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More of that vaccine/autism research that doesn’t exist

17 Jul

There are some parents who want research on vaccines and autism. I may not agree that this is the best way to spend our limited resources, but there’s no denying that this group exists and is very vocal. One thing that surprises me is that these parents appear to be unaware of vaccine/autism research that is ongoing. Not just the studies that come out that show us over and over again that autism risk is not increased by vaccines. But other projects. Biology. Studies on regression. And more. I pointed out recently that using NIH Reporter, one can find a number of projects on autism and vaccines or autism and mercury.

But NIH is not the only Federal agency funding autism research. And there are private funders as well. As I mentioned in my previous article, another place to look for funded research projects is the IACC/OARC Autism Spectrum Disorder Research Portfolio Analysis Web Tool as this includes work the various groups represented on the IACC–both Federal and Private. Unfortunately, this tool only has 2008, 2009 and 2010 projects (had the GAO not required OARC to provide a lot of information last year, perhaps this tool would be updated by now. But such is the government.) But, even with this limitation in years, let’s see what projects come up with searches for vaccines or mercury. I’ll give the titles first, and then the abstracts for these projects below.

It’s understandable that parent advocates are not aware of these projects. I’ve written about this before (“What projects are being funded in autism research? Part 1: vaccines and GI issues”) but I think it’s safe to say that parents who believe in the vaccine/autism connection do not frequent Left Brain/Right Brain. There are places on the web that carry that message (for example, the Age of Autism blog and the sites of the organizations that sponsor it). They aren’t telling their constituencies about the ongoing research efforts. As an example, as I was finishing this article, SafeMinds came out with a letter discussing how no work is being performed on vaccines and autism.

Again, this list is only for 2008, 2009 and 2010. More recent projects from NIH were discussed here.

Vulnerability phenotypes and susceptibility to environmental toxicants: From organism to mechanism (funded by Autism Speaks)

Evaluation of the immune and physiologic response in children with autism following immune challenge (funded by Autism Speaks)

Vaccination with regression study (funded by Autism Speaks)

Vaccine safety datalink thimerosol and autism study (Federally Funded)

Analysis of developmental interactions between reelin haploinsufficiency, male sex, and mercury exposure (Funded by Autism Speaks)

MeHG stimulates antiapoptotic signaling in stem cells (Federally funded: DoD)

Etiology of autism risk involving MET gene and the environment (Funded by Autism Speaks)

Epidemiological research on autism in Jamaica (Federally Funded, NIH)

investigation on the potential harmful effects of mercury in the nonhuman primate (Funded by SafeMinds)

Investigating the effect of mercury on ASD, AD and ASD regression (Funded by SafeMinds)

The effect of mercury and neuropeptide triggers on human mast cell release of neurotoxic molecules (Funded by SafeMinds)

Does mercury and neurotension induce mitochondrial DNA release from human mast cells and contribute to auto-immunity in ASD? (Funded by SafeMinds)

Toxicant-induced autism and mitochondrial modulation of nuclear gene expression (Federally Funded: DoD)

Below are the abstracts for these research projects.

Vulnerability phenotypes and susceptibility to environmental toxicants: From organism to mechanism (funded by Autism Speaks)

One hypothesis regarding the association between genetic changes, environmental factors and autism is that many mutations or polymorphisms make the organism more vulnerable to later exposure in some individuals. Called the “vulnerability phenotype”, the Noble lab hypothesizes that one potential unifying theme of the vulnerability phenotype of children with ASD is that they are more oxidized. This elevated oxidation state has been shown to be sufficient to cause dramatic changes in cellular function. In this project, Dr. Noble will test the hypotheses that genetically-based differences in oxidative status are associated with differences in vulnerability to physiological stressors in vitro and in vivo, with even greater increases in vulnerability to combinations of physiological stressors. Specifically, thimerosal and other vaccine adjuvants will be studied. The second part of the study will determine if these effects on a novel regulatory pathway called redox/Fyn/c-Cbl is a necessary mechanistic convergence for increases in vulnerability caused by a more oxidized metabolic status. These results will provide a better understanding of the biochemical effects and mechanisms of possible toxicity of vaccines and vaccine additives. What this means for people with autism: These studies will initially focus on the combination of vaccine additives, but then examine whether a background genetic vulnerability phenotype affects the response to these additives. The results would provide new targets for intervention against the adverse effects of increased oxidative status in children with autism.


Evaluation of the immune and physiologic response in children with autism following immune challenge
(funded by Autism Speaks)

The overall goal of this proposal is to address immune function in children with autism, including the response to vaccine challenge, and how that relates to behavior. Evidence suggests that autism is associated in some cases with altered immune function, but the response of the immune system in children with autism to specific immune challenges, such as vaccines, has not been investigated directly. While it has been reported that some children with autism respond poorly following vaccination with symptoms ranging from rash, diarrhea, irritability, seizures, and loss of skills, no careful, thorough approach has been undertaken to fully characterize this issue, both at the biology and behavior level. We propose to use our current CHARGE (Childhood Autism Risks from Genetics and the Environment) and Autism Phenome Project (APP) study population to address this critical issue. The overall approach would include an examination of the immune response to both viral and bacterial vaccines in children with autism, as compared to typically developing age-matched controls, in real time following vaccination at 5 years of age. Vaccines have advantages for directly studying the immune response as they provide a known, scheduled immune challenge, whose dose is well characterized – making it possible to collect and interpret immune response data at the time that it occurs. Therefore, we think that exposure to an immune challenge with vaccine would result in an increase in inflammation compared to controls in a subpopulation of children with autism. However, we also anticipate that some children will respond to vaccine challenge differently, depending on form of the vaccine, i.e. viral vs. bacterial. Thus, we propose to address the issue of immune function in children with autism through a careful analysis of the immune system, medical and mitochondrial issues, and behavioral response to both viral and bacterial vaccines.

Vaccination with regression study (funded by Autism Speaks)

A major challenge to studying autism with a suspected vaccine-related regression is identifying children with acute regressive-type symptoms following MMR vaccination; there are no specific codes, tests, or procedures that identify this occurrence with a high degree of specificity. This study will explore the Kaiser Permanente electronic databases to ascertain whether we can identify children with regressive type autism and identify the timing of the regression in relation to the period directly following MMR vaccination. In order to see if identification of regressive autism from medical records is possible, the investigators will attempt to identify children vaccinated with MMR who then abruptly undergo a ‘cluster’ of visits, tests, and/or procedures in the time period directly following vaccination. The researchers feel that there may be a number of children who receive a diagnosis (such as ‘prolonged crying’) in the emergency department on the day after vaccination, followed shortly thereafter (1-2 days later) by another set of diagnoses (such as ‘fever’ & ‘irritability’) in the pediatric office or other outpatient department, and then receive either diagnostic or laboratory tests indicating (at least) a moderate degree of severity of concern, such as CT scans, metabolic testing, or referral to neurology. If this study is successful in using medical databases to identify a specific group of children with demonstrable autism-related regression that clearly follows vaccination, it may point to the feasibility of further studies concentrating on this specific population.

Vaccine safety datalink thimerosol and autism study (Federally Funded)

The Thimerosal and Autism Study is a case-control study conducted in three U.S. managed care organizations (MCOs). Data collection began in 2005 and took three years to complete. In this study, children who were diagnosed with autism were matched with control children. The autism diagnosis of the case samples was confirmed by a standardized clinical assessment protocol. Vaccination histories and information on other potential confounding factors were confirmed by reviewing the medical records for all children. In addition, the mothers of both cases and matched controls were interviewed.

Analysis of developmental interactions between reelin haploinsufficiency, male sex, and mercury exposure (Funded by Autism Speaks)

This project will investigate the role of three separate factors in an animal model of autism spectrum disorder: a) genetic susceptibility, b) hormonal environment, and c) possible environmental triggers. A mouse model with a mutation of the reelin gene, implicated in autism spectrum disorders, will be studied after exposure to methyl and ethyl mercury. Both behaviors and neuropathological endpoints will be explored. Finally, the role of endogenous sex hormones will be examined by eliminating the testosterone “surge” around the time of puberty. The individual effects of each will be examined, as well as the interaction of the three components (genetic liability, environmental exposure, hormonal influences) to determine gene x environment interactions. What this means for people with autism: This study will use a unique design to study multiple factors in the etiology of autism spectrum disorder in a mouse model, isolating and combining factors which previously have been implicated in the pathophysiology and behavioral phenotype.

MeHG stimulates antiapoptotic signaling in stem cells (Federally funded: DoD)

This project is a study of the antiapoptotic effect of low concentration of methly mercury and cadmium in cells.

Etiology of autism risk involving MET gene and the environment (Funded by Autism Speaks)

Two independent lines of evidence indicate that the maternal immune system and a functional genetic variant contribute to autism spectrum disorder (ASD) risk. Here, the Van De Water lab will partner with scientists at Vanderbilt University to examine whether these two seemingly unrelated contributions may converge to define a unique ASD susceptibility. Preliminary evidence collected by the Van De Water lab indicates an association between the Mesenchymal epithelial transition factor (MET) gene ‘C’ type, which reduces MET protein expression, and the presence of specific maternal anti-fetal brain autoantibodies. This relationship suggests that this as a pathway for production of the maternal autoantibodies, leading to a gene x environment interaction underlying ASD susceptibility. The next line of experiments will examine the relationship in an even larger sample and assess the functional effect of the MET gene polymorphism on immune cell activity as well as further examine the impact of environmental toxins (including ethyl mercury) on the gene expression-dependent function of maternal immune cells.

Epidemiological research on autism in Jamaica (Federally Funded, NIH)

The prevalence of autism spectrum disorders (ASD) appears to be on the rise in developed countries and has become a serious public health concern. In most developing countries, however, the nature and prevalence of factors associated with ASDs are unknown. The long term goal of this planning project is to develop capacity for conducting large scale population-based ASD studies in Jamaica. First, the diagnostic criteria used in Jamaica and the United States will be compared. Then, questionnaires regarding the demographic and socioeconomic position, occupation, and drinking habits of each child’s parents will be used, and information will be gathered about family history of developmental disorders, family size, birth order of the affected child, and whether the child is taking any medications. An age and sex matched case-control study, including a dietary questionnaire, will also be conducted to investigate whether environmental exposures to mercury, lead, arsenic, and cadmium play a role in autism. Blood and saliva samples will be collected to determine if any DNA polymorphisms that might affect interactions with heavy metals are present in children with ASD. New knowledge of potential environmental risk factors for ASD may arise from this research, thereby reducing physical, psychological, and economic burdens on the child, family, and society and helping parents make decisions about avoiding exposure to environmental contaminants.

An investigation on the potential harmful effects of mercury in the nonhuman primate (Funded by SafeMinds)

An investigation into the effect of mercury on neurons, astrocytes, and microglia on the central nervous system of the nonhuman primate.

Investigating the effect of mercury on ASD, AD and ASD regression (Funded by SafeMinds)

An investigation into the influences of demographics and environmental variables in the development of neurodevelopmental problems such as AD, ASD, and ASD-regression

The effect of mercury and neuropeptide triggers on human mast cell release of neurotoxic molecules (Funded by SafeMinds)

An investigation to determine the pro-inflammatory effects of mitochondrial DNA with and without mast cell triggers.

Does mercury and neurotension induce mitochondrial DNA release from human mast cells and contribute to auto-immunity in ASD? (Funded by SafeMinds)

Further investigation into preliminary data that neurotensin (NT) stimulates mast cell activation and that NT is elevated in young children with autism spectrum disorder.

Toxicant-induced autism and mitochondrial modulation of nuclear gene expression (Federally Funded: DoD)

Autism has been associated with epigenetic changes: Tiny chemical tags in the regulatory regions of genes that affect how genes express themselves by turning them on or off. One gene often decreased in expression in the brain tissue of autistic individuals is MECP2, a gene that governs the expression of genes crucial to brain development. Exposure to environmental pollutants is also thought to play a role in autism. These two phenomena both involve a small cellular organ called mitochondria. The suspect environmental pollutants are toxic to mitochondria, which play a critical role in epigenetics: Pollution exposure can lower the amount of mitochondrial DNA (mtDNA) in a cell, causing an increase in placement of epigenetic tags by DNMT1 that leads to gene silencing. We hypothesize that exposure during pregnancy to pollutants toxic to mitochondria causes a decrease in mtDNA copy number and increased placement of epigenetic tags by DNMT1 on key developmental genes, affecting pathways that have direct roles in the development of autism. We will expose mice, during pregnancy, to selected toxicants and evaluate adult behavior and associated biochemical changes in brain tissue. Valproic acid will be used as a positive control, with saline as a negative control. The environmental pollutants lead, arsenic, cadmium, manganese, mercury, and permethrin will be investigated for their potential to induce autistic behavior changes. Brain tissue will then be used for molecular studies of mtDNA copy number, expression of DNMT1, and alterations to the epigenome on both a genomewide and gene-specific level.


By Matt Carey

Note: I serve as a public member to the IACC. My views here and elsewhere are my own, not those of the Committee.

Why won’t the government fund vaccine/autism research?

15 Jul

This question gets brought up a lot by some parent advocates. The are informed by groups promoting the idea of vaccine causation that the government is blocking this work. The evidence points strongly away from vaccines as a primary cause of autism, and investment in this area doesn’t seem wise. At least that’s the viewpoint of the majority of parents (including myself), autistics and researchers. But some remain unconvinced and want vaccine/autism research performed. And they are upset that none of this work is being performed.

Here’s a different question: why are the groups who promote the idea that vaccines cause autism failing to inform their members that, yes, indeed vaccine/autism research is being performed?

Or, to put it simply: vaccine/autism research is being performed and it’s being funded by the government. But you wouldn’t know that if you read, say, the Age of Autism blog, Generation Rescue’s website, SafeMinds’ website, or the other groups advocating for this research. If you are interested in vaccine/autism research and you are reading about these projects for the first time here, ask yourself “why have these orgs not informed me of this?”.

As noted here recently, Tom Insel discussed an upcoming vaccine/autism study. Already commissioned, performed and in the publication stage. That announcement was in April. What was the response from the community that has pleaded for vaccine/autism research? For the first few months: Silence. In July, SafeMinds finally put out an article showing that they were “worried” about this study. I don’t see much discussion of this announcement from other groups or outlets.

I’m not surprised by this. I’ve noted before that work on areas such as vaccines, mercury, environmental risk factor research and GI dysfunction don’t get discussed by the groups that are focused on these topics. I’ve covered the research in these areas more than they have.

So let’s get back to what other work is going on in vaccines and autism. Let’s start with the simple question: how would you find out? One place is the IACC/OARC Autism Spectrum Disorder Research Portfolio Analysis Web Tool. That could use updating, but it is an easily searchable database. Another place is NIH Reporter. It’s less easy to use than the Portfolio Analysis Tool and includes all of NIH. I.e. it covers non autism topics and doesn’t include projects being done outside of NIH (say, by Autism Speaks or other private funders). But, search Reporter for autism and vaccines or mercury and what do you get? Quite a number hits. Let’s consider a few.

How about:

There’s a study by Ian Lipkin’s group at Columbia titled: GENE-ENVIRONMENT INTERACTIONS IN AN AUTISM BIRTH COHORT.

There’s a study by Gene Sackett’s group, A PRIMATE MODEL OF GUT, IMMUNE, AND CNS RESPONSE TO CHILDHOOD VACCINES. This appears to be a follow on project to the Laura Hewitson studies that were discussed a great deal online a few years ago.

Isaac Pessah’s group at the UC Davis MIND Institute has a project NEURODEVELOPMENTAL TOXICOLOGY OF AUTISM. Prof. Pessah also had a multiyear project ENVIROMENTAL FACTORS IN THE ETIOLOGY OF AUTISM

Judy Van de Water’s group at UC Davis MIND Institute has a project IMMUNOLOGICAL SUSCEPTIBILITY OF AUTISM.

The Lewin Group study (which I believe is the one mentioned by Tom Insel) STUDY OF HEALTH OUTCOMES IN CHILDREN WITH AUTISM AND THEIR FAMILIES. (Just a note–see how this has been publicly available information for a year?)

There’s the CHARGE study, which is looking at a large array of potential environmental risk factors, including specifically mentioning mercury. THE CHARGE STUDY: CHILDHOOD AUTISM RISKS FROM GENETICS AND THE ENVIRONMENT

Here’s a 2014 grant to Ray Palmer, well known to the groups promoting mercury as a cause of autism, PRENATAL TIMING OF HEAVY METAL EXPOSURES FROM AUTISTIC AND NON-AUTISTIC CHILDREN.

The EPIDEMIOLOGICAL RESEARCH ON AUTISM IN JAMAICA – PHASE II project is continuing (hence the Phase II) and includes work on mercury.

There are more projects. Some I left out because they are older. But I think the point is made and is very clear: vaccine/autism and mercury/autism research are being funded.

And that is without even discussing how research on the biology of autism feeds into all etiological questions. Whether it’s vaccine, genetics or what have you, if you understand the biology, you have a better chance of understanding the cause. (when I searched NIH Reporter with the terms Autism and Immune, I got 25 pages of hits. Sure, not all are on-topic, but that’s 25 pages, 606 topics).

Here are the full abstracts–with emphasis added by me–for the NIH Reporter projects mentioned above.

GENE-ENVIRONMENT INTERACTIONS IN AN AUTISM BIRTH COHORT.

Abstract Text:
Reports of increasing prevalence of autism spectrum disorders (ASDs), a set of highly genetic conditions, are intensifying interest in the role of environmental exposures, including infectious, immune, and toxic factors. Retrospective studies exploring associations between environmental factors and ASDs are compromised by selection bias, small sample sizes, possibly invalid diagnosis, and absence of biologic measures. This prospective study will employ an unselected birth cohort of 75,500 in which cases are ascertained through screening of the entire population, diagnoses established using uniform procedures, extensive histories and clinical data obtained, and biologic samples collected serially throughout pregnancy and early childhood. The application of high throughput laboratory assays to derive maximal information from developmentally-influenced, finite, and nonrenewable biologic samples, and inclusion of early screening and diagnostic assessments, will permit an unprecedented, rich view of the longitudinal trajectory and nascent signs and symptoms of ASDs, facilitate discovery of biomarkers, and afford unique insights into the role of gene:environment interactions in ASD pathogenesis. Specific aims are to: (1) establish the autism Birth Cohort (ABC) through ascertainment of cases of autism spectrum disorder (ASD, N=150-233) and selection of controls (N-1000) from the Norway Mothers and Child (MoBa) cohort; (2) examine biologic pathways that may predispose to ASD, through evaluation of immune, endocrine, and neuroregulatory factors in mothers during early gestation or at birth and in children, at birth or 30 months postnatal; (3) identify environmental factors that may be directly or indirectly associated with ASD, including pre- or postnatal infection, vaccination, very low birth weight or other obstetric risk factors in which infections are implicated, dietary and/or environmental exposure to methylmercury; (4) describe the natural history of clinical, anthropometric, and neurobehavioral features of ASD; and (5) explore genotypic influences that may be directly or indirectly associated with ASD by testing associations of ASD and/or its endophenotypes with family history of autoimmune disease or selected candidate genes, and investigating conditional gene-environment effects using antecedent factors found to influence ASD risk.

NIH Spending Category:
autism; Brain Disorders; Clinical Research; Genetics; Immunization; Mental Health; Mental Retardation (Intellectual and Developmental Disabilities (IDD)); Neurosciences; Pediatric; Prevention; vaccine Related

Project Terms:
autism spectrum disorder; Autistic Disorder; Autoimmune Diseases; base; Biological Assay; Biological Markers; Birth; Candidate Disease Gene; case control; Child; Clinical; Clinical Data; cohort; Cohort Studies; Collaborations; Collection; Confusion; Control Groups; design; Development; Diagnosis; Diagnostic; Discipline of obstetrics; Disease; disorder risk; Drops; early childhood; Endocrine; endophenotype; Environment; Environmental Exposure; Environmental Risk Factor; Epidemic; Epidemiologic Studies; Evaluation; Exposure to; Family history of; gene environment interaction; Genes; Genetic; Hereditary Disease; Immune; immune function; Infection; insight; interest; Investigation; Laboratories; Life; Measles; Measures; member; Mercury; Methylmercury Compounds; Mothers; Mumps; Natural History; Nested Case-Control Study; neurobehavioral; Neurodevelopmental Disorder; Norway; novel; Pathogenesis; Pathway interactions; Phase; Population; postnatal; Pregnancy; prenatal; Prevalence; Procedures; prospective; Prospective Studies; Recording of previous events; Relative (related person); Reporting; Research; Research Design; Retrospective Studies; Risk Factors; Role; Rubella; Sample Size; Sampling; Screening procedure; Selection Bias; Signs and Symptoms; Specimen; Testing; Vaccination; Vaccines; Vacuum; Very Low Birth Weight Infant

A PRIMATE MODEL OF GUT, IMMUNE, AND CNS RESPONSE TO CHILDHOOD VACCINES.

Abstract Text:
This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject’s principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Diagnoses of childhood developmental disorders involving autism-spectrum symptoms are increasing, estimated to affect 1 in 100 children in the United States. Childhood Vaccines have been hypothesized to be contributory factors to this increase. The childhood vaccine regimen has an experimentally unstudied potential for cumulative and synergistic toxicities and possible immunologic interference to normal development. A prior study developed a primate model to assess neurodevelopmental consequences of the 1994-1999 pediatric thimerosal vaccine regimen (1994-1999). Significant neurodevelopmental deficits were evident for vaccinated animals in survival reflexes and standardized cognitive tests, and exposed animals developed gastrointestinal inflammation associated with focal transmural colitis, lymphoid hyperplasia, and syncytia.

NIH Spending Category:
autism; Brain Disorders; Cancer; Digestive Diseases; Immunization; Lymphoma; Mental Health; Mental Retardation (Intellectual and Developmental Disabilities (IDD)); Pediatric; Rare Diseases; vaccine Related

Project Terms:
Affect; Animals; Autistic Disorder; Child; Childhood; Cognitive; Colitis; cost; Development; developmental disease/disorder; Diagnosis; Funding; gastrointestinal; Giant Cells; Grant; Immune; Immunologics; Inflammation; lymphoid hyperplasia; Modeling; National Center for Research Resources; Neurodevelopmental Deficit; Primates; Principal Investigator; Reflex action; Regimen; Research; Research Infrastructure; Resources; response; Source; Symptoms; Testing; Thimerosal; Toxic effect; United States; United States National Institutes of Health; Vaccinated; Vaccines

NEURODEVELOPMENTAL TOXICOLOGY OF AUTISM

Abstract Text:
The long range goal is to determine if exposure to environmental toxicants early in development contributes to the etiology of neurodevelopmental disorders such as autism. A related goal is to determine whether susceptibility to autoimmune disease increases the neurotoxicity of environmental contaminants and increases the risk for developing disorders such as autism. Understanding how exposure to environmental toxicants may contribute to the etiology of neurodevelopmental disorders is important so that the exposure risks can be identified and minimized. If immune system dysfunction is found to increase the risk of exposure to environmental toxicants, then exposure limits to toxic substances can be lowered, and children with immune system dysfunction who may be at increase risk can be identified and protected. The specific aims are to expose mouse strains with low (C57BL/6J) or high (SJL mice) susceptibility to autoimmunity perinatally to either methylmercury (MeHg), polychlorinated biphenyl 95 (PCB 95) or polybrominated diphenyl ether 47 (BDE 47). We will then compare the effects of toxicant exposure between these mouse strains on brain development, complex social behaviors, and immune system function. The hypothesis is that perinatal exposure to each of these toxic substances will impair brain development and behavior, and that suscepbility to autoimmune disease will increase the neuro- and immunotoxicity of these agents. We will also explore a potentially new model of autism in mice injected prenatally with unique autoantibodies isolated from the serum of mothers who have given birth to two more more autistic children. Brain development will be examined histologically using stereological procedures and immunohistochemistry. Complex social behaviors will be studied using behavioral testing procedures established in our laboratory that measure social recognition, social interaction and social communication in mice. Immune system status will be established by measuring cytokines, chemokines, immunoglobulins, and quantifying immune system response to antigenic stimulation. In addition, seizure susceptibility will be measured in toxicant-exposed mice as well as measures of synaptic excitibility and plasticity in hippocampal brain slices. These studies will provide critical new information on the role of the immune system and its interaction with environmental contaminants in autism and other neurodevelopmental disorders.

NIH Spending Category:
autism; Autoimmune Disease; Behavioral and Social Science; Brain Disorders; Epilepsy; Mental Health; Mental Retardation (Intellectual and Developmental Disabilities (IDD)); Neurodegenerative; Neurosciences; Pediatric; Perinatal Period – Conditions Originating in Perinatal Period

Project Terms:
Age; Animal Testing; Antibodies; Anxiety; autistic Children; Autistic Disorder; Autoantibodies; Autoimmune Diseases; Autoimmune Process; Autoimmunity; Behavior; behavior test; Behavioral; Biological Assay; Birth; Brain; CCL2 gene; CCL3 gene; CCL4 gene; Cerebellum; chemokine; Chemokine (C-C Motif) Ligand 4; Child; Complex; cytokine; density; Development; developmental disease/disorder; developmental neurotoxicity; Disease; Environmental Pollution; Enzyme-Linked Immunosorbent Assay; Etiology; Exposure to; fetal; Fibroblast Growth Factor; Flurothyl; Fright; Glutamate Receptor; Goals; Granulocyte-Macrophage Colony-Stimulating Factor; Hippocampus (Brain); Histologic; Homer 1; human TNF protein; IL8 gene; Immune response; Immune system; Immune System and Related Disorders; Immunoglobulin A; Immunoglobulin G; Immunoglobulin M; Immunoglobulins; Immunohistochemistry; Immunophilins; immunotoxicity; In Vitro; in vivo; Infection; Interferon Type II; Interleukin-10; Interleukin-17; Interleukin-4; Interleukin-5; Interleukin-6; Kindling (Neurology); Laboratories; Learning; Leptin; link protein; Long-Term Potentiation; Measures; Memory; Metabotropic Glutamate Receptors; Methods; Methylmercury Compounds; Mitogens; Modeling; Mothers; mouse model; Mouse Strains; Mus; N-Methylaspartate; neurobehavioral disorder; neurodevelopment; Neurodevelopmental Disorder; Neurologic; Neuronal Injury; Neurons; neurotoxicity; offspring; Pentylenetetrazole; Perinatal; Perinatal Exposure; phenyl ether; Plasma; Poisons; Polychlorinated Biphenyls; postnatal; Predisposition; pregnant; prenatal; prenatal exposure; Preparation; Principal Investigator; Procedures; programs; Proteins; RANTES; receptor; receptor function; repaired; Research Design; Research Personnel; research study; response; Risk; Role; Ryanodine Receptor Calcium Release Channel; Ryanodine Receptors; Seizures; sensory gating; Sensory Motor Performances; Serological; Serum; Signal Pathway; Signal Transduction; SJL Mouse; SJL/J Mouse; Slice; Small Inducible Cytokine A3; social; Social Behavior; social communication; Social Interaction; Source; Splenocyte; Structure; Synapses; synaptotagmin; System; T-Cell Proliferation; Testing; Tetanus; Tetanus Toxoid; Tetanus vaccine; Toxic Environmental Substances; toxicant; Toxicant exposure; Toxicology; Tumor Necrosis Factor-alpha; Vascular Endothelial Growth Factors; Western Blotting; Work; Xenobiotics

IMMUNOLOGICAL SUSCEPTIBILITY OF AUTISM.
Abstract Text:
Recent studies indicate that immune function in children with autism spectrum disorder (ASD) is profoundly altered compared to developmentally healthy controls. There is a strong interface between the immune system and the neurologic network, and successful neurodevelopment is contingent upon a successful interaction between these two systems. We have identified several aspects of immune dysfunction in patients with autism compared with typically developing controls. These include a reduced response to vaccine antigens of bacterial origin, altered cytokine levels in plasma and upon stimulation of PBMC, increased levels of leptin in patients with early onset autism, and autoantibodies to brain antigens. This wide and complex variety of immune anomalies noted in our first funding period is in keeping with the broad range of phenotypes encompassed by the autism spectrum. Thus, we will build upon our earlier findings of both serologic and cellular changes in immune function. While our studies in the previous project period were aimed at a broad analysis of immune function in patients with autism, the current proposal will address the mechanisms responsible for the numerous alterations in immune homeostasis uncovered in our earlier studies. Therefore, our primary focus will be on the mechanisms responsible for such anomalies in immune function through an in depth analysis of cellular immune function. Our overall hypothesis is that patients with autism have a fundamental defect at the cellular level that ultimately leads to abnormalities in immune function and heightened susceptibility to environmental triggers. To examine this, we propose to: (1) examine longitudinally the serologic profile of children with ASD to ascertain whether the various immune changes noted in our first studies are maintained and/or deteriorating further; (2) determine which immune cell population(s) plays a critical role in the immune dysfunction seen in patients with autism; and (3) fully characterize the autoantibody response in a subpopulation of children with ASD and some mothers of children with ASD. It must be noted that due to the highly heterogeneous nature of autism, there will potentially be immunologic differences that relate to sub-groups of patients with autism. Therefore, we will carefully define the study groups based on our current data to include children with early onset autism, children with delayed onset/regressive autism, general population controls, and children with developmental disorders without ASD. The studies will be performed on CHARGE subjects formerly analyzed by our laboratory (CHARGE-BACK study). This will allow us to extend our prior studies longitudinally to determine if the immune dysregulation, such as increased leptin levels in the early onset patients, remains over time. The following aims address both the serologic and cellular aspects of immune function in patients with autism.

NIH Spending Category:
autism; Brain Disorders; Mental Health; Mental Retardation (Intellectual and Developmental Disabilities (IDD)); Neurosciences; Pediatric

Project Terms:
Address; Age; anti-IgM; Antibodies; Antigens; autism spectrum disorder; autistic Children; Autistic Disorder; Autoantibodies; B-Lymphocytes; Back; base; Behavior; Blood Cells; Brain; calcium indicator; Calcium Signaling; Cell Culture Techniques; Cell physiology; Cell Proliferation; Cell surface; Cells; Child; Color; Complex; Cultured Cells; cytokine; Data; Defect; Development; developmental disease/disorder; Digestion; Disease; Dose; Dyes; early onset; Environmental Health; Etiology; fetal; Flow Cytometry; Flu virus; Frequencies (time pattern); Funding; Gel; General Population; HLA-DR Antigens; Homeostasis; Human; IgE; Immune; immune function; Immune system; Immune System Diseases; Immunoglobulin A; Immunoglobulin G; Immunoglobulin M; Immunologics; Label; Laboratories; Lasers; Leptin; Maps; Mercury; Microarray Analysis; Mitogens; Modeling; Mothers; Mus; Nature; neurodevelopment; Neurologic; Oligonucleotides; Pathogenesis; Pathology; Patients; Pattern; Peptides; Peripheral Blood Mononuclear Cell; Phenotype; Plasma; Play; Poly I-C; Population; Population Control; Predisposition; Pregnancy; Principal Investigator; Production; programs; Reagent; research study; response; RNA; Role; Serological; Serum; Source; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization; Staining method; Stains; System; T-Lymphocyte; Testing; Time; TNFSF5 gene; Tube; Up-Regulation (Physiology); Upper arm; vaccine Antigen; Xenobiotics

STUDY OF HEALTH OUTCOMES IN CHILDREN WITH AUTISM AND THEIR FAMILIES

Abstract Text:
This contract modification is to extend and supplement Contract HHSN271201000033C, consistent with the scope of work of “Study of Health Outcomes in Children with autism and Their Families¿ in order to access the currently validated database developed under the contract to provide for further analysis . Autism Spectrum Disorder (ASD) is a significant public health concern, with an estimated prevalence of 1 in 88 children in the United States. Much of the research to date has focused on the core social and communication deficits of ASD, but there are anecdotes and some survey data suggesting that the rate of comorbid health conditions may also be elevated in this population. Furthermore, despite several large-scale epidemiological studies that have assessed but not found any potential association between ASD and vaccinations, public concerns persist about such a causal link. At least partly as a consequence, health officials in the United States have reported an increased rate of vaccine refusal in the general population. The Study of Health Outcomes in Children with autism and their Families was begun two years ago. Under this contract, the Contractor analyzed a large dataset of retrospective commercial health plan claims of 46,236 children with ASD, their parents and siblings, and a comparison cohort of children and family members. They successfully completed the analyses requested in the original statement of work, which included a study of the validity of ASD diagnoses in the claims data, and descriptions of health outcomes and health care utilization of the ASD cohort, their family members, and the comparison cohorts.

NIH Spending Category:
autism; Brain Disorders; Immunization; Intellectual and Developmental Disabilities (IDD); Mental Health; Pediatric; Prevention; vaccine Related

Project Terms:
Anecdotes; autism spectrum disorder; Autistic Disorder; Child; cohort; Contractor; Contracts; Data; Data Set; Databases; Diagnosis; Epidemiologic Studies; Family; Family member; General Population; Health; health care service utilization; Health Planning; Link; Modification; Outcome; Parents; Population; Prevalence; public health medicine (field); Recording of previous events; Reporting; Research; Siblings; social communication; Surveys; United States; Vaccination; Vaccines; Work

CORE D: MOLECULAR GENOMICS CORE

Core 4 is the Molecular Core. It serves as the central resource for the projects that isolate and process RNA on Affymetrix microarrays, and for performing RT-PCR confirmation of the microarray data for those projects. The UCD Affymetrix Core Facility is run by Dr. Jeffrey Gregg and is equipped with fluidics stations, hybridization ovens, and the new scanner required to scan the human Affymetrix U133 2.0PLUS arrays. Preliminary data from the previous CHARGE study has shown that there are changes in gene expression in the blood of children with autism compared to control children in the general population (GP) and to control children with mental retardation and developmental delay (MR/DD). The blood genomic profile in children with autism without regression (A) was different from controls, autism spectrum disorder (ASD) and different from children with autism with regression (A-R). In addition, there is a group of regulated genes in most children with A, A-R and with ASD that are expressed by natural killer (NK) cells in peripheral blood, suggesting an abnormality in this cell type that is common to all types of autism. These NK-cell related genes are expressed by all of the autism phenotypes including A, A-R and ASD, and hence may point to common pathways that underlie the common language and behavioral abnormalities in all three disorders. This core will be utilized by the projects as follows. Project #1: Aim #1: Perform genomic (RNA expression on microarrays) studies on blood from children with autism in the 4-9 year old range, and compare to the blood genomic profiles we have obtained in children with autism in the 2-5 year old age range. Aim #2. Compare gene expression as a function of blood metal levels in both age groups in A, A-R, ASD, MR/DD and GP groups. Aim #3. Examine genomic profiles in pregnant mothers who have previously given birth to an autistic child to determine if there is a specific genomic profile that correlates with whether the mother’s fetus is destined to develop autism. Project #2. Aim #1. Describe the gene expression profiles in the blood using specific white blood cell subsets including NK cells for children with autism without regression, autism with regression, and ASD children compared to GP and delayed children. Aim #2. Examine gene expression following stimulation or activation of specific white blood cell subsets of A, A-R, ASD, MR/DD and GP children with: low level mercury; immune cell stimulation/activation with vaccine antigens and cell-specific mitogens; and xenobiotics. Project #3. Compare gene expression profiles in the blood of children with autism to the blood of experimental animals exposed to toxicants including organic mercury, PCB 95, and PBDE 47 (Project #3).

NIH Spending Category:
autism; Biotechnology; Brain Disorders; Genetics; Mental Health; Mental Retardation (Intellectual and Developmental Disabilities (IDD)); Pediatric

Project Terms:
5 year old; 9 year old; Accounting; Age; age group; Animals; autism spectrum disorder; autistic Children; Autistic Disorder; Autoantibodies; base; Behavioral; Birth; Blood; Blood specimen; cell type; Cells; chemokine; Child; Core Facility; cytokine; Data; Developmental Delay Disorders; Disease; Environmental Health; Fetus; Gene Expression; General Population; Genes; Genetic; Genetic Transcription; Genome; Genomics; Human; Immune; immune function; Inherited; Language; Leukocytes; Mental Retardation; Mentally Disabled Persons; Mercury; Metals; Mitogens; Molecular; Molecular Profiling; Mothers; Natural Killer Cells; Pathway interactions; Patients; pentabromodiphenyl ether; peripheral blood; Phenotype; Polychlorinated Biphenyls; Population Group; pregnant; Principal Investigator; Process; programs; Resources; Reverse Transcriptase Polymerase Chain Reaction; RNA Processing; Running; Scanning; Subgroup; Surveys; Toxic Environmental Substances; toxicant; vaccine Antigen; Xenobiotics

THE CHARGE STUDY: CHILDHOOD AUTISM RISKS FROM GENETICS AND THE ENVIRONMENT

Abstract Text:
DESCRIPTION (provided by applicant): Few rigorous epidemiologic studies have addressed the environmental causes and biologic underpinnings of autism spectrum disorder (ASD). The CHARGE (Childhood autism Risks from Genetics and Environment) Study is a large, population-based case-control investigation of environmental risk factors, broadly defined, in relation to ASD and developmental delay without ASD symptoms, with referents from the general population. Fieldwork began in 2003, and by now CHARGE has published widely on exposures such as air pollution, mercury, flame retardants, maternal nutritional status in the peri-conception, untreated fever during pregnancy, mitochondrial dysfunction, candidate genes, a wide array of functional immune markers in both the child and the mother, and maternal metabolic conditions including obesity and diabetes. This last finding is notable, given the epidemic of obesity and type 2 diabetes that has occurred in parallel with the steady rise in ASD over the last few decades. Moreover, an emerging literature implicates several endocrine disrupting chemicals as contributing to obesity and metabolic dysregulation, including hyperinsulinemia, and to neurodevelopmental disorders as well. This project therefore builds upon these observations in several ways. First, obesity and type 2 or gestational diabetes will be examined in a larger sample, and glucose challenge test (GCT) results for the first time, to determine associations not only with development of ASD and intellectual impairment in the children, but also with specific speech and language delays, behavioral phenotypes such as attention deficits or hyperactivity, and gene expression. Second, these maternal metabolic conditions will be evaluated for associations with markers of both metabolic and immune dysregulation to be measured in neonatal bloodspots. Third, the predictive value of neonatal bloodspot markers for a later diagnosis of ASD or other child developmental and behavioral outcomes will be assessed. Fourth, the maternal metabolic conditions will be analyzed for potential links with upstream exposures to phthalates and anti- bacterial compounds, ubiquitous chemicals in common household products. Finally, this project will examine how gene variants that play a role in biochemical pathways relevant to the processes under study may influence susceptibility of the mother, the neonate or the child. To ensure adequate power for this analysis of gene-environment interaction, the sample size will be increased to 2400 children. This project addresses several goals set by the NIH Interagency autism Coordinating Committee: 1) to discover environmental factors contributing to ASD, particularly in the prenatal period, 2) to understand biological mechanisms for ASD risk, including gene-by-environment interactions, and 3) to identify children at risk for ASD at earlier time points. Results of this detailed inquir into early exposures, maternal pathophysiology and prognostic markers in the newborn will set the stage for developing prevention strategies.

Public Health Relevance Statement:
PUBLIC HEALTH RELEVANCE: This project addresses several issues of direct public health relevance, and the science to be produced will lead to benefits in a wide cross-section of the U.S. population. Because obesity is reaching epidemic proportions and other metabolic conditions such as Type 2 diabetes, gestational diabetes, and dyslipidemia are rising steeply, understanding environmental causes has tremendous public health potential for moving us closer to effective prevention strategies. If environmental chemicals used in common household products do prove to adversely affect body weight, measures can be taken to either reformulate those products, removing them from the market, or to educate consumers on how to avoid them. Similarly, steady increases in ASD might be curbed if the postulated causal pathway is supported by the evidence.

NIH Spending Category:
autism; Behavioral and Social Science; Brain Disorders; Clinical Research; Diabetes; Genetic Testing; Genetics; Intellectual and Developmental Disabilities (IDD); Mental Health; Neurosciences; Nutrition; Obesity; Pediatric; Perinatal Period – Conditions Originating in Perinatal Period; Prevention

Project Terms:
Address; Affect; Age; aged; Air Pollution; Anti-Bacterial Agents; Attention; autism spectrum disorder; Autistic Disorder; Behavior; Behavioral; Biochemical Pathway; Biological; Biological Markers; blood glucose regulation; Body Weights and Measures; C-Peptide; Candidate Disease Gene; case control; CCL2 gene; chemical association; Chemicals; Child; Childhood; Conceptions; cytokine; Data; Development; Developmental Delay Disorders; Diabetes Mellitus; Diagnosis; disorder risk; Dyslipidemias; Endocrine Disruptors; Ensure; Environment; environmental chemical; Environmental Risk Factor; Epidemic; Epidemiologic Studies; ESR1 gene; Exposure to; Fever; Flame Retardants; Functional disorder; gene environment interaction; Gene Expression; General Population; Genes; Genetic Risk; Gestational Diabetes; Glucose; glucose metabolism; Goals; high risk; Household; Household Products; human TNF protein; Hyperactive behavior; Hyperinsulinism; Hypertension induced by pregnancy; Immune; immune function; Immunologic Markers; Impairment; inattention; Inflammation; Inflammatory; Insulin Resistance; insulin sensitivity; interest; Interleukin-6; Investigation; Language Delays; Lead; Leptin; Link; Literature; Marketing; Maternal Exposure; Measures; mercury; Metabolic; Metabolic Marker; Metabolism; mitochondrial dysfunction; Mothers; Neonatal; neonate; neurodevelopment; Neurodevelopmental Disorder; Newborn Infant; Non-Insulin-Dependent Diabetes Mellitus; Nutritional status; Obesity; Outcome; Pathway interactions; Phenotype; phthalates; Play; Population; population based; PPARG gene; Predictive Value; Predisposition; Pregnancy; prenatal; Prevention strategy; Process; prognostic; Prognostic Marker; public health medicine (field); public health relevance; Publishing; Regulation; Risk; Role; RORA gene; RPL10 gene; Sample Size; Sampling; Science; Self Care; Speech Delay; Staging; Symptoms; Test Result; Time; Triclosan; Tumor Necrosis Factor-alpha; United States National Institutes of Health; Variant; Variation (Genetics)

PRENATAL TIMING OF HEAVY METAL EXPOSURES FROM AUTISTIC AND NON-AUTISTIC CHILDREN

DESCRIPTION (provided by applicant): Little is known about the etiology or risk factors for autism, a disease affecting 1 in 50 children in the U.S. While genetic and environmental factors are thought to act together, the specific mechanisms are not known and the measurement of environmental risk factors during critical periods of neurodevelopment has been lacking. This case-control study seeks to apply a novel dental biomarker of early life metal exposure, including in utero, to identify risk factors for ASD. Beyond looking at exposure intensity, we will be able to identify differences in exposure timing between cases and controls. This will allow us to identify critical windows when exposure, even at low levels, increases the risk of ASD. Using the proposed biomarker, we will directly assess fetal exposure, and will not rely on maternal biomarkers which may only provide an indirect measure of fetal exposure to metals. This work will have substantial impact on epidemiologic investigations of the relation of early life chemical exposures to ASD and other neurodevelopmental disorders as it can be used to objectively reconstruct both exposure intensity and timing.

Public Health Relevance Statement:
PUBLIC HEALTH RELEVANCE: Little is known about the causes of autism. This proposal seeks to apply a novel dental biomarker of early life metal exposure, including in utero, to identify risk factors for ASD. Beyond looking at exposure intensity, our application is novel in that we will be able to identify differences in exposure timing between cases and controls. This will allow us to identify critical windows when exposure, even at low levels, increases the risk of ASD.

Project Terms:
Accounting; Address; Affect; Aluminum; analytical method; Animals; Apatites; Arsenic; autism spectrum disorder; autistic Children; Autistic Disorder; Binding (Molecular Function); Biological; Biological Markers; bone; Cadmium; Calcified; Calcium; case control; Case-Control Studies; Chemical Exposure; Chemicals; Child; Childhood; Chromium; critical period; Data; deciduous tooth; Dental; Dentin; Development; Disease; early life exposure; Elements; Environment; Environmental Exposure; Environmental Risk Factor; Epidemic; Epidemiologic Studies; Etiology; Exposure to; fetal; Fetus; Genes; Genetic; Health; Heavy Metals; Human; Immune system; in utero; Investigation; Lead; Life; Literature; longitudinal design; Manganese; Measurement; Measures; mercury; Metal exposure; Metals; Methodology; Methods; mineralization; Mothers; neurodevelopment; Neurodevelopmental Disorder; Nickel; novel; Perinatal; Perinatal Exposure; Play; postnatal; Predisposition; Pregnancy; prenatal; Property; prospective; public health relevance; Recording of previous events; repository; Risk; Risk Factors; Role; Sampling; skeletal; Staging; Time; Tissues; Tooth structure; Toxic Environmental Substances; toxicant; Toxicant exposure; Work

comment on: Childhood vaccine beliefs reported by somali and non-somali parents.

14 Jul

Autism in the U.S. Somali Community has gathered significant attention in recent years (as has autism in other Somali communities outside of Somalia, for example in Sweden). Most of the attention in the U.S. can be traced back to vigorous advocacy by people like my fellow IACC public member Idil Abdul. Not all attention is good. For example, Minnesota Somali parents received a lot of attention from groups promoting the failed vaccine/autism link. When news of the possibly high prevalence in the Minnesota Somali community arose, David Kirby used the story to promote the idea of vaccines causing autism. Generation Rescue brought in Andrew Wakefield to talk to Somali parents in closed door meetings.

With the discussion of vaccines and autism comes fear and with fear of vaccines comes a reduced uptake. One recent story reports that the MMR uptake in the Minnesota Somali community dropped from 90% to 54% in the past 10 years. Sadly, that same story discusses how the Minnesota Somali community is presently involved in one of the largest measles outbreaks in recent history.

The question is, what are the views of the Somali community on vaccines and autism? To answer that, a new study has just been released: Childhood vaccine beliefs reported by somali and non-somali parents. (note the lack of capitalization of Somali is in the original). The full paper is available online.

There are limitations to the study, such as the use of a “convenience sample” of parents attending one specific clinic. This could induce bias. Also, the response rate was about 50%. This is reasonable, but again some bias might be involved in who actually responded. People who distrust vaccines might distrust those performing the survey, for example.

To answer the question–yes, Somalis in Minnesota do think that the MMR causes autism more than their non-Somali counterparts. Nearly 5 times more likely. But, the majority do not believe–about 35% of Somali parents and 8% of non-Somali parents believe that autism is caused by vaccines.

At recent IACC meetings, Idil Abdul has related how she knows Minnesota Somali families who stopped vaccinating after having a first autistic child. These families went on to have more autistic children. Unvaccinated autistic children. In one family, she relates a family with 5 autistic children.

This stands as an example of where we in the autism parent community have failed. We scared the parents in the Minnesota Somali community, sending in Generation Rescue, Andrew Wakefield and David Kirby. Parents stopped vaccinating, offering zero protection from autism but leaving their children open to infectious diseases. To say nothing of the guilt that parents feel and the children who grow up under that falsely placed guilt.

Yes, I stand apart from the minority of parents spreading the message of a vaccine-epidemic. But, as a community, we have to accept our failures as a community. And this is an example of a big failure.

Here is the abstract.

Abstract

BACKGROUND:

In 2011, an outbreak of measles in Minnesota was traced back to an unvaccinated Somali child. The purpose of this project was to (1) ascertain whether Somali parents are more likely than non-Somalis to refuse childhood vaccinations, particularly the measles-mumps-rubella (MMR) vaccine and (2) determine what factors influence the decision not to vaccinate.

METHODS:

We explored parental perceptions and utilization of vaccines through a survey distributed to a convenience sample of Somali and non-Somali parents of children ≤5 years old in a family medicine clinic in Minneapolis, MN.

RESULTS:

A total of 99 surveys were completed, 28% (n = 27) by Somali parents. Somali parents were more likely than non-Somali parents to have refused the MMR vaccine for their child (odds ratio, 4.6; 95% confidence interval, 1.2-18.0). Most of them refused vaccines because they had heard of adverse effects associated with the vaccine or personally knew someone who suffered an adverse effect. Somali parents were significantly more likely to believe that autism is caused by vaccines (35% vs. 8% of non-Somali parents). Somalis were also more likely to be uncomfortable with administering multiple vaccines at one visit (odds ratio, 4.0; 95% confidence interval, 1.4-11.9) and more likely to believe that children receive too many vaccines.

CONCLUSIONS:

Statistically significant differences in perceptions and use of vaccines were reported by Somali and non-Somali participants. Somali parents are more likely to believe that the MMR vaccine causes autism and more likely to refuse the MMR vaccine than non-Somali parents. These beliefs have contributed to an immunization gap between Somaliand non-Somali children


By Matt Carey

Andrew Wakefield and Lance Armstrong: two unethical people exposed by the Sunday Times

30 Jun

The Sunday Times has a series of films (Unquiet Films, www.foreverunquiet.co.uk) has a series of short films about the impact of The Times has had over the years.

Newspapers are all about stories – but sometimes the best stories are the ones we don’t tell.

Let’s not forget that news is often something that someone, somewhere, doesn’t want you to know. The real-life tales of how world-changing exclusives – whether from foreign reporters under fire, or determined hacks banging against stone-walling bureaucracy – are brought out into the open can be just as extraordinary as the articles that end up in the newspaper. Sometimes the story behind our amazing photo-journalism, campaign to change the law on adoption, to make cities safe for cycling, to reveal the corruption at the heart of FIFA, or the lies of a champion like Lance Armstrong are as exciting as a thriller, as tense as an episode of House of Cards.

We decided it was time to showcase just what the best journalists do… the real lives, real struggles, real bravery behind the newspaper stories that change the course of history. It’s all very well to boast that The Times and the Sunday Times strive to speak truth to power, without fear or favour and to report the truth, whatever the cost. But too often exactly what that takes – the death threats to reporters, the legal battles, the toughness and integrity it takes to get the article on the page – gets lost in the telling.

So here, in a series of extraordinary and independently made short films are some of the amazing, true-life stories behind the stories – we hope you find them as moving and inspiring as we do.

As an example of the “best journalists do”, they have a segment entitled “question everything“. It focuses on Brian Deer (whose work exposed the unethical actions of Andrew Wakefield, later found proved by the GMC) and David Walsh (who pursued and uncovered the Lance Armstrong doping scandal).

From BAFTA-winning filmmaker Will Clark: We now live in a world where more often than not, only the surface facts of a story are reported. Real investigative journalism seems to be a dying art and I feel this is something we should all be deeply concerned about. I wanted to create a film that focused on two Sunday Times journalists whose pursuit for the truth turned into an obsession. From Lance Armstrong’s doping revelations to Andrew Wakefield’s fraudulent MMR claims, both were lengthy investigations that were published at risk by the newspaper. Both investigations also managed to reveal large scandals that would most likely have remained hidden were it not for the perseverance and tenacity of the journalists covering the stories. I’m sure every reporter has secretly wished for his or her very own All The President’s Men moment. This is the tale of two journalists who got their wish.

Here’s the video:


By Matt Carey

UK families suing MMR litigators for pursuing “hopeless” claims

27 Jun

The saga of the U.K. MMR litigation continues. In this case a family is suing a law firm involved for mishandling the case. Per one story, one of the original MMR litigants (McCafferty) is now suing:

McCafferty, 23, from Falkirk, central Scotland, is seeking damages to “include compensation, distress, expense and inconvenience of engaging in hopeless litigation”.

I’m not sure how sound this case is, but here we have a family arguing that they suffered by being sucked into the MMR litigation. The effort and expense they put into the case was not only wasted, but the case was “hopeless” and, thus, the attorneys were at fault for dragging them through this.

The story at The Times is behind a paywall, but it starts:

MMR families sue their legal aid lawyers

Families who failed to win compensation cases driven by flawed research into the MMR vaccine are suing their lawyers for pursuing “hopeless” claims and enriching themselves on legal aid.

Matthew McCafferty, 23, who received the vaccine and three years later developed autism, is taking action against his former legal team over a claim that he says had no chance of succeeding, was issued out of time and raised false hopes

MMR vaccine: lawyers sued for pursuing claim based on link to autism
Man claims Hodge Jones & Allen was negligent in litigating a hopeless claim while profiting from part of £15m legal aid funding

A man is suing his former legal team for pursuing “hopeless claims” based on flawed research into the MMR vaccine, it has emerged.

Matthew McCafferty, who was diagnosed with autism three years after receiving the vaccine, is taking legal action over a legal claim that he says had no chance of succeeding, according to a report in the Times.

The law firm is Hodge Jones & Allen. In MMR and Autism: What Parents Need to Know, Michael Fitzpatrick discusses how Richard Barr, the attorney who worked closely with Andrew Wakefield, started at Dawbarns, moved to Hodge Jones & Allen and then moved on to Alexander Harris, “always taking his burgeoning portfolio of MMR cases with him.”


By Matt Carey

Andrew Wakefield, apparently he’s making films to convince you that doctors think vaccines cause autism and are covering it up.

28 May

It can be very interesting to hear what people say when they are in their home element. Ken Reibel showed this when he reported back from an AutismOne parent convention six years ago. More recently, we heard Jenny McCarthy accuse parents who don’t take her advice on alternative medicine of being victim moms who love the attention they get from having a disabled child. So much so that they won’t treat their children. So, with that in mind, I took the time to listen to a talk from this year’s AutismOne convention. The talk by Andrew Wakefield.

Andrew Wakefield, the doctor behind the MMR/autism scare of the 1990’s, spoke at the AutismOne parent convention last week. His talk at AutismOne was The Legacy of Vaccine Injury. It’s much of the same non-autism talk about vaccines one reads online. But one minute of the talk stood out for me. A minute where he describes why he is making films.

Yes, in case you weren’t aware, Mr. Wakefield has a new career as a film maker. He has a documentary on the death of an autistic young man, Alex Spourdalakis. Mr. Spourdalakis was brutally murdered by his mother and caregiver. Mr. Wakefield, as it turns out, had been “helping” the family and was filming their story. That film is finished. Mr. Wakefield tells us why he makes his films in his AutismOne talk. One might ask: is it to demonstrate the needs of autistics? The challenges parents of autistics face? The lack of supports for autistics?

No. It’s best to get it straight from him (although I admit the title of this article gives it away). With that in mind, here’s my best effort at transcribing what he says. For context: he’s speaking to an audience of autism parents at AutismOne, and he’s been talking about how surveys/studies show a sizable minority of the U.S. population believes that vaccines cause autism:

“And there is no mention in these studies of the uncertain or the undecided. There was another poll* that came out, I think from the University of Chicago, in fact. Where they asked the question: ‘Do you believe doctors think that vaccines cause autism and are covering it up?’ 20% of the respondents said yes. The important number is that 36% didn’t know. And it’s that 36% that I am targeting in the films that I am making. They are not for you. You already know. I’d be honored if you watched them but they are not for you. They are for the agnostic. And for that reason they must get out into the mainstream.”

For that reason they must get out into the mainstream

“That reason”: convincing the agnostic that doctors think that vaccines cause autism and they are covering it up. Alex Spourdalakis died a horrific death, and that can be used in this campaign, by inserting him into one of Mr. Wakefield’s films.

Go ahead and listen. It’s about 9 minutes in this video (for some reason the embed code isn’t working so you have to follow the link).

And some people wonder why I am critical of Mr. Wakefield. Yeah, I know that criticizing Mr. Wakefield plays directly into the persona he has created, where he has given everything for the children. But in this case the time as well as the criticism is well deserved.


By Matt Carey

*In case you are wondering: he appears to be referring to Medical Conspiracy Theories and Health Behaviors in the United States.

On Andrew Wakefield and the use of the term “fraud” in the press

6 May

Andrew Wakefield has sent a threatening letter to Forbes and Emily Willingham claiming harm over their use of the word “fraud” in a recent article. I wrote about this recently but then thought, “I wonder how often the term ‘fraud’ shows up in the press. Here are some examples from a recent Google News search.

Vail Daily column: Vaccine: Not a 4-letter word

But before I continue, realize that a few years later Wakefield was found guilty of falsifying data in order to fit a desired conclusion and was stripped of his license to practice medicine. The hypothesis that MMR caused autism was declared fraudulent, and Wakefield is now living in Texas pushing homeopathic medicine (read: watered-down to the point it needs no FDA approval) to the gullible.

STONE: Vaccines save lives

First, let’s put to bed one of the more outlandish conspiracy theories brought on by the anti-vaccine movements that vaccines cause autism. Jenny McCarthy, fueled by a biased and fraudulent study in 1998 by Dr. Andrew Wakefield claiming autism was linked to the combined measles, mumps, rubella (MMR) vaccine, used her celebrity stature to “raise awareness” for parents to reconsider vaccines for their children.


LETHBRIDGE: The victory of reason over my vaccination fears

In retrospect, it was the correct decision. Wakefield’s work was later found to be fraudulent. His research practices were ethically dubious, he falsified data and failed to declare certain vested interests.

The vaccine and its controversy

The MMR vaccine became the centre of a controversy following claims (which were subsequently established as fraudulent) that the vaccine was responsible for causing Autism-spectrum disorders in children. The controversy was kicked off in 1998 by the publication of a paper by British surgeon Andrew Wakefield in the medical journal The Lancet. Investigations later revealed that Wakefield had multiple undeclared conflicts of interest, had manipulated evidence, and had broken other ethical codes. The Lancet paper was partially retracted in 2004 and fully retracted in 2010, and Wakefield was found guilty by the General Medical Council of serious professional misconduct in May 2010 and was struck off the Medical Register.

Collin Boots | Immune to reason
The Devil’s Advocate | The anti-vaccine movement, whether religious or secular, needs a dose of reality

Not only have countless follow-up studies directly contradicted this result, but The Lancet actually retracted the original article in 2010 when it was revealed to be fraudulent. Wakefield was also stripped of his medical license

Richard Feldman: Vaccines and autism: Numerous studies indicate no connection

British researcher Dr. Andrew Wakefield authored completely bogus research in 1998 that linked the measles-mumps-rubella vaccine to autism. His fraudulent research was finally exposed; he was completely discredited and lost his British medical license.

Don’t let parents opt out of ‘mandatory’ vaccinations

In 2011, the British Medical Journal published an investigative piece by Sunday Times reporter Brian Deer, debunking Dr. Andrew Wakefield’s vaccine/autism study as “an elaborate fraud.”

Only 12 children were studied. Doubts were raised about the manner in which they were recruited and the science with which the study was conducted.

As well, it was discovered Wakefield was on the payroll of a group that had launched a lawsuit against manufacturers of the MMR vaccine — and their claim would be based on his evidence.

What’s most shocking about this is that well-meaning, concerned parents around the world stopped vaccinating their children on the basis of this fraudulent study and Wakefield became the darling of the anti-vaccine activists movement.

Even though it’s been shown to be a giant fraud, there are those who still persist in parroting the untruths.

EDITORIAL: Vaccinate your children

Reasons vary. Some parents prefer a “natural immunity” to vaccine-acquired immunity; others believe vaccines overload a child’s immune system; others say we shouldn’t worry about diseases that have “disappeared.” Then there’s the Jenny McCarthy phenomenon. The former Playboy model has convinced some parents that vaccines cause autism. The one study that linked the measles-mumps-rubella vaccine to autism, by British doctor Andrew Wakefield in 1998, has been discredited as fraudulent, and the published paper was retracted. Autism rates are the same in vaccinated and unvaccinated children.

My position on immunization – Dr. Mark Fishaut

Editors of BMJ, the British medical journal, have even called the study “an elaborate fraud,” accusing author Andrew Wakefield of deliberately falsifying medical data.

Prevention is better than cure

It was also reported that his research methodology was questionable as patient data was manipulated to create the appearance of a link to autism. This conflict of interest plus the fraudulent research resulted in the withdrawal of Wakefield’s paper from The Lancet and revocation of his medical licence.

That’s, what, 10 examples in only the past few weeks?

None have any notation that Mr. Wakefield has contacted them. I have not heard of any such letters being sent other than the one to Forbes and the lawsuit instigated against Brian Deer and the BMJ.

Odd, isn’t it, that all of a sudden Mr. Wakefield decides to threaten one of the Age of Autism’s favorite targets and no one else?


By Matt Carey

Andrew Wakefield threatens another libel suit

6 May

One of the advantages of taking some time off writing and the internet autism discussions is not hearing about Andrew Wakefield. Otherwise it seems a day can’t go by without some news article or blog post going up where the same 4-5 people will descend and tell us, once again, about how Andrew Wakefield isn’t an unethical guy but a combination of Nelson Mandela and Jesus Christ rolled up into one.

If you don’t recall and think I’ve gone way over the top with that phrase: it’s a quote. Yeah, really. J.B Handley, co-founder of Generation Rescue actually said that to a reporter at the New York Times for his article The Crash and Burn of an Autism Guru.

A decade ago Brian Deer exposed the first of the ethical lapses to come to light involving the MMR/Autism research Mr. Wakefield had undertaken. That’s when it became clear that Mr. Wakefield had financial conflicts of interest, hidden from the public and even his own colleagues. While this ground has been gone over many times in the past 10 years, it’s worth reading about it again if only to hear Mr. Wakefield’s colleague, Simon Murch, chime in on what it was like to discover that Mr. Wakefield had hidden financial interests:

Simon Murch, one of the leading doctors involved with Wakefield’s research at the Royal Free, said yesterday that news of the £55,000 legal funding was “a very unpleasant surprise”. “We didn’t know. We were pretty taken aback. The timing of it before the paper is something we have all been shocked by. If you have a colleague who has not told you, if you have not been informed you are going to be taken aback.”

He went on: “I am not going to join the queue of people rushing up to kick Andy. But it is right that this has come out: there has been a complete conflict of interest.”

Murch said it was never made clear that the payment was in place before the report was published. “We never knew anything about the £55,000 — he had his own separate research fund,” said Murch. “All of us were surprised . . . We are pretty angry.”

In response for his 2004 reporting of such stories, Mr. Deer was served with a lawsuit. A lawsuit that Mr. Wakefield eventually dropped, paying Mr. Deer’s legal fees. But before it was dropped, a judge made the following statements in a judgment and those comments are worth reading again (at least I think so):

It thus appears that the Claimant wishes to use the existence of the libel proceedings for public relations purposes, and to deter other critics, while at the same time isolating himself from the “downside” of such litigation, in having to answer a substantial defence of justification.

The Claimant in the above being Mr. Wakefield. Who appears to have been facing a rather strong rebuke for “us[ing] the existence of the libel proceedings for public relations purposes..” etc..

Before we get to the matter at hand, here’s one more paragraph of background. Readers of Left Brain Right Brain may be aware that Mr. Wakefield has again sued Mr. Deer, this time for articles which appeared in the BMJ. Mr. Wakefield lost the first round of this lawsuit against the BMJ and Brian Deer and is appealing (docket here). Mr. Wakefield took exception to his work being called fraudulent and himself being called a fraud. Well, he took exception to the word fraud in the BMJ and spoken by Mr. Deer, but as Todd W notes at Harpocratese Speaks, Mr. Wakefield has since let a lot of other mentions of the word “fraud” go by unchallenged. Most notably, to me, a Time magazine article: Great Science Frauds.

Mr. Wakefield has now taken offense at an article written by Emily Willingham, Ph.D., a researcher and science writer whose work appears, among other places, on Forbes.com. Emily Willingham wrote an article, Blame Wakefield For Missed Autism-Gut Connection in which she used the “f” word (fraud):

So why is it that no one attends to this clear (to me) link when it come to autistic children? Well, the Pediatrics review by McElhanon et al. happens to cite that reason several times: Wakefield’s MMR/autism/gut red herring and the subsequent noxious cloud that his fraud (link added 5/2/14) left over any research examining autism and the gut. So we don’t know anything about the real underlying causes of these digestive problems among autistic children. The Pediatrics authors state it unequivocally, as they have done before (link added 05/02/14):

It is clear that greater clinical and research scrutiny is needed to increase awareness on this topic and thus support development of the best standards of care. Previous controversy surrounding the MMR vaccine and proposed causal link between ASD and infection of the GI tract probably deterred investigators from dedicating resources to examine GI functioning in this population while fostering uncertainty in the ASD community regarding the validity of this line of inquiry.

Mr. Wakefield responded with a letter (linked at Forbes) in which he has informed Willingham and Forbes that while he isn’t bringing a suit forward now but he intends to bring suit. He also sent a copy of the letter sent to the Age of Autism blog which posted it.

Let’s go to the heart of Mr. Wakefield’s assertion, where he pulls a line out of the Forbes article and comes to a conclusion of malicious intent (he starts with a quote from the Forbes article):

Well, the Pediatrics review by McElhanon et al. happens to cite that reason several times: Wakefield’s MMR/autism/gut red herring and the subsequent noxious cloud that his fraud… The Pediatrics authors state it unequivocally:

On any ordinary reading, the intent of your statement is clear: to imply that the authors of the Pediatrics paper cite fraud on my part. What McElhanon et al actually say is substantially different from your false and defamatory allegation i.e.,

Well, I guess by Mr. Wakefield’s standards I did not give the article an “ordinary reading” as I did not see that purported intent. I stand apart from Mr. Wakefield on many standards. Why didn’t I make the association Mr. Wakefield claims?. Because I know without reading the Pediatrics article that no where in it does it have the phrase “noxious cloud that his fraud”. I know this because I read scientific journals, write for scientific journals, have edited an issue of a journal and more. Perhaps Mr. Wakefield missed the obvious conclusion that the phrase he focuses upon is clearly in Emily Willingham’s voice and that is obvious “on any ordinary reading”.

Mr. Wakefield asserts that the Forbes article was written “maliciously” and that “[Emily Willingham's] defamatory statements about me will undoubtedly cause me to suffer significant personal and financial damage.” Now, I can’t speak for Emily Willingham, but I can speak for myself–when I write my opinions of Mr. Wakefield and his work, I don’t think about it in terms of causing him damage. Frankly, if forced to consider it, I’d guess that when I write I likely enhance his stature among his supporters and donors, by supporting the image of Mr. Wakefield as some wronged maverick with myself as cast in the role as part of the machine which is grinding him down.

When I saw that Mr. Wakefield had threatened Forbes and Emily Willingham I thought, has he never heard of the Streisand Effect? I mean, here was a blog post at Forbes that had a couple of thousand views and was quickly on its way to the archives. Then I thought, yep, I bet he has heard of the Streisand Effect. I wouldn’t be surprised if he’s counting on me and others writing about him. What was it that judge said 10 years ago in a different suit? It thus appears that the Claimant wishes to use the existence of the libel proceedings for public relations purposes. I could be wrong. Probably am. I can no more read minds than can Andrew Wakefield, who projects malicious intent where I see none.

Consider a very recent interview he gave for a podcast. He’s introduced as “one of those dudes… [who] won’t back down” who has been “through living hell”. That group, by the way, is helping raise money for Mr. Wakefield.

So, here I am, playing into the mythos that is Andrew Wakefield, a man bravely facing critics like me in order to do what he does best: listen to the mothers of autistic children with GI disease. Except when those mothers disagree with him, apparently. Oh, did you miss that? Emily Willingham *is* the mother of an autistic child. And *two* of her kids have dealt with GI diseases. It’s in the comments of the article on Forbes.

In case it is not clear in the above, this is far from a trivial matter. Threats of legal action are never minor. I recall when Kathleen Seidel (autism parent and writer) was subpoenaed by Cliff Shoemaker, a vaccine attorney (Mr. Shoemaker was sanctioned). I recall when J.B. Handley threatened Kev Leitch (disabled adult, father of an autistic child and founder of Left Brain Right Brain). Even when you know you are in the right, lawsuits create a lot of uncertainty and distress.


By Matt Carey

Yep, measles is still a killing disease

21 Mar

Vaccines are a side show to the autism discussion, I know. And, yes, I know I spend a lot of time on this side show. One reason is that the autism parent community has a segment which does a lot to harm public health by creating fear of vaccines. With the resurgence of measles in the U.S., we are seeing the discussion rise again. For example, Dr. Robert “Bob” Sears has chimed in on facebook (see a discussion at Respectful Insolence here) as has Dr. Jay Gordon on twitter (see a discussion at The Poxes).

Inevitably these discussions include statements about how people suffer injuries or even death from measles. This is then countered by claims that with good nutrition, sanitation and vitamin A, no one will suffer lasting consequences. The CDC makes this very clear:

Even in previously healthy children, measles can be a serious illness requiring hospitalization. As many as 1 out of every 20 children with measles gets pneumonia, and about 1 child in every 1,000 who get measles will develop encephalitis. (This is an inflammation of the brain that can lead to convulsions, and can leave the child deaf or mentally retarded.) For every 1,000 children who get measles, 1 or 2 will die from it. Measles also can make a pregnant woman have a miscarriage, give birth prematurely, or have a low-birth-weight baby.

But people think this is an acceptable risk, or downplay this risk. One way they do this is to estimate risk of harm by the fraction of the total population, not the fraction of the population infected. That made some sense in the old days when a sizable fraction of the population was infected each year and everyone would be infected at some point in their lives.

Consider this old graph. In a bit we will get to the edit that was done and how deceptive that is (click figure to enlarge):

measlesmortalityusa1971-75_1

The rate of measles infection dropped by about 30x between 1964 (before the introduction of the vaccine) and 1971. With that came a drop in deaths from measles. A factor that is very interesting, and very much misused, is the fact that the death rate from measles was steadily dropping before the introduction of the vaccine. Hence the “vaccines didn’t save us” myth. Had we just waited, the death rate would have dropped to the same level anyway. There’s a line extrapolating from the data that “shows” that.

First off–hooray for medical advances. They have improved the survival rate from measles. Damned glad they did. But, what about that line? Well, you can draw a line through pretty much anything if you try hard enough. It doesn’t mean anything if you don’t understand the mechanism causing the trend. Why should we expect the trend before 1965 to continue for the next 45 years?

While engaging in online discussions about measles outbreaks, I ran across this website from the U.K.. The table is “Measles notifications and deaths in England and Wales, 1940-2013″. The public health officials in the UK are supposed to be “notified” of every person infected with measles, so “notifications” are “cases”. Let’s consider the notifications. (click figure to enlarge)

Measles Notifications UK

This isn’t normalized to the total population, it’s just the raw number of cases in any given year. I’ve taken the liberty to point out some events which happen to coincide with changepoints in the graph. First is the introduction of the measles vaccine, after which the number of cases per year dropped dramatically. Second is the introduction of the MMR vaccine which, again, was followed by drops in the number of cases. Lastly we see the publication of Andrew Wakefield’s now-retracted Lancet study. Shortly after which, the number of cases started to rise again. Yes, correlation is not causation, but time after time, with vaccine after vaccine we see the same thing: introduce a vaccine and the incidence of that disease decreases.

OK, we’ve looked at notifications. What about deaths? Let’s take the number of deaths and normalize by the number of notifications. In other words, let’s look at what fraction of those infected died.

Measles Deaths UK

Pre 1960 there was a steady drop in the fraction who died. Again, yay medicine. And, yes, yay nutrition and sanitation. After 1960, though, the fraction who died leveled off. 2-3 people per 1000 infected died. (it averages to about 2.6/1000 from 1960 onward).

None of this is news. In Measles Elimination in the United States, a team from the CDC writes:

By the late 1950s, even before the introduction of measles vaccine, measles-related deaths and case fatality rates in the United States had decreased markedly, presumably as a result of improvement in health care and nutrition. From 1956 to 1960, an average of 450 measles-related deaths were reported each year (∼1 death/ 1000 reported cases), compared with an average of 5300 measles-related deaths during 1912–1916 (26 deaths/ 1000 reported cases)

Catch that–that’s people from the CDC saying “yay healthcare! Yay nutrition!” and “yay vaccines!”.

Did nutrition, sanitation and improved medical care reduce the fraction of people who died from measles infection? Absolutely. Was it enough? No. Can we draw lines from old data and claim that the number who would die today would be 4 in 100 million today? Well, sure, you can draw the line. It’s dishonest, but given the source that’s not surprising. As I wrote above, you can draw a line through anything. Doesn’t make it true. If you don’t know the reason why a trend is happening, or the limitations on that trend, it’s meaningless. In this case there was a “hard floor”. There are deaths from measles that sanitation, nutrition and modern medicine can’t prevent. People still die from measles. Measles deaths in France (modern sanitation, nutrition and medicine) were seen at a rate of 3/1000 in recent years. Pregnant women, fetuses, small children and the infirm are more likely to suffer. Which is why when people like “Dr. Bob” Sears and “Dr. Jay” Gordon downplay the risks of measles–in effect telling their readers to keep relying on the rest of us to provide herd immunity–people like me speak up. Yes it’s a diversion from autism, but it’s a diversion fed by some of my fellow autism parents. And it’s an important diversion.


By Matt Carey

A cause célèbre for those claiming vaccines cause autism

1 Mar

If you participate in online discussions about autism and vaccines (and I’d advise you to spend your time more productively), you will often hear about how the U.S. Court of Federal Claims (the “Vaccine Court”) has compensated numerous cases of autism, the government just doesn’t admit it. These are often referred to as “secret” compensations, even though the decisions are in the public record. And, quite frankly, the families were not compensated for autism claims.

One family whose story has become a cause célèbre thanks to David Kirby is now the topic of a new Court decision. In this new decision, the court responds to the parents request to have past court documents redacted. They would like to stop being approached by members of the media.

Before we get to the new decision, consider Mr. Kirby’s story:

The parents, who did not want to be interviewed, specifically asserted that [child] “suffered a Vaccine Table Injury, namely, an encephalopathy” as a result of his MMR vaccination on December 19, 2003.” (“Table injuries” are known, compensable adverse reactions to immunizations.)

Alternatively, they claim that “as a cumulative result of his receipt of each and every vaccination between March 25, 2003 and February 22, 2005, [child] has suffered . . . neuroimmunologically mediated dysfunctions in the form of asthma and ASD.”

(child’s name redacted by me)

The parents didn’t want to be interviewed. They also presented two claims, one encephalopathy and one autism. Mr. Kirby focused on the autism claim, even though it wasn’t compensated. Mr. Kirby states:

Whether HHS agreed with [child]‘s parents that his vaccine-induced brain disease led to ASD is unknown. The concession document is under seal.

Actually, it was known. The proffer of an award was titled “Proffer on Award of Compensation; Measles-Mumps-Rubella (MMR); Table Injury; Encephalitis.”

The child was being compensated for a table injury: encephalitis. Within that document, it is clearly stated:

On June 9, 2011, respondent filed a supplemental report pursuant to Vaccine Rule 4(c) stating it was respondent’s view that Ryan suffered a Table injury under the Vaccine Act – namely, an encephalitis within five to fifteen days following receipt of the December 19, 2003 MMR vaccine, see 42 C.F.R. § 100.3(a)(III)(B), and that this case is appropriate for compensation under the terms of the Vaccine Program

Emphasis mine.

Even with this information showing the family were not compensating autism clearly in the public domain Mr. Kirby tells us it’s “unknown”. Then, true to Mr. Kirby’s style, he leads his readers to the evidence supporting the possibility that it was ASD while never coming right out and saying it.

Perhaps the feds were loath to concede yet another vaccine case involving autism. Four cases in the Autism Omnibus Proceedings were recently compensated. Three of those cases are marked with asterisks, indicating the government did not conclude that autism can be caused by vaccines. But the fourth autism case that was paid out in 2013 ([child]‘s case? We don’t know) has no such caveat.

Mr. Kirby was referring to the HRSA statistics page that lists vaccine court petitions filed and compensated. At the time Mr. Kirby wrote his piece, the statistics report did include autism cases. They no longer do, so you have to check archived pages to see what he’s referring to.

At the time of Mr. Kirby’s article, there appear to have been two cases where someone in the Omnibus Autism Proceeding did receive compensation (I don’t have reason to believe Mr. Kirby was in error, but the archived page doesn’t show four cases). Both of those cases had asterisks.

*May include case(s) that were originally filed and processed as an OAP cases but in which the final adjudication does not include a finding of vaccine-related autism

Mr. Kirby concluded with:

Meanwhile, as HHS says it “has never concluded in any case that autism was caused by vaccination,” it is still underwriting autism treatments such as ABA for children in its vaccine-injury program.

Which basically reads as “the government is making a distinction without a difference”. I.e. the reader comes away with the impression that the government really are compensating autism.

We knew then that these parents didn’t want to talk to the media. They didn’t want to speak with Mr. Kirby, to become his latest cause célèbre. And now we know that they still do not want this attention and we read once again that the case was not compensated for autism. From a recent decision:

“Petitioners have made these requests because they have had the misfortune of being frequently contacted by members of the media who mistakenly believe they were compensated for their alternative autism allegation when Petitioners were actually compensated for a Table Injury encephalopathy.”

Given the family’s clear intent to get out of the public’s eye, I am hesitant to put this article out. But perhaps, just perhaps, some of those using this family as part of their constant fight to keep the autism/vaccine idea alive might reconsider.


By Matt Carey

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