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Disturbances in certain genes play a role in autism

19 Aug

OK, so not ‘new’ news. I want to look at this story’s opening as a kind of case-study into what binds and separates the autism community.

[researchers have]…found in a new study that autism can be partially explained by abnormalities in certain genes. The group’s results could, in the long run, pave the way for more appropriate treatments for autism.

Now, camp one, to which one could add the Age of Autism anti-vaxxers would snarl at the uselessness of this study. They ‘know’ that genes play little to no part in autism and that the real issue is that of vaccines.

Camp two, to which one could say shades into camp one and who you could add Harold Doherty to would bemoan the fact that yet another gene study had been done, would ignore the successes it has brought in terms of giving us more data and grump about how ‘the environment’ had been ignored.

Camp three, to which you could add Lisa Jo Rudy’s autism.about.com site would acknowledge that this was an interesting study but maybe ask valid questions about the context into which you could place this one single study. Knowing Lisa Jo she would also be interested in what exact therapies might be on offer as a result of this study.

Camp four, to which I would hope you could add LBRB and which possibly shades into camp three a little too, would be interested in the the story behind the science as well as the science itself, would hope to get an interview with one of the authors and would ask them what future science might ‘spin off’ from this study. Depending on the answers we might also editorialise a little on the need to be responsible with the science.

Just an interesting little game, of no import, as to how the community – itself a spectrum – is separated. Some say this is a bad thing and that we need unity. I disagree. I think we need diversity, as I do in most things. We even need an Age of Autism to play the token fool.

The autism ‘epidemic’ no more

17 Aug

OK, so its well known to LBRB readers that I don’t think its ever been scientifically established that there has been such a thing as an autism epidemic but even so, looking at why autism numbers have changed over a certain period of time – the period of time people believe is part of the ‘epidemic’ – should be a good way to determine what contributed to that time periods rise in autism.

So thats what Peter Bearman did. Summed up well in this weeks New Scientist, Bearman’s study offers the first look at what actually did cause the ‘epidemic’.

Better diagnosis
Diagnostic changes are the most important influence. After 1987, the definition of autism used in California was broadened several times. Bearman and his colleague Marissa King examined the medical records of around 7000 Californian children with autism and found that one in ten had initially been diagnosed with mental retardation. Extrapolated to the state as a whole, they estimate that this change in diagnosis created almost 5000 extra cases of autism between 1993 and 2005, or 26 per cent of the increase of recorded over that period.

Greater awareness
Social influence accounts for another big chunk of the overall increase. Parents are more aware of the disorder than they used to be, and so those whose children who have mild forms of autism have become more likely to seek out diagnosis.

Bearman and his colleague Ka-Yuet Liu quantified this effect. They first estimated how the chances of a child being diagnosed with autism increase if he or she lives close to a child that has already been diagnosed. They then plotted the addresses of children with and without autism in California to calculate the number of children who had grown up close to a child diagnosed with the condition. They were then able to calculate the fraction of extra cases that would have been diagnosed as a result of social interactions. They put this figure at 16 per cent.

Older parents
The final contribution to the rise in diagnoses comes from demographics. Couples in California are having children later in life, as they are in much of the rest of North America and Europe. That is pushing up autism rates, because autism is triggered by genetic mutations that older parents are more likely to pass on to their children.

Bearman and King calculated that these older parents are responsible for 11 per cent of the extra autism cases.

So these total 53% of the so-called ‘epidemic’. What about the missing 47%? Well, Professor Roy Grinker says:

Autism used to be highly stigmatised, in part because it was thought to be due to poor parenting. The removal of that stigma has made doctors and parents more willing to recognise the disease, which will have contributed to [some of] the extra cases…This and other social causes, together with uncertainty in the number of cases that can be attributed to the factors already studied by Bearman, could account for much or all of the unexplained half

But note Grinker doesn’t say it definitely does. This is because he knows as a careful scientist it hasn’t been looked at.

So what can we take from Bearman’s work? In my opinion we can take the fact that as soon as the questions regarding non-environmental causes were actually looked at and studied, there were numerical values that could be applied to their contribution. There are other non-environmental causes which Bearman didn’t look at which would probably be found to contribute to the other half.

What about the alleged environmental causes? It would not surprise me in the least if it were found that there were some. But as to what they are, the environmental lobby are still so hung up on vaccines they don’t seem to want to look at other possible environmental issues. Maybe its time they dropped the vaccine nonsense and got involved in some decent research. Just a thought.

New study – “90% diagnostic accuracy”

11 Aug

According to study author Christine Ecker in today’s Guardian:

We know already that people with autism have differences in brain anatomy and some regions are just bigger and smaller or just different in shape…[o]ur technique can use this information to identify someone with autism.

The study used 20 non autistic controls and 20 autistic people – all adults – and found ‘significant differences’ in the grey matter areas of the brain which control behaviour and language. This is nothing new in itself, differences in brain structure have long been known about in regards to autism. Whats new in this study is the method – and resultant accuracy – of the detection of autism.

In the experiment, Ecker showed that her imaging technique was able to detect which people in her group had autism, with 90% accuracy. “If we get a new case, we will also hopefully be 90% accurate,” she said. The research, supported by the Medical Research Council, Wellcome Trust and National Institute for Health Research, is published today in the Journal of Neuroscience.

If this is established as a viable method (Carol Povey of NAS states that further testing is still required) then it’ll be the first true objective test for autism ever developed. So far, as everyone knows, autism is diagnosed based on the opinion of a clinician (or team of specialists). Whilst they will probably still play a role, this test offers an objectivity that would be unparalleled. It would also have the interesting effect of making the DSM diagnosis largely obsolete.

Evidence of Harm

9 Aug

A new Cochrane Review looks at the issue of SSRI’s in use for autistic populations.

OBJECTIVES: To determine if treatment with an SSRI: 1. improves the core features of autism (social interaction, communication and behavioural problems); 2. improves other non-core aspects of behaviour or function such as self-injurious behaviour; 3. improves the quality of life of children and their carers; 4. has short and long term effects on outcome; 5. causes harms.

SSRIs (Selective serotonin reuptake inhibitors) do exactly what they say – they combat depression by ‘boosting’ serotonin. They are usually fairly effective in that role, although not all people with depressive tendencies use SSRIs, the majority tolerate them well. The most famous SSRI is Prozac.

The outcome of the study was:

There is no evidence of effect of SSRIs in children and emerging evidence of harm. There is limited evidence of the effectiveness of SSRIs in adults from small studies in which risk of bias is unclear

This is worrying. It indicates to me that autistic people are being treated for autism with SSRIs. Bearing in mind I haven’t read the full paper, it does read to me as though we are verging into the territory of chemical cosh.

A chemical cosh is shorthand for the administration of drugs to people who don;t actually require its benefit but who are kept quiet by its effects or side effects. This isn’t the fault of the drug or even the manufacturer but the prescriber. This is also not a situation unique to autism but is frequently found throughout all areas of mental health.

Microglial Activation and Increased Microglial Density Observed in the Dorsolateral Prefrontal Cortex in Autism.

4 Aug

Here is a study that will likely be discussed for a long time to come. There has been a lot of interest in the study by John’s Hopkins researchers (Pardo, et al.) on microglial activity in the brains of autopsied autistics. A paper just released by Prof. Pardo together with Prof. Courchesne at UCSD shows markedly increased microglial cell activiation in 5 of 13 autistics, including children under 6.

The exact implications of this are not yet determined. The authors conclude the abstract with

“Given its early presence, microglial activation may play a central role in the pathogenesis of autism in a substantial proportion of patients. Alternatively, activation may represent a response of the innate neuroimmune system to synaptic, neuronal, or neuronal network disturbances, or reflect genetic and/or environmental abnormalities impacting multiple cellular populations.”

Here is the full abstract:

Biol Psychiatry. 2010 Aug 15;68(4):368-376.
Microglial Activation and Increased Microglial Density Observed in the Dorsolateral Prefrontal Cortex in Autism.

Morgan JT, Chana G, Pardo CA, Achim C, Semendeferi K, Buckwalter J, Courchesne E, Everall IP.

Department of Neuroscience, School of Medicine, University of California, San Diego, La Jolla, California.
Abstract

BACKGROUND: In the neurodevelopmental disorder autism, several neuroimmune abnormalities have been reported. However, it is unknown whether microglial somal volume or density are altered in the cortex and whether any alteration is associated with age or other potential covariates. METHODS: Microglia in sections from the dorsolateral prefrontal cortex of nonmacrencephalic male cases with autism (n = 13) and control cases (n = 9) were visualized via ionized calcium binding adapter molecule 1 immunohistochemistry. In addition to a neuropathological assessment, microglial cell density was stereologically estimated via optical fractionator and average somal volume was quantified via isotropic nucleator. RESULTS: Microglia appeared markedly activated in 5 of 13 cases with autism, including 2 of 3 under age 6, and marginally activated in an additional 4 of 13 cases. Morphological alterations included somal enlargement, process retraction and thickening, and extension of filopodia from processes. Average microglial somal volume was significantly increased in white matter (p = .013), with a trend in gray matter (p = .098). Microglial cell density was increased in gray matter (p = .002). Seizure history did not influence any activation measure. CONCLUSIONS: The activation profile described represents a neuropathological alteration in a sizeable fraction of cases with autism. Given its early presence, microglial activation may play a central role in the pathogenesis of autism in a substantial proportion of patients. Alternatively, activation may represent a response of the innate neuroimmune system to synaptic, neuronal, or neuronal network disturbances, or reflect genetic and/or environmental abnormalities impacting multiple cellular populations. Copyright © 2010 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

PMID: 20674603 [PubMed – as supplied by publisher]

Diagnosis of autism occurs much later than it should among Medicaid-enrolled children

4 Aug

This from a recent study by Prof. David Mandell’s group. The abstract is below:

Psychiatr Serv. 2010 Aug;61(8):822-9.
Age of diagnosis among medicaid-enrolled children with autism, 2001-2004.

Mandell DS, Morales KH, Xie M, Lawer LJ, Stahmer AC, Marcus SC.
Abstract

OBJECTIVE: This study examined child- and county-level factors associated with age of diagnosis of autism among Medicaid-enrolled children and the change in age of diagnosis over time. METHODS: National Medicaid claims from 2002 to 2004 were used to identify age of diagnosis and characteristics of children younger than ten years old with a diagnosis of autism (ICD-9 codes 299, 299.0x, or 299.8x). These data were linked to county-level education and health care variables. Linear regression with random effects for state and county was used to examine associations between these variables and age of diagnosis. RESULTS: A total of 28,722 Medicaid-enrolled children newly diagnosed with an autism spectrum disorder were identified. Their average age of diagnosis was 64.9 months. Adjusted average age of diagnosis dropped 5.0 months for autistic disorder and 1.8 months for other spectrum disorders during the study period. Asian children were diagnosed earlier than children in other racial or ethnic groups, although these differences were much more pronounced for other spectrum disorders than for autistic disorder. Children eligible for Medicaid through the poverty category were diagnosed earlier, on average, than children who were eligible through disability, foster care, or other reasons, although this difference decreased over time. Children in large urban or rural counties were diagnosed later than children in small urban or suburban counties. CONCLUSIONS: Findings showed that diagnosis of autism occurs much later than it should among Medicaid-enrolled children, although timeliness is improving over time. Analyses suggest that most of the observed variation is accounted for by child-level variables, rather than county-level resources or state policies.

PMID: 20675842 [PubMed – in process]

The age of diagnosis in California for the general population was 3 years by 2000 (falling from 6 in 1992) according to a recent paper by Bearman’s group at Columbia. Why are medicaid children diagnosed later?

I find it odd that children on medicaid due to poverty are diagnosed earlier than children “eligible through disability, foster care, or other reasons”. Naively, I would expect the opposite: that children already identified with a disability would be under greater scrutiny and more likely to receive evaluations to determine an ASD diagnosis.

Much more can be said about this, but I will stop with “Diagnosis of autism occurs much later than it should among Medicaid-enrolled children”. This is just wrong. We as a society should take better care of our most vulnerable.

Prof. DeSoto discusses mercury and autism

3 Aug

A recent issue of the journal Acta Neurobiologiae Experimentalis (ANE) focused upon autism. Not just autism, but autism causation with papers on vaccines, acetaminophen and, of course, mercury. The idea for this focus edition came from Professor Dorota Majewska who holds the EU Marie Curie Chair at the Institute of Psychiatry and Neurology in Warsaw, Poland. The authors for this focus issue are largely the same as those from a conference Prof. Majewska organized in 2008, Autism and Vaccinations.

One of the papers in the focus edition of ANE was the paper by Hewitson et al., that we have discussed at length here at LeftBrainRightBrain.

Another paper in this focus edition is Sorting out the spinning of autism: heavy metals and the question of incidence by M.C. DeSoto and R.T. Hitlan. DeSoto and Hitlan gathered some attention for a paper a few years back where they analyzed an existing data-set, that by Ip et al.. D’oC and Interverbal discussed this paper at the blog Autism Street, starting with A Tale Of Two Tails. In that piece, D’oC and Interverbal discuss the statistical analysis used by DeSoto and Hitlan. Prometheus at the Photon in the Darkness blog also discussed the DeSoto and Hitlan paper in Winter Potpourri. Pure Pedantry blog at ScienceBlogs also discussed this study in Mercury, Autism, and a Note on Scientific Honesty. Perhaps the best analysis of the original DeSoto and Hitlan paper was performed by EpiWonk, an epidemiologist.

The recent paper by DeSoto and Hitlan, Sorting out the spinning of autism: heavy metals and the question of incidence, is basically a review article. It has been touted as support for the mercury hypothesis with a commonly quoted phrase,

Fifteen were offered as evidence against a link between exposure to these metals and autism. In contrast, a sum of 43 papers were supporting a link between autism and exposure to those metals

I somehow doubt the authors intended the debate to boil down to counting papers. It would be a weak support, and rather ironic at that as this paper is placed in exactly the sort of journal that leads to large numbers of papers supporting the heavy-metal/autism link. The current DeSoto and Hitlan paper is in a focus issue on autism in ANE which selected papers which support autism as vaccine injury. Many papers on the mercury appear in lower impact journals and by authors such as the father-son team of Geier and Geier (which if I counted correctly account for 19 of the 43 articles on DeSoto and Hitlan’s list). If you are unfamiliar with that team, the neurodiveristy.com blog has many articles on the team such as Significant Misrepresentations: Mark Geier, David Geier & the Evolution of the Lupron Protocol (Contents).

That said, I was planning to avoid the recent DeSoto and Hitlan paper. It isn’t really new (adding to the number of articles on toxins and autism without adding to the knowledge base). I was going to avoid the paper, that is, until Prof. DeSoto gave an interview for the Age of Auitsm blog. I don’t understand why the Age of Autism considers Prof. DeSoto to be an expert on so many areas of autism and the environment. The breadth of her work is not great. Below is an exchange which shows what I mean. Prof. DeSoto was asked to comment on the recent study by Hewitson et al., comparing vaccinated and unvaccinated monkeys.

Q: There is a study published in Acta Neurobiologiae Experimentalis alongside yours that deals with vaccinated and unvaccinated primates. Do you have a reaction to the study or its conclusions?

Dr. DeSoto: All the primates were vaccinated, the difference was whether there was a heavy metal additive. This is a potentially important study. There are a few weaknesses that prevent strong conclusions. The size of the control group is small (apparently n=2). Given that rhesus neural development within the brain region of interest is not all that well documented, a larger control group would have been desirable. This weakness is acknowledged by the authors.

Isolating the infant monkeys shortly after birth is a significant change from normal environment. The severing of the maternal bond and being raised essentially alone (only visual contact was maintained with the peer infants) affects every aspect of development – including neural development. There is evidence that brain volume is specifically affected by isolation. The rearing situation in the study, in my mind, is not very comparable to normal development, especially if the outcome of interest includes brain volume.

That said, this is the only study that has compared the net effect of multiple vaccination additives on brain development. Above all, I have to editorialize and say this seems difficult to understand (that is – why is this the only study?). If some scientists and some parents question the safety of the vaccine schedule, such studies as this one are the way to investigate the concerns.

Now, the one study that exists (even if there are caveats that go with pilot research) suggests there are differences. Whether one is of the opinion that individually testing vaccines is as good as testing the combined effect or not – at this point it is imperative that additional studies be conducted on the additive effect of the full vaccine schedules.

To be clear and to repeat, if one thinks that the vaccines with additives given in close succession have no effect on neural development– this ought to be established empirically. One thing that I noticed in the study is the main effect for difference in brain volume (no time effect). It should be noted that this suggests the early administration of additive-containing vaccine (first four rounds) was a culprit of interest.

Prof. DeSoto did not take a careful look at the Hewitson et al. study. How do I know this? In the above interview, DeSoto states:

“All the primates were vaccinated, the difference was whether there was a heavy metal additive”

The paper states, “”Four infants were assigned to the unexposed study group and received saline injections according to the schedule in Table I””. The differences included the heavy metal additive, as well as all the ingredients that make a vaccine differ from saline.

What amazes me is that the interviewer at the Age of Autism missed that as well. Even though AoA has touted the Hewitson study greatly, they don’t appear to have read it closely.

This is not a minor detail. It is key to the study design and conclusions.

Another comment:

Given that rhesus neural development within the brain region of interest is not all that well documented

I think that Prof. DeSoto can be excused for not realizing that there is a study tracking the development of precisely the amygdala in macaques. This is because Hewitson et al. did not include that reference (which was easily found in a pubmed search).

“The size of the control group is small (apparently n=2)”

The control group was 4. One was excluded for “scheduling reasons” and the other for unknown reasons. This was a major problem with the study. Fatal, one might say, as the brain sizes of the control group didn’t grow between the two time periods tested (about 4 months and about 6 months of age) for the monkeys. At the same time, their amygdalas shrank. This was a big warning sign that something was amiss with the control subjects, but this was ingored by Hewitson, et al.. Based on this faulty premise, Hewitson et al. claimed that the brains and amygdalas of the vaccinated monkeys were on an abnormal growth path. It is amazing that Prof. DeSoto missed that.

A fact that I am not surprised that Prof. DeSoto missed is that in a previous IMFAR abstract on this group, Hewitson et al. came to the exact opposite conclusion: that the brains of the vaccinated monkeys did not grow as fast as the unvaccinated monkeys.

Back to the recent DeSoto and Hitlan paper. They make the following statement:

It is worth noting that there have been only three empirical articles directly comparing those with and without an ASD on mercury levels in the body to a control group of normally developing matched controls that report that report no link (Ip et al. 2004, Soden et al. 2007, Hertz-Piciotto et al. 2010). While, the most recent article appears to be the strongest, lacking any obvious errors or flaws (we think that this recent article does provide at least some legitimate evidence contradicting the hypothesis that autism and heavy metals are linked), the other two are seriously flawed.

In the end, this mention of the Hertz-Picciotto study is why I decided to write about the DeSoto piece, and in the process bring in the interview.

Part of what made the Hertz-Picciotto study strong was the fact that they controlled for fish consumption. Correct me if I am wrong, but I believe this is something that Ip did not do, nor did DeSoto and Hitlan in their re-analysis. I don’t see mention of fish consumption in the recent DeSoto and Hitlan paper.

Again, I’ll point out that the analysis by EpiWonk was thorough and clear. I wish he had published it. I don’t think consider fish consumption to state that the DeSoto/Hitlan re-analysis of the Ip data is likely not thorough enough to make the conclusions they draw.

The fact of the matter is, the Ip data just aren’t that profound. It was worthwhile to do a re-analysis given the errors in the Ip dataset and paper. But it was three years ago that DeSoto and Hitlan did their re-analysis. In the meantime, Hertz-Picciotto et al. have a better dataset and a more thorough analysis.

DeSoto and Hitlan editorialize a bit in their paper:

If a person has publicly staked his/her career on a certain position being right, it may become harder to keep a truly open mind, even when new data become available and even when the original intent was to be objective. A way this bias might manifest itself is an overstatement or slight misstatement of results. We feel that both sides have been guilty of this, and this happens when a person becomes so confident in the correctness of his/her own view that he/she no longer reviews evidence to the contrary. Unconscious bias may exist even in the best scientists.

This begs the question of whether DeSoto and Hitlan are as guilty of those they chide. Re-analyzing the Ip data is not staking their career on a certain position. Repeatedly publishing on such a limited dataset does make this reader start to question whether some piece of their reputation is now tied to this position. With apologies to Prof. DeSoto, but the fact that her misimpressions of the Hewitson et al. paper are skewed towards the mercury hypothesis makes me wonder even more.

The autism research community needs to have fresh eyes looking at questions and data. DeSoto and Hitlan did well to reanalyze the Ip data once the mistakes were shown. They just appear to this observer to have (a) overstated the interpretation of their analysis and (b) gotten very quickly in to exactly the sort of rut they accuse others of being in.

OSR pulled from the market….or is it?

3 Aug

Here on LeftBrainRightBrain we recently discussed a letter from Boyd Haley, Ph.D. announcing his decision to voluntarily remove his product, OSR #1 from the market. The letter from Mr. Haley stated (in part):

The product will not be available for sale after that date until new drug approval has been obtained. Please continue to access our website, http://www.ctiscience.com , for updates on OSR#1® in the future.

The CTI website is down, and has been for a few days. The message I get when try it is:

HTTP Status 404 –

type Status report

message

description The requested resource () is not available.

Two locations I checked are still selling OSR.

The Forrest Health site has the letter from Mr. Haley noting that he has pulled the product from the market. They not only let you buy it, but they require that you purchase 3 or more “Note: you must order at least 3 items”.

Living Well International has OSR on their site as well. In response to my email, they response to my email request, “Do you still have OSR#1 for sale?”, they responded “Yes we do. It is $60 for a box of 30”

I do wonder how long before someone decides to make his or her own batch of OSR. Mr. Haley has been quoted as stating it was not difficult. The published recipe for the chemical indicates a few potential concerns. First, the chemicals are themselves not without hazards.

Triethylamine

Liquid causes first degree burns on short exposure; [CHRIS] Corrosive to skin; [Quick CPC] Short-term exposure at high concentrations may cause pulmonary edema. [ICSC] A lachrymator; [CHEMINFO] Experimental animals exposed repeatedly to 100 ppm show evidence of liver, kidney, lung, and heart damage. [HSDB] A corrosive substance that can cause pulmonary edema; [ICSC]

Chloroform has relatively high LD50 values (the amount where 50% of exposed animals die). But the MSDS lists reproductive toxicity as:

Birth defects have been seen in rats and mice exposed by inhalation of chloroform at concentrations greater than 100 ppm in air. Ingestion of chloroform by pregnant laboratory animals has resulted in fetotoxicity but not birth defects, and only at levels causing severe maternal effects.

Isophthaloyl chloride is only listed as an eye/skin irritant. I won’t go down the list of all the chemicals. I think you get the idea. It is likely that a competent chemist with a reasonable laboratory (including a fume hood and access to nitrogen gas) could produce “bathtub OSR” reasonably safely. I frankly cringe at the thought of someone attempting this at home. I will add, the yield of the published process for producing this chemical is about 72% without optimization. This begs the question to me as to how clean the product is in this form.

Desiree Jennings back in the news

26 Jul

Remember Desiree Jennings? She was a cheerleader ambassador for the Washington Redskins who claimed that a flu shot gave her dystonia. She was highlighted by the Age of Autism blog and by Generation Rescue, who connected her with alternative medical practitioner Rashid Buttar. Mention of Desiree Jennings has been removed from the Generation Rescue website. Neurologist and blogger Steve Novella discussed how her case more closely resembled a psychogetic disorder. Dr. Novella’s take on the case prompted the American TV show Inside Edition to take a second look. We discussed the Jennings case then here on LeftBrainRightBrain as Successful blogging by Steven Novella: the Desiree Jennings story
.

Now the TV Show 20/20 has taken a look a the Desiree Jennings story in Medical Mystery or Hoax: Did Cheerleader Fake a Muscle Disorder?

First, one must stress that many people following this case have not been calling out “hoax”. A psychogentic disorder is quite real, just not dystonia and not physical.

That said, here is the trailer for the 20/20 episode:

http://abcnews.go.com/assets/player/walt2.6/flash/SFP_Walt.swf

I find the beginning to be really cheesy. The way they took the video to make it look like it was some film taken decades ago was, well, cheesy. Ms. Jennings is less than 30 years old. Somehow I doubt her wedding was recorded on film and, even if it was, it wouldn’t be so deteriorated in a few years. But, we get the idea–the wedding was in the past.

Ms. Jennings has been used as an example of how successful Rashid Buttar is. One article, copied to Dr. Buttar’s blog, states that shortly after beginning treatment with him:

The good doctor ran to his patient, fearing she had suffered another seizure but instead was elated to find that she was awake, coherent and carrying on a normal conversation with the nurses and her family. By the next day she was walking the corridors with limited affliction. (See the video at: http://www.desireejennings.com.) The AMA has remained silent.

(note–www.desireejennings.com is no longer active).

But just as she was leaving Dr. Buttar’s clinic on her last visit in December 2009 — with “20/20’s” cameras rolling — it all seemed to fall apart. Jennings was in distress again. She could no longer walk forward, and had to be taken out in a wheelchair.

In the early discussions of Ms. Jennings, much interest focused on the idea that she was diagnosed with Dystonia by doctors at Johns Hopkins. People complained that Dr. Novella shouldn’t make statements that contradicted doctors who actually saw Ms. Jennings. The 20/20 story states:

In search of a cure, Jennings and her husband Brendan visited countless doctors and four hospitals, among them Johns Hopkins Hospital. There, a rare movement disorder that causes the muscles to twitch or convulse involuntary. The symptoms resembled her own.

“a physical therapist told Jennings about dystonia”. That’s a bit different from a doctor diagnosed her with dystonia.

Yes, this isn’t about autism at all. But this story does shed some light onto groups like Generation Rescue who supported Desiree Jennings, sending her to Dr. Buttar. The story was compelling for them, even though it was not about autism. It was about alleged vaccine injury. Generation Rescue appears to have abandoned Ms. Jennings now. It sheds light on Dr. Buttar, whose claims of recovery for Ms. Jennings appear to be unsupported by the facts. Dr. Buttar is one of the more prominent names in the alternative medicine community marketing their services to the autism community.

Laura Hewitson has left the University of Pittsburgh

26 Jul

Laura Hewitson is the lead researcher on a series of studies on comparing vaccinated and unvaccinated macaque monkeys. This work became public first in the 2008 IMFAR conference. At that time and since, the work from these studies has been strongly criticized. Dr. David Gorski of Science Based Medicine discussed those abstracts. It is very likely that the new conflict of interest declaration policy for IMFAR resulted from Ms. Hewitson’s lack of declaration of her own COI at IMFAR (she has filed a claim with the vaccine court on behalf of her child). One paper resulting from that study was withdrawn before it was published (discussed by Countering Age of Autism and Respectful Insolence). More recently, a study from this series was published in which conclusions were drawn based on only 2 control animals. Those control animals underwent brain shrinkage during a critical period of infant growth. In other words, there was something seriously wrong with the control animals and, hence, the entire study. The study (and subsequent discussions by groups such as SafeMinds) spun the brain shrinkage around to claim that the “The vaccinated primates also showed altered maturation of their brains’s [sic] amygdalas.”

Ms. Hewitson has listed here professional affiliations as:

1Department of Obstetrics and Gynecology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA;
2Thoughtful House Center for Children, Austin, TX, USA;

In 2008 she was listed as Associate Professor of Obstetrics, Gynecology & Reproductive Sciences on the University of Pittsburgh’s website. That is the last date for an internet archive version of that page. A google cache version of the page from June 2010 listed her as “adjunct” Associate Professor. Adjunct faculty are typically part time or people from other institutions who are working in some capacity with the University.

Ms. Hewitson’s webpage link at Pitt is no longer active. She is no longer listed on the faculty page for the Pittsburgh Development Center (PDC). The PDC confirmed that she is no longer on the faculty there.

Before people start speculating, the most likely explanation is that it simply became too difficult to balance a career at Thoughtful House in Texas with a faculty appointment in Pennsylvania.

This will mean that in the future Ms. Hewitson will be unable to use her University of Pittsburgh affiliation to bolster the credibility of her research. Studies begun while at Pitt will likely continue to show that affiliation (such as the recently published study on the amygdalas of macaques).

Whatever the reason for her departure, I welcome it. I don’t believe that a fine institution like Pitt should have its name attached to the level of research in the recent paper. It is difficult to simply put into simply how poor the quality of that study was.

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