medical procedures on autistic children, and misrepresentation of data — and ultimately led to the disciplinary hearings.

On 7 April 2010, the GMC Disciplinary Panel will consider whether the conduct described in the decision warrants professional sanctions, including revocation of Dr. Wakefield’s, Dr. Walker-Smith’s or Dr. Murch’s license to practice medicine in the U.K. Dr. Wakefield now resides in Texas, and although not licensed to practice medicine in the United States, is the Executive Director of Thoughtful House, which provides medical care to autistic children.

The following passages are excerpted from the GMC decision.


On the responsibilities of a physician/researcher:

[A]mongst the responsibilities of a Responsible Consultant, is the requirement to conduct research within ethical constraints, and report it responsibly, accurately and fairly. At no stage should a doctor take any action that is contrary to the clinical interests of the patient involved.

On Dr. Wakefield’s, Dr. Walker-Smith’s and Dr. Murch’s authorization of hospital admission and medical procedures on children for whom they were not clinically indicated, and commencement of research for which no ethical approval had been obtained:

Child 1 underwent a colonoscopy, MRI scan of his brain, an EEG and a variety of blood and urine tests. These were some of the investigations listed in the programme of the project. He was further admitted on 23 October 1996 for further investigations regarding the “etiology of the autism”, again for no obvious clinical gastro-intestinal reasons. During this admission, Child 1 underwent a barium meal and follow-through and a lumbar puncture. These were also the investigations listed in the programme of the project. The Panel has concluded that Child 1 underwent a programme of investigations for research purposes and for which there was no Ethics Committee approval. (p. 16)

You [Dr. Murch] attempted to carry out a colonoscopy on Child 1 when such an investigation was not clinically indicated… You wrote in your colonoscopy report dated 22 July 1996 that the child’s history is “disintegrative disorder” and noted that the letter to the child’s GP from Professor Walker-Smith concluded the child had features of toddler’s diarrhoea. The Panel concluded that these were not clinical indications to undergo a colonoscopy… You attempted to carry out a colonoscopy on Child 1 when such an investigation was not clinically indicated. (pp. 120, 125)

[T]here is no evidence in Child 3’s clinical notes to indicate that a lumbar puncture was required. Experts on both sides… both considered that such a test was not clinically indicated… The Panel is persuaded by the letters written by [Dr. Walker-Smith] at the time, to Child 3’s paediatric neurologist, his school doctor and his GP, that you did conclude there was no evidence of bowel inflammation on routine blood results but nevertheless you decided to admit Child 3. In particular, the Panel noted the wording of the letter dated 18 July 1996 to the paediatric neurologist: “…the initial blood screens for bowel inflammation were negative, however Dr Wakefield is of the opinion that subtle changes in relation to inflammation may be present… and we have arranged (Child 3’s) admission”. (p. 68)

The Panel is satisfied that… you [Dr. Wakefield] exposed Child 4 to an unnecessary test. (p. 24)

You [Dr. Wakefield] ordered the neurophysiological investigations [on Child 7] without having requisite paediatric qualifications and writing an incorrect diagnosis on the investigation form. (p. 40)

Child 8 was admitted to the Royal Free Hospital on 19 January 1997, without prior outpatient assessment. (p. 37)

The Panel concluded that subjecting the child [Child JS] to a colonoscopy was not clinically indicated as his main presentation was behavioural difficulties and you [Dr. Walker-Smith] accepted his GI symptoms were “rather minor… In your evidence to the Panel you accepted that you did “lower the threshold” in relation to this child… The Panel concluded that these findings, which include those of your irresponsible conduct and not acting in the child’s best clinical interests in several instances, would not be insufficient to support a finding of serious professional misconduct. (p. 111)

On Dr. Wakefield’s taking of blood samples from guests at his son’s birthday party:

On a date unknown prior to 20 March 1999 at your son’s birthday party you… caused blood to be taken from a group of children to use for research purposes… [Y]ou showed a callous disregard for the distress and pain that you knew or ought to have known the children involved might suffer.. The Panel is satisfied by your evidence that the children were “paid for their discomfort”, which it concluded was evidence of a callous disregard. (54-55)

On Dr. Walker-Smith’s “parent-driven” testing and treatment recommendations:

The Panel was satisfied on the basis of your letter to his GP dated 21 June 1996, where you stated “…if (child 1’s mother) feels that is appropriate we could consider performing endoscopy and further assessments…” The Panel concluded that your reliance on her views that there was a link between autism and immunisation and bowel inflammation was inappropriate. (p. 67)

On Dr. Wakefield’s assertion that the definition of “conflict of interest” changed after publication of the Lancet study:

The Panel is satisfied that the concept of a conflict of interest, and the extension of this to the perception of a conflict of interest, was known in the scientific community in 1997. At that time the Lancet and other organisations had published guidance on the requirement for authors for recognising and declaring financial and other conflicts of interests, as well as the importance of declaring “potential”, “perceived” or “apparent” conflicts of interest. The Panel therefore rejects the proposition put forward by your Counsel that third party perceived conflicts of interest did not fall within the relevant definition at the time. (p. 44)

On Dr. Wakefield’s failure to disclose relevant information about the purpose and subjects of the Lancet study:

[T]he project reported in the Lancet paper was established with the purpose to investigate a postulated new syndrome and yet the Lancet paper did not describe this fact at all. Because you drafted and wrote the final version of the paper, and omitted correct information about the purpose of the study or the patient population, the Panel is satisfied that your conduct was irresponsible and dishonest. (p. 45)

On Dr. Wakefield’s assertion that his autistic subjects were “routine referrals” for whom invasive testing was medically indicated:

Having regard to its findings in relation to Child 1, 9, 5 and 10, namely that these children were admitted to undergo a programme of investigations for research purposes, and that they all lacked a history of gastrointestinal symptoms, the Panel is satisfied that these referrals did not constitute routine referrals to the gastroenterology department… In reaching its decision, the Panel concluded that your description of the referral process as “routine”, when it was not, was irresponsible and misleading and contrary to your duty as a senior author. (p. 46)

On Dr. Wakefield’s response to allegations of selection bias:

The Panel is persuaded by all the correspondence in the Lancet Journal volume 351 dated 2 May 1998 regarding a suggestion by correspondents to the Lancet that there was a biased selection of patients in the Lancet Paper of 28 February 1998, of which you were one of the senior authors. The Panel has found that your [published response] does not respond fully and accurately to the queries made by correspondents to the Lancet. The Panel is satisfied that the statement you made would be considered by ordinary standards of reasonable and honest people to be dishonest. Additionally, you knew that this statement omitted necessary and relevant information, such as the active role you played in the referral process, and the fact that the referral letters in four cases made no mention of any gastrointestinal symptoms and the fact that the investigations had been carried out… for research purposes. Therefore, the Panel is satisfied that your conduct in this regard was dishonest and irresponsible. (p. 47)

On Dr. Wakefield’s failure to disclose conflicts of interest to the editors of the Lancet:

…[T]he Panel is satisfied that your conduct in failing to disclose your involvement in the MMR litigation, your receipt of funding for part of [your research] from the Legal Aid Board and your involvement in the Patent, constituted disclosable interests. Your failure to disclose these to the Editor of The Lancet was contrary to your duties as a senior author of the Lancet paper. (p. 50)

On the administration of an unlicensed drug to a study subject:

The Panel noted that Child 10’s deterioration was not assessed by any clinician prior to being administered Transfer Factor. Therefore the Panel has concluded that Child 10 was given Transfer Factor for experimental reasons… Furthermore, an essential requirement of a doctor is to share information with colleagues in the ways that best serve patients’ interests. The Panel has noted the evidence that Child 10’s GP did not have any knowledge of any prescription of Transfer Factor other than that contained in a letter from the community paediatrician. The Panel is satisfied that you [Dr. Wakefield] did not inform the GP or arrange for someone else to do so. (pp. 52-53)

The Panel is persuaded that Child 10 was administered Transfer Factor by the weekly diary card completed by his mother, submitted to the Royal Free Hospital in January 1998 which states, “over Christmas and New Year we felt very optimistic about the apparent effect of Transfer Factor… is it possible that the dose now needs to be increased?”. The Panel concluded that you [Dr. Murch] caused the child to be administered with Transfer Factor on the basis of the letter of 23 July 1997 that you and Dr Wakefield wrote to the Dispensary Manager. You informed her that “we would like to start Child 10 …on measles-specific Transfer Factor and we are prepared to take full responsibility for the outcome of this treatment. The supplies of the drug are presently in our hands (Dr Wakefield).” … The Panel is persuaded that this was experimental treatment and not given for clinical reasons, because you had not seen or assessed the child before causing him to be administered with the unlicensed drug and you stated “we do not know whether the treatment will work” in your letter to the Dispensary manager of the pharmacy, dated 23 July 1997, jointly signed by you and Dr Wakefield. (p. 100)

Conclusion re Dr. Wakefield:

The Panel concluded that these findings, which include those of dishonesty and misleading conduct, would not be insufficient to support a finding of serious professional misconduct. (p. 55)

Conclusion re Dr. Walker-Smith:

The Panel concluded that these findings, which include those of your irresponsible conduct and not acting in the child’s best clinical interests in several instances, would not be insufficient to support a finding of serious professional misconduct. (p. 111)

Conclusion re Dr. Murch:

The Panel concluded that these findings, which included Dr. Murch failing in his duty as a responsible consultant and in some cases, not acting in the best clinical interests of the children, would not be insufficient to support a finding of serious professional misconduct.

Waist Deep In The Autism Fundraising Hole · 170 days ago

An Update on the “Autism Spectrum Disorder Foundation” & Its Telemarketing Campaign

The Autism Spectrum Disorder Disorder Foundation (ASDF) — the subject of the report “Dialing for Autism Dollars,” published on this weblog in March 2009 — has filed its 2008 audit, tax return, revised telemarketing contracts, and fundraising campaign report with the North Carolina Secretary of State Charitable Solicitation Licensing Section. These documents reveal that the purportedly charitable organization, whose principals claim to provide educational services and financial aid to benefit autistic children and their families, is almost exclusively devoted to the begging business, and that ASDF is thousands of dollars in debt to the professional fundraising firms whose staff have been blanketing the United States with telephone solicitations since mid-2008.

As described in detail in “Dialing for Autism Dollars,” ASDF was incorporated in 2007, granted tax exemption shortly thereafter, and promptly commenced a nationwide telephone and direct mail fundraising campaign. Its founder and President — Schererville, Indiana resident Michael Slutsky — has acknowledged having no personal or professional experience or expertise in autism or disability services or advocacy; until early 2008, he was a wholesale distributor of candles and other fundraising supplies to churches, school groups and nonprofit organizations.

In 2008 — its first full year of operations — Mr. Slutsky’s newly-hatched “charity” received $370,082 in donations, incurred $370,858 in liabilities for telemarketing services, and incurred an additional $126,930 in liabilities for printing and mailing fundraising appeals. At the end of the year, the organization faced a $165,854 deficit, with $159,225 owed to fundraising consultants, and $14,678 to Mr. Slutsky himself.

ASDF’s expenditures on grants, donations and scholarships to directly benefit autistic children and families totaled $1,391 — $160 to subsidize one parent’s attendance at a workshop, $850 for a camp scholarship for one child, an $86 donation to the Autism Society of Oregon, and another $295 in unspecified grants and donations. These outlays represent less than 0.3% of the $370,082 in contributions received by the organization from the general public during 2008. In its audit, however, ASDF asserts that its telephone calls and direct mail packages help fulfill its charitable mission, and therefore allocates half of its fundraising costs — over $250,000 — to the “program services” category.

ASDF’s Direct Mail Package

The paper goods at the heart of ASDF’s “volunteer solicitation” campaign (reproduced in the images below and in a 4MB .pdf file) come packaged in a glossy envelope illustrated with photographs of a girl playing with a butterfly, and embellished with the words “Wings of Hope” and “Thank you for volunteering… Start your kit today and give hope to children with autism.” The envelope flap declares that “Every 20 minutes a child is diagnosed with autism,” and urges the recipient to open the package immediately.



The package contains two “assignment cards” with a computer-generated list of names, addresses and telephone numbers of fifteen of the recipient’s neighbors, and a list of “Early Signs and Red Flags for Infants and Toddlers at Risk for an Autism Spectrum Disorder.”


The package also contains fifteen blank white envelopes, fifteen blank green envelopes, and fifteen campaign letters.



The campaign letters inform the reader that one in 150 children are diagnosed with autism, and invite potential donors to

bring a candle of hope into that dark world by helping the Autism Spectrum Disorder Foundation today. By giving to the Wings of Hope Campaign, you can help us provide financial assistance to families in need, free Early Detection Kits, and scholarships to send children with autism to camp.


The recipient is instructed to hand-address each white envelope to the neighbors listed on their “assignment card,” and to self-address each green envelope; to personalize each campaign letter with a signature and a handwritten message; to stuff each white envelope with a campaign letter and a green return envelope; and to mail all fifteen envelopes with stamps purchased and donated by the recipient. The recipient is next instructed to record donations on the assignment card as they are received from neighbors; to follow up with a phone call to those who do not respond; to convert cash donations into a personal check made payable to the Autism Spectrum Disorder Foundation; and to mail off the donations and the completed assignment sheet in a large envelope provided in the package.

The large envelope is addressed to the “Autism Foundation Processing Center, P.O. Box 96730, Washington, D.C. 20090-6730” — a rented mailbox at the main post office in the nation’s capital, where neither the Autism Spectrum Disorder Foundation nor any “Autism Foundation” has an office, or is legally authorized to solicit funds. ASDF’s actual legal address in Everett, Washington, the name of the telemarketing firm hired to conduct ASDF’s fundraising campaign — InfoCision Management Corporation of Akron, Ohio — and a list of ASDF’s official filings with state regulatory agencies appear in small print on the back of the campaign letter. The small print also indicates that donations to ASDF may be used for far less specific purposes than those described in the campaign letter:

Funds donated to ASDF will be used to address any and all kinds of issues in assisting children with Autism and their families.


Completing the presentation, a slip of yellow paper reiterates the assertion that “Every 20 minutes a child is diagnosed with autism,” and urges the recipient to visit the organization’s website at www.myasdf.org/wingsofhope.

The only information about autism provided in the direct mail package is the list of “Early Signs and Red Flags” on the assignment sheet, and the recitation of the “one in 150” statistic in the campaign letter. Such sparse factual content notwithstanding, the note on “Accounting for Costs of Activities That Include Fundraising” accompanying ASDF’s audit asserts that:

[ASDF’s] direct mail campaigns share a dual purpose of fundraising and program services that call for the recipients to help fulfill the ASDF’s mission. Given the dual nature of the mail campaigns, the ASDF has adopted a policy to split the costs of the direct mail campaign 50% to fundraising and 50% to program services.

ASDF’s “Early Detection Kit”

The “Early Detection Kit” described in the fundraising appeal consists of a cover letter addressed to “individual[s] who work in the care industry,” a DVD and a growth chart listing “various developmental capabilities children should have throughout the first five years of life.” The list of milestones on the growth chart is appropriated word-for-word from the Child Development Informational Card published by the U.S. Centers for Disease Control, a resource widely distributed to physicians, educators, clinics, and social service providers. Whereas ASDF fails to cite the source of the list, the CDC gives proper attribution to Drs. Steven Shelov and Robert E. Hannerman, authors of the American Academy of Pediatrics guide, Caring for Your Baby and Young Child: Birth to Age 5, published by Bantam Books.

ASDF’s 2008 Audit

The following financial statements are reproduced from ASDF’s audit, prepared on July 14, 2009 by the St. Louis firm Swink Fiehler & Company P.C.

STATEMENT OF NET ASSETS AS OF DECEMBER 31, 2008

Assets  
Cash and cash equivalents $6,780
Funds held in escrow $1,349
Total assets $8,129
   
Liabilities and Net Assets  
Liabilities  
Accounts payable $157,518
Loans payable to Executive Director $14,678
Payroll liabilities $80
Wells Fargo checking overdraft $1,707
Total Liabilities $173,983
Net Assets  
Unrestricted net assets ($165,854)
Total Net Assets ($165,854)
Total Liabilities & Net Assets $8,129
 

(The notes to the financial statements describe the $14,678 in loans payable to Michael Slutsky as “non-interest bearing advances” that the foundation intends to repay, and indicate that ASDF “makes periodic payments as cash flow permits” — implying that such advances and repayments occur on a regular basis.)

STATEMENT OF ACTIVITIES AS OF DECEMBER 31, 2008

Revenue  
Contributions $370,082
Total revenue $370,082
   
Expenses  
Program services $250,285
Management and general $25,384
Fundraising $255,913
Total expenses $531,583
   
Decrease in net assets ($161,501)
   
Unrestricted Net Assets, Beginning of Year ($4,353)
   
Unrestricted Net Assets, End of year ($165,854)
 

(As itemized in the “Statement of Functional Expenses” that follows, and explained in the note on “Accounting for Costs of Activities That Include Fundraising” cited above, $248,894 of the $250,285 categorized under “Program Services” represents half of the cost of the telemarketing and direct mail campaign.)

STATEMENT OF FUNCTIONAL EXPENSES FOR THE YEAR ENDING DECEMBER 31, 2008

  Program Services Management and General Fundraising Expense Total Expenses
         
Grants $341     $341
Compensation of officers   $585   $585
Payroll taxes   $69   $69
Professional fees – legal and accounting   $16,666   $16,666
Advertising and promotion   $1,689 $1,689 $3,378
Office expenses   $795   $795
Travel   $898 $898 $1,796
Bank and merchant service fee   $2,221 $2,221 $4,442
Donations $200     $200
Printed materials and fulfillment $38,515   $38,515 $77,030
Professional fees – telemarketing services $185,429   $185,429 $370,858
Postage and delivery $24,950 $250 $24,950 $50,150
Registration fees   $801 $800 $1,601
Scholarships $850     $850
Telecommunications ________ $1,411 $1411 $2,822
         
TOTAL $250,825 $25,385 $255,913 $531,583

(Grants, donations and scholarships are not itemized in ASDF’s financial statements, but are partially described in its tax return.)

ASDF’s 2008 Tax Return

The Form 990 informational return filed by the Autism Spectrum Disorder Foundation with the Internal Revenue Service reports $370,082 in contributions and $271,348 in program expenses in 2008; $270,252 of the latter amount represents half of the cost of ASDF’s telemarketing and direct mail campaign. The remaining $1,096 is comprised of three grants made during the first two months of 2008: an $850 payment to Mount Hood Autism Camp, a $160 payment to Think Social Publishing, and an $86 donation to the Autism Society of Oregon Walkathon.

The 990 claims that ASDF President and Executive Director Michael Slutsky devoted 45 hours per week to the Foundation’s activities, but received no compensation whatsoever; and that Chief Financial Officer Janet Coyer toiled a noteworthy 75 hours per week on ASDF business for only $585 in annual salary. $387,533 in “professional fees” to consultants is reported, $279,506 of which consists of payments to InfoCision. The 990 provides no further detail regarding the remaining $108,027 in “professional fees,” and does not indicate whether any of these “professional fees” were paid either directly or indirectly to Mr. Slutsky or Ms. Coyer in lieu of salary.

In addition to identifying Mr. Slutsky and Ms. Coyer as Directors, the Board roster provided with the 990 names Everett, Washington school psychologist James Roan, and indicates that he received no compensation and devoted no time whatsoever to the organization. (In a March 2009 phone conversation, Mr. Roan claimed to have had no significant involvement with ASDF since early 2008, when he helped to develop its website.) Also named as a Director is Mrs. Helen Ignas, who has shared a residence with Mr. Slutsky and like Mr. Roan, devoted no time to the organization’s activities.

ASDF’s Telemarketing Contract With InfoCision

In March 2009, Mr. Slutsky and Ms. Coyer entered into a revised contract with InfoCision for ASDF’s telemarketing and direct mail fundraising campaign. Charges for phone calls, printed matter, postage, and other services remain roughly the same as in the original September 2008 contract; however, whereas the original contract included a “Breakeven Guarantee For Prospecting” ensuring that ASDF’s liability would not exceed the cost of the fundraising campaign, the revised contract paints a far less generous scenario:

3.1 Pay From Proceeds The parties agree that InfoCision [IMC] shall advance [ASDF] $3,000 per month. This amount shall first be paid from the proceeds fulfilled from donations accrued for all programs during the contract term. In the event the proceeds from all programs do not total $3,000, IMC will advance the amount of the shortage from its own funds. The $3,000 advancement will be added to the accumulating deficit on [ASDF]‘s account.

The remainder of proceeds from all programs will go to IMC to pay all fundraising costs irrespective of the program… Parties also agree that this schedule of payment will be adhered to on each individual campaign, until both parties are satisfied but in no event later than the time in which [ASDF]‘s deficit is eliminated.

In the event that there are not enough funds to pay all of the donor acquisition debt, IMC may at its sole discretion forgive the remainder of the donor acquisition debt…” (emphasis added)

The note on “Mail and Communication Campaigns” in the ASDF audit indicates that of the $157,870 in accounts payable to fundraising consultants at the close of 2008, only $24,164 stood to be forgiven if the campaigns fail to generate enough donations to cover costs.

InfoCision’s Fundraising Campaign Report

In June 2009, InfoCision filed a final accounting for the ASDF telemarketing campaign in North Carolina. According to this report, out of $14,943.25 in donations received from North Carolina citizens between October 15, 2008 and March 21, 2009, $14,898.95 was paid to InfoCision for calls, letters, postage, training, computer services, and shipping. $44.30 — 0.3% of the total amount raised in North Carolina — was ultimately received by the Autism Spectrum Disorder Foundation.

Associated Community Services Contract & Withdrawal

As previously discussed in “Dialing For Autism Dollars,” the Autism Spectrum Disorder Foundation has also retained Associated Community Services (ACS), a Southfield, Michigan for-profit firm that conducts telemarketing campaigns on behalf of nonprofit organizations. ACS’s fundraising campaign for the Knoxville-based Youth Development Fund has been the subject of investigation by the Tennessee Attorney General’s office; in August 2008, ACS was fined $100,000 by the Missouri Attorney General for harassing Missouri residents with rude, high-pressure telephone solicitations.

The contract between the Autism Spectrum Disorder Foundation and Associated Community Services names ACS as ASDF’s “exclusive sales agent and exclusive representative,” responsible for “locat[ing] telemarketing firms qualified to conduct campaigns” throughout the United States and Canada. The contract further reveals that ASDF has agreed to pay ACS 52% of gross proceeds resulting from the firm’s efforts, and that ASDF has also commissioned “an outside firm to collect the proceeds of solicitation, deposit same, and… account for all funds received through ACS’s efforts.” The identity of this “fundraising campaign finance manager” is not disclosed.

In June 2009, Associated Community Services formally withdrew its applications to raise funds in North Carolina for ASDF and for the unrelated Law Enforcement Education Program, and submitted an affidavit confirming that ACS had not solicited and would not solicit funds for either organization in that state. Although ACS President R. William Burland did not specify his reasons for the withdrawals, they occurred shortly after the Federal Trade Commission’s announcement of “Operation False Charity,” a crackdown on fraudulent charity telemarketers. At the same time, the Connecticut Attorney General announced the filing of a lawsuit against Associated Community Services alleging failure to comply with state regulations requiring disclosure of its status as a paid solicitor, and the South Carolina Attorney General publicized an ongoing investigation against the firm.

The North Carolina withdrawal notwithstanding, ASDF’s contract with ACS remains in effect through July 2010. Absent similar withdrawals in other states, it can be assumed that ACS will continue to raise funds on behalf of the Autism Spectrum Disorder Foundation everywhere it is legally permitted to do so.

Free Speech, Secrecy & Sunshine

In its 1988 decision in Riley v. American Federation of the Blind (108 S.Ct. 2667), the United States Supreme Court struck down North Carolina’s Charitable Solicitations Act, which defined the “reasonable fee” that a professional fundraiser could charge a nonprofit organization, and required fundraisers to disclose to potential donors, before appealing for funds, the percentage of contributions collected during the previous twelve months that were actually turned over to the charity. The court held that such requirements represented unconstitutional infringements on freedom of speech, were “unduly burdensome,” were likely to hamper legitimate efforts to raise money for charitable purposes, and would inevitably discriminate against small or unpopular organizations. The American Federation of the Blind’s case was argued by Errol Copilevitz, whose firm represents the Autism Spectrum Disorder Foundation and a host of other nonprofit organizations engaged in telemarketing and direct mail fundraising.

While overruling a law that it described as “prophylactic, imprecise, and unduly burdensome,” the court acknowledged the need to prevent fraud on charities and potential donors by requiring tax-exempt organizations and their for-profit consultants to disclose the details of their financial relationships. The court suggested that, in order prevent fraud,

the State may itself publish the detailed financial disclosure forms it requires professional fundraisers to file. This procedure would communicate the desired information to the public…

The North Carolina Attorney General’s office took this advice to heart; the state now leads the way in making charitable solicitation filings readily available to the public on the Internet. In so doing, it subverts intentions such as those expressed in the contract between InfoCision and the Autism Spectrum Disorder Foundation:

10.2 Non-Disclosure of Relationship

[E]ach party agrees that it will not disclose either expressly or by implication the existence of this Agreement or the relationship created hereunder to any third party without the express written consent of the other party. Further… both parties agree to maintain complete confidence and secrecy with respect to the pricing, terms and conditions of this Agreement.

Evidently, Mr. Slutsky, Ms. Coyer and their fundraising consultants would prefer that the public remain unaware of the extent to which contributions to the Autism Spectrum Disorder Foundation enrich those who hold out the begging bowl to the caring, generous and unsuspecting public. The organization’s financial statements, contracts and regulatory filings, however, reveal the dollars-and-cents reality behind ASDF’s altruistic-sounding pleas for donations for the supposed benefit of “children and the families of children suffering autism spectrum disorder.” These documents paint a picture of a money-churning operation masquerading as a philanthropy, an “Autism Foundation” established and enabled by individuals with no experience or expertise in the field of developmental disabilities, who solicit donations at great expense with materials that provide minimal, already widely available information about autism — and who would like potential donors to believe that they are engaging in a primarily educational endeavor, rather than digging an ever-widening financial hole in the ground.

The following non-profit organizations provide education, recreation, respite and advocacy for autistic children, adults, their families, educators and care providers. Each and every one is worthy of support; none engages in telemarketing solicitation.

Asperger’s Association of New England (AANE)
ARC of King County, Washington
Autism National Committee
Autism Network International
Autism Society of America Foundation
Autism Society of Indiana
Autism Society of New Hampshire
Autism Society of North Carolina
Autism Society of Oregon
Autistic Self-Advocacy Network
Autistics.org
Provincial Autism Center

Many thanks to the reader who provided me with ASDF’s fundraising kit.

Federal Claims Court Dismisses Third MMR-Autism Appeal · 218 days ago

In a 59-page decision issued yesterday afternoon, August 11, Judge Margaret M. Sweeney of the United States Court of Federal Claims sustained the ruling of Special Master Denise K. Vowell dismissing the Vaccine Injury Compensation Program claim, Snyder v. U.S. Department of Health and Human Services (Case No. 01-162V) — the last of the three Omnibus Autism Proceeding test cases in which petitioners sought to establish that a combination of the MMR vaccine and thimerosal-containing vaccines, acting in concert, are capable of causing autism spectrum disorders.

Arguments raised in the Snyder appeal were virtually identical to those raised by the petitioners in Cedillo v. HHS and Hazlehurst v. HHS.

The decision includes an extensive discussion of the role of the special master in Vaccine Injury Compensation Program proceedings, elucidating the differences between VICP vaccine injury claims and conventional tort claims. Judge Sweeney herself served as a VICP special master from 2003-2005, and ruled on dozens of such cases.

From the decision:

[W]hen considering the provisions and legislative history of the Vaccine Act, the language of the Vaccine Rules, and the case law, one factor that has remained constant in the Vaccine Program is the necessary and important role of special masters in conducting proceedings and rendering decisions in Vaccine Act cases. The special masters have great leeway in how they conduct proceedings, including what evidence to consider and how to weigh that evidence, and their credibility determinations and fact-intensive conclusions are afforded great deference. However, this is not to suggest that the special masters are infallible and that their final decisions are sacrosanct. To be sure, the Court of Federal Claims on review, and the Federal Circuit on appeal, do not merely rubber stamp special master final decisions. Decisions from both courts demonstrate a willingness to reverse the decision of a special master when the special master has failed to adequately develop the record, failed to consider facts critical to the case, failed to give adequate consideration to a viable medical theory, or otherwise misapplied the law. Nevertheless, the law is settled that neither the Court of Federal Claims nor the Federal Circuit can substitute its judgment for that of the special master merely because it might have reached a different conclusion. Reversal is appropriate only when the special master’s decision is arbitrary, capricious, an abuse of discretion, or not in accordance with the law. (pp. 16-17)

[P]etitioners’ contention that they were required to prove their case to all three special masters lacks merit. Although all three special masters heard and considered the general causation evidence, they issued separate decisions applying that evidence to their respective test case. The special masters were free to reach different conclusions based on the same evidence. That all three reached the same conclusion – rejecting petitioners’ theory of causation – does not mean that petitioners were required to satisfy all three special masters. There is nothing in the record suggesting that the special masters were bound to speak with one voice. Nor can petitioners point to evidence that Special Master Vowell rendered her decision in consultation with the other two special masters. Rather, petitioners generally contend that their review of the three special masters’ decisions caused them to conclude that they had to prove their individual case to all three special masters. The court finds no evidence in the record to support this purported heightened burden. Moreover, the decision of the special masters to conduct the general causation hearing together, rather than require three separate hearings concerning the general causation issue with the resultant duplication of the time and resources of the OSM, petitioners, and respondent, hardly suggests fundamental unfairness. To the contrary, it reflects a common-sense, cost-saving approach to complex litigation. Accordingly, the use of a panel of three special masters to hear the general causation evidence was not arbitrary, capricious, an abuse of discretion, or contrary to law. (pp. 19-21)

Petitioners complain that the filing of Dr. Bustin’s “highly technical” reports from the U.K. MMR litigation “on the eve of trial” and the submission of Dr. Bustin’s “impossibly technical power-point [sic] presentation at the hearing” were “grossly unfair” because counsel for the Cedillo petitioners had “no time to review the documents, let alone prepare for crossexamination.” However, petitioners could not have been surprised that respondent would need to address the laboratory results from Unigenetics – evidence that the petitioners, not respondent, put in play. As is clear from the record and as they acknowledge in their motion for review, the Unigenetics test results were “the single-most critical issue in the case.”

…[I]t is clear to the court that petitioners have no basis to complain about the special master admitting Dr. Bustin’s expert reports into the record. It was not until February 2007 – when petitioners filed their expert reports – that respondent could have been aware that the test results from Unigenetics were crucial to petitioners’ theory of causation. Indeed, respondent did not actually become aware of the importance of the test results until March 2007 after he retained expert witnesses to review, analyze, and respond to petitioners’ expert reports. There is no question that respondent was not dilatory in obtaining as much information relevant to petitioners’ theory of causation as possible prior to the Cedillo hearing in June 2007. It would have been grossly unfair to respondent had he been hampered in his ability to counter petitioners’ theory of causation as a result of petitioners’ failure to fully explain their theory of causation until four months before hearing, especially in light of his due diligence. It is worth remembering that in Vaccine Program proceedings, petitioners have the burden of going forward, and only after petitioners have made a prima facie case does the burden of persuasion shift to respondent. Thus, without the formal discovery that is available in other civil litigation, it is not surprising that respondent in this case could not anticipate the precise nature of petitioners’ theory of causation and supporting testimony.

Moreover, as previously described, the special master afforded petitioners ample opportunity to respond to the contents of Dr. Bustin’s reports once the Cedillo hearing had concluded. She, along with the two other special masters, repeatedly queried petitioners about their efforts to obtain additional information from the U.K. MMR litigation, encouraged petitioners to obtain the information, and offered to join in petitioners’ application for the release of the information from the court in the United Kingdom. There were almost five months between the Cedillo and Snyder hearings, eight months between the Snyder hearing and the close of the evidentiary record, and six months between the close of the evidentiary record and the special master’s issuance of a decision. Thus, petitioners had approximately nineteen months within which to obtain whatever information they believed necessary to respond to Dr. Bustin’s expert reports and testimony. Given this extraordinary amount of time to secure any additional information, petitioners’ claim of prejudice fails. The special master’s conclusion to this effect was not arbitrary, capricious, or an abuse of discretion. (pp. 22, 24-25)

Immediately problematic is that petitioners do not explain how the special master’s alleged failure to consider certain evidence would have altered her decision. They allege that the special master disregarded evidence, but fail to explain the evidence’s materiality to their case. This failure, in itself, nullifies petitioners’ criticism. Yet, even presuming that petitioners’ contention is that this evidence would have tipped the scales in their favor such that they would have been able to demonstrate causation by a preponderance of evidence, their contention is flawed in two respects. First, the special master’s decision reflects that she carefully considered the entire voluminous record in this case. Second, petitioners fail to demonstrate that the special master improperly weighed the evidence in the record. (pp. 25-26)

It is of no import that the special master may not have attributed [certain] assertions to Dr. Griffin or indicated that Dr. Griffin concurred with them – it is clear that she did, in fact, consider the statements, or the underlying ideas represented by the statements… [I]t is of no import that the special master may not have attributed [certain] assertions to Dr. [Brian] Ward or indicated that Dr. Ward concurred with them – it is clear that she did not ignore the statements, or the underlying ideas represented by the statements… Had [Dr. Robert Fujinami’s] article been as valuable to petitioners’ case as they claim, surely they would have sought to subpoena Dr. Fujinami’s testimony or retain his services… It does not matter that the special master may not have attributed the assertions to Dr. [Bertus] Rima or indicated that Dr. Rima concurred with them – it is clear that she considered the statements, or the underlying ideas represented by the statements. Altogether, there is no indication that the special master ignored the evidence cited by petitioners regarding the reliability of the test results from Unigenetics when rendering her decision.(pp. 29, 31, 32, 37, 38)

Petitioners did not advance a theory of “mercury induced immune dysfunction” in [this] case. Therefore, the special master had no obligation to make such a finding. Similarly, because the special master was not obligated to consider an argument that was not advanced by petitioners, she could not have ignored evidence related to that argument…

[F]ar from disregarding the statements and various subject matter cited by petitioners, the special master both considered them and assigned them the weight that she felt appropriate. Although they never expressly discuss the materiality of these statements, it is apparent that petitioners’ grievance is that the special master did not find petitioners’ expert testimony persuasive. However, the weight afforded such evidence is within the sound discretion of the special master. Because the special master did not abuse her discretion, the court will not disturb those findings. (pp. 40-41)

Although the special master had complete control over the discovery process in this case, such control does not extend to compelling a court in a foreign jurisdiction to unseal documents. Petitioners acknowledged this fact at oral argument before the undersigned. Accordingly, the special master did not improperly shift the burden to petitioners to obtain the documents from the U.K. MMR litigation – there was no burden to shift because the special master could not have obtained the evidence sought by petitioners in the first instance. (p. 46)

Petitioners filed their motion [for reconsideration] on Friday, March 13, 2009, at 6:02 p.m. Almost all of the “new” evidence submitted with the motion was published before [the special master] rendered her decision. The deadline for filing such a motion, pursuant to Vaccine Rule 10(c), was March 5, 2009. And, pursuant to Vaccine Rule 23, the thirty-day filing deadline for any motion for review fell on Monday, March 16, 2009… The court finds no abuse of discretion here. The special master held that petitioners failed to comply with the requirements of the Vaccine Rules, and even had they so complied, the evidence was insufficient to result in the granting of their motion. Both of these reasons for the special master’s denial of petitioners’ motion were well within her discretion to make. (pp. 46-47)

Petitioners first make the blanket accusation that the special master “improperly applied Daubert to the experts’ conclusions,” rather than to the methods employed by the experts. They do not expand on this allegation to show how error was committed or provide any citation to the portions of the decision containing the alleged misapplication. Thus, petitioners place the burden on the court to divine precisely how the special master’s application of Daubert might have been improper. (pp. 50-51)

The court finds no error in the special master’s application of the framework suggested by Daubert. Federal Circuit precedent explicitly permits a special master to evaluate scientific evidence using the Daubert factors. Here, the special master considered all of the relevant evidence submitted by both parties, using the Daubert factors only to determine the reliability of that evidence and, hence, the weight it should be assigned. Indeed, by allowing all relevant evidence to be admitted into the record, regardless of its reliability, the special master was actually being quite generous to petitioners. As the special master noted throughout her decision, petitioners’ expert witnesses compared unfavorably to respondent’s expert witnesses in many respects: their credentials, their demeanor, how forthcoming they were at hearing, and the quality of their testimony. Accordingly, to the extent that petitioners are complaining that the special master’s use of the Daubert factors resulted in a failure to consider their evidence, they are mistaken. Rather, the special master evaluated all of the evidence presented by both parties and determined that the science behind petitioners’ theory was lacking. Contrary to petitioners’ contention that the investigation into the link between the MMR vaccine, along with all thimerosal-containing vaccines, and autism spectrum disorders “is ‘bereft’ of science,” the record demonstrates that there is an abundance of science in this area – just not science that supports
petitioners’ position. The special master’s application of Daubert was in accordance with the law. (pp. 53-54)

When determining fundamental fairness to the parties, there is no direct correlation between the sheer volume of evidence offered and amount of evidence that must be admitted and ultimately credited at hearing. Merely because a party offers a huge volume of evidence does not mean that the special master is duty bound to accept any of that material as persuasive. (p. 50, fn. 63)

The court finds no error in the special master’s findings. The special master’s conclusion that petitioners did not present a biologically plausible medical theory is clearly supported by the record. She found that the various aspects of petitioners’ theory were not scientifically sound and that the lynchpin of their theory was wholly unreliable. Next, the special master’s conclusion that petitioners had not established a logical sequence of cause and effect is also supported by the record. As noted above, petitioners’ theory of causation depended upon, among other things, [the child’s] immune system being damaged by the MMR vaccine (but not thimerosal-containing vaccines), the persistence of the measles virus in [the child’s] body, [the child’s] development of inflammatory bowel disease, and the presence of the measles virus in [the child’s] brain. The special master found that petitioners had demonstrated none of these necessary elements by a preponderance of the evidence. Further, the special master’s conclusion that the onset of [his] symptoms did not occur within a biologically acceptable time period following the MMR vaccination is supported by the record. She found that based on the medical records, the onset of [the child’s] symptoms did not occur at the time suggested by petitioners. Given that petitioners had not established any of the prongs of the test set forth in Althen, the special master correctly concluded that the burden of proving an alternative cause never shifted to respondent.

Petitioners’ complaints with the special master’s decision amount to nothing more than dissatisfaction with the weight she assigned to the evidence… The special master exercised her discretion appropriately here and her decision was not contrary to law. (p. 56)

The court has addressed all of petitioners’ numbered objections, finding them to be without merit. However, petitioners lodge other complaints about the special master’s conduct that despite their lack of merit, cannot be ignored. Specifically, petitioners advance the remarkable complaint that “the special master abandoned her obligation to impartially weigh the evidence. . . . [I]nstead, the special master inappropriately assumed the respondent’s role as protector of the integrity of vaccines.” Petitioners later elaborate:

During the past decade, the publicity afforded the issue of whether vaccines can cause autism has been intense. . . . [D]ue to this publicity, . . . the special master feared that a finding in [petitioners’] favor would drive down immunization rates. For this reason, to protect the integrity of vaccines, [the child’s] case, a so-called “test” case, was treated far differently than other vaccine program petitioners. First, after thousands of other autistic children had filed claims, and after years of intense public controversy over the vaccine/autism connection, the respondent was permitted to present the opinions of seventeen experts to defeat [the petitioner’s] claim. In so doing, the special master treated [the petitioners] far differently than other petitioners. In addition, disregarding the Federal Circuit’s recent decisions in Althen and Capizzano, the special master instead invoked Daubert and found virtually all of [petitioners’] evidence unreliable. For her to do so . . . was fundamentally unfair. [Petitioners were] entitled to equal treatment.

To reinforce their attack on the special master, petitioners reiterate their allegations of bias, charging:

[T]he special master ignored [petitioners’] considerable, albeit circumstantial, evidence that a persisting vaccine-strain measles virus caused [his inflammatory bowel disease] and autism… [S]he did so because of the intense national publicity this case has received… [S]he did so to assure the American public that vaccines are safe. She did so because she views her role as a protector of the integrity of our nation’s vaccines. This, however, is the role of the respondent, not a special master.

…[T]he special master, to protect vaccine integrity in a very public case, chose to impose upon [petitioners] an unattainable standard of proof. To protect the vaccine’s integrity she rejected all of petitioner’s credible evidence and simply accepted the conclusions of the respondent’s seventeen experts, denying [petitioners] the fundamental fairness required by the Vaccine Rules, ignored Congress’[s] intent in establishing the Vaccine Program, and rejected the Federal Circuit’s interpretation of that intent.

Finally, at oral argument, petitioners attempted to justify their charge of bias by arguing that it was fundamentally unfair for the special master to admit the purportedly unreliable evidence from Dr. Bustin and Dr. Rima and, thereafter, “allow[] the credibility of those witnesses to substitute for the reliability of those witnesses on key issues…”

Petitioners’ charge – that the special master feared a public backlash against vaccines if she ruled in their favor – is preposterous. There is not a shred of evidence to support petitioners’ claim; it rests solely on petitioners’ speculation. Merely because the special master found that petitioners did not carry their burden of proof does not diminish her integrity or render her decision unsupported. Claims of error by a losing party against a decision maker are hardly unusual, but should be grounded in reality. There is an enormous chasm between disagreement with a judicial officer’s findings of fact and conclusions of law and the accusation that the judicial officer is, in essence, intellectually dishonest. An allegation of bias raises ethical concerns, not errors in judgment (i.e., legal or factual errors). Although petitioners appeared to understand this distinction at oral argument, they maintained that the special master was biased against them by unfairly “shift[ing] the burden of discovery” and “weighing… the evidence…” However, alleged errors of this nature are grounded on purportedly mistaken evidentiary rulings, factual findings, and legal conclusions, not bias. And, the court has already held that it identified no legal or factual error in the special master’s decision.

Indeed, it is abundantly clear from her decision that the special master took great care in considering all of the evidence in the record–whether presented by petitioners or respondent – and applying the appropriate legal standards in evaluating that evidence. As the Court of Federal Claims stated in Ultimo:

This sort of personal attack on the [special master] is highly inappropriate, contentious, and unpersuasive. . . . Petitioner . . . accuses the [special master] of subverting the intent of Congress in establishing the Program. The court will not condone such frivolous, unsubstantiated accusations. Accordingly, the court finds that petitioner’s… objection is completely without merit. Petitioner is forewarned that any repetition of such groundless accusations may cause the court to entertain sanctions against petitioner and petitioner’s counsel pursuant to RCFC 11. 28 Fed. Cl. at 153. (pp. 56-59)

As the special master’s decision makes clear, [the child], and by extension, his family, have dealt with significant adversity for many years, and, like the special master, the court is very sympathetic to their circumstances. However, the court cannot be ruled by emotion and base its determination solely upon the adversity endured by petitioners’ family. Moreover, it is not the task of this court to determine whether vaccines cause autism or other neurodevelopmental disorders. Rather, the court must decide whether the special master, considering the record as a whole, rendered a decision that was arbitrary, capricious, an abuse of discretion, or otherwise not in accordance with the law. She did not. Her decision was entirely rational and fully supported by the record. Thus, the court DENIES petitioners’ motion for review. (p. 59)

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