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National Geographic, “The War on Science”, includes discussion of vaccines and autism

19 Feb natgeo

I just got my copy of the March 2015 issue of National Geographic a couple of days ago. Imagine my reaction when I saw this cover (click to enlarge):

natgeo

In case you are having trouble imagining my reaction–it includes a big THANK YOU to National Geographic.

Yes, they put “vaccinations can lead to autism” up there with “evolution never happened” and “the moon landing was fake”.

This paragraph includes references to Jenny McCarthy (anti-vaccine activist and actress Jenny McCarthy) and Andrew Wakefield’s Lancet article.

Doubting science also has consequences. The people who believe vaccines cause autism—often well educated and affluent, by the way—are undermining “herd immunity” to such diseases as whooping cough and measles. The anti-vaccine movement has been going strong since the prestigious British medical journal the Lancet published a study in 1998 linking a common vaccine to autism. The journal later retracted the study, which was thoroughly discredited. But the notion of a vaccine-autism connection has been endorsed by celebrities and reinforced through the usual Internet filters. (Anti-vaccine activist and actress Jenny McCarthy famously said on the Oprah Winfrey Show, “The University of Google is where I got my degree from.”)


By Matt Carey

CNN: The money behind the vaccine skeptics

6 Feb

CNN Money has a short video up that makes a point that a few of us have been making for the past few years: much of the vaccine antagonistic message is funded by a few wealthy people. A good discussion can be found at A Snapshot of the Deep Pockets of the Anti-Vaccine Movement on Haprocrates Speaks. The CNN piece is called “The money behind the vaccine skeptics“. I can’t get the video to embed here, but one can find it here.

Here’s a screenshot from CNN showing the organizations, people and money that CNN discusses (click to enlarge)

cnn money

CNN points out that the self-styled National Vaccine Information Center and others (such as Chris Shaw’s group at the University of British Columbia) get a lot of money from the Dwoskin family. The Dwoskin Family Foundation told CNN that they are not antivaccine but are, instead, advocates for safer vaccines. It’s a story we hear a lot.

Claire Dwoskin is or was a board member of the NVIC and made this statement about vaccines. John Stossel had aired a piece about how his daughter had fought off a whooping cough infection and in her response to one of his producers she stated:

What his daughter went through is NOTHING compared to what the families of autistic children go through every day of their lives. No disease can match this record of human devastation. Vaccines are a holocaust of poison on our children’s brains and immune systems. Shame on you all.

I’m not sure how that sentiment fits in with being “advocates for safer vaccines”. One has to accept that vaccines are safe before advocating for safer vaccines.

Also mentioned is Barry Segal who funds Focus Autism (now Focus for Health) and A Shot of Truth. And Generation Rescue’s JB Handley and Jenny McCarthy. Both Focus Autism and Generation Rescue are noted for funding Andrew Wakefield’s “Strategic Autism Initiative”. All these groups are discussed in previous articles here at Left Brain/Right Brain.

The piece is short and perhaps that’s why they don’t mention Generation Rescue’s hundreds of thousands of dollars spent on full page ads claiming vaccines cause autism, or their poorly performed phone survey on vaccines. Lots of money spent on promoting fear and distrust of vaccines.

I’ve never seen evidence of these groups actually funding work into safer vaccines. I’ve never seen, say, funding for research into a new vaccine or even something simple like improved storage and transportation for vaccines into the developing world to reduce the use of thimerosal, a preservative these groups claim (without good evidence) cause autism and other disabilities.


Matt Carey

Jenny McCarthy tells the story two different ways…again

29 Jan

Yep, this doesn’t have anything to do with autism. Well, aside from the fact that we will discuss how one public face for autism is once again showing that her stories don’t match over time. You see, Jenny McCarthy has a reality TV show now and the story of her divorce presented in that show doesn’t match what she wrote in her book 8 years ago. I found the new story in a recent article in the Washington Post: Jenny McCarthy tries to mend her anti-vaccine reputation with reality TV. It’s too little, too late in which Emily Yahr writes:

The show is filled with such heart-to-hearts, with McCarthy recounting her ordeals as a single mom, starting with her ex filing for divorce in 2005 the same week that Evan was diagnosed with autism.

Now, it’s been a while since I read Jenny McCarthy’s “Louder than words” book. A long while, but that statement didn’t strike me as consistent with what she wrote in her book. The sentiment is the same: harsh on her kid’s father while putting herself in a good light, but the details didn’t match.

What did she say in her 2007 book? She says that she asked for the divorce. She was the mommy warrior, taking charge in that book. Now in her reality show she’s the object of sympathy, dumped by her husband just when she needed him most.

LTW-divorce

In fact, if you read the book, she talks about thinking about divorce for some time before she finally asked for it. Because that whole “same week as the diagnosis” thing in the TV show isn’t what she wrote in 2007 either. Between the autism diagnosis and her asking for a divorce, there are weeks, if not months of stories in her book. Stories that include Ms. McCarthy asking her husband to leave, and him refusing.

Who knows what the actual story was. All we hear is the story that fits the image she wants to portray at the moment. Her ex husband is taking the high road and not returning fire.

Oh, and if you are worried about how her son took the divorce, don’t. According to Ms. McCarthy, autism renders one incapable “emotionally connecting” with such events.

LTW-downplay-evan-reaction

Sorry to be sarcastic there. But, really, Ms. McCarthy? Autism renders one incapable of emotionally connecting with what was going on? Couldn’t be that the kid was unable to understand why his mother was making his father leave, just as any kid would?

No real surprises here. Ms. McCarthy has been inconsistent over the years. She had multiple stories of her first encounter with Barbara Walters when Ms. McCarthy was a guest on The View. She has informed us that her son is no longer autistic. Then, a few years later, she tells us that he is. (Jenny McCarthy Slams Rumor That Her 11-Year-Old Son Evan Doesn’t Have Autism). She hammers away at vaccines, but tells us she’s pro-vaccine. And to cap it all, she heads an autism charity that focuses on treatment, but won’t speak out against the faux treatments (like bleach enemas) that are promoted at her orgs conventions.


by Matt Carey

Measles are back but where is Jenny McCarthy?

28 Jan

It takes a lot of courage to stand up and make yourself heard on unpopular topics. But it’s only really courageous if you are willing to accept responsibility for being wrong. Jenny McCarthy stood up. She made herself heard. In the process she got a lot of media attention, led a march on Washington (the Green Our Vaccines rally), and sold a lot of books. That was years ago. Now we are seeing the outbreaks of disease that so many, even Ms. McCarthy, predicted based on the path she set. Back then she at least had the guts to say, “it’s not my fault” (I disagree). Now she’s just absent from the public’s eye on this topic. Instead we get her new reality show.

Today, a measles outbreak originating in Jenny McCarthy’s old backyard (southern California) has reached about 100 people infected (50 in the state, 23 more whose connection to the epicenter of the outbreak is unknown and more out of state). And, no comment from Ms. McCarthy. But she wasn’t always so quiet. Consider this statement from an interview in Time Magazine:

I do believe sadly it’s going to take some diseases coming back to realize that we need to change and develop vaccines that are safe. If the vaccine companies are not listening to us, it’s their f___ing fault that the diseases are coming back. They’re making a product that’s s___. If you give us a safe vaccine, we’ll use it. It shouldn’t be polio versus autism.

The idea that somehow a resurgence of disease would lead to a change in vaccines didn’t make sense to me back then. It seemed like some nasty game of “chicken” where Ms. McCarthy was going to frighten enough people about vaccines that outbreaks would be possible. Frighten with statements like “they’re making a product that’s shit” and that the vaccines are not safe. Somehow, once this fear was instilled and the drop in vaccination rates happened, outbreaks would happen and these would prove her point that the vaccines are “shit” and the vaccines would be reinvented.

Apparently Ms. McCarthy realized that this logic wasn’t sound as she started distancing herself from the vaccine message years ago. Instead of being at the forefront of her movement today, ready to force the changes she predicted, she brings handlers to interviews to deflect questions on vaccines. She points people to her nonpology and nosplenation of her views in an op-ed published by the Chicago Sun Times, Jenny McCarthy: The gray area on vaccines

Here’s a defensive paragraph (and a straw man argument) in that op-ed:

“People have the misconception that we want to eliminate vaccines,” I told Time Magazine science editor Jeffrey Kluger in 2009. “Please understand that we are not an anti-vaccine group. We are demanding safe vaccines. We want to reduce the schedule and reduce the toxins.”

Here’s the thing. Many people have called out Jenny McCarthy over the years for her irresponsible statements about vaccines. She spread a lot of fear. One doesn’t read “They’re making a product that’s shit” or a correction of that view at the Sun Times. One doesn’t hear blanket statements that vaccines are all unsafe (“If you give us a safe vaccine, we’ll use it.”) One doesn’t read her statements that vaccines are behind the rise in diagnosed autism rates. One doesn’t hear her state that if she had another child, she wouldn’t vaccinate (a statement she made back when she was more vocal). No, all we get is her “grey area” on vaccines.

Also, not comment about the impending outbreaks.

Which brings me back to: where’s the courage in hiding and dodging the consequences of your actions, Ms. McCarthy? Are you going to point me back to your claim that “it’s not my fault” made on Larry King Live?

KING: Isn’t the problem here, Jenny, that people sometimes listen with one ear are going to panic. And not vaccine at all?

MCCARTHY: Probably. But guess what? It’s not my fault. The reason why they’re not vaccinating is because the vaccines are not safe. Make a better product and then parents will vaccinate.

I didn’t buy it then, I don’t buy it now.

And a similar sentiment

KING: Probably due to you, jenny, and programs like this, the percentage of children getting vaccinations is dropping.
Do you think that’s good?

MCCARTHY: I think it’s only good because it’s the only thing that’s going to shake up the CDC to do something about it.

Yes, they and others have been doing something about “it”. It being the drop in vaccination rates, not the alleged problems with vaccines you were intending. Many people have spent a lot of time trying to prevent or reduce the outbreaks we are seeing now. The question is why weren’t you working on avoiding this?

As I stated at the outset, it’s only courageous to stand up against prevailing opinion if you are willing to take responsibility and fix problems if/when you are proved wrong.

Ms. McCarthy, you were wrong. You were wrong to spread fear. And you can’t get out of it with a simple “it’s not my fault”. It is partly your fault that outbreaks are happening.

And are these outbreaks causing people to accept your position and make the changes you asked for?

No.

And all this doesn’t even touch on the problems of your promotion of unsafe “therapies” for autism, an issue much closer to my heart.


By Matt Carey

Is Autism Speaks supporting vaccine-autism causation proponent Congressman Bill Posey?

19 Aug

Someone forwarded an email from the “Autism Action Network” recently. The email asked people to support Congressman Bill Posey’s election campaign by attending a fundraiser. Looks like a few big donors to Mr. Posey were going to attend, including Sallie Bernard of SafeMinds and Autism Speaks. Ms. Bernard certainly is with both organizations, but I wonder if she was attending as an Autism Speaks officer or if Autism Speaks was even aware that their name was being used to promote the fundraiser.

Perhaps Ms. Bernard wasn’t aware that her Autism Speaks affiliation was being used this way. I’ve seen some of my affiliations used where I didn’t expect nor want them. Perhaps Ms. Bernard was aware that the AS affiliation was being used in this advertisement, but Autism Speaks wasn’t. Perhaps Autism Speaks was aware and supported this effort. I’m not betting heavily on that last option though.

Here’s the list of donors for the fundraiser in the email I got:

Jennifer Larson of the Canary Party and Health Freedom
Sallie Bernard of Safeminds and Autism Speaks
JB Handley of Generation Rescue
Tony Lyons of Shy[sic] Horse Publishing
Barry Segal of Focus Autism
Mark Blaxill of the Canary Party and Health Freedom
Dr. Gary Kompothecras
Teri Costigan

The Autism Speaks name adds a legitimacy to this fundraiser that the other groups just can’t. The Canary Party and Health Freedom (which I assume to be Americans for Health Choice) are basically the same people with “Canary Party” as a political party and “heath freedom” as a charity. The Canary Party/Health Freedom team is led by the same people who funded large donations to Oversight & Government Reform Committee Chair Daryl Issa ($40k plus). JB Handley is not as vocal as he once was, but he founded Generation Rescue on the notion that “autism is just a misdiagnosis for mercury poisoning“. Sky Horse publishing is boutique publisher of many of the books on vaccines and autism, including “Age of Autism” and books by Andrew Wakefield. Barry Segal (Focus Autism) has been a large supporter of groups like Generation Rescue, the Age of Autism, SafeMinds and is very vocal on his belief that vaccines cause not only autism, but many other health problems as well. Gary Kompothecras has been funding Mr. Posey for years and is an autism parent and benefactor of groups promoting the vaccine/autism idea.

Without Autism Speaks’ name added to this, this would be very clearly all about a small but wealthy group of people pushing the failed ideas of vaccines and autism. People with failed and damaging ideas have the right to lobby members of congress along with everyone else. I, for one, am glad that the vast majority of Congress has moved on from the vaccine/autism-epidemic idea. I look forward to the day when that majority reaches 100%.


By Matt Carey

A bit of irony from Generation Rescue: still citing Jenny McCarthy as the face of autism recovery

5 Aug

Somehow I’ve found myself on Facebook and, even more, navigating to the Generation Rescue page. And today I found this:

GR_FB

In case you didn’t click to enlarge and read, here’s their statement:

The New York Times recently posted an article on autism recovery – and yes, it’s real! There really is hope!

Thank you Jenny McCarthy for being the celebrity to bring attention to the truth and thank you for all you have done for this cause.

Here’s a hint–there really is hope even without losing a diagnosis. One can have be autistic or the parent of an autistic kid and have hope. Trust me, I know. And I think if you ask Jenny McCarthy, she will tell you the same.

Back to the story. Generation Rescue are referring to this article (The Kids Who Beat Autism) in the NY Times magazine.

You may ask, where’s the irony in that? Jenny McCarthy is the public face of autism “recovery” after all, right? She told us all about how her kid was no longer autistic, typical, all that after using alternative medicine. She went so far as to berate the government for not calling her to study her no-longer-autistic son (more on that later).

I find it ironic because she’s been in the news just in the past few weeks, discussing how her autistic son is being bullied because of his autism.
http://www.people.com/article/jenny-mccarthy-the-view-autistic-son-bullied

AutisticEvan

I wish her kid well. I really do. I also wish Jenny McCarrthy compassion and forgiveness. I wish she would be more honest.

Let me return to the “Jenny McCarthy Berates the US Government for Not Studying her Autistic Kid” thing. You seethe NY Times Magazine article is discussing an NIH study of kids who were diagnosed as autistic but later were diagnosed to be not autistic. Not just a coincidence, but years back my friend Kev Leitch not only discussed that study while it was in progress, but pointed out that if Jenny McCarthy were serious about wanting the government to study her kid she might want to participate in the NIH study. Here’s what Jenny McCarthy had to say back then:

Evan is now 5 years old and what might surprise a lot of you is that we’ve never been contacted by a single member of the CDC, the American Academy of Pediatrics, or any other health authority to evaluate and understand how Evan recovered from autism. When Evan meets doctors and neurologists, to this day they tell us he was misdiagnosed — that he never had autism to begin with. It’s as if they are wired to believe that children can’t recover from autism.

So where’s the cavalry? Where are all the doctors beating down our door to take a closer look at Evan? We think we know why they haven’t arrived. Most of the parents we’ve met who have recovered their child from autism as we did (and we have met many) blame vaccines for their child’s autism.

So, where was the cavalry, Jenny? Where was your desire to see that the NIH, CDC, AAP and “any other health authority…understand how Evan recovered from autism”?

Ms. McCarthy, back then the autism community knew you’d never volunteer your kid for such a study. Controlling the message was just too important to you. The only surprises are that these “new” revelations so soon and are so clear.


By Matt Carey

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

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