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App May Help Nab Handicap Parking Violators

27 Oct

From Disability Scoop: App May Help Nab Handicap Parking Violators.

A smartphone app may soon be all that’s needed to crack down on illegal parking in handicap spots.

Officials in Austin, Texas are set to vote this week on a resolution that would allow residents to use an app to report handicap parking violators directly to law enforcement.

Under the plan, app users would take a photo of the offending vehicle and submit it to city officials who could send an officer to issue a ticket.

“The only way we’re going to be able to address the problem is if we enlist help from ordinary citizens,” Austin City Councilman Chris Riley told the Austin American-Statesman. To read more click here.

I bring this up because it is a bit of a pet peeve for me. There is a strip mall near where I live where I have often seen people parking in the handicap spot in violation of the law. The strange things I have noticed (in my small sampling, and totally anecdotal experience):

They are almost always SUV’s. Yes, those rugged outdoors people can’t walk the extra 10 feet from a different spot.

I see them in the early morning, when the parking lot is basically empty and other spots are, quite literally, only 10 feet away.

They are in front of the donut shop. Probably has something to do with the early morning times I spot them, but I always find the SUV/donut shop/not wanting to walk an extra 10 feet combination to be highly ironic.

Autism: Faces and lungs

27 Oct

Two stories out in the past couple of days point to physical differences in autistics: faces and lungs. One study found that facial features were quantitatively different in autistic children than in non-autistic children. In MU study links facial features to autism, Janese Silvey wrote:

A new University of Missouri study shows that children with autism have slight differences in facial characteristics — a finding that indicates the disorder develops in the womb.

Kristina Aldridge, assistant professor of pathology and anatomical sciences in MU’s School of Medicine, worked with other researchers at the Thompson Center for Autism and Neurodevelopmental Disorders to analyze 64 boys with autism and 41 typically developing boys ages 8 to 12.

They used a camera to capture 3-D images of each child’s head and then mapped 17 points on the faces. When Aldridge compared the two groups, she found statistically significant differences in facial features.

It is perhaps not surprising that facial differences could be detected. Head circumferences are known to be often larger in autistics, and follow a different trajectory after birth. However, the authors point to prenatal development as possibly at play:

“We can look at a point in time when facial features are being developed and genes that are shared at that time between the face and brain,” Aldridge said. “This narrows the window of time and the candidate genes we might look at.”

A story from WebMD points to Autism linked to unusual shapes in lungs. The study was presented at a conference of the Annual Meeting of the American College of Chest Physicians as Can Bronchoscopic Airway Anatomy Be an Indicator of Autism?

Here is the abstract:

Can Bronchoscopic Airway Anatomy Be an Indicator of Autism?
Barbara Stewart, MD*

Nemours Childrens Clinic, Pensacola, FL

PURPOSE: The purpose of this study is to investigate possible correlation between certain airway anamolies and a definitive diagnosis of autism and/or autistic spectrum disorder.

METHODS: IRB approval was obtained for a restrospective study to evaluate 49 patients with a diagnosis of autism or autistic spectrum disorder. These patients were seen in the pulmonary clinic with a diagnosis of cough that was unresponsive to therapy and who required further pulmonary work-up.Bronchoscopic evaluation of the airway was included as part of that work-up.

RESULTS: Bronchoscopic evaluations revealed the presence of initial normal anatomy followed by double take-offs in the lower airway (or “doublets”)in 100% of the autistic population studied.

CONCLUSIONS: There appears to be a correlation between autistic spectrum disorder and airway anatomy. This is a small study of 49 patients. More investigation is warranted.

CLINICAL IMPLICATIONS: At present autism is diagnosed through subjective observation of “autistic behaviors.” Autistic children with cough may be diagnosed objectively.

DISCLOSURE: The following authors have nothing to disclose: Barbara Stewart, Barbara Stewart

Not surprisingly, it is a pretty small study. (49 patients). This isn’t a study which says, “all autistic kids have these lung differences”. Rather it is, “of the autistic kids we saw in our clinic for persistent coughs had this anomaly”. Even still, it is an interesting finding if real. On thing this points to, that the author notes in the interview is that for this subset of kids, development went on a different path very early:

“I think the whole thing occurs embryologically — when the cell and egg come together and the fetus is formed,” she says. “It’s important for parents to know that.”

As also discussed on CRACKING THE ENIGMA as The many faces of autism

Tough fiscal times in California

26 Oct

Two stories out recently point to the tightening budgets that the

This one isn’t caused by economy. This is mismanagement. In AUDIT: Inland Regional Center must repay $10 million, the Press Enterprise discusses the results of an audit of one of California’s Regional Centers. The Regional Centers are private non-profit organizations which administer funds for California’s developmentally disabled population. Inland Regional Center (IRC) has had problems for the past few years and been placed on probation.

From the Press Enterprise story:

As for the center’s ability to repay the $9.8 million in improper expenses cited in the audit, that would be all but impossible, she said.

“We’re going to have to get direction from the department on that. We don’t have $10 million,” Fitzgibbons said. “We’re really working hard to improve things and do the best job we can do.”

Well, they’ve been audited and IRC has to repay the state $10M. That’s a lot of money, and could mean a reduction in services for the clients of IRC. People who are not responsible for the mismanagement.

The nonprofit agency that serves developmentally disabled residents in Inland Southern California improperly spent almost $10 million and must repay the state, according to a highly critical audit released Friday that found continued widespread problems at the San Bernardino-based Inland Regional Center.

One example of misspent funds was when $1M allocated for services for people with hearing, speech and/or vision impairment was used for the operation expenses in their resource library.

Another recent story: San Diego Unified School District is facing insolvency and possible takeover by the state:

http://www.kqed.org/assets/flash/kqedplayer.swf

California required school districts to budget as though there would be no cuts in funding. However, California also has automatic cuts in place should revenues not meet specific “trigger” levels. If the state misses the revenue levels, they will cut funds to the districts. While special education is not specifically mentioned, Special Education tends to be a focus of budget minded administrators, with comments of “encroachment” commonly heard.

Disability History Museum: We Committed Our Child

25 Oct

This story was discussed online a few years ago. It has haunted me ever since. The story can be found online in Google Books (which carries The Rotarian) or at the Disability History Museum as “We Committed Our Child“.

The image says it all: a happy 1940’s family with a baby of their dreams:

At about 20 months, things changed:

By that time another baby was on the way, for we believed that she should have a companion. Those were happy months as we planned for the second child and tried to prepare Mary Lou for the newcomer, but then came a cloud. One evening when Mary Lou was 20 months old, she became violently ill, having shown signs of only a slight cold. Developing a high fever, she was lethargic and “loppy” for three days. We were frantic. The doctor prescribed rest, and Mary Lou, who loved her bed, cooperated nicely. Within a few days she was trotting about again.

It wasn’t like old times, however, for she tired quickly and was nervous and touchy. She seemed on occasion to be “out of this world” and was upset more and more often by the books that previously had brought hours of delight.

By the time our boy was born, three months later, we were deeply worried. Mary Lou’s nervousness increased; she went into screaming spells with no apparent cause, cast aside her books and toys, gradually stopped talking, became choosy about her foods, and refused to feed herself.

The parents faced 5 options:

1. Keep Mary Lou at home.
2. Place her with some relative or friend willing to assume the burden of her care.
3. Place her in a private institution.
4. Place her in a State institution.

Yes, that’s only 4. The fifth option they considered in theory (and rejected, thankfully): euthanasia.

They discuss the life they expected for their child at home, impact they felt their child had on them and their community:

Also, having witnessed the ridicule and ill treatment which residents of our home town turned on the “village half-wit” and his family, we understood what keeping her with us would mean to our family.

We decided we must look further, in justice to Mary Lou, her brother, ourselves, and the community.

And chose an institution:

So it was that we decided in favor of a State hospital. Taking Mary Lou to it was a heartbreaking experience, but we were fortified with the conviction that in this move lay the sole hope for happiness for all four of us. And we were greatly heartened by the appearance of the place. It resembled a college campus, with pretty brick buildings set amid sweeping grounds. There were no walls, no guards. Patients strolled, played, or rested outside their homelike cottages. In this community, we saw also, there were no thoughtless neighbors gossiping about the unfortunates and jeering at them and their families.

They kept contact with their child, and kept questioning their decision:

More than a year has passed since that day. We have kept in close touch with the hospital by mail and telephone and have made the 100-mile trip to visit our daughter at least once a month. The simple routine of good food, sunshine, and fresh air have done wonders for Mary Lou’s physical health. She is calmer and again is feeding herself. We still do not know what potentialities Mary Lou possesses, but we feel confident that whatever they are, the skilled, hard-working staff will labor earnestly to develop them.

And so tragedy came into a family that barely knew the word. We think, we pray, we have faced it wisely.

The full story can be found at the Disability History Museum. It isn’t very long.

That story was written 66 years ago.

Verbal and non-verbal intelligence changes in the teenage brain

24 Oct

A recent Letter in the Journal Nature takes on the question of how stable is intelligence in teenagers. The title is pretty self explanatory: Verbal and non-verbal intelligence changes in the teenage brain.

Consider teenagers. Is their IQ “set in stone”? By the time a kid is, say, 13, isn’t his/her intelligence pretty well demonstrated? What if you heard that IQ changes can change, up or down, by as much as 20 points during the teenage years? Would you be surprised? I was.

The article attracted my attention on its own merits, but also given the nature of the discussion that forms around early intervention and autism. Statements about “windows of opportunity” and times when the brain is “plastic” are common in discussions of autism focused educational therapies. For example, a study entitled “Early intervention and brain plasticity in autism” or “Autism: a “critical period” disorder?“. Certainly early childhood is a period of great learning and growth, but does the “window” of plasticity “close”?

Here is the abstract:

Intelligence quotient (IQ) is a standardized measure of human intellectual capacity that takes into account a wide range of cognitive skills1. IQ is generally considered to be stable across the lifespan, with scores at one time point used to predict educational achievement and employment prospects in later years1. Neuroimaging allows us to test whether unexpected longitudinal fluctuations in measured IQ are related to brain development. Here we show that verbal and non-verbal IQ can rise or fall in the teenage years, with these changes in performance validated by their close correlation with changes in local brain structure. A combination of structural and functional imaging showed that verbal IQ changed with grey matter in a region that was activated by speech, whereas non-verbal IQ changed with grey matter in a region that was activated by finger movements. By using longitudinal assessments of the same individuals, we obviated the many sources of variation in brain structure that confound cross-sectional studies. This allowed us to dissociate neural markers for the two types of IQ and to show that general verbal and non-verbal abilities are closely linked to the sensorimotor skills involved in learning. More generally, our results emphasize the possibility that an individual’s intellectual capacity relative to their peers can decrease or increase in the teenage years. This would be encouraging to those whose intellectual potential may improve, and would be a warning that early achievers may not maintain their potential.

” More generally, our results emphasize the possibility that an individual’s intellectual capacity relative to their peers can decrease or increase in the teenage years.” Those are quite powerful words.

The authors tested 33 subjects at two time periods:

They were first tested in 2004 (‘time 1’) when they were 12–16?yr old (mean, 14.1?yr). Testing was repeated in 2007/2008 (‘time 2’) when the same individuals were 15–20?yr old (mean, 17.7?yr).

And they found that the while the IQ scores were relatively stable, on average, individuals showed large changes:

The wide range of abilities in our sample was confirmed as follows: FSIQ ranged from 77 to 135 at time 1 and from 87 to 143 at time 2, with averages of 112 and 113 at times 1 and 2, respectively, and a tight correlation across testing points (r = 0.79; P<0.001). Our interest was in the considerable variation observed between testing points at the individual level, which ranged from -20 to +23 for VIQ, -18 to +17 for PIQ and -18 to +21 for FSIQ.

Individuals had changes in verbal IQ of -20 to +23 points, with large changes seen in performance IQ (PIQ) and full-scale IQ (FSIQ) as well. Twenty point swings in IQ, up or down? That’s a lot. As noted before, the study is rather small (33 subjects), but what makes this an impressive study is that they have physical data–brain structure data–to correlate with the changes in IQ. The authors performed MRI scans on the subject. These are shown in a Figure from the paper (click to enlarge):

The authors found that grey matter changed in specific areas of the brain and that these changes correlated with the changes in VIQ and PIQ.

The brain is not just “plastic” in terms of IQ scores, it is still able to physically change during teenage years.

Our findings demonstrate considerable effects of brain plasticity in our sample during the teenage years, over and above normal development.

If an early intervention program were to claim that some kids gained 20 IQ points, it would be huge. (Of course, if they had to admit that some kids lost 20 IQ points, it would also be huge, but in a different way)

But if non-autistic kids can see such large swings in IQ during the teenage years, why not autistic kids? Why not kids with intellectual disability and autism? Just as important as the potential for swings up in IQ are the losses in IQ. What if a kid ends up in a placement that is inappropriate to the level that IQ is lost?

I would love to see a study such as this one on autistic kids, especially those with intellectual disabilities, to track IQ and brain structure during age ranges outside of early childhood.

Autism and diabetes…not ready for prime time

21 Oct

A recent news story on autism discussed: Common Link Suggested Between Autism and Diabetes: Study Implicates Hyperinsulinemia in Increased Incidence of Autism. I figured I’d take a day or two to read up on this and try to write about it. I didn’t figure on Emily Willingham. If you aren’t following her articles and you are into autism and science, you might want to consider doing so now. She’s already covered the story and in much better detail and expertise than I ever could in: Autism and type 2 diabetes linked because “both are increasing”?

Which tells you a lot right there. This is another “there is a temporal correlation, maybe there’s a link” type of story. The journal article is an opinion piece, not a research study. The Opinion Article, Insulin signaling and autism, is by Michael Stern of Rice University and appears in Frontiers In Cellular Endocrinology. In it he makes it clear it is a hypothesis. Unfortunately, Rice University has promoted this far beyond it’s current importance. A press release, including a YouTube video are out.

As Ms. Willingham points out, the language of the press release could be much better. Starting with the title:

Research proposes common link between autism, diabetes
Study implicates hyperinsulinemia in increased incidence of autism

This isn’t a study. It is an opinion piece. It’s great to have new ideas thrown out. I’ve seen many come and go in just the past few years. But let’s consider the opinions calmly and on their merits.

The YouTube video, in my opinion, goes further into overplaying this story:

Well, I think the key point of the hypothesis is that both autism and type 2 diabetes or obesity have the same common underlying cause, which is hyperinsulinemia.

It then goes on into the discussion of the proposed link. It goes on long enough, in my opinion, that the key word, “Hypothesis”, is pretty much forgotten (I had to go back and listen again to hear it).

Stories on this hypothesis carry titles like
Research proposes common link between autism, diabetes
Common link between autism, diabetes identified
and
Potential Link Found Between Type 2 Diabetes and Autism

So far this hasn’t really taken off. It would be good to put the idea in front of some researchers who could actually address it. I don’t think that press releases are the way to do that.

Advice for new and expectant parents

20 Oct

This from the National Down Syndrome Congress. Their page for new and expectant parents.

After reading this, imagine a future where autism is diagnosed via some biomarker, potentially prenatally.

If you have arrived here, there is a good chance you have received news you did not expect. As an expectant or new parent you have been told your child has Down syndrome.

If your child has arrived, please accept the sincere congratulations of our entire community.

Whether you are celebrating the birth of your child or anticipating its arrival, here you will find the basic information you need — to manage your pregnancy, plan for the delivery and to get started on the rewarding processes of having a child with Down syndrome in your life.

As you embark on this passage, the NDSC offers two thoughts.

First, you are not alone. Instead, you have become part of a large, deeply caring and warmly welcoming community. When you are ready, please contact us. We can answer what seem to be terribly daunting questions and, if you like, put you in contact with other parents who have been exactly where you are now. We can promise you will find them supportive, knowledgeable and above all sensitive.

Second, take care of yourself. Whether you are expecting or have been joined by a new arrival, the one thing that is known that a baby – a little packet of human potential just waiting to explore his or her world – is counting on you. So, rest, relax and enjoy.

Imagine a future where autistic infants are referred to as little packets of human potential. Where the birth of a child is an occasion, where congratulations are in order. Where people aren’t arguing over person first language, but accept person-first as a value. It is the person that is celebrated, the person who is valued. The disability is neither something to celebrate or disparage.

Under “Self Advocates”, their website includes Join the NDSC Board. Imagine a world where autistic self-advocates are not in a separate organization or added to large organizations as advisers.

Imagine a world where we accept the phrase, We’re More Alike Than Different.

It is not only possible, it is coming. It is the future.

Autism Risk and low birth weight newborns

19 Oct

A recent article in the journal Pediatrics has gathered a lot of news coverage this week. Prevalence of Autism Spectrum Disorder in Adolescents Born Weighing<2000 Grams

Here is the abstract:

Objective: To estimate the diagnostic prevalence of autism spectrum disorders (ASDs) in a low birth weight (LBW) cohort.

Methods: Participants belonged to a regional birth cohort of infants (N = 1105) born weighing <2000 g between October 1, 1984, and July 3, 1989, and followed up by periodic assessments to 21 years of age. At 16 years (n = 623), adolescents were screened for ASD using a wide net (previous professional diagnosis of an ASD or a score above a liberal cutoff on the Social Communication Questionnaire or the Autism Spectrum Symptoms Questionnaire). At 21 years (n = 189), 60% of screen positives and 24% of screen negatives were assessed for diagnoses of ASD by the Autism Diagnostic Observation Schedule or the Autism Diagnostic Interview–Revised.

Results: Samples retained at ages 16 and 21 years were representative of samples assessed at earlier ages except for lower levels of social risk. Of positive screens, 11 of 70 had ASD; of negative screens, 3 of 119 had ASD. The fractions of the 2 screening groups with ASD (14.3% in screen-positives and 2.5% in screen negatives) were weighted by fractions of screen-positives and screen-negatives among the adolescents (18.8% and 81.2%, respectively). This calculation produced an estimated prevalence rate of ASD in the entire cohort of 5% (31 of 623).

Conclusions: The diagnostic prevalence of ASD in this LBW preterm cohort was higher than that reported by the Centers for Disease Control and Prevention for 8-year-olds in the general US population in 2006.

The idea that low birth wieght might increase risk of autism isn’t new, but this is a different design: following a low birthweight cohort into adulthood.

The paper, and definitely the media coverage, has some limitiations. A great discussion of this paper and the media coverage can be found at The Biology Files in an article by Emily Willingham: Autism and low birthweight: study–and quote–limitations It’s written much better than I could do, an whatever I’d write at this point would just be a distillation of it.

This is different from the risk of autism due to premature birth, something the media mixed up on occasion and that Emily Willingham discusses in her article.

There are certainly some concerns about how the 5% figure was derived, and one can’t really make a direct comparison between a closely watched cohort at adulthood to the prevalence of 8 year olds based on record review (as in the CDC prevalence estimates). However, the idea that low birth weight is a risk factor is worth investigation.

ASF Founding Board Member Dr. Paul Offit Elected to the Institute of Medicine

19 Oct

Dr. Paul Offit, founding board member of the Autism Science Foundation, has been elected to the Institute of Medicine.

From the Autism Science Foundation Blog:

Autism Science Foundation Founding Board Member Dr. Paul Offit has been elected to the Institute of Medicine (IOM) at the Academy of Natural Sciences. For three decades, Dr. Offit has been a leading researcher in the fields of virology and immunology, and a well-respected and outspoken voice on the science, safety and value of childhood vaccinations. He is also one of the most public faces of the scientific consensus that vaccines have no association with autism.

The IOM is part of the National Academies:

The Institute of Medicine (IOM) is an independent, nonprofit organization that works outside of government to provide unbiased and authoritative advice to decision makers and the public.

Established in 1970, the IOM is the health arm of the National Academy of Sciences, which was chartered under President Abraham Lincoln in 1863. Nearly 150 years later, the National Academy of Sciences has expanded into what is collectively known as the National Academies, which comprises the National Academy of Sciences, the National Academy of Engineering, the National Research Council, and the IOM.

Also elected this year is autism researcher Dr. Daniel Geshwind:

Daniel H. Geschwind, M.D., Ph.D., Gordon and Virginia MacDonald Distinguished Professor, departments of neurology, psychiatry, and human genetics, and director, program in neurogenetics and Center for Autism Research and Treatment, Semel Institute, David Geffen School of Medicine, University of California, Los Angeles

The Wakefield Rehabilitation? Not really.

18 Oct

Reading about Andrew Wakefield gets old and tiring. I’m sure that isn’t news to readers here. Writing about Andew Wakefield gets very tiring. Who wants to keep reminding him/her self about a man who has caused so much harm to both the autism communities and public health in general? Who wants to read about dishonesty and unethical behavior?

I can only imagine that Brian Deer must want to put his award on a shelf and move on.

Which all begs the question: why do I think people reading Left Brain/Right Brain might want to read about him again? Because in this case it isn’t about Mr. Wakefield. Rather it is about his supporters. People who put aside the proved charges of dishonesty and unethical behavior. People such as Kent Heckenlively of the Age of Autism blog who are looking for The Wakefield Rehabilitation. It’s about how and why authors cite previous literature, and not reading too much into citations.

Beyond the hopes of those supporting Andrew Wakefield, there is some good research here and a bit of information about how and why people cite certain papers in the scientific literature.

First, how is Mr. Wakefield being “rehabilitated”? Answer: his papers were recently cited in a recent study. Seriously, something that small. That’s how hard people have to look for validation for Mr. Wakefield. A few citations and he’s on the road to rehabilitation.

The new paper isn’t by just any team, though. The study, recently out in PLoS One is Impaired Carbohydrate Digestion and Transport and Mucosal Dysbiosis in the Intestines of Children with Autism and Gastrointestinal Disturbances. The study is a follow-on to the PLoS One paper by Hornig et al., Lack of association between measles virus vaccine and autism with enteropathy: a case-control study.

Why is that important? “Lack of association…” is the paper which definitively put an end to the Wakefield MMR hypothesis. The team tried, with meticulous attention to detail, to replicate the most important factors of various Wakefield MMR-autism papers. They studied children with autism and gastro-intestinal complaints. They restricted their study to children who had demonstrated clear need for endoscopy (one major difference from the Wakefield studies). They were very careful about correctly reporting the patient histories (another major difference). They tested intestinal biopsy samples for measles virus (similar to as study by the Wakefield team), but were very careful to avoid contamination (unlike the Wakefield studies). The recent study used multiple laboratories to test for measles virus (Wakefield used two: his own and the O’Leary laboratory). Unlike Mr. Wakefield, the recent study reported on results from all the laboratories (Mr. Wakefield neglected to mention the results from his own laboratory which were contradictory to his theory).

Hornig et al. wrote:

The work reported here eliminates the remaining support for the hypothesis that ASD with GI complaints is related to MMR exposure. We found no relationship between the timing of MMR and the onset of either GI complaints or autism. We also could not confirm previous work linking the presence of MV RNA in GI tract to ASD with GI complaints.

About as clear a conclusion as I’ve ever seen. “The work reported here eliminates the remaining support for the hypothesis that ASD with GI complaints is related to MMR exposure.”

So, what about the new paper and the citations? Well, members of the team that produced the Hornig et al. study did further research on the tissue samples taken. Brent L. Williams heads up the author list on the new study.

Here is the (highly technical) abstract from the new study by Williams et al.:

Gastrointestinal disturbances are commonly reported in children with autism, complicate clinical management, and may contribute to behavioral impairment. Reports of deficiencies in disaccharidase enzymatic activity and of beneficial responses to probiotic and dietary therapies led us to survey gene expression and the mucoepithelial microbiota in intestinal biopsies from children with autism and gastrointestinal disease and children with gastrointestinal disease alone. Ileal transcripts encoding disaccharidases and hexose transporters were deficient in children with autism, indicating impairment of the primary pathway for carbohydrate digestion and transport in enterocytes. Deficient expression of these enzymes and transporters was associated with expression of the intestinal transcription factor, CDX2. Metagenomic analysis of intestinal bacteria revealed compositional dysbiosis manifest as decreases in Bacteroidetes, increases in the ratio of Firmicutes to Bacteroidetes, and increases in Betaproteobacteria. Expression levels of disaccharidases and transporters were associated with the abundance of affected bacterial phylotypes. These results indicate a relationship between human intestinal gene expression and bacterial community structure and may provide insights into the pathophysiology of gastrointestinal disturbances in children with autism.

If this were really about the autistics and not about Andrew Wakefield, those claiming that there is something different about the GI disturbances in autistics should be extatic. Here is a top notch team pointing to a possible real difference. In the kids tested, the genes were expressing enzymes and transporters–i.e. the genes are performing differently–for autistic kids. Also, they are seeing differences in the bacteria in the autistic kids.

Not only that, but these kids benefited from dietary intervention, although it isn’t specific to the autistic kids: “Beneficial effects of dietary intervention on GI disturbances were reported for all AUT-GI and Control-GI subjects with FA.”

But, it apparently isn’t about the autistics or the research when it comes to the Age of Autism. It’s about rehabilitating Andrew Wakefield’s reputation. (With apologies in advance–the image that comes to mind is a team that has been performing CPR on his reputation for years now. It’s time to move on.)

The important piece of this study, according to Mr. Heckenlively, is that they cite some of Andrew Wakefield’s papers. In particular:

Wakefield AJ, Anthony A, Murch SH, Thomson M, Montgomery SM, et al. (2000) Enterocolitis in children with developmental disorders. Am J Gastroenterol 95: 2285–2295.

Wakefield AJ, Ashwood P, Limb K, Anthony A (2005) The significance of ileo-colonic lymphoid nodular hyperplasia in children with autistic spectrum disorder. Eur J Gastroenterol Hepatol 17: 827–836

Ashwood P, Anthony A, Torrente F, Wakefield AJ (2004) Spontaneous mucosal lymphocyte cytokine profiles in children with autism and gastrointestinal symptoms: mucosal immune activation and reduced counter regulatory interleukin-10. J Clin Immunol 24: 664–673.

Mr. Heckenlively appears to have built a nice straw man argument in which every thing Mr. Wakefield has done is now discredited. Somehow citing a paper by Mr. Wakefield then becomes some sort of a statement that everything he did was actually right. Both sides of that argument are false. The authors should cite what is in the literature. By citing, say, the Ashwood (2004) paper, they aren’t saying that, say, the 1998 Wakefield Lancet paper is now “rehabilitated’.

Notice that the authors didn’t cite the 1998 Lancet paper. One big reason: it’s been retracted. Which begs the question, why are the authors citing Wakefield et al. (2000)? The paper in the American Journal of Gastroenterology has also been been retracted:

On 28 January 2010, the UK General Medical Council’s Fitness to Practice Panel raised concerns about a paper published in the Lancet by Dr Wakefi eld et al. (1). The main issues were that the patient sample collected was likely to be biased and that the statement in the paper, that the study had local ethics committee approval, was false. Th ere was also the possibility of a serious conflict of interest in the interpretation of the data. Th e Lancet has now retracted this paper (1). Th is paper in the American Journal of Gastroenterology (AJG) (2) also includes the 12 patients in the original Lancet article and therefore we retract this AJG paper from the public record.

One really shouldn’t cite things that have been retracted from the public record. So, is there some message that Williams et al. are trying to send us? Are they saying that Andrew Wakefield was correct all along? Hardly. That paper was retracted in May of 2011, the same time that Impaired Carbohydrate Digestion and Transport and Mucosal Dysbiosis in the Intestines of Children with Autism and Gastrointestinal Disturbances was submitted to PLoS One. The authors weren’t aware of the retraction. Says a lot about how closely they follow Andrew Wakefield, don’t it?

Apparently, the authors have contacted PLoS about the citation, and it will be corrected to notify readers of the retraction. That is the right thing to do. It isn’t a statement about Mr. Wakefield’s research, other than this paper was retracted.

Authors can’t control the message bloggers may try to create from their research (heck, one of the authors, Ian Lipkin, consulted on the recent movie “Contagion”, a main character is a blogger whose message is unscientific and irresponsible). From what I’ve heard, the authors are still very clear on the message of their first PLoS paper: “The work reported here eliminates the remaining support for the hypothesis that ASD with GI complaints is related to MMR exposure. ”

I think the point was made pretty clearly. Mr. Heckenlively in his excitement read way too much into this new paper. Not surprisingly, he just goes on and on making more mistakes. Consider this paragraph:

Isn’t Dr. Wakefield supposed to be some super-villain, leading all of us gullible parents to believe that vaccines aren’t quite as safe as sugar water? Didn’t he make up fake diseases? So, after being stripped of his license to practice medicine in the U. K., it turns out there really is something called autistic entercolitis and ileo-colonic lymphoid nodular hyperplasia in children with autism. At least Dr. W. Ian Lipkin seems to think so.

Wow. All this is extrapolated from a single sentence in the introduction of the paper: “Macroscopic and histological observations in ASD include findings of ileo-colonic lymphoid nodular hyperplasia, enterocolitis, gastritis, and esophagitis [2], [3], [4], [5], [6], [7].”

What does that sentence mean? Simple interpretation: others have reported these findings. Not “we confirm that these findings are real”. Given that reference [3] (a retracted Wakefield paper) may be removed or noted to be retracted, the only support for “enterocolitis” will be gone from the paper.

Mr. Heckenlively wrote “Although this study used a relatively small sample of gut biopsies from children with autism (Hey, isn’t that what Wakefield got in trouble for? Or is my memory failing me?),”

Mr. Heckenlively, your memory is failing you. The findings of the General Medical Council are easily found online.

Let me remind you of some of that document:

The Panel concluded that Dr Wakefield’s shortcomings and the aggravating factors in this case including in broad terms the wide-ranging transgressions relating to every aspect of his research; his disregard for the clinical interests of vulnerable patients; his failure to heed the warnings he received in relation to the potential conflicts of interest associated with his Legal Aid Board funding; his failure to disclose the patent; his dishonesty and the compounding of that dishonesty in relation to the drafting of the Lancet paper; and his subsequent representations about it, all played out against a background of research involving such major public health implications, could not be addressed by any conditions on his registration. In addition, the Panel considered that his actions relating to the taking of blood at the party exemplifies a fundamental failure in the ethical standards expected of a medical practitioner. It concluded that conditional registration would not mark the seriousness of such fundamental failings in his duty as a doctor

and

The Panel made findings of transgressions in many aspects of Dr Wakefield’s research. It made findings of dishonesty in regard to his writing of a scientific paper that had major implications for public health, and with regard to his subsequent representations to a scientific body and to colleagues. He was dishonest in respect of the LAB funds secured for research as well as being misleading. Furthermore he was in breach of his duty to manage finances as well as to account for funds that he did not need to the donor of those funds. In causing blood samples to be taken from children at a birthday party, he callously disregarded the pain and distress young children might suffer and behaved in a way which brought the profession into disrepute.

Mr. Heckelively also poses the question: “Didn’t he [Andrew Wakefield] make up fake diseases?”

That would be “autistic enterocolitis”, a term Andrew Wakefield coined and a condition which still, 13 years later, doesn’t have support. Autistic enterocolitis is not just any and all GI disturbances in autistics. Enterocolitis is “…an inflammation of the colon and small intestine”. Note the “and”, there. Even more important, the PLoSOne paper is not about inflammation at all.

Mr. Heckenlively finishes with the rather hopeful, wishful thinking statement: “But if a big shot scientist like Dr. W. Ian Lipkin is quoting Dr. Andrew Wakefield as a reliable source, maybe the rest of the world will soon be doing the same thing.”

Again, wow. Here we have Ian Lipkin, one of the team that just put an end to the Wakefield-MMR hypothesis. Again, let’s remind ourselves, Ian Lipkin is part of the team which wrote: “The work reported here eliminates the remaining support for the hypothesis that ASD with GI complaints is related to MMR exposure.” There is such a major disconnect between that statement (which, yes, Dr. Lipkin stands by) and what Mr. Heckenlively wrote that I am just left in amazement.

This isn’t a story about rehabilitation. This is a story about diversion. Diversion of attention away from important subjects in autism. These include the medical treatment of major health problems. How does one treat something like bowel problems in individuals with communication and/or sensory difficulties? That’s a big question that gets lost in this whole “Andrew Wakefield” discussion. Research like this new paper is important in that respect: is there something specific to kids with autism, regression and GI disease? Leave aside any discussion about GI being linked to the regression, how do you treat it? I, for one, am glad to see something come out of this research project than just the “MMR doesn’t cause autism and GI disease” conclusion. Instead of trying to read the tea leaves of this paper and try to recoup the damage Andrew Wakefield did to his reputation, why don’t we just read the paper in the context of what this might tell us about the health problems of autistics?

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