Recovery from autism 40% - two sources agree?

If you asked an expert today whether it is possible to recover from autism all you are going to get is a big fat question mark. To date we have not been able to accurately determine exactly how many children and adults have autism let alone how many might have once had autism and recovered from it.

But maybe recovery from autism is more common that we thought.

If you remember, there was a big deal made out of what last summer's National Survey of Children's Health (NSCH) had to say about autism. According to that survey, autism was much more common that previously believed AND there were a significant number of children who once had a label of autism but no longer did.

The NSCH data was formalized in a paper in Pediatrics that said "nearly 40% of those ever diagnosed with ASD did not currently have the condition".

Results from a survey can be misleading and the report in Pediatrics didn't draw any conclusions from the figure. There was widespread talk on autism sites of what this figure meant with some people claiming that it showed recovery from autism while others were using it to show how flaky diagnosis could be. I didn't really know what to make of it at the time.

But then a funny thing happened when I was looking at the data in the study I wrote about yesterday. This was a prevalence study done in the UK on a group of children that were born in 1990 and 1991 whose main point was that autism was much more common than previously thought. As part of this study the researchers examined 112 children that had a diagnosis of autism and yet, after looking at their medical records and test results (ADOS, ADI-R, and others), 44 of the children had their label removed (this result was not stated directly but if you look at the data in the study you can arrive at the figure).

In other words, 40% of the children in this second study had a confirmed medical diagnosis of autism but, years later, when the children were evaluated again, they no longer had a diagnosis.

This study, published the year before the NSCH results, shows the same "recovery" rate (40%) and at the same time avoids the problems with the NSCH data. The existing diagnosis for these children was confirmed and a new evaluation of the children was done by qualified professionals - this wasn't just a parent saying it was so like the NSCH survey.

The same result appearing in two different sets of children from two different countries using two different methods of discernment makes me wonder.  This result is also similar to the "recover rate" that has been demonstrated by ABA.

I am starting to think that this figure is real and means something - I just don't know what.

It is completely possible that all this means is that a diagnosis of autism isn't reliable, that a huge number of children are given the label "just in case", or that the children receive the label just to access services (which don't exist in many areas). Or it could just mean that I am misinterpreting the data from the second study.

Or, just maybe, this result shows that it is possible for a child to recover from autism.

Just food for thought.

Debunking Michelle Dawson's 1 in 86 adults with autism

Recently, Michelle Dawson wrote a post called 1 in 86: the prevalence of autism among adults where she asserted, among other things, that the prevalence of autism in adults is 1 in 86.  Ms Dawson is basing this estimate on a study published in 2006 -

All 56,946 individuals comprising the targeted population cohort in this study are, as of today, the last day in the decade, 18 years of age or older. They were born between July 1, 1990 and Dec 31, 1991 and they are now all adults. 

Within this cohort, Baird et al. (2006) reported an autistic spectrum prevalence of ~116/10,000. That's 1 in 86, and all these autistics, originally assessed as such when 9 to 14yrs old, are now adults.

Well, she is correct about at least one thing - all of these children in the study were born between 1990 and 1991 and would be now all be 18 or 19 years old. However, I am not at all sure that even if autism is at a certain rate in a specific population 18 year olds that the same rate would apply to adults of all other ages.  The available data points to an increasing rate of autism and that the rate is increasing with each passing year.

But even ignoring that point for a minute, what exactly was found in the study that she is referring to?  Given the fact that the study population was 56,946, did the researchers find 662 children with a diagnosis of autism?

The short answer is no, they didn't.

What they found was 158 children who would fit the broadest possible definition of autism.  Using what would be a normal definition of autism used in studies, they only found 81 children.

So how did they get from from the 158 they identified to claiming that there were over four times that number and what exactly is the difference in the between the two groups?  The answer is complicated and has to do with the differences between actually counting the number of cases and using statistical techniques to estimate a number.  The difference also has to do with what you call autism - are you talking about what could clinical be diagnosed as autism or something who has some symptoms of autism.

Lets start with the basics, this study looked at 56,946 children born in South Thames, UK between July 1, 1990 and December 31, 1991.  When the study started, there were 255 children who had a diagnosis of autism.  If you look at what the historical rate of autism was thought to be when these children were 9 years old, it was about 1 in 250 (40 per 10,000).  The children in this group had slightly higher rate but were generally in line with the 1 in 250 number (45 per 10,000).

From there the study identified all of the children who has a special education label (or the equivalent in the UK) or had an existing diagnosis of autism.  This narrowed the population to 1,770 children.  The authors assumed that all of the children with autism would be in this sub group.  I think this is a safe assumption - any 9 year old who had any diagnosable form of autism would likely need at least some extra help at school.

I am going to stop here for a basic sanity check.  The study is asserting that there are about 662 children with autism in this population.  If you do the math you will see that they are saying that over 35% of the special ed population has autism.  Compare that to the number of existing cases (255) in the population and you will see that the rate of existing cases is about 15%.  If you consider the fact that the comparable percentage in the US for all children served under IDEA around the same time frame was about 17% you can see that the 35% is about double what would be expected.  Although to be fair, I am comparing two different countries so the comparison isn't strictly apple to apple.

Moving along, the study then used the Social Communication Questionnaire (SCQ) to help group the children.  The SCQ is a screening test that is designed to identify children with autism.  The idea is that if a child has a score above a certain level the should be further evaluated for a form of autism.  Out of the initial 1,770 there were 1,035 who returned the SCQ and consented to further evaluation.

Out of this set of 1,035, a "two-way stratified random" sample of 363 children were selected for further evaluation.  In this group of 363 there were 141 children who already had a diagnosis of autism - a little over half of the known cases.

Of the 363 only 255 were actually evaluated due to a variety of factors.  In this population of 255 there were 112 children who had an existing diagnosis of autism, which amounts to about 44% of the known population.  For each of these 255 children an ADOS and ADI-R was performed as well as assessments of IQ, language, and adaptive behaviors.  Information was collected (via the telephone interviews) from the children's teachers about their social, communicative, and other behaviors.  The children's health records were also collected.

Before I go into the specific numbers found, I wanted to talk about the "two-way stratified random" sample of 363 children. The groups (stratification) used a prior autism diagnosis and SCQ score range as the defining criteria for the groups and here lies one of the potential problems.

Remember how I said that the SCQ was a screening tool?  That means above a certain score you have a certain likelihood that the test will accurately identify children with autism and will not identify children who don't have autism.  All of this means that above the cut-off score the SCQ will agree with another, presumable more accurate, test, such as  the ADOS, a certain percentage of the time but below that score we really have no idea how what it says.

So the validity of the screening test is always relative to another, more accurate, test - usually the ADOS or ADI-R.  So the validity of the test isn't really relative to having autism but rather the chance of achieving a score on another test.  As a result, if you don't use the other test, or worse ignore it, then you have no real idea whats the score on the test means.  These may seem like an academic points but, as you will see below, they lead to potential problem.

To give an example, assume that we have a group of 100 children, 20 of whom score an 10 on the SCQ which is under the normal cutoff  We further test 5 of these children using the ADOS and find that 2 of them have autism.  Can we then say that 8 ( 2/ 5 * 20) children out of the 20 should have a score on the ADOS that puts them into the realm of autism?  No, we cannot because the relation of this SCQ score to the ADOS score has not been established.  If we were talking about a score above the cutoff then we would be able to make the relation.

Furthermore, if we gave the same group of children the ADOS but the, instead of giving 2 of them a label of autism, we decided to say that 4 of them did - even though that extra two did not score high enough on the ADOS to indicate autism - can we then say that 16 of the children have autism based on the SCQ scores?  Again the answer is no.

Going back to the 363 children, the stratification groups where based on prior autism diagnosis (yes, no) and range of score on the SCQ ( under 8, 8-14, 15-21, over 21 ) which gives us a total of 8 groups.  The normal cutoff of the SCQ is about 15, so I am not sure what is says when you have a score in the under 8 or 8-14 groups and you certainly can't (accurately) relate that back to other children who scored in those ranges.
 
Now lets consider the number of children that the study identified as having autism.  Three of the researchers involved in the study looked at all of the available information and arrived at what diagnosis, if any, that the children should have.   I think it is important to note that the researchers did not interview the children themselves but rather relied on the data that was collected by others.

Lets first take a step back, how do you know if a child has a form of autism?

Typically what is done in research is to rely on one of the "gold standard" tests - the ADOS or ADI-R.  Some of the time you will see that the children met DSM-IV criteria and usually that means that one of the researchers evaluated the child themselves and determined that the met the criteria for a form of autism.  The important part here is that either a standardized test is used OR a knowledgeable person examines the child and their history and comes to a conclusion. 

In this study, the DSM IV criteria were not used but rather a related set of criteria called the ICD-10 were used.  These criteria are similar to the DSM IV but label things differently.

Going back to the diagnosis in the subgroups, the researchers identified 53 children who met a strict (narrow) definition of autism.  This strict definition was that the ADOS and ADI-R both indicated that the child had autism.  These would be the most severe children, the ones who should be readily identifiable.  In this group 34 already had a diagnosis of autism and 19 did not.

The next group were a "consensus" group were all the three researchers agreed that it was likely that the children had autism.  This group had a total of 81 children, which included the 53 children from the strict group.  In this group there were 50 children who already had a diagnosis of autism.  For this consensus group it was not required that both of the standardized tests indicated autism and indeed, the ADOS indicated autism in only 64% of these children with a further 25% meeting the cutoff for a sub-threshold form of autism (think PDD-NOS).  The ADI-R showed better agreement with the group.

In the consensus group there were 7 who had no delay in language and no evidence of abnormal development before the age of 3.  I am not sure why these 7 would be labeled as having autism instead of a sub-threshold condition (see below).  The ICD-10 and the DSM IV both say that for a diagnosis of "autism" the symptoms must be present before the age of 3.  Under the DSM IV, these cases would likely be labeled as PDD-NOS and not autism.  I normally wouldn't think much of this, but this set makes up almost 10% of this set.  The researchers suggest that these 7 might have Asperger's but still label them as autism.

The consensus group (probably minus those 7) are likely to be what you would see included in other studies as the "autism" group since that is the group that the ADOS would have labeled as having autism.  This is also the group that the SCQ would have selected if the normal cutoff had been used.

The last group was the "other asd" group and was made up of 77 children, 18 of which had a prior diagnosis.  Six were in this group because of late onset (although how this 6 differ from the 7 above I don't know), 61 met the ICD-10 criteria for atypical autism (PDD-NOS on the DSM IV) because the severity wasn't there, 7 had an incomplete history (lack of early medical records), and 3 met criteria for other ICD-10 disorders.  I don't know why these last three were included in the "other ASD" group because, according to the data provided, they did't have autism.

That brings the total number of children with any possible (however questionable) diagnosable form of autism to 158, of which less than half (68) had an existing diagnosis.  Or to state that another way, 44 of the children who initially had a label of autism had the label revoked and 90 were added.

Now here comes the funny part.  From these numbers the researchers estimated the prevalence of autism in the entire population and came up with the following (all per 10,000) : 24.8 have "strict" autism, 38.9 have "consensus" autism, and 77.2 have some other form for a grand total of  116.1 for all forms of autism.

So, how did the researchers get from the 158 number to a figure that was over four times that amount (662)?  Simple, they used their groupings and, after making some adjustments, extrapolated back to the original population of special education children.  They then assumed that all of the autism cases were in that subset and arrived at what they thought were the totals for the whole population.

Unfortunately, the study does not detail the exact methods that they used to do this extrapolation nor does it give the breakdown of how many of each of the asd groups (narrow, consensus, other asd) fall into each stratification groups and without those figures it is difficult to duplicate their exact numbers.  If you remember, half of the stratification groups would not have a good path back to the population since it really isn't know how a score of below the cutoff would be related to a diagnosis of autism and we can't assume that there is no relation.  Furthermore, I don't know what an SCQ score would mean once you have ignored the ADOS or ADI-R score - which was done for a number of the children.

But here is the rub - no matter how they extrapolated from this subset of 255 back to the entire population, it is at best only a guess.  The underlying principle of doing this sort of analysis is that you have a known (and verified) path from your subset back to the original population.  You can't pick an subset using some non-arbitrary method and then expect to accurately relate it back to the whole.

To give you an example, assume I have a set of 100 men and women.  I select all of the people who have dark hair and find I have 10 men and 15 women.  Can I then say that, based on hair color, there are 40 (10 / (10+15) * 100)  men in the initial set of 100?  The answer is no - you would have to know what percentage of men had dark hair to start out with.
 
If the researchers they had selected a completely random set of individuals from the initial population of 1,035, they would have then been able to relate it back to the whole as a simple percent because there would have been no relation between having autism and being in the selected group.  Or if they had used the SCQ as a screening test (as it was designed) and then tested all of those who scored over the cut off they would have found all of the "likely" cases of autism - remember, counting actual cases is much more accurate than estimating.

As a result, we have to treat their extrapolation from the subset back to the original population as questionable.  When you have a questionable result, you look to other sources to see if other studies have arrived at the similar results.  Well, if you look at other research done on the same age group / birth year, you will see that the prevalence numbers from this study are significantly higher than those from other studies - somewhere from about 1.5 to 4 times higher than other estimates.

If you further consider other research that was done in a subset of the population by the same researchers, you will see that they estimated, just 2 (age) years before, that the prevalence of all cases of autism in this was half (57.9 per 10,000) of what they are suggesting now.

Remember the percentages of special ed statistics I listed above?  They also suggest that the proposed numbers are twice what they should be.

On the other hand, one of the goals of the researchers was to find cases of autism that had been missed by other sources and that goal was accomplished.  They identified 90 new cases that had been missed and, at the same time, they rejected the diagnosis of 46 children.  If you put those two numbers together, you are left with a number of cases that is 40% higher than the previously number.  If you extrapolated that back to the original 255 cases of autism, you would expect there to be a total of 360 cases of autism.  While that number is higher it certainly is much less than the proposed 662.

As a result, when you consider all of the above reasons, it is unlikely that the prevalence of autism in this population is  in 86.

So is Michelle Dawson's 1 in 86 adults overall accurate?  I don't think so.

Dr Wakefield found guilty, anyone surprised?

As I predicted a week ago, Britan's General Medical Council has found that Dr Wakefield acted "dishonestly and irresponsibly" and showed a "showed a callous disregard" for the suffering of children.  I think the GMC also suggested that he steals candy from babies and pushes elderly women down stairs in his spare time.

If you are interested you can read about it here or here or here or here or here, just to name a few places.

Now, is anyone surprised that the GMC came down on Dr Wakefield like a ton of bricks?

You shouldn't be.  I believe the outcome was preordained when the case started two and a half years ago.  The medical establishment is determined to have their pound of flesh from Dr. Wakefield and they are going to get it.

I haven't been able to get a copy of the ruling but most of the media reports that I have read have focused on the  blood draw at the birthday party without talking about the other charges.  There were a good number of other charges so it will be interesting to see what the final ruling has to say.  I expect it will say that he is guilty (or whatever the term is) of most of the other charges as well.

In somewhat sad news, Age of Autism is carrying a story about organizations filing complaints with the GMC alleging that participants in the proceedings against  Dr. Wakefield's hearing gave false statements and testimony.  I don't know if these allegations have any merit or not but at this point I have to say - give it a rest already.  You have lost this round and it is time to move on.  Even if everything that you say is true, you aren't going to win.  It is time to cut your loses and move on.

I know it is long past time for the autism community to move on.

Updated : If you are interested in the text of the ruling it is available from Age of Autism here.

Flame retardants and autism

As I have written about before, exposure to flame retardants could be problematic.  Now, a new review published in Physiology & Behavior talks about how exposure to flame retardants could be a risk factor for autism.

Mini-review: Polybrominated diphenyl ether (PBDE) flame retardants as potential autism risk factors.

Brominated flame retardants, including Polybrominated diphenyl ethers (PBDEs) have been used at increasing levels in home furnishings and electronics over the past 25 years. They have also become widespread environmental pollutants. High PBDE levels have been detected in food, household dust, and indoor air, with subsequent appearance in animal and human tissues. This minireview summarizes studies on the extent to which these compounds can act as potent thyroid hormone mimetics, and emerging studies on long-term neurological effects of acute administration of PBDEs during development. When these data are considered in combination with the extensive literature on stage-dependent effects of thyroid hormone on aspects of brain development that are also implicated in autistic brains, a hypothesis that PBDEs might also serve as autism risk factors emerges.

I have not read the study as of yet but I think the abstract makes it pretty clear what the authors are thinking.

Pregnancy + flu might be bad

Yesterday in Medical News Today there was an article that talked about a new study showing a possible relation between material infection and changes in brain development in her offspring.

Expectant Mom's Flu Exposure Stunts Baby's Brain Development

For expectant mothers, catching even a mild case of the flu could stunt brain development in their newborns, according to a new study conducted in rhesus macaques.

The study was a controlled experiment with 19 pregnant monkeys were 12 were exposed to a strain of the seasonal flu while the other 7 were not.  The results were notable -

Birth weight and gestation length were not affected, nor were infant neuromotor, behavioral, and endocrine responses. However, magnetic resonance imaging analyses revealed significant reductions in cortical gray matter in flu-exposed animals. Regional analyses indicated the largest gray matter reductions occurred bilaterally in cingulate and parietal areas; white matter was also reduced significantly in the parietal lobe.

In other words, the offspring of the monkey's that were exposed to the flu had a 4 - 7 percent decrease in the number of cells in the cerebral cortex and these differences may be permanent.  What is interesting is that it doesn't appear that the flu virus that caused the problems but rather the mother's response to it -

Maternal infections were mild and self-limiting. At birth, maternally derived influenza-specific immunoglobulin G was present in the neonate, but there was no evidence of direct viral exposure.

 The authors elaborate in the Medical News Today article, saying -

Coe and his colleagues ... speculate that the flu infection affects the developing fetus indirectly through the mother's inflammatory and immune response to the virus. In primates, including humans, the inflammatory response is more pronounced in the third trimester of pregnancy, the time when the animals in the new study were infected. 

This is not the first piece of research to show that a pregnant women's immune response can effect the developing fetus and I am sure it is not going to be the last.   The kicker is the authors suggestion based on the research -

The take-home message of the research, Coe argues, has compelling public health implications: Pregnant women or those who expect to conceive during flu season should be vaccinated. Flu vaccinations are widely regarded in the medical community and by the U.S. Centers for Disease Control (CDC) as safe for pregnant women.

 I know that this isn't necessarily bad advice. But, I have to point out, what exactly is it that vaccines do if not stimulate an immune response?  The reaction might not be as strong as it would be to the full flu but at the same time the current research doesn't deal with the strength of the immune response, just the fact that there is a response.

Sounds like more research is needed (what else is new).

The smear campaign against Brian Deer?

Have you ever had one of those moments when you are reading material from the Internet and you run across a statement that renders you speechless?  I am talking about the type of statement were you have to go back and read in a second, third, or possibly fourth time because you just have to be reading it wrong.  The type of statement that is so at odds with reality that you are sure that the author must have typed it wrong because there is no way that they meant to say that.

Well, I just ran across one of those statements in something written on Left Brain Right Brain by Sullivan concerning the Dr. Wakefield and Brian Deer.  It said, and I quote -

Mr. Deer faces a pretty major smear campaign from Dr. Wakefield’s supporters. I can only expect it to get worse after the decision is handed down—whatever that decision may be.

The first time I read that statement, I thought I had read it wrong and transposed the names in my head.

The second time I read that statement, I looked for the punchline in the surrounding text.

The third time I read that statement, I finally glanced up at the source of the post in Google Reader, saw it was written by Sullivan on LBRB and thought to myself, "nah, that still has to be a mistake.  No one could seriously think that".

So I went to the source to confirm that the text actually said that, and lo and behold, it did.  The ever present reality distortion field at LBRB has now become a full-fledged war on reality where white is black and black is white and Brian Deer is the victim.

This is the same Brian "problem with their brains" Deer who has seemingly made it his mission to ruin Dr. Wakefield's life and livelihood.  This is the same Brian Deer whose complaints initiated the GMC proceedings against Dr Wakefield.  This is the same Brian Deer who continually publishes attack articles against Dr. Wakefield and, when asked to provide backing for this claims, is unable to do so.  When the PCC tells him to take the story down, he thumbs his nose at them.

But, by some distortion of reality, Sullivan has come up with the idea that it is Brian Deer who is being attacked and smeared?  By any measure of reality, it is Brian Deer who has it out for Dr. Wakefield.  Even if every single thing that Mr. Deer has said is true (doubtful), he is clearly out to get Dr. Wakefield by any means necessary.

Sullivan, whatever it is that you are smoking or drinking or doing, you may want to stop.  You are starting to hallucinate.

Could Rett Syndrome be reversible?

Adrian Cousins,
Wellcome Images

Rett Syndrome is the only autism spectrum disorder that has a known genetic cause.  Normally when you think of a genetic disorder you get the impression of an irreversible condition that is with a person for their entire life.  But that might not be the case.

Newer research is showing that this might not be the case and that genetic disorders can sometimes be mitigated,  reversed, or even cured.  In the case of Rett Syndrome, a recent paper in Epigenetics is suggesting that it might be possible to compensation for the defects that lead to Rett Syndrome -

MeCP2 deficiency downregulates specific nuclear proteins that could be partially recovered by valproic acid in vitro.

MeCP2, the major causative factor of Rett syndrome and related phenotypes including autism, is a two-face nuclear modulator acting via transcriptional and chromatin remodeling mechanisms. This study investigated the expression of several nuclear proteins and their dependence on MeCP2 dose and presence of the Rett causative R306C mutation. To this end, we developed in vitro models representing MeCP2 deficiency induced by siRNAs, and cells expressing the R306C mutation. Using an extended antibody microarray validated by specific assays, revealed that MeCP2 dose was correlated with specific nuclear proteins profiles including the BRM/SNF2 component of SWI/SNF complex, PRMT1 methyl transferase and HDAC2. Furthermore, while exposing the MeCP2 knock-down system to therapeutic concentrations of valproic acid (VPA), a known HDACs inhibitor, we observed a partial restoration of MeCP2 expression levels. Exposure to VPA also increased the levels of BRM, as well as of BDNF, an important co-factor in MeCP2-mediated pathway. Our findings provide additional evidence of diverse mechanisms of MeCP2 function as transcriptional repressor and activator of specific genes. As it has been recently demonstrated that post-natal restoration of MeCP2 deficiency may reverse neurological defects in a mouse model of Rett syndrome, we suggest to study the restorative effect of HDAC inhibitors in MeCP2-deficient mouse model.

The thing that I find most interesting here is that valproic acid, the substance that might help restore normal functioning, is one of the substances that is known to increase the risk of autism during pregnancy.  Or in other words, if you are on valproic acid while you are pregnant, you stand a good chance of having a child with autism.  Yet the same substance might be able to help correct the problems that lead to Rett Syndrome, go figure.

Obviously it goes without saying that this research is very theoretical in nature and that there has been no case where Rett's was actually reversed in a person.  However, it is encouraging that there may be the possibility of one day being able to "cure" a genetic form of autism.  It gives me hope that someday other forms of autism can be cured.

Dr. Wakefield will be found guilty, but does it matter?

Picture via
Wikimedia Commons

The decision in the GMC hearing against Dr. Wakefield is expected to be issued later this month. I don't think it will matter what the facts of the case are or whether Dr. Wakefield actually did anything that would considered wrong.  I don't think that he intentionally tried to deceive people or engaged in some massive fraud.

Regardless, I fully expect that they will find him guilty (or whatever the proper term would be) of doing something wrong.

If you think about it, no person's actions are so far beyond reproach that a sufficiently meticulous examination of their actions won't turn up something that they could have done differently. I think this is going to be the case for Dr. Wakefield. There will be something that he did that could have been done better, something that he said that he might not have, or something that perhaps should have been done differently (Note to self : don't take blood samples and children's birthday parties).

The GMC has been noodling about the case for over two years now so they are sure to have found something that they can pin on him. So, I firmly believe that Dr. Wakefield will be found guilty of something.

I don't mean to sound cold or uncaring here - I am sure the issue is very important to the doctor, his family, and his supporters. I am sure that these people firmly believe that Dr. Wakefield has done absolutely nothing wrong.

But that isn't really true.

There is one thing that Dr. Wakefield did that is beyond doubt - he made the medical establishment think for a short while that vaccines, their golden child, might have something to do with autism. They have since manged to convince themselves, rightly or wrongly, that this isn't true.  But, for at least a little while, he had them scared. And for that, if no other reason, he is going to be found guilty.

The question that I find myself asking is how much this will matter to the field of autism. Fortunately, I don't think it is going to have a large impact.

The more controversial areas of Dr. Wakefield's research have already been written off but the more grounded idea of a link between gastrointestinal problems and autism lives on. The proof of this is the consensus report published this month in Pediatrics that (finally) acknowledges that there just might be something worth looking into. I know that Dr. Wakefield wasn't the first to propose such a relationship but the controversy sounding him has helped by making people more aware of the idea.

So, regardless of whether you think that Dr. Wakefield has done something wrong and regardless of whether you think there is any relation between the MMR and autism, I think we should be glad that Dr. Wakefield helped advance the idea that there is a relation between gastrointestinal problems and autism.

Consensus Report on Gastrointestinal Disorders in Autism, Part 3

Picking up where I left off last time ...

Gastrointestinal problems can lead to problematic behaviors such as sleep disturbances, vocal or motor behaviors, aggression, or self-injury in people with autism. It is sometimes difficult to relate these behaviors back to an underlying condition however it is important that care providers consider the possibility that these behaviors could be caused by gastrointestinal symptoms. Care providers need to become more aware of what the typical and atypical signs and symptoms are in people with autism.

Primary care providers also need to be alert to potential nutritional problems in patients with autism. Children with autism are known to be picky eaters and restricted diets might be nutritionally inadequate. However, even children who are not on a restricted diet have been shown to have nutritional problems.

Strangely, this is one of the areas where the panel does not call for additional research. My opinion is that this area is critical to understanding the role of gastrointestinal dysfunction in autism. If a child has a problem absorbing nutrients from their diet there are going to developmental consequences.

Moving along, we come to what is probably the most cited part of the report, the section on special diets. I think the exact wording of this section is important so I am going to include it -

"Anecdotal reports have suggested that there may be a subgroup of individuals with ASDs who respond to dietary intervention. Additional data are needed before pediatricians and other professionals can recommend specific dietary modifications."

"Available research data do not support the use of a casein-free diet, a gluten-free diet, or combined glutenfree, casein-free (GFCF) diet as a primary treatment for individuals with ASDs."

Notice what the panel is actually saying here - there are some anecdotal (parental) reports that suggest that diets work in subsets but there is not enough evidence to recommend using the diet as a primary treatment for autism. This is not a blanket statement that diets don't work but rather a qualified on that there is some reason to believe that a certain subset of people with autism could benefit from special diet. However, modern medicine will not (and should not) recommend a treatment based solely on anecdotal data and so the panel does not recommend it.

So, contrary to what is suggested by media reports, the problem isn't that research has looked at the question and found that diets don't work but rather that the the question has not been properly examined as of yet. The panel does give some suggestions on how a trial of a special diet should be conducted but does not call for additional research in this area. Go figure.

The report goes onto talk about how care providers should look compile a detailed history of their patients and look for physical signs of food allergies to identify potential associations between exposure and behavioral symptoms. A guide on how to evaluate and treat common gastrointestinal problems with children with autism published in the same issue of Pediatrics.

I want to call out one other statement that was made concerning gastrointestinal symptoms and autism because it runs directly counter to what you will often see quoted on the Internet -

"The patient's parents, teachers, or other caretakers are an important source of information, because they are in a position to observe an association between exposure and the person's response"

Got that?  Parents DO have some idea what they are talking about.

There are a few points in the report on how there is a possible link between immune dysfunction and autism but that this is (yet another) area that needs further study. But that is a topic for another time.

The report concludes with how it is likely that there is more than one type of autism. Given the differences in people with autism and the conflicting research findings "it is likely, therefore, that different pathogenic mechanisms underlie ASDs in individuals who have received this diagnosis".

So there you have it, in three rather long parts, what this report says rather than the simplistic version presented in the media. If you have made it here and read all three parts, I think you deserve a gold star.

Consensus Report on Gastrointestinal Disorders in Autism, Part 2

As promised (or threatened) last time, I am going to attempt to cover what was said in the consensus report was published last week in Pediatrics. The report contained 23 statements that covered a wide range of topics relating to gastrointestinal disorders and autism.

I am going to give a general summary of what the report said with some minimal comments. If you have access to the report itself, I highly recommend that you read it. So, without further ado, the report says ...

People with autism who have GI symptoms deserve the same treatment for their symptoms as other patients would receive. Gastrointestinal conditions that are common in "typical" individuals are just as common in people with autism. However, the problem is that people with autism may have a hard time communicating their symptoms effectively and there is a lack of guidelines for how to evaluate someone with an impaired ability to communicate. Further compounding the problem is the fact that gastrointestinal disorders in people with autism can cause or aggravate other seemingly unrelated problems, problems such as sleep disturbances, irritability, vocal or motor tics, tantrums, aggression, and self injurious behavior.

While these may seem like trivial statements, I believe that they are squarely aimed at children's doctors who have grown accustomed to automatically dismissing parental reports of GI symptoms. The statements are an admonishment to remember that children with autism can have GI problems too, and that these symptoms need to be taken seriously. Ahem, moving along...

It is not well understood how common gastrointestinal abnormalities are in autism. There are studies that show that these abnormalities are very common in people with autism while others say that these abnormalities are no more common than in the general population. Unfortunately, most of the research that has been done in this area is flawed and that makes it hard to draw any reliable conclusions.

Even still, based on the evidence that is available today, the preponderance of the data suggest that gastrointestinal symptoms are more common in people with autism than in "typical" people. More research is needed to properly address this question.

But while it is possible that gastrointestinal symptoms are more common in autism, there is no evidence establishing a gastrointestinal disturbance specific to people with autism. Specifically, this point refers to Wakefield's "autistic entercolitis" - there simply is not enough direct evidence to support the idea that it exists.

This should not come as a surprise to anyone. I would suggest that the reason for this has more to do with politics than with science. Given the stigma attached to Wakefield's work, I can understand why other scientists are reluctant to take up this question. Which is really tragic, because the main thrust of Wakefield's work was that there is a gastrointestinal disturbance that contributes to autism, not that the MMR vaccine causes autism. Continuing with the paper ...

The panel found that there is limited evidence of abnormal gastrointestinal permeability (leaky gut) in people with autism. While some studies have found that this can be an issue in a subset of children, the available evidence is not sufficient to confirm that a abnormal permeability is an issue or that it contributes to autism. This is yet another area that needs more research.

Just to interject, the idea of a "leaky gut" goes to the heart of how some special diets, such as the gluten-free casein-free diet, are thought to work. It also goes to the heart of why the existing research on dietary interventions in autism are badly flawed. The idea is that some, but not all, people with autism have GI issues and a subset of this group would benefit from dietary treatments. Yet the research that has been done has not attempted to locate the subset that would benefit from the diet and has just lumped everyone with autism into one big bucket. And as most people know, people with autism are nothing if not diverse.

So far I have covered the controversial parts of the report, next time I will continue with some of the more common sense things the report had to say.

Consensus Report on Gastrointestinal Disorders in Autism

Last week a consensus report was published in Pediatrics that dealt with the subject of gastrointestinal disorders in individuals with autism. This report was the product of a multidisciplinary panel that met in May of last year. After reading it, I can honestly say that I think this is report is some of the best news that has come down the pike recently concerning GI issues and autism is a long time.

The panel basically said that there might well be something to the idea that GI problems are more common in individuals with autism and that, when present, these problems can exacerbate the symptoms of autism. They also pointed out (numerous times) that children with autism would likely have a hard time communicating that they are experiencing pain and that, left untreated, could lead to problem behaviors. Of course, they also strongly emphasized that no association has been proven, that the available evidence is badly lacking, and that much more research is needed.

Of course, if you read the news and blog coverage of this report, that isn't the story you will see. Mostly I found stories like this one Evidence lacking for autism diets, panel says that focus on the "no evidence for special diets" line or the ones that say that there is "no evidence that digestive problems are more common in children with autism". The first statement is true and I will get to that is a minute, but the second is just plain wrong.

 The paper clearly states that the limited (weak) evidence does suggest that GI disorders are more common in autism, saying "Despite the limitations in type and quality of available evidence, the preponderance of data were consistent with the likelihood of a high prevalence of gastrointestinal symptoms and disorders associated with ASDs." The authors hedge this statement by emphasizing that the available data is flawed and more research is needed but this statement is clearly a far cry from "no evidence".

As for the common statement about no evidence that a special diet can help treat autism, well, that is true, but not for the reasons that most people would assume. The reason that evidence is lacking is not because the question has been examined an no relationship has been found, the reason is that the question has not been examined. There have been only one or two studied that directly looked at the question and none that done properly. So perhaps the better way of phrasing the lack of evidence would have been to talk about the fact that it is an unanswered question, not a lack of evidence.

Regardless of what the media has to say about this report, I think this is an important report that possibly marks a turning point in mainstream attitudes about an association between autism and gastrointestinal disorders. In my next post, I am going to attempt to give a summary of what the report actually says.

Kirkman Labs Recall - January 2010

I saw a notice about this last night and I wanted to pass it along as I have not seen very many places online yet.  I did talk to Kirkman Lab's consumer service department who confirmed the problem.  If you use any of the Kirkman Labs supplements listed below, you may want to stop using the product and contact either Kirkman Labs or the store where you purchased the product for more information.

From what I understand, the following products could have problems -

1. Zinc Liquid
2. Super Nu-Thera w/o A and D 
3. DMAE 50 mg. Chewable
4. Super Nu-Thera Powder Orange
5. B Complex Powder Pro Support
6. TMG w/Folinic and B-12 Powder
7. Chewable Vitamin C Tablets

The following is a copy of the notice (it would be nice if Kirkman Labs posted a notice on their web site, hint, hint) -

Dec 30, 2009

Dear Kirkman Distributor,

It has come to Kirkman's attention that a raw material supplier has been supplying Kirkman with substandard quality material that is higher in antimony content than what would be considered acceptable to the special needs community. Raw material supplier are actually not required to test for antimony levels routinely, so this problem did not come to our attention until a physician using Kirkman products brought the issue to our attention. We immediately had our laboratory research the issue which they quickly isolated and linked it to a specific raw material.

We have stopped using this material and have located and purchased a quality replacement which we will begin using immediately.


UPDATE : Kirkman has posted a notice about the recall on their website.