Archive | Science RSS feed for this section

Los Angeles Times: Discovering Autism

23 Dec

The Los Angeles Times produced a series of articles called “Discovering Autism”. The series is in four parts and represents was researched for years. The articles are:

Autism boom: an epidemic of disease or of discovery?
Autism rates have increased twentyfold in a generation, stirring parents’ deepest fears and prompting a search for answers. But what if the upsurge is not what it appears to be?

Warrior parents fare best in securing autism services
Public spending on children with autism in California varies greatly by race and class. A major reason: Not all families have the means to battle for coveted assistance.

Families cling to hope of autism ‘recovery’
An autism treatment called applied behavior analysis, or ABA, has wide support and has grown into a profitable business. It has its limits, though, and there are gaps in the science.

Autism hidden in plain sight
As more children are diagnosed with autism, researchers are trying to find unrecognized cases of the disorder in adults. The search for the missing millions is just beginning.

The first article brought a great deal of criticism, from many quarters. As you can imagine challenging the way the “autism epidemic” is viewed is not welcomed by those promoting vaccines as a primary cause of autism. This article also brought out at least one commenter who asserted that the rise in autism diagnoses is driven by people seeking social security payments (SSI), which goes to show that readers tend to bring their own preconceptions to what they read.

Interest in the online discussion of the series dropped off dramatically after day one.

Autism boom: an epidemic of disease or of discovery? looked at the rise in autism diagnoses observed in many places. Writer Alan Zarembo points out quite rightly that autism rates vary dramatically by school district in California, as well as state to state.

Such variability of autism rates across geography speak strongly against the idea of a single cause, such as vaccines. Autism Diva wrote about the strong variation by regional center district within California years ago (her piece is not up, but this article from LBRB discusses her article)

The variation by school district and by race/ethnicity was a major factor in helping me see that the vaccine-epidemic of autism did not make sense, back when I first started to read up on autism.

The LA Times quotes Prof. Peter Bearman of Columbia University, who studied the California Department of Developmental Services data closely and showed, amongst other things, that a large autism “cluster” existed in Southern California. The Times notes that similar clusters were found by U.C. Davis Professor Irva Hertz-Picciotto. (I was present when Autism Diva discussed the regional center graph with Prof. Hertz-Picciotto, by the way).

Prof. Bearman also showed that social forces were at work–awareness, if you will–which has aided the increase in autism diagnoses.

In other words, autism is not contagious, but the diagnosis is.

“`Is it real or not?’ is a meaningless question,” Bearman said of the surge in cases. “The sociological processes are as real as the biological processes.”

A diagnostician (neurologist) is quoted in the Times:

Dr. Nancy Niparko, a child neurologist in Beverly Hills, said that whether she identifies a child as autistic can come down to whether she believes it will do any good.

“If it’s going to improve the possibility of getting services that will be helpful, I will give the label,” she said.

“I don’t work for labels. Labels work for me.”

In Warrior parents fare best in securing autism services makes the point that it takes work, hard work, to get the services that a child may need. An autism diagnosis is not a ticket to services, it is a first step. Parents who fight harder and longer tend to get higher levels of services for their children.

The Times points out that within a single district (albeit one of the largest in the U.S., Los Angeles Unified), the fraction of students with 1:1 aides varies by geography and race/ethnicity:

District officials acknowledge that advocacy efforts make a big difference in who gets services, but see things differently than parents on the value of 1:1 aides:

L.A. Unified officials offered a similar explanation for the disparity. As parents successfully lobbied for outside aides, the idea spread, and in certain schools it became standard practice to offer them.

“Parents learned from each other,” said Nancy Franklin, a top special education administrator. “It became a cottage industry in LAUSD.”

The district is trying to break the pattern by persuading parents that its own staff can meet children’s needs in many cases.

“We’re paying lots of money for services that are of questionable value,” said Eileen Skone-Rees, who oversees the district’s contracts with companies that supply one-on-one aides.

In Families cling to hope of autism ‘recovery’, the Times focuses on ABA. Biomedical approaches are not really discussed.

The article talks about ABA from the early work of Ivar Lovaas to the present day, where it is common in some school districts and regional centers. The high costs and the level of research support are discussed along with examples of children who are success stories and those who are not.

In Autism hidden in plain sight, the Times looks at how autism is often missed in adults.

The Times presents an intriguing look at the past in medical records from a child diagnosed by Leo Kanner (whose work coined the term “autism”).

The times provided a number of slide show vignettes of people they interviewed.

I can’t link to them directly, but I’ve watched a few and enjoyed them. Jeane Duquet, autistic adult diagnosed at age 39 (right side, middle). Jesse Castillo, age 11 (bottom right corner)

The author of the series, as well as Catherine Lord were interviewed by NPR:

http://www.npr.org/v2/?i=144022386&m=144022377&t=audiowidth=”400″ height=”446″ />

I would certainly have done some things differently had I written the series. I would have chosen different wording, for example. Yes, the pieces brought out some less than pleasant perspectives. I’ve read a few complaints about the series, from not supporting vaccine causation or biomedical approaches to presenting autism as a costly burden. Ironically, these complaints come from the same people who repeatedly say that “autism costs society $3.5 million per individual”. A big piece of that $3.5M is ABA and if we as a community (or part of the community) are to defend the need for ABA, we have to accept that there is a cost. I believe, and I commented, that the choice of language at times put a negative slant where one was not needed. However, the series put some very good information out, including: 1) the “epidemic” has a large portion which is driven by social factors, with a much smaller part that may be a real change in the number of autistics, 2) services are not handed out on a silver platter. Parents and autistics have to fight for what supports the law says they should get, 3) 1:1 therapies such as ABA may be effective, but they are expensive and the research behind them is still incomplete and 4) adult autistics are out there in greater numbers than is currently reported.

The biggest complaint about the series is that it portrays parents as seeking diagnoses for their kids for some sort of financial gain. Dr. Jay Gordon (a major promoter of the vaccine-epidemic idea) has noted this where Mr. Zarembo has been interviewed (http://www.scpr.org/programs/patt-morrison/2011/12/22/21866/autism-diagnoses-spike-an-epidemic-in-the-making). Mr. Zarembo makes it clear in the interview that this is not his point. That the autism diagnosis “opens the door” and that parents are doing what they should for their children–including fighting hard to obtain appropriate services once the door is opened.

For those complaining that the LA Times series didn’t cover the vaccine-epidemic idea or biomedical approaches to autism: I’d recommend you be thankful. Quite frankly an evidence driven newspaper series on these issues will not go the way you want.

Autism Frequently Missed in Children With Epilepsy

14 Dec

A recent study presented at the American Epilepsy Society annual meeting suggests that developmental delay in general and autism in specific might be undetected in a large fraction of children with epilepsy.

In Autism Frequently Missed in Children With Epilepsy, Allison Shelley of Medscape writes:

In a study presented here, the investigators tracked children younger than 5 years seen at an epilepsy monitoring unit and a ketogenic diet clinic for about half a year. They asked parents of the 44 children to complete the Ages and Stages Questionnaire, as well as an autism screening tool.

Most of the children (77%) screened positive for developmental delay; of these participants, a strong proportion (36%) had autism.

More than a third of patients had not been previously diagnosed as having developmental delay or autism and were referred for confirmatory evaluation.

Here is a video from the American Epilepsy Society discussing this:

The study is relatively small and is, to my knowledge, as yet unpublished. But it does present a potentially important idea that people with epilepsy should be screened for autism.

Lower birth weight indicates higher risk of autistic traits in discordant twin pairs

7 Dec

Twin studies have shown that there is a strong genetic component to autism. When one “identical” twin has autism, the odds are high that the other twin does as well. But, what about those cases where only one twin has autism? The pair is “discordant”.

One of the major twin studies ongoing is the “Child and Adolescent Twin Study of Sweden” (CATSS). The study is not just an autism study, as their website notes:

The aim of this study is to investigate how both genetic and environmental effects influence health and behavior in children and adolescents. In this study parents to all Swedish twins turning 9 or 12 years are asked to complete a telephone interview concerning the health and behavior of their twins. The interview screens for several different health (e.g., asthma, allergies, diabetes) and behavior (e.g., attention, social interaction) problems. Some of the families will be followed up with additional questionnaires, as well as with genotyping and clinical interviews.

By studying discordant pairs, they are able to look for other risk factors. In this case, low birth weight. They found that low birth weight confers a significant risk for autism. Three times higher risk for a discordant autism pair for low birth weights.

They conclude ” a non-genetic influence associated with birth weight may contribute to the development of ASD”

Here is the abstract:

Lower birth weight indicates higher risk of autistic traits in discordant twin pairs.
Losh M, Esserman D, Anckarsäter H, Sullivan PF, Lichtenstein P.
Source

Roxelyn and Richard Pepper Department of Communication Sciences and Disorders, Northwestern University, Evanston, IL, USA.
Abstract
BACKGROUND:

Autism spectrum disorder (ASD) is a neurodevelopmental disorder of complex etiology. Although strong evidence supports the causal role of genetic factors, environmental risk factors have also been implicated. This study used a co-twin-control design to investigate low birth weight as a risk factor for ASD.

Method
We studied a population-based sample of 3715 same-sex twin pairs participating in the Child and Adolescent Twin Study of Sweden (CATSS). ASD was assessed using a structured parent interview for screening of ASD and related developmental disorders, based on DSM-IV criteria. Birth weight was obtained from medical birth records maintained by the Swedish Medical Birth Registry.

RESULTS:

Twins lower in birth weight in ASD-discordant twin pairs (n=34) were more than three times more likely to meet criteria for ASD than heavier twins [odds ratio (OR) 3.25]. Analyses of birth weight as a continuous risk factor showed a 13% reduction in risk of ASD for every 100 g increase in birth weight (n=78). Analysis of the effect of birth weight on ASD symptoms in the entire population (most of whom did not have ASD) showed a modest association. That is, for every 100 g increase in birth weight, a 2% decrease in severity of ASD indexed by scores on the Autism – Tics, attention-deficit hyperactivity disorder (AD/HD), and other Comorbidities (A-TAC) inventory would be expected in the sample as a whole.

CONCLUSIONS:

The data were consistent with the hypothesis that low birth weight confers risk to ASD. Thus, although genetic effects are of major importance, a non-genetic influence associated with birth weight may contribute to the development of ASD.

The Prevalence of Autism Spectrum Disorders in Toddlers: A Population Study of 2-Year-Old Swedish Children.

6 Nov

A recent study, The Prevalence of Autism Spectrum Disorders in Toddlers: A Population Study of 2-Year-Old Swedish Children, considers changes in prevalence in very young children and the effect of early screening:

Autism Spectrum Disorder (ASD) is more common than previously believed. ASD is increasingly diagnosed at very young ages. We report estimated ASD prevalence rates from a population study of 2-year-old children conducted in 2010 in Gothenburg, Sweden. Screening for ASD had been introduced at all child health centers at child age 21/2 years. All children with suspected ASD were referred for evaluation to one center, serving the whole city of Gothenburg. The prevalence for all 2-year-olds referred in 2010 and diagnosed with ASD was 0.80%. Corresponding rates for 2-year-olds referred to the center in 2000 and 2005 (when no population screening occurred) were 0.18 and 0.04%. Results suggest that early screening contributes to a large increase in diagnosed ASD cases.

The prevalence for this young age group in Gothenburg Sweden showed a dramatic rise: from 0.04% in the year 2000, to 0.18% in 2005 and a big jump to 0.80% in 2010.

I’m sure many things have changed in Gothenburg in the past 10 years. However, the implementation of an early screening program is cited as having the major impact, as this was in place in 2010, but not for 2005 or 2000.

For those who will undoubtedly ask: the vaccine schedule for Sweden did not change remarkably in that time period.

2007: A revised schedule is implemented from 2007, including a diphtheria-tetanus-pertussis booster at school entry (DTaP) and at school leaving (dTap), and also a lower age for the second MMR (6-8 years). The new schedule starts with children born from 2002. Children born 1995-2001 receive a single dose pertussis catch-up in form of DTaP instead of DT at 10 years.

2009: PCV7 was introduced into the national childhood vaccination programme and recommended at 3, 5 and 12 months of age to all children born from October 2008 onwards.

2010: HPV introduced into the national childhood vaccination programme on 1st January 2010.

The 2007 change doesn’t affect children 2 1/2 and under. The 2009 addition of PCV7 doesn’t affect the children in 2005, where the prevalence was over 4 times higher than in 2000. HPV doesn’t affect children aged 2 1/2. Thimerosal was removed from vaccines in Sweden in the early 1990’s, so that exposure was unchanged over the entire period. My guess is this won’t stop people from pointing to the PCV7 vaccine as the “toxic tipping point” for Swedish kids.

Call me biased. I’m going with the authors on this one and giving credit to the hard work of the screening program implemented.

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

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 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.

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?

Defending alternative medicine and autism: the charges against Anju Usman

14 Oct

In Illinois charges DAN doctor with unethical behavior, LBRB writer Ken Reibel discussed the case recently brought against alternative medical practitioner Dr. Anju Usman. These charges follow on a civil suit brought by the parent of an autistic child seen by Dr. Usman. This charges in this case will require that Dr. Usman defend many of the common practices in alternative medicine.

The complaint is:

DEPARTMENT OF FINANCIAL AND PROFESSIONAL REGULATION of the State of Illinois,

v.

ANJUM I. USMAN, M.D.

No. 200904994

One short paragraph in the complaint sums up a big piece of where this suit has the possibility to strongly influence how alternative medicine “treats” autism: None of the treatments described above has been proven to influence the course of autism.

Here is a section of count 1:

17. Hair analysis does not provide a basis for the diagnosis of heavy metal toxicity.
18. Provoked urine testing does not provide a basis for the diagnosis of heavy metal toxicity. The American College of Medical Toxicology has determined that provoked testing has not be scientifically validated, has no demonstrated benefit and may be harmful when used for assessing patients for metal poisoning.
19. Porphyrin testing does not provide a reliable basis for the diagnosis of heavy metal toxicity.
20. Although chelation therapy is FDA-approved for treating lead poisoning, it should not be used unless a non-provoked blood (not urine) test shows an extremely high level of lead.
21. Respondent did not obtain a confirmatory blood lead test or record any source of lead exposure.
22. The record contains no basis for concluding that chelation therapy was appropriate.
23. The record does not contain adequate infonlled consent for any of the prescribed nonstandard tests or treatments. The consent fonns used did not accurately present the risks and/or benefits of tests and treatments. Although it mentioned experimental drug use, these were not administered as part of a proper experimental protocol.
24. The informed consent form states that chelation therapy “is considered controversial for the generalized treatment of chronic low or high level lead toxicity, mercury toxicity, or for other heavy metal toxicities, either acute or chronic.” This statement is misleading because there is a clear scientific consensus that it is inappropriate for treating lead toxicity without demonstrating that toxicity exists and that the level is very high.
25. Throughout the treatment period, Respondent made statements to AC’s mother that the prescribed treatments had positive clinical benefits for children with autism, despite the lack of empirical research supporting Respondent’s position.
26. The record does not document any reason why AC should have received unproven treatments.
27. Spironolactone, which is potentially dangerous, was prescribed without justification.
28. Despite a nonnal selenium level, Respondent repeatedly and unnecessarily prescribed selenium supplements and continued to do so even when AC eventually showed a high level.
29. That Respondent abused the physician/patient relationship by taking unfair advantage of a patient’s vulnerability in that Respondent utilized unproven drugs and medicine to treat AC, a pediatric patient diagnosed with autism.
30. That the foregoing acts and/or omissions of Respondent are grounds for revocation or suspension of a Certificate of Registration pursuant to 225 Illinois Compiled Statutes (2002), Section 60122(A)(20), relying on the Rules for the Administration of the Medical Practice Act, Illinois Administrative Code Title 68, Section 1285.240(b)(1 )(C), and (2) (C).

There are many methods by which “heavy metal toxicity” is diagnosed by alternative medical practitioners. These methods are not demonstrated to be accurate, and are not accepted by actual medical toxicologists. These include hair analysis, provoked urine testing and porphyrin testing.

A prime example is provoked urine testing. A thorough discussion can be found here. A provoked urine test involves giving an individual a chelator and then testing the urine for heavy metals. Everyone (every thing, every animal) has some level of mercury. A chelator will force the body to excrete some level of the heavy metals inside, so it is no surprise that the levels obtained are “elevated”. The problem is that there is no standard by which one can compare the provoked urine to determine if the person actually has heavy metal poisoning.

The method is also called “challenge” testing. The American College of Medical Toxicologists have a position statement on this:

It is, therefore, the position of the American College of Medical Toxicology that post-challenge urinary metal testing has not been scientifically validated, has no demonstrated benefit, and may be harmful when applied in the assessment and treatment of patients in whom there is concern for metal poisoning.

More quotes from the complaint:

From Count III

That Respondent made false or misleading statements regarding the efficacy or value of the medicine, treatment, or remedy prescribed by Respondent in the treatment of any disease or other condition of the body in that Respondent made false or misleading statements regarding the efficacy of chelation therapy in the treatment of autism.

From Count V

29. That Respondent engaged in a pattern of practice or other behavior that demonstrates incapacity or incompetence to practice in that Respondent:
a. Repeatedly prescribed and administered unproven and medically unnecessary treatments to AC despite the lack of empirical research demonstrating the effectiveness of the prescribed treatment plans; and
b. Demonstrated extreme departure from rational medical judgment in the care and treatment of AC.

This isn’t a criminal complaint. Rather it is an ethics or “professional regulation” complaint. The disciplinary action called for if the case is proven involves Dr. Usman’s license:

WHEREFORE, based on these allegations, the Department of Financial and Professional Regulation of the State of Illinois, by Laura E. Forester, its Chief of Medical Prosecutions, prays that the Physician and Surgeon license of ANJUM I. USMAN, M.D., be revoked, suspended, placed on probation or otherwise disciplined.

Illinois charges DAN doctor with unethical behavior

13 Oct

According to the Chicago Tribune, the Illinois Department of Financial and Professional Regulation has charged a well-known Naperville physician with “unprofessional, unethical and/or dishonorable conduct.”

Dr. Anju Usman, a familiar face at anti-vaccine conferences in the US and abroad,   allegedly lied about or exaggerated the value of treatments, and “demonstrated extreme departure from rational medical judgment” and “abused the patient/physician relationship.” Regulators are moving to have Usman’s medical license revoked or suspended, or otherwise disciplined.

The report, written by science writer Trine Tsouderos, says:

The complaint, filed Wednesday, revolves around Usman’s care of a boy diagnosed with autism whose treatment was described in the Tribune’s series “Dubious Medicine.” The series detailed the many unproven therapies prescribed for the boy and found that many alternative treatments for autism amount to uncontrolled experimentation on children.

According to the complaint, the boy began seeing Usman shortly after he was diagnosed with mild to moderate autism in the spring of 2004. He was not yet two.

Usman allegedly diagnosed the child with a calcium-to-zinc imbalance, yeast, dysbiosis, low zinc, heavy metal toxicity and abnormally high levels of aluminum, antimony, arsenic, cadmium, copper, lead, nickel, silver, tin, titanium, and selenium.

Dr. Anju Usman

Usman is the defendant in a civil suit filed by the boy’s father in 2010. Also named are Dan Rossignol, a Florida DAN doctor; and Doctors Data, a Chicago-based laboratory that performs tests used to convince patients that they have dangerously high levels of lead, mercury, or other heavy metals that require “detoxification” to reduce these levels.

Usman is also associated with the 2005 death-by-chelation of five-year-old Tariq Nadama. According to court records, Usman diagnosed the boy with “high aluminum” and referred him to Roy Kerry, a Pennsylvania physician. Kerry, an ear-nose-and throat surgeon, inexplicably treated the boy for lead poisoning.

According to Kerry’s notes, which were published by the Pennsylvania Medical Board:

“We don’t have the entire record at all. Mother left her entire volume of his records home. But we have been in communication with Dr. Usman regarding EDTA therapy. He apparently has a very high aluminum and has not been responding to other types of therapies and therefore she is recommending EDTA, which we do on a routine basis with adults. We therefore checked him to it … But on testing for the deficiency indicator we find him only indicating the need for EDTA at the present time. Therefore we agree with Dr. Usman’s recommendation to proceed with the treatment. She recommends 50mg per kilo. He is 42 pounds today. So we’ll treat him with a 20-kilo child and give 1 gram of EDTA.

Nadama arrested and died in front of his mother during the third chelation round in August, 2005. A year later, Kerry was certified as a DAN doctor after completing an eight-hour training course. Prosecutors declined to charge Kerry for the death, and the state medical board suspended his license for six months and ordered extra training.

Usman spoke at AutismOne in Chicago last May, a cult-like annual gathering that expels skeptical writers and news reporters. Her topic: Prevention & Raising Healthy Kids in a Toxic World.

← Older Entries
Newer Entries →