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Autism Vox

Yes, the Vaccine Question Again

by Kristina Chew, PhD on May 10th, 2008

Do childhood vaccines cause autism? (KSDK, St. Louis)

No.

Vaccinations do not cause autism.

Source. Source. Source.

Tags: asd, asperger, autism, Cause, Epidemic, Health, magical thinking, measles, mercury, mmr, Parenting, pdd-nos, savant syndrome, shots, Vaccines

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Marla
May 10, 2008 at 11:02 am

Ahhhhhhhhhh!
Kristina Chew, PhD
May 10, 2008 at 12:38 pm

Another Autism Omnibus Proceeding begins on May 12.

“Two of those autistic children will take their mercury-injury claims to trial in “Vaccine Court” in the U.S. Court of Federal Claims in Washington, DC beginning on Monday, May 12. Decisions in these two “test cases” will help decide the outcomes of hundreds of other claims in Vaccine Court.”

So we’ll be hearing plenty more.
María Luján
May 10, 2008 at 3:20 pm

I wonder about how questions are done , as if it is possible to make simple and easy to answer questions in autism.
It isn´t.
I would phrase different the question and the answer
question:Do vaccines affect adversely to children who are born immunologically, gastrointestinally, biochemically, metabolically immature-(probably genetically linked through SNPs or other ) or with off the average kidney/liver and xenobiotics management ( transport and absorption and metabolism and excretion) function?
answer:We do not know.

We need more research on the topic ( serious, high quality and high level)
Cliff
May 10, 2008 at 3:35 pm

Of course, the standard of proof in regards to knowledge, when dealing with an inductive method and a nebulous question, is going to be impossible to reach. And I don’t think that people here think that, under specific circumstances, vaccines can’t cause harm. Now, where does that put them in terms of safety? Up with pretty large number of substances, truth be told.

The question, framed more specifically to autism, is less nebulous and, quite honestly, the evidence seems to point otherwise. Again, no nebulous standard of proof of harm is ever going to be met fully with an inductive method, but the studies that have been conducted thus far have suggested that it’s most likely not the “casual factor”.

Cliff
daedalus2u
May 10, 2008 at 4:15 pm

María Luján, to answer your question with another question, which is cause and which is effect?

If a child is ”born immunologically, gastrointestinally, biochemically, metabolically immature-(probably genetically linked through SNPs or other ) or with off the average kidney/liver and xenobiotics management ( transport and absorption and metabolism and excretion) function”, there may be many “triggers” of many different problems.

Again, which is cause and which is effect?

It appears that most individuals with autism or on the autism spectrum do not have any issues related to ”immunologically, gastrointestinally, biochemically, metabolically immature-(probably genetically linked through SNPs or other ) or with off the average kidney/liver and xenobiotics management ( transport and absorption and metabolism and excretion) function.”

If an individual doesn’t have certain traits, the traits that the individual lacks cannot be related to any traits that the individual does have. If an individual has autism and doesn’t have metabolic issues, their autism can’t be related to the metabolic issues that they don’t have.

If an individual does have traits that are associated with autism, do we “blame” those traits, or do we blame a “trigger” that many children without those traits have no adverse effects from?

I appreciate that there is no one to sue if a child is ”born immunologically, gastrointestinally, biochemically, metabolically immature-(probably genetically linked through SNPs or other ) or with off the average kidney/liver and xenobiotics management ( transport and absorption and metabolism and excretion) function.” That the pharmaceutical companies that make vaccines have deep pockets seems to be the only reason that vaccines have been selected to be looked at as the “cause” of autism. All the well done research indicates it isn’t an important factor.
H6
May 10, 2008 at 5:52 pm

Maria,

Are you aware that HHV-6 may be the source of those problems you list? Maybe the vaccines activate HHV-6 and make the problems worse.

http://www.ageofautism.com/2008/04/my-funny-virolo.html
María Luján
May 10, 2008 at 7:27 pm

Hi H6
Thank you for your question.
I hope Kristina thinks is OK to answer about my personal opinion on the topic.
There are very recent published research on the need of further research on the topic of HHV-6

Neuropediatrics. 2007 Dec;38(6):292-7. Links
Confirmed Primary HHV-6 Infection in Children with Suspected Encephalitis.Virtanen JO, Herrgård E, Valmari P, Ahlqvist J, Fogdell-Hahn A, Vaheri A, Koskiniemi M.

HHV-6 infection has been associated with neurological symptoms in children. Two variants of human herpes virus 6, HHV-6A and HHV-6B, have been identified. Their role in neurological infections is poorly understood. We studied 53 children with suspected encephalitis for HHV-6A (strain GS) and HHV-6B (strain Z29) antibodies using an indirect immunofluorescence test. Primary infection was separated from past infection by an IgG-avidity test. The identified primary infections were studied for HHV-6 specific DNA by PCR. Forty-one children of 53 had IgG antibodies to HHV-6. Six children had low avidity of HHV-6 IgG antibodies indicating acute primary infection; four to type A, one to B, and one to both types. By serology, HHV-6 viral etiology was suggested in 6/53 (11.3%) of cases. One of the six patients with primary infection had HHV-6 DNA in serum and two in CSF. The children with primary HHV-6 infection were significantly younger than the whole series, 2.3 years vs. 6.4 years. We conclude that primary HHV-6 infection appears to be an important associated or causative agent in neurological infections of young children, and it can be confirmed from a single serum specimen using the IgG-avidity test.
More

http://www.ncbi.nlm.nih.gov/pubmed/18422852?ordinalpos=10&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

J Neurosci Res. 2007 Apr;85(5):1143-8. Links
Evidence for Mycoplasma ssp., Chlamydia pneunomiae, and human herpes virus-6 coinfections in the blood of patients with autistic spectrum disorders.Nicolson GL, Gan R, Nicolson NL, Haier J.

We examined the blood of 48 patients from central and southern California diagnosed with autistic spectrum disorders (ASD) by using forensic polymerase chain reaction and found that a large subset (28/48 or 58.3%) of patients showed evidence of Mycoplasma spp. infections compared with two of 45 (4.7%) age-matched control subjects (odds ratio = 13.8, P < 0.001). Because ASD patients have a high prevalence of one or more Mycoplasma spp. and sometimes show evidence of infections with Chlamydia pneumoniae, we examined ASD patients for other infections. Also, the presence of one or more systemic infections may predispose ASD patients to other infections, so we examined the prevalence of C. pneumoniae (4/48 or 8.3% positive, odds ratio = 5.6, P < 0.01) and human herpes virus-6 (HHV-6, 14/48 or 29.2%, odds ratio = 4.5, P < 0.01) coinfections in ASD patients. We found that Mycoplasma-positive and -negative ASD patients had similar percentages of C. pneumoniae and HHV-6 infections, suggesting that such infections occur independently in ASD patients. Control subjects also had low rates of C. pneumoniae (1/48 or 2.1%) and HHV-6 (4/48 or 8.3%) infections, and there were no coinfections in control subjects. The results indicate that a large subset of ASD patients shows evidence of bacterial and/or viral infections (odds ratio = 16.5, P < 0.001). The significance of these infections in ASD is discussed in terms of appropriate treatment

I am always very reluctant to assign one particular cause to a very complex set of conditions ; I think more in terms of system affecting conditions- coinfections for example- I know that herpes group of virus are particularly being more and more studied in terms of latency, reactivation and infection, considering what is known about the neurotropic character of them.
I consider herpes -DNA virus- important to be properly studied related to how may impact in autism (prenatally, posnatally, in teens and adults), considering the immune system
- not only from the environmental impact, but also from genetics, that is how genetics may predispose to be more affected by certain infections.
Curr Opin Infect Dis. 2008 Jun;21(3):217-22. Recently identified factors predisposing children to infectious diseases.Arkwright PD, Abinun M.
aPaediatric Immunology, University of Manchester, UK bPaediatric Immunology, University of Newcastle, UK.

PURPOSE OF REVIEW: To identify articles published between January 2006 and January 2008 that have significantly enhanced our understanding of why some children are prone to severe or recurrent infectious diseases. RECENT FINDINGS: Significant inroads into the genetic basis of immune disorders leading to severe and recurrent infections in children have been made over the last few years. We now understand the specific susceptibility to herpes simplex virus encephalitis, the underlying cause of hyper IgE and Hermansky-Pudlak type 2 syndromes, as well as further explanations for the genotypic/phenotypic variations in severe combined immunodeficiency, common variable immunodeficiency and congenital neutropenia syndromes. Virulence factors for Staphylococcus aureus and Plasmodium falciparum have also been identified, and disease pathophysiology of respiratory syncytial virus related bronchiolitis and of acute pyelonephritis are better understood. SUMMARY: Progress in this area continues to be rapid. Clinicians now have the knowledge and techniques to explain why many children develop infectious diseases.

Herpes. 2006 Nov;13(3):81-2.
Highlights from 5th International Conference on HHV-6 and -7.Komaroff AL, Jacobson S, Ablashi DV, Yamanishi K.
Harvard Medical School, Boston, MA, USA.

This article reports on key presentations at the 5th International Conference on Human Herpesvirus (HHV)-6 and -7, organized by the HHV-6 Foundation. New assays for HHV-6 and -7 promise to be more accurate and better able to distinguish between HHV-6A and B or differentiate active from latent infection. Nevertheless, more research is needed to enhance the sensitivity and specificity of these assays. Cellular receptors for both HHV-6 and -7 have been identified. Both viruses have in vitro tropism for neurons and dendritic cells of the central nervous system (CNS), and their role in producing CNS disease in the immunocompromised (particularly transplant recipients and the HIV-infected) is well established. HHV-6 may enhance the progression of simian immunodeficiency virus in monkeys, as suggested by in vivo data. In immunocompetent children and adults, HHV-6 and/or -7 may play a role in triggering and perpetuating several diseases of the nervous system, namely encephalitis, multiple sclerosis, chronic fatigue syndrome and epilepsy.

Now, I am concerned about how to properly diagnose herpes mismanagement in ASD children/teens and adults, how to safely treat these- considering also the potential adverse effects of antivirals in ASD population- and how to properly give the adequate relevance to the treatment of this as a potential CMP in ASD without the non-productive discussion of cause-cures only UNTIL more information about a mechanism of how the potential harm is done (when, how and what) be known.
And yes, the topic hits home with the herpes in general although my son has tested negative to HHV-6.
However,HHV6 altered answer has been found part of the CMPs in a subgroup of children diagnosed with ASD- with other problems. It seems an aspect to research with care.
María Luján
May 11, 2008 at 1:53 am

Cliff

Sorry; I consider you misunderstood completely my question. However, you didn´t give me any answer, only an opinion of why my question is not suitable- for you.Your privilege to consider “nebulous”, “inductive” and so on.BTW, no, classic epidemiology is not going to answer these kind of questions and only well formulated questions are going to produce useful clinical data.

Daedalus
Beyond any kind of cause-effect first proper detection of CMPS/neurological differences/other in different subgroups of autistic children/teens/adults would be appropiate, IMO. Once these subgroups detected, the origin of the CMPs could be properly hypothesized and tested.
Recent report
Beyond the genome
http://harvardmagazine.com/2008/01/beyond-the-genome.html

And no, I was not thinking about who to sue - or not- or which factor was first because when the medical problem is present, you must deal with. The cause of is another field. And the cause debate- at this point-I think is so much charged with the kind of comments you did-not related to my question in terms of the generation of a productive interaction, IMO- that I hope you understand I am not going to explain further to avoid to repeat myself. If you are interested I have presented here some reflexions where many of your questions are presented in context
http://www.autismspeaks.org/community/forums/showthread.php?t=2572
However, thank you for your questions.

H6
Thank you
Yes, I have been very interested on herpes research regarding neurodevelopment. (prenatal and posnatal). However, I never simplify -because I do think that oversimplification is a problem, such as generalizations. Yes, I consider that HHV6 should be more researched but in combination with other aspects and no in the context of causes per se- even when depending on the individual for example epilepsy could be related to.
For example I am interested on research on the studies on coinfections in ASD and what kind of implicancies these findings have for the immune system in ASD-

J Neurosci Res. 2007 Apr;85(5):1143-8.
Evidence for Mycoplasma ssp., Chlamydia pneunomiae, and human herpes virus-6 coinfections in the blood of patients with autistic spectrum disorders.
Nicolson GL, Gan R, Nicolson NL, Haier J.
We examined the blood of 48 patients from central and southern California diagnosed with autistic spectrum disorders (ASD) by using forensic polymerase chain reaction and found that a large subset (28/48 or 58.3%) of patients showed evidence of Mycoplasma spp. infections compared with two of 45 (4.7%) age-matched control subjects (odds ratio = 13.8, P < 0.001). Because ASD patients have a high prevalence of one or more Mycoplasma spp. and sometimes show evidence of infections with Chlamydia pneumoniae, we examined ASD patients for other infections. Also, the presence of one or more systemic infections may predispose ASD patients to other infections, so we examined the prevalence of C. pneumoniae (4/48 or 8.3% positive, odds ratio = 5.6, P < 0.01) and human herpes virus-6 (HHV-6, 14/48 or 29.2%, odds ratio = 4.5, P < 0.01) coinfections in ASD patients. We found that Mycoplasma-positive and -negative ASD patients had similar percentages of C. pneumoniae and HHV-6 infections, suggesting that such infections occur independently in ASD patients. Control subjects also had low rates of C. pneumoniae (1/48 or 2.1%) and HHV-6 (4/48 or 8.3%) infections, and there were no coinfections in control subjects. The results indicate that a large subset of ASD patients shows evidence of bacterial and/or viral infections (odds ratio = 16.5, P < 0.001). The significance of these infections in ASD is discussed in terms of appropriate treatment.
Also, on genetic links to immune differences in ASD.
Genomics. 2008 Jan;91(1):22-9. Epub 2007 Nov 14.
Gene expression changes in children with autism.
Gregg JP, Lit L, Baron CA, Hertz-Picciotto I, Walker W, Davis RA, Croen LA, Ozonoff S, Hansen R, Pessah IN, Sharp FR.
Department of Pathology, University of California at Davis Medical Center,
The objective of this study was to identify gene expression differences in blood differences in children with autism (AU) and autism spectrum disorder (ASD) compared to general population controls. Transcriptional profiles were compared with age- and gender-matched, typically developing children from the general population (GP). The AU group was subdivided based on a history of developmental regression (A-R) or a history of early onset (A-E without regression). Total RNA from blood was processed on human Affymetrix microarrays. Thirty-five children with AU (17 with early onset autism and 18 with autism with regression) and 14 ASD children (who did not meet criteria for AU) were compared to 12 GP children. Unpaired t tests (corrected for multiple comparisons with a false discovery rate of 0.05) detected a number of genes that were regulated more than 1.5-fold for AU versus GP (n=55 genes), for A-E versus GP (n=140 genes), for A-R versus GP (n=20 genes), and for A-R versus A-E (n=494 genes). No genes were significantly regulated for ASD versus GP. There were 11 genes shared between the comparisons of all autism subgroups to GP (AU, A-E, and A-R versus GP) and these genes were all expressed in natural killer cells and many belonged to the KEGG natural killer cytotoxicity pathway (p=0.02). A subset of these genes (n=7) was tested with qRT-PCR and all genes were found to be differentially expressed (p<0.05). We conclude that the gene expression data support emerging evidence for abnormalities in peripheral blood leukocytes in autism that could represent a genetic and/or environmental predisposition to the disorder.

Human Herpesvirus 6 (HHV-6) Induces Dysregulation of Glutamate Uptake and Transporter Expression in Astrocytes.
http://www.ncbi.nlm.nih.gov/pubmed/18247129?ordinalpos=28&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
This manuscript for example
Nature. 2008 Jan 24;451(7177):388-9.
Virology: the battle within.Wenner M.
Is extremely interesting, such as this:

Human herpesvirus 6 infection of the gastroduodenal mucosa.
http://www.ncbi.nlm.nih.gov/pubmed/18181741?ordinalpos=35&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

and this
A complex interaction between drug allergy and viral infection.
http://www.ncbi.nlm.nih.gov/pubmed/18094951?ordinalpos=41&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
and

Again , the complicated interaction between coinfections of herpes- besides HHV-6 alone-and with other-bacteria/virus- is an area of continuous research.
H6
May 11, 2008 at 12:57 pm

Maria,

The first big issue for the HHV-6 Foundation has been the development of better tests. I believe that one of the founders of the HHV-6 Foundation became convinced that the tests were not reliable and nothing credible could be done on HHV-6 research until testing methodology improved.

So when someone tests negative for HHV-6, you have to ask what kind of a test they were given. Testing is still a work in progress. This virus is a crafty enemy.

What is becoming clearer is that we are in the middle of an epidemic of activated HHV-6 and the epidemics of AIDS and Chronic Fatigue Syndrome, and the rise in incidence of autism, may all be expressions of that complex neuroimmunological viral epidemic.

As evidence piles up that HHV-6 is either the second AIDS virus that causes the disease’s progression or is the primary cause, it’s a good bet that the autism research community will eventually begin to ask what this very destructive neuroimmunological virus is doing in the bodies of people with autism.

Controlling activated HHV-6 in autistic people who are infected may turn out to be a very important form of treatment. It may even become part of the standard of care for autism. Undoing the damage from HHV-6 in autism may become an important research goal.

The more one knows about HHV-6 the more one asks this question: “What can’t this virus do?”
Cliff
May 11, 2008 at 1:10 pm

“Sorry; I consider you misunderstood completely my question. However, you didn´t give me any answer, only an opinion of why my question is not suitable- for you.Your privilege to consider “nebulous”, “inductive” and so on.BTW, no, classic epidemiology is not going to answer these kind of questions and only well formulated questions are going to produce useful clinical data.”

Did I go to answer the term in its explicit form with the clinical evidence? No, because as I’ve said, the question you posed is so incredibly vague that it’s effectively unprovable. For starters, “affect adversely” is such a broad term. It works as a potential proposition already because “affect adversely” can be described in so many ways in so many terms. Heck, we can already go back to psychoanalytic terms. And the rest of the modifiers doesn’t change that, because we already have a vague definition of potential harm that we have more hypotheses than one could address in hundreds of years.

In other words, your proposed question isn’t as well formulated as you would propose. Honestly, I could put anything (yes, anything) in front of “adversely affected” and it’s a legitimate question, because the standard of proof is impossible. “Do vaccines cause autism?”, even with the tricky terminology of causation, is far more likely to get an actual answer instead of another hypothesis. If we are going to use the inductive method effectively, we need to ask those more specific questions that can be controlled for.

Cliff
H6
May 11, 2008 at 1:45 pm

Maria,

CMPs in autism seem to be a very controversial subject. But for parents who deal with them, they must be all too real. Is there a website devoted just to autism and CMPs?

Research on the effects of vaccines on the CMPs of autism could reveal new insights into this complex issue. At least for some, autism may be the forest and the CMPs may be the trees.
Regan
May 11, 2008 at 3:59 pm

Hubby pointed out to me that our Commentary page was devoted to “Vaccines do not cause autism”. It was a well written article and discussed many aspects of this messy issue.

I have no idea what the consequent Letters to the Editor will say.
stopautismquackery
May 11, 2008 at 9:53 pm

@H6:

Do you work for or with the HHV-6 Foundation? What’s your interest in HHV-6? What’s your interest in autism?

You state here:

“Controlling activated HHV-6 in autistic people who are infected may turn out to be a very important form of treatment. It may even become part of the standard of care for autism.”

Shouldn’t testing for HHV-6 be part of the standard of health care for everyone? Why wouldn’t everyone want to to treat a herpes infection? Do you know anyone on the spectrum who’s been treated for HHV-6? I do. Lots of cases, in fact. But I’d like to hear about your experience in that area, so please elaborate.
María Luján
May 11, 2008 at 11:24 pm

Hi H6
I would be interested to discuss further the issue about herpes. May I contact you by e-mail? Please let me know Thanks.
María Luján
May 11, 2008 at 11:35 pm

Cliff
I disagree.With the technology available such as this research is considering
Methods Mol Biol. 2008;448:469-79.
Pharmacogenomics in the evaluation of efficacy and adverse events during clinical development of vaccines.Nilsson LJ, Regnström KJ.
Division of Paediatrics, Faculty of Health Sciences, Linköping University, Sweden.

The understanding of vaccine-induced immune responses in adults and infants is limited. Current vaccination schedules for infants are frequently debated. Especially, the relationship among the timing, the frequency of the dosing, and the generation of an immunological memory are debated. Vaccine antigen-induced cytokine responses to vaccinations given in infancy are of particular interest because little is known about cellular responses in this age, and the information available is based on antibody responses. Pharmacogenomics is ideally suited to study cellular responses related to immune response; in addition, toxicity, inflammation, apoptosis, stress, and oncogenesis can be monitored, since the expression of thousands of genes can be measured in a single experiment.

Much more useful than “vaccines cause autism”? kind of questions may be done with increasing knowledge, especially in combination with clinical studies. There are a lot of questions that may be done about adverse effects and biochemistry and metabolism- and others- and not only from vaccines- considering ASD. Even more, there are a lot of published studies related to these topics in ASD, but fragmented and not in the context of a systemic consideration .
Cliff
May 11, 2008 at 11:54 pm

Admittedly, I still disagree. “Adverse affect” still, still doesn’t become any more qualified by that, to be sure. And it only got worse. In that brief, I was once again bombarded with conditional after conditional, and every time there is a conditional like that there is something that isn’t being controlled for and thus something that in terms of the inductive method. As it stands, it’s tricky enough tying a biomarker with a direct source to a causation of certain forms of development, and certainly not when you’ve stacked so many bricks that none of the individual theses are addressed.

The reason why they’re fragmented is because, when you are looking for substance that causes certain behavioral trends, you have to consistently control for every possible substance in an inductive trial as it stands. And when you’re dealing with something as nebulous as “adversely affects”, it becomes far less clear. How can you tell when something is “adversely affected”? The type of behavior examined on that end is thrown out the window, and you have an uncontrolled variable lurking in your study. Putting autism back in helps as that’s a defined category in its place. “Cause” is a far more better term than “adversely affect”, because a. with “adversely affect”, you can argue it compounded an unknown variable that hasn’t been determined yet which would, in fact be the cause, and that’s tricky to prove and b. casual conditions are essentially what’s being looked for in practical terms of purpose, taking the assumptions of these studies. Then you’re just knocking out all of the potential substance variables, and I guess vaccines a place to start, if anywhere.

In other words, in “vaccines cause autism”, we actually have means for an inductive trial. In “Do vaccines affect adversely to children who are born immunologically, gastrointestinally, biochemically, metabolically immature-(probably genetically linked through SNPs or other ) or with off the average kidney/liver and xenobiotics management function?”, you’ve got an insane number of conditionals and no means to conduct an inductive test.

Cliff
María Luján
May 12, 2008 at 12:48 am

Well, Cliff I disagree with you because you are oversimplyfing the issue.
I accept you don´t like my question, but your criticism is vague also. Simply you are thinking in simple aspects of causation and there is no room now to think about the test of only one variable in autism.The combination of techinques in multidisciplinary approach is being more and more proposed as the right approach- such as the link to Harvard is presenting- because of heterogeneity.
About my question I do think that there are ways to test them without “the insane number of conditionals” you mentioned, especially with the clues available.
Landru
May 12, 2008 at 1:06 pm

The KSDK story includes a link to Dr. Rashid Buttar, who “helped” the family that the story focuses on.

Kiiiiiiiiiiiiiiiiiii.
Cliff
May 12, 2008 at 1:16 pm

I assume you understand what happens in controls in clinical studies when conditional variable have to be further controlled for? And that every time such a variable is included the number of tests for that subject increases and even makes it impossible to necessarily do the controls at all?
And, yes, you can test many of those details, individually, in terms of causation and in terms of a concrete result. It actually can warrant an inductive trial. You can’t test a string of conditional variables. Simply can’t. It’s against the whole scientific method, to its core.

Cliff
H6
May 12, 2008 at 9:11 pm

It’s interesting to hear that people on the spectrum have been treated for HHV-6. How did they do?
María Luján
May 13, 2008 at 7:52 am

The need of new approaches is more and more presented
http://cebp.aacrjournals.org/cgi/content/full/14/3/557
Cliff
May 13, 2008 at 8:08 am

Nothing there, be told, is contradicting anything I said necessarily.

Cliff
Kristina Chew, PhD
May 13, 2008 at 9:15 am

@Landru,

Yes, noted the link to Rashid Buttar—here is Orac with some thoughts on Dr. Rashid Buttarand the failure of state medical boards.