Myths and Legends of Autism: Part 3
September 7th, 2007
Diagnostic Myths
There are almost as many myths about the diagnosis of autism as there are people with that diagnosis. But, I suppose that the first myth we need to address is the myth that a diagnosis of autism actually means anything.
The Myth of the Meaningful Diagnosis:
In medicine, a diagnosis is supposed to provide – in an ideal world – three things:
[1] Prognosis: a meaningful diagnosis will allow the practitioner and patient to anticipate what will happen in the future – how long the disease will persist, whether it will get worse, and the likelihood of recovery.
[2] Treatment: a meaningful diagnosis will indicate treatments that are helpful to cure or moderate the disease. If there are no known treatments, a valid diagnosis will indicate this, as well.
[3] Pathogenesis: a meaningful diagnosis will indicate the physiological abnormalities that cause the disease to occur (e.g. bacterial infection, enzyme dysfunction, toxicity, etc.).
Now, there are lots of meaningful diagnoses that do not meet all threee of these criteria. We don’t know, for example, what causes pancreatic cancer, but we do know what the prognosis (grim) and the treatments (few and not very effective) are.
But what about autism?
Prognosis: A diagnosis of autism in early childhood gives no indication of what the child’s eventual functional abilities will be. Even the severity at diagnosis is no predictor. This has become even more of a problem as the diagnosis of autism has become more “inclusive”. If you extend the category of “autism” to include all those diagnosed by educational or social service agencies, the diagnosis loses all prognostic ability.
Treatment: The most scientific answer to the question of treatment is that none of the currently touted treatments for autism has been shown to be consistently effective.
None.
Even the most rabid of “biomedical” apologists will have to admit (although never in public) that no one treatment or group of treatments has been shown to work for even half of the autistic children treated. And this problem is not just limited to “alternative” treatments – none of the treatments recommended for autism have been shown to work for over half of the children treated.
Even cancer treatments have a better record, if you remember that, in many cases, their expected effect is to slow the growth of the tumor rather than to affect a “cure”.
Cause: Despite years of research, there is no consensus about the location of the pathology in autism (other than to say that autism affects the brain). Mirror neurons, microcolumns, corpus callosum, amygdala, etc. have all been proposed, but have not been consistently found to be the site of the dysfunction. Even the “fringe element” in autism pseudoscience is not consistent – except in a superficial way – about the “site of the lesion” in autism.
The non-scientific element in autism “research” has proposed a number of causes, ranging from vaccines to metals, all without adequately explaining how these could explain the wide range of autistic phenotypes or how it is that most children exposed to the same substances do not develop autism. Their usual rejoinder is to blame the variation on “genetic differences”, without bothering to explain what those might be.
Having been backed into a corner by the very research they claimed to desire, many of the so-called autism advocacy groups have resorted to extreme vagueness, blaming “environmental factors” or “vaccine components”. The bottom line is that there is no consensus – not even a general agreement – as to the cause of autism or even the area of the brain that is affected.
Thus, it appears that a diagnosis of “autism” provides no medically meaningful information.
The Legend of the Autism Epidemic:
The Autism Epidemic, so the legend goes, started in the mid-1980’s and has continued, unabated, to the present day. There are many variations on the legend, mostly revolving around specific causes. Vaccines, mercury, cell phones, television, Sesame Street and Britney Spears have all been named as the cause of the “epidemic” in one or more versions of the legend.
Like many modern legends, the purpose of the Legend of the Autism Epidemic is to make a complex situation simpler and more easily understood. Unfortunately, in the real world (and especially in medicine and biology), “simpler” is often just a euphemism for wrong.
When so-called autism advocacy groups developed their “autism epidemic” legends, they looked at autism numbers from – initially – the California Department of Developmental Services (CA-DDS), which showed a rise in autism intake numbers starting somewhere around 1985 (depending on how you interpret the curve). They then came up with a variety of things that had changed at about the same time, coming up with – strangely enough – thimerosal (thiomersal), a mercury-containing preservative present in some vaccines since the 1930’s, and the measles-mumps-rubella (MMR) vaccine, which had been introduced in the US in the 1970’s and in the UK in the late 1980’s.
The thimerosal “connection” has failed to keep up with recent developments, with the number of CA-DDS clients with a diagnosis of “autism” continuing to rise despite thimerosal being eliminated (if you believe “the government”) or greatly reduced (if you believe the conspiracy theorists) in childhood vaccines.
The MMR “connection” was always a bit “iffy” in the US, since MMR uptake was around 95% in the mid-1980’s and continued at that level (or lower) to the present date. At any rate, it lacks any supporting data now that the small bit of data that did seem to support it has been shown to be spurious.
Regardless of the “cause” attributed to the “epidemic”, the legend remains. Doubtless, there will be other putative causes assigned later. But what about the reality of the epidemic?
One of the changes that occurred at about the same time as the start of the “epidemic” were changes in the diagnosis of autism. The Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition (DSM-III) was published in 1980. This was a revolutionary change in the DSM (which was first published in 1952) and included – for the first time - autism. Strangely enough, this change is rarely mentioned when the “autism epidemic” is discussed.
In 1992, the Individuals with Disabilities Education Act (IDEA) was changed to include autism as an eligibility category. Prior to this, it must be assumed that children with autism either did not exist or were listed under a different eligibility category. It is interesting to note that the number of children with an IDEA eligibility of “mental retardation” has declined in lockstep with the increase in children who have the “autism” eligibility. Strangely enough, this fact is rarely (or never) mentioned in the context of the “autism epidemic”.
It would also seem that, while the IDEA and CA-DDS numbers support an increase in autism over the past 15 years (past 20+ for the CA-DDS), there have been significant changes in the diagnosis of autism in that time.
In 1987, the DSM-IIIR (revised) was published, with changes in the criteria for autism diagnosis. In 1994, the DMS-IV (4th Edition) was published, with even more changes. The DSM-IVTR (text revision) was published in 2000, with extra information on the various diagnoses.
The awareness of autism among doctors, educators and parents has skyrocketed from 1985 to today. As has happened with ADD/ADHD, the diagnosis is often made in error, by people who are not qualified to do so (even if the are legally allowed to do so) and who do not use the consensus medical criteria (more on that later).
Also occurring in the same time, the California state legislature – and state legislatures from Alabama to Wyoming – were passing laws, codes and rules pertaining to the evaluation of autism in school-age (and pre-school) children. These “educational” diagnoses of autism have potentially ballooned the number of children carrying the “label” (but not the diagnosis) of “autism”.
And all of this was happening during the “autism epidemic”.
So, what does all of this mean to the Legend of the Autism Epidemic?
[1] Children diagnosed with autism (medical diagnosis – not “educational” diagnosis) in 1985 cannot be compared with children diagnosed with autism in 2007. The criteria – even for medical practitioners - have changed dramatically. A study from the MIND Institute (Byrd, 2000) showed the dramatic differences between people with autism born in the years 1983-1985 and those born in the years 1993-1995.
[2] Education and social services criteria for “autism” are even looser than the medical criteria, and have changed more over the years. Since almost all of the “epidemic” data comes from either education (usually IDEA reports) or social service (usually CA-DDS) sources, it is clear that no meaningful comparison can be made, a point that the CA-DDS itself makes.
[3] Increasing awareness has led to a number of practitioners – some of whom have little or no experience or training in the recognition of autism – to “diagnose” autism in children who do not meet the criteria. This is compounded by the number of children who have received “educational” diagnoses of autism, often using criteria that are appallingly broad and vague.
The Myth of Autism as a Single Disorder:
Almost anyone who has spent a few hours with a group of children carrying the “autism” label will note the wide range of abilities and disabilities among them. Added to that simple observation is the fact that a child diagnosed with “autism” can have any of a number of associated conditions (e.g. GI disturbance, coordination difficulty, sensory sensitivities, etc.) or none at all. Further, a child diagnosed with “autism” may eventually become an independent adult, may need to be admitted to an institution or any outcome between the two.
This has led some of the more astute scientists and clinicians to suggest that “autism” is not a single disorder.
When viewed in that light, many of the puzzles of autism begin to make sense. If autism is a symptom (more properly, it would be a sign) that there has been a disturbance in a neural pathway (or a set of neural pathways), then you would expect the following:
[1] Any disorder that disrupts the neural pathway(s) could result in the sign known as autism. Thus, autism could have a number of different and even disparate causes (much as the sign fever does).
[2] The disorder that disrupts the neural pathway(s) and causes autism could disrupt other physiological functions, causing other signs and symptoms – much as fever can be accompanied by a rash, nausea, coughing, or any combination (or none) of the three.
[3] Each separate disorder will have its own prognosis, cause and treatments. Thus, giving a person with disorder A the treatment for disorder B will generally be ineffective. This has the effect of masking treatments that are truly effective for one of the disorders causing autism in the following way:
If disorder A causes 10% of the autism in a particular population and treatment X gives detectable improvement in 80% of patients with disorder A, treating 100 people with X gives the following results:
People with A: 10
People with A who improve: 8
People with disorders other than A (and who presumably don’t improve): 90
Overall number who improve: 8
Apparent effectiveness: 8%
So, even a treatment that is 80% effective (probably an unrealistically high rate for autism) would appear no better than placebo if it is effective in only 10% of people with autism.
[4] For genetic disorders causing autism, each will have its own specific location on the genome. This is exactly what multiple studies of familial autism have found and is also borne out by the more recent genetic studies looking at copy number variations in autism.
It would seem, then, that viewing autism as a symptom or sign is a better “fit” with the data than any of the current “single cause” hypotheses.
Next: Part 4 - Therapeutic Myths and Misadverntures
Prometheus
Filed under: Autism Science, Autism Treatments, Critical Thinking
September 7th, 2007 at 5:32 pm
A minor correction:
The MMR vaccine is a live vaccine, and just like the chicken pox and polio vaccines, has never contained thimerosal.
September 7th, 2007 at 5:57 pm
That’s a great overview of the inadequacy of the medical model of autism. (I realize you might have not intended it to be that.)
September 7th, 2007 at 6:04 pm
Joseph,
That, in a nutshell, was exactly what I had in mind.
Autism is, in my humble opinion, sometimes a symptom (sign) and sometimes just a variation in “mental wiring”. The diagnosis long ago lost any utility it may once have had. It seems to now serve primarily as a “label” to organize IDEA reports and parent “support” and “advocacy” groups.
Prometheus
September 7th, 2007 at 6:11 pm
HCN,
I’ve inserted a paragraph break to make it clearer that the thiomersal (thimerosal) and MMR issues are completely unrelated (except to those people who don’t know that the MMR never had thiomersal).
To expand on that thought:
Thimerosal (thiomersal) is a preservative that kills bacteria, fungi and protozoa - it also renders viruses inactive (you can’t kill something that isn’t - strictly speaking - alive). Adding it to a live virus vaccine (like the MMR, chickenpox and oral polio vaccines) would be - at best - counterproductive.
Thanks for pointing out where I was unclear, HCN.
Prometheus
September 7th, 2007 at 9:36 pm
“That’s a great overview of the inadequacy of the medical model of autism.”
In essence, I think it shows that we have to move away from that model and base ourselves in a developmental and educational paradigm to understand and deal with the notion of autism better.
September 7th, 2007 at 10:52 pm
It’s also a great overview of what’s wrong with mass-market pharmaceuticals. Because they’re tested on “average” people, rather than on people identified as having genes similar to yours, there’s no way of knowing whether a drug will help you, kill you, or do nothing.
The same is true of herbal products and other alternative stuff, except that often they haven’t been tested on anyone.
I generally avoid everything but an occasional aspirin.
September 7th, 2007 at 10:55 pm
Your over simplification of the autism epidemic is just another euphemism.
“It is interesting to note that the number of children with an IDEA eligibility of “mental retardation” has declined in lockstep with the increase in children who have the “autism” eligibility. Strangely enough, this fact is rarely (or never) mentioned in the context of the “autism epidemic”.”
It has not been a perfect correlation between the decrease in MR as you imply. Many have stated that the professionals that previously inaccurately diagnosed those with MR that would currently be diagnosed with ASD should be sued for the quacks that they are.
Your examples [1], [2], and [3] are proof that there is an epidemic occurring. The definition of “autism” is both chronologically and culturally dependent. The definition that the current culture has chosen for “autism” has vastly expanded the number of individuals that are considered “autistic”. It is an artificial, man made epidemic, but an epidemic none the less. To those that say that today’s numbers are not of “epidemic” proportions, please provide a globally accepted criteria of who is “autistic” that would have the same rate 100, 200, or 500 years ago as it does today. Today’s criteria are not globally accepted and are the third or fourth attempt made by the publishers of the DSM and international criteria have varied as much or more then the DSM.
September 7th, 2007 at 10:59 pm
“It would seem, then, that viewing autism as a symptom or sign is a better “fit” with the data than any of the current “single cause” hypotheses.”
Those aren’t the only two possibilties (”single cause” vs “symptom or sign”). No one can seriously support the “single cause” hypothesis, because there are many known causes. But if the “sign and symptom” hypothesis were accurate, then consistent findings at the level of cognitive and neural mechanisms would be non-existent in autism (and I’d have a lot more spare time).
“Further, a child diagnosed with “autism” may eventually become an independent adult, may need to be admitted to an institution or any outcome between the two.”
No autistic needs to be in an institution. Many of us have experienced both of your supposedly extreme and mutually exclusive outcomes, often in close succession. That is, we have been “independent adults” (which means, we’re dependent on the services “normal” people are dependent on and therefore are not seen as dependent). And at other times it has been decided that we “need to be admitted to an institution.”
September 7th, 2007 at 11:31 pm
Chuck,
If you go to the IDEA stats, you’ll find that by adding the mental retardation numbers to the autism numbers, you get a line that exactly parallels the total number of children with IDEA eligibility. It is “perfect correlation”.
You then go on to provide one of the most tortured definitions of “epidemic” that I have ever heard. I think that we are both aware that the use of “epidemic” in this context is meant to imply that the real number of autistic children is increasing. Really increasing, not just “inflation”.
Chuck, any definition of autism would do to compare autism prevalence today to autism in the past - all that is lacking is a time machine to allow us to go back and evaluate those people in the past using our current criteria.
Or, we could look to see how many people with the label of “autism” today would meet the DSM III criteria. The answer to that question is “not many”. This is an important point.
If we change the cutoff point for high cholesterol or high blood pressure to lower numbers, does that mean that we suddenly have an “epidemic” of high cholesterol or hypertension?
If a large number of people have a disorder, like myopia (nearsightedness), are we in the midst of an “epidemic”? Even if the number is stable?
Either we have an epidemic (i.e. increasing numbers of children with autism) or we have a diagnostic shift from “mental retardation” to “autism”. The data support the latter hypothesis.
Your argument seems to be that even if there is no real increase in the numbers of children with developmental disorders, the increase in autism numbers constitute an “epidemic”. Even if it’s just an artifact of shifting diagnostic criteria?
Your final argument - that there are no “globally accepted” diagnostic criteria - pretty much makes my argument. If we can’t even define what autism is, there is no point to talk about an “epidemic”.
Prometheus
September 7th, 2007 at 11:35 pm
Prometheus - Another excellent summary, thanks for that.
Chuck - Your implication that this summary oversimplifies the ‘epidemic’ argument is completely off base. What you just read is a clear, concise, logically presented argument that what is being perceived to be an epidemic is actually an understandable inflation of reporting numbers accompanied by a change in diagnostic criteria. Any argument that an epidemic exists is predicated upon the fact that we are talking about the same condition at the beginning point and the current point in any measurement of prevalence. The ’sameness’ is clearly not evident. What you are stating, therefore, is that it is your opinion that there is an epidemic. You are entitled to your opinion. The known facts would disagree with you.
September 8th, 2007 at 1:19 am
About the IDEA numbers, I think it’s more complicated than that. You have to consider autism, MR, developmental delay, speech & language impairments and specific learning disability at least. If you add them all together, there’s no caseload increase relative to population growth, particularly if you choose a cohort that would not be affected much by earlier age of diagnosis. (I know, Shattuck did something different to that, but it didn’t work very well in a few states).
An epidemic is generally understood to mean that there’s a condition that has started to affect a group of people. Cultural relabeling does not count.
The “autism epidemic” arguments generally come down to confusing being diagnosed with autism with being autistic. While the former generally implies the latter, the latter often does not imply the former. Autistic adults, for example, seem to be more often diagnosed with schizophrenia than autism.
Michelle’s points are interesting. But consistent cognitive findings could be explained by heterogenous causes as well, just as, say, macrocephaly could have multiple causes (e.g. Sotos syndrome or a PTEN mutation). Also, cognitive findings are on autistics “as a group”. In Michelle’s intelligence paper, for example, there are clusters of performance all over the Weschler vs. RPM graph. There could be subgroups albeit ones that are hard to identify consistently.
September 8th, 2007 at 9:47 am
Steve,
“Your implication that this summary oversimplifies the ‘epidemic’ argument is completely off base. “
What base is it off of? The starting point being where the DSM III gave diagnosis criteria, the ending point being toady’s version of the DSM. Between those two points the number have increased dramatically in areas that use the DSM. Those areas that use the DSM are in an epidemic situation, those that do not use a variation, are not.
My opinion, probably less then 20% of children diagnosed with ASD would have been diagnosed with MR. Of the 38 children attending my child’s school, all are ASD, none are diagnosed MR, and less then half satisfy DSM-III criteria per the school’s consulting psychiatrist.
The fact that the diagnosis criteria is subjectively defined and subjectively diagnosed does absolutely everyone currently diagnosed a disservice. Having a constantly moving line in the sand that professionals can choose to put people behind is not science so there are no “facts” to substantiate, or not substantiate, an epidemic. It is your opinion there is no epidemic. Our opinions differ. If the DSM-V criterion cuts the ASD population in half, or is eliminated like homosexuality was, does that mean that they are cured? I’m sure the professionals will spin it that way. What will you do for your child does not meet the diagnosis criteria of the next DSM? There are no guarantees that the line in the sand has to be more inclusive every time.
September 8th, 2007 at 3:18 pm
According to The Webster’s dictionary on my desk, the definition that does not relate to disease is: “an out-break, or product of sudden rapid spread, growth, or development: a natural population suddenly and greatly enlarged” Given this definition along with state statistics showing three or four digit percentage increases depending on the region and time frames for the state, I have had no arguments from local, state, or federal politicians or agencies as to the accuracy of my facts or the terminology I use to describe them.
In the circles that I associate in at the state level or on the Hill, I have yet to interact with any activist that says there is not an epidemic.
September 10th, 2007 at 2:12 pm
Chuck,
You misunderstand my position. I’m not saying that there isn’t an “epidemic” - I’m saying that there is no convincing data saying there is.
If data comes up supporting an autism epidemic, then I am completely willing to examine it and change my mind.
As things stand right now, the ruling on the “autism epidemic” is “Not Proven”.
Shifts in diagnosis do not neccessarily do a “disservice” to autistic people. As long as they are receiving the social services and medical care they need, it matters little what their “label” might be. However, it might be better for them to have a “label” that doesn’t mislead doctors, therapists and educators - whatever that might be.
My objection to the “epidemic” is the political exploitation of it. Various “pressure groups” attribute the “epidemic” to their own pet cause (mercury, vaccines, television, Thomas the Tank Engine, etc.) without ever bothering to show that there really is an epidemic. In fact, they vigorously attack anyone who points out the lack of data supporting an epidemic as being “epidemic deniers”.
As an aside, the fact that politicians and “activists” believe that there is an “autism epidemic” does not qualify as “data”.
At some point, all the political hay will have been made on the “autism epidemic” and the politicians and pressure groups will toss it in the dustbin. When that happens, it will be exceedingly difficult to get any attention (or funding) for autism itself.
Prometheus
September 10th, 2007 at 5:08 pm
“At some point, all the political hay will have been made on the “autism epidemic” and the politicians and pressure groups will toss it in the dustbin. When that happens, it will be exceedingly difficult to get any attention (or funding) for autism itself. ”
When do you foresee this happening? I don’t see this senerio happening until the 22nd century, maybe, unless the next DSM changes directions again.
September 10th, 2007 at 6:12 pm
Chuck,
I think that you have seriously overestimated the attention span of the average politico, not to mention the general (i.e. not affected by autism) public.
At some point (and the “…one in 58…” number was pretty close to it), the politicians are going to realize that this is a “cause” that is likely to backfire on them. Once the claimed prevalence of autism reaches the point where the “average guy/gal on the street” starts thinking “Huh? That doesn’t make sense.”, you will see politicians run away so fast you’ll think they were never there.
Eventually, one of two things are going to happen - either the autism prevalence numbers will level off or they won’t.
If they do level off, people will probably claim that whatever stopped at that time (mercury in vaccines - oops, too late for that one - Chinese toy imports, Britney Spears…) was “the cause” and interest will fade away. That is, unless we can convince people that the “epidemic” numbers are not reliable, in which case we can keep on looking for a/the cause.
If they don’t level off, it won’t be too long before every third or fourth boy in school has the “autism” label (as it currently seems with “ADD/ADHD”) and people will dismiss the label as meaningless.
What keeps public (and political) interest in autism going is the fact that autism is mysterious, uncommon, but not rare and catastrophic. As the “diagnosis” widens, the average severity lessens and the rarity declines. When it reaches the point that every “typical” kid has “autistic” classmates, friends and teammates, it will no longer hold the public interest.
Maybe that would be a good thing.
Prometheus
September 10th, 2007 at 7:18 pm
For Joseph, my comment included the established fact that autism can have many causes. But this does not mean there must be many “autisms” or (as Prometheus judges us) many “disorders.”
My comment was that the two views of autism Prometheus provides are not the only ones, and also that the sign/symptom view as put forward by Prometheus–with the requirement of many “autisms,” or as Prometheus judges us, many “disorders”–is not consistent with existing evidence.
Dividing autistics into subgroups for specific purposes (e.g., Caron et al., 2006, where we divided non-autistics into subgroups also), or noticing that not all autistics have absolute pitch (or whatever specific ability or savant abilities in general), also does not necessarily mean that there are many “autisms” or (as Prometheus judges us) many “disorders.”
September 10th, 2007 at 8:47 pm
“When do you foresee this happening? I don’t see this senerio happening until the 22nd century, maybe, unless the next DSM changes directions again.”
Did it a couple of years or so ago.
Likely to do it again well before the 22nd century starts.
September 11th, 2007 at 1:45 am
“So, even a treatment that is 80% effective (probably an unrealistically high rate for autism) would appear no better than placebo if it is effective in only 10% of people with autism.”
Kind of like… chelation maybe?
September 11th, 2007 at 12:30 pm
Ms. Dawson,
You seem to feel that my use of the word “disorder” in association with “autism” is somehow a judgement. It is, in my mind, no more a “judgement” of the person so affected than is calling hypertension, heart disease, seizures or depression a “disorder”.
If you have a better term - one that is less “judgmental” - please let me know. I am trying to use as neutral a term as I can, consistent with brevity. It is not my intention to “judge” the people with autism.
As to your findings of “…consistent findings at the level of cognitive and neural mechanisms…”, I assume that you have found these to be consistent in people with Tuberous Sclerosis, Fragile X, Rett Syndrome and Purine Autism - am I correct? Can the tests you use differentiate between these [insert correct term here]?
Grace,
If chelation is ever shown to be effective in any percentage of people with autism, that would be news worthy of a front page (above the fold) headline.
I have been waiting so long for all of the chelationists to publish - even in the web - their results. Not testimonials, but actual results - you know, number of patients treated, standardized test results before and after treatment, number of patients improved vs not improved, etc. That wouldn’t be an actual study - to do that, you’d have to include a group that didn’t get the treatment - but it would be a start.
And simply having somebody get up at a DAN! conference and say, “I’ve treated hundred of autistic kids with chelation and 70% have gotten better.” is worthless. Would you believe it if somebody from “Big Pharma” got up and said “Over 70% of autistic kids treated with X have gotten better.”? I don’t think you would.
Show me the data. Until then, chelation is just another “Not Proven”.
Prometheus.
September 11th, 2007 at 3:45 pm
Hi Prometheus,
Like autism, Down syndrome is a neurodevelopmental disability. The Canadian Down Syndrome Society, in their definition of Down syndrome, writes:
“Down syndrome is not a disease, disorder, defect or medical condition. It is inappropriate and offensive to refer to people with Down syndrome as “afflicted with” or “suffering from” it. Down syndrome itself does not require either treatment or prevention.”
The same is true of autism.
Simon Baron-Cohen’s group uses the term “Autistic Spectrum Conditions,” having argued in several places (e.g., Baron-Cohen, 2005) that “disorder” is inaccurate. I’ll use “disorder” when I’m required to directly quote a DSM-IV category (e.g., “Autistic Disorder,” “Pervasive Developmental Disorder”), but otherwise I prefer to be accurate.
Also, you are free to equate autism with heart disease, mental illness, etc., but these approaches to autism have been hard on autistics (e.g., autism as “childhood schizophrenia,” autistics as “psychotics,” autism as any dreaded and/or fatal disease, etc.) and notably unproductive, no matter how popular they have been and continue to be. See also Gernsbacher et al. (2006) and Mottron et al. (in press), for some of the consequences of presuming that autistics are defective, disordered, disturbed, etc., non-autistics.
For how to differentiate autism from fragile X, see Armando Bertone’s work (for one example). For Rett’s, see Tony Charman’s Rett’s papers (see also Mottron et al., 2007), for starters. Etc. Even with CDD (which is extremely rare, and there is very little science), it’s been noted that the cognitive profile differs from autism. But I’m not sure what your point is (I’m quite sure I’m missing it), maybe you can elaborate?
September 11th, 2007 at 4:08 pm
Hi Prometheus -
“Education and social services criteria for “autism” are even looser than the medical criteria, and have changed more over the years. Since almost all of the “epidemic” data comes from either education (usually IDEA reports) or social service (usually CA-DDS) sources, it is clear that no meaningful comparison can be made, a point that the CA-DDS itself makes.”
I literally laughed out loud when I read this. While what you say may be technically true, in my case getting autism written on my son’s IEP continues to be very difficult, indeed, as of yet impossible. Our guess is that this is an attempt to keep from having to provide additional services, but whatever the reason, despite having ‘passed’ the ADOS more than once times with very high scores, my son’s IEP continues to have a DD tag applied. Other families we know report similar problems.
This, of course, may not be the case in every district, but I think the possibility should be kept in mind that using educational reporting mechanisms may lead to the opposite effect, an undercounting of autism.
- pD
September 11th, 2007 at 4:25 pm
pD,
I have heard from parents in my state (which has very loose “criteria” for the educational assessment of “autism”) that there are some districts that are very resistant to giving a child an “autism” eligibility. Conversely, our school district (same state) practically pushes the “autism” eligibility. There seems to be no consistency, even within the same state.
My point remains that the data sources currently in use by most (if not all) of the “autism advocats” promoting the idea of an “autism epidemic” are not reliable. Therefore, no meaningful conclusion can be drawn from their “data”.
These “data” sources may undercount, overcount or even count sideways. The bottom line is that you cannot compare the numbers from year to year, state to state, city to city. It’s like comparing apples and orangutans.
As for your particular situation, I know that our state does not allow a “developmental delay” eligibility to be applied to children over 6 years old. Perhaps the same is true where you live?
Prometheus
September 12th, 2007 at 2:30 am
Sorry I was not more clear. Just wondering how you can say this,
“So, even a treatment that is 80% effective (probably an unrealistically high rate for autism) would appear no better than placebo if it is effective in only 10% of people with autism.”
and then demand that chelation be proven more effective than placebo(esp. after stating that a small percentage of cases might be caused by mercury)?
Wouldn’t we first have to find a way to determine which kids are actually mercury damaged to figure out who the potential responders would be so that we can come up with a study that produces real results rather than appearing “no better than placebo if it is actually only effective in [a small number] of people with autism”?
Until that can be done, isn’t it premature to make a judgment on the efficacy of chelation?
September 12th, 2007 at 11:08 am
Hi Prometheus -
I’ve been thinking about this issue some; what bothers me is that it seems we quickly approach a sitaution wherein an increase, or decrease, in mental disorders such as autism can never be determined.
If we accept that the problems in data collection and shifts in diagnostic parameters you describe in this post result in intractable flaws; I cannot for the life of me determine how the question of if there is more or less autism now than twenty years ago can ever be answered.
Can you describe a set of data that could realistically be collected that would allow you to have confidence in answering the question as to if autism is actually increasing or not?
Take care.
- pD
September 12th, 2007 at 12:37 pm
Grace,
You said:
“Until that can be done, isn’t it premature to make a judgment on the efficacy of chelation?”
I agree absolutely! That’s why I say (over and over and over…) that chelation has not been shown to be effective. It hasn’t.
Now, if you are in possession of data showing that chelation is more effective than placebo, then I am all ears.
Perhaps chelation will eventually be shown to work in a small percentage of autistic children - perhaps it will not. As of now, it hasn’t been shown to work. That’s what I keep saying, in contrast to the number of DAN!ites who insist that it does work, but never show their data.
As far as finding “… which kids are actually mercury damaged…”, the practitioners promoting chelation assert that they know which kids are “mercury damaged” (said figure running between “all” and “most”), so why don’t they do a study? And whatever happened to the Arizona study with Jim Adams? That seems to have quietly folded its tents and moved on.
Grace, you seem to be trying to paint me as the “bad cop” in this situation. I see myself as a lonely voice in the mob crying out, “But the Emperor has no clothes!”
pD,
As for telling whether there is really more autism now than there was twenty years ago, I suspect that there is no way that we can know.
It is as though we were trying to follow global warming and all of the thermometers had been changed multiple times in the past decades, with no clear conversion between the different temperature scales.
As I’ve said to Grace (over and over and over…), saying that the present data is inadequate, tainted, flawed or missing does not require that I have better data or a better way to measure the same parameters.
The actual prevalence of autism today may be higher than twenty years ago or it may be the same or even less. We simply have no way of knowing because of the way the “standards” for measuring autism have changed.
There may be a way to overcome the problem with the large educational and social services data piles, but I can’t think of one. I suspect that those “data” sources are useless for tracking autism prevalence over time (and many experts in the field agree with me).
There are probably data sources that I am not aware of that can give us a measure of how autism prevalence has varied with time, but until the public gives up its fascination with the USDE and CA-DDS databases, nobody will be listening.
Prometheus
September 13th, 2007 at 8:50 am
Hi Promemtheus -
Of course you are under no obligation to have better ideas or different data; I was simply curious.
What about the possibility of using biomarker based tests with stored samples or from an older cohort? Of course, we don’t have a reliable mechanism, yet, for identifying autism, but research is being put into this. There certainly do appear to be many identifiable abnormalities in the blood and plasma of autistics.
It seems possible that at some point in the future there will be autistic phenotypes identifiable via presence of biomarkers. At that point, perhaps, it may be possible to identify how common the same abnormalities are in fifty year olds; or in stored samples from the past.
Take care!
- pD
September 13th, 2007 at 4:38 pm
I cannot for the life of me determine how the question of if there is more or less autism now than twenty years ago can ever be answered.
Here’s my suggestion. Try to replicate Lotter (1967). Same criteria. Same methodology. Study exactly how Lotter understood autism. Lorna Wing knows. There is still some subjectivity involved and there’s no way to control for bias. But it would give us a rough idea of whether autism as viewed by Lotter has risen in the last 40 years.
September 13th, 2007 at 7:51 pm
Hi prometheus,
what do you know of carcinosin? i have recently heard of it as a hoemopathic treatment of autism. any thoughts?
September 15th, 2007 at 4:21 pm
This is exactly what I expected to find out after reading the title Myths and Legends of Autism: Part 3. Thanks for informative article
September 17th, 2007 at 12:36 am
<p><i>”I see myself as a lonely voice in the mob crying out, “But the Emperor has no clothes!”</i><br />
Fair enough, but try to understand - some see you as a not so lone voice crying out he has no clothes when you haven’t even seen him yet…</p>
[This comment was "hung up" in the spam filter because there were five identical copies of the same comment in the moderation queue.]
September 17th, 2007 at 1:22 pm
Grace,
“Some” may see me in a myriad of different ways - “some” believe in alien abduction.
The fact is that I am a single person and although my voice may, at times, be joined by others, I stand alone.
As for having “seen the Emperor…”, I have seen him, indeed. And he has no data (clothes).
Now, if you want to argue that maybe some of these therapies might help some autistic children, then I can’t really argue with you. Maybe pigs will fly - maybe they already have - but the data is lacking.
Maybe all of these “might be” therapies don’t work at all, on anybody. That’s just as likely as your “might be” story.
Prometheus
September 17th, 2007 at 6:00 pm
Prometheus:
A few days back one of your responses appears to leave open the door for human experimentation. I don’t believe that’s what you meant. Specifically, you wrote:
“Grace,
You said:
“Until that can be done, isn’t it premature to make a judgment on the efficacy of chelation?”
I agree absolutely! That’s why I say (over and over and over…) that chelation has not been shown to be effective. It hasn’t.
Now, if you are in possession of data showing that chelation is more effective than placebo, then I am all ears.”
The FDA has approved chelation only for single dose treatment of acute heavy metal poisoning. It is a treatment that carries substantial risk to the patient, and has been linked to deaths. For any medical treatment or procedure the expected benefits should outweigh the risks and costs. I see no reason to conclude that chelation qualifies.
For chelation to be suitable as a treatment for ASD, at least 2 conclusions have to be found to be supported by facts:
1. That ASD (or some identifiable sub-set of ASD) is caused by mercury or other heavy metal exposure; and,
2. That even after the mercury or other heavy metal has been excreted or is no longer present in amounts sufficient to cause symptoms, that chelation will reverse, in whole or in substantial part, the effects of the exposure.
Until at least those 2 conclusions are found to be supported by facts, there is no applicable standard of care for chelation as a therapy for ASD, but, rather its use strongly resembles human experimentation.
September 17th, 2007 at 9:54 pm
wfjag,
I’m afraid that your proposal doesn’t work.
As a licensed pharmacist for almost 2 decades now, I can assure you that off label usage of medications are nearly as common as FDA approved uses. The reason being that it costs a drug company significant time & money to get the FDA approval - a delay that is problematic on multiple levels (which is the whole reason why off label usage is permitted).
Additionally, chelation therapy when used with proper professional oversight is certainly safe - Dr. Mary Jean Brown, chief of the Lead Poisoning Prevention Branch of the Atlanta-based Centers for Disease Control and Prevention, said “there have been no reputable medical trials demonstrating the effectiveness of chelation as a therapy for anything but lead poisoning. But if it were administered accurately, the procedure would be harmless.” [Note that she said there is no serious study supporting its use outside of lead poisoning which means that it is unknown - an open question] If it was so terribly dangerous, it would certainly not be available without a prescription as it currently is.
And, I’m sorry, but your 2nd requirement is absurd. Try applying those requirements to lead poisoning! You never get all the lead out and you cannot reverse all of the effects of the exposure - it gets stored in the bones and it damages the brain. Yet they do use chelation therapy for lead poisoning and do typically but not always see improvements. We can hope & pray that some day we may find a more perfect solution, but for now it’s all we’ve got.
As for your objection to human experimentation, take a look at the current FDA approval process. If you take a medication (or vaccine) that’s less than 5 yrs on the market, like it or not, you are a guinea pig. There is no way to eliminate that risk, we can only try to minimize it - that’s the needful purpose of the risk - benefit ratio we use.
September 18th, 2007 at 8:33 am
Hi wfjag -
“That ASD (or some identifiable sub-set of ASD) is caused by mercury or other heavy metal exposure; and,
2. That even after the mercury or other heavy metal has been excreted or is no longer present in amounts sufficient to cause symptoms, that chelation will reverse, in whole or in substantial part, the effects of the exposure.”
I’ve seen in other neurodiverse blogs that parents are putting their children on risperdol and/or other psychotropic drugs; in fact, they were referred to as ‘traditional’ treatments alongside a slam of ‘alternative’ biomedical treatments. Most certainly risperdal would fail the tests that you have described above, and it certainly has it’s share of potentially scary side effects; especially in people who may not know how to tell you they have blurry vision, a sore throat, or any of the other warning signs.
Would you consider this type of ‘treatment’ any less of an expirement than chelation?
- pD
September 18th, 2007 at 6:07 pm
pD:
Risperdahl (not “risperdol”) is FDA approved as a treatment for ASD, and used for treatment of symptoms related to lack of sociability. Sorry, your assertion is completely in error. The risks and side-effects of risperdahl are known. That is why, among other symptoms a treating physician will monitor for, complete blood testing is done every year to 18 months. So, “No”, risperdahl does not fail the tests I stated. Its expected benefits have been shown to exceed its risks and cost.
Grace:
I am very aware of off-label uses of drugs. Such is accepted medical practice when there are good scientific reasons to conclude that the drug will provide benefits and the risks are negligible. For example, Ambien is not FDA approved for use by women in early stage labor, but is frequently prescribed so that they can get rest. Ambien was approved for use in the US by the FDA about 15 years ago, approved in Europe about 10 years before that, and has been prescribed about 1 Billion times in the past 10 years. Its risks and side-effects are well known, so that the off-label use of prescribing it to women in early stage labor is one in which the expected benefits are greater than the risk and costs. Similarly, Namenda is FDA approved for the treatment of moderate to severe dementia of the Alzheimer’s type in adult patients. However, its off-label use includes mild dementia, even when Alzheimer’s is not diagnosed. Again, its risks are understood, so that the expected benefit of slowing the progress of the dementia (of whatever cause) exceeds the risk and costs — at least in the US. In the UK, the agency charged with controlling the costs of medical care has refused to approve such wider use of Namenda because of its cost.
However, as for chelation, while there are significant risks (contrary to your assertion), there is no reason to conclude that it is effective for anything other than lead (and maybe other kinds of heavy metal) poisoning. Its use on people diagnosed with an ASD condition is based on completely unsupported speculation that lead, mercury or some other heavy metal causes ASD (or some subset of ASD).
There were no generally accepted medical studies proving that chelation therapy (of any kind) offers any beneficial treatment of autism.
Since you contend that chelation is safe, please address this: “FDA links child deaths to chelation therapy Mar. 2, 2006)”
http://www.msnbc.msn.com/id/11640868/
The article states:
“Since at least 1978, federal health officials have warned against giving it to children with lead poisoning. Endrate’s calcium-removing abilities can dangerously disrupt the body’s chemistry, Brown said.
In August, a 5-year-old boy with autism died in Portersville, Pa., while receiving an infusion of Endrate in a physician’s office. A coroner later ruled that the treatment killed the boy.
In February 2005, a 2-year-old girl with lead poisoning was treated with three chelating agents — one of them Endrate — and died at a hospital hours later from what an autopsy concluded was cardiac arrest due to depleted levels of calcium.”
The Dr. Brown cited in the article is the same Dr. Mary Jean Brown you refer to.
You may complain that in the case of the autisic child, the “wrong” type of EDTA was used, since Disodium EDTA was used. The only FDA approved use of Disodium EDTA is for treatment of patients with hypercalcemia (high levels of calcium) or digitalis toxicity.
Another chelation treatment involves using Calcium Disodium EDTA (also known as “Calcium Disodium Versenate” and “edetate calcium disodium”). However, use of this compound also carries significant risk. A typical warning for this compound is:
“WARNINGS: Calcium Disodium Versenate is capable of producing toxic effects which can be fatal. Lead encephalopathy is relatively rare in adults, but occurs more often in pediatric patients in whom it may be incipient and thus overlooked. The mortality rate in pediatric patients has been high. Patients with lead encephalopathy and cerebral edema may experience a lethal increase in intracranial pressure following, intravenous infusion; the intramuscular route is preferred for these patients. In cases where the intravenous route is necessary, avoid rapid infusion. The dosage schedule should be followed and at no time should the recommended daily dose be exceeded.”
Calcium Disodium EDTA has also been linked to deaths. See the CDC report titled “Deaths Associated with Hypocalcemia from Chelation Therapy — Texas, Pennsylvania, and Oregon, 2003–2005″ (March 3, 2006 / 55(08);204-207). It states:
“Chelating agents, especially those intended for use in children, should be effective in reducing lead and other heavy metals from the body without producing substantial adverse effects on levels of critical serum electrolytes, such as calcium. The only agent recommended for intravenous (IV) chelation therapy for children is CaEDTA (1). However, hospital formularies usually stock multiple chelation agents. One such agent, Na2EDTA, was formerly used for treatment of hypercalcemia, but its use has become infrequent because of concerns regarding nephrotoxicity and because of the availability of less toxic alternatives (3). Furthermore, Na2EDTA contains a warning stating, “The use of this drug in any particular patient is recommended only when the severity of the clinical condition justifies the aggressive measures associated with this type of therapy.” According to the package insert, Na2EDTA is “indicated in selected patients for the emergency treatment of hypercalcemia and for the control of ventricular arrhythmias associated with digitalis toxicity.” According to FDA and CDC, the safety and effectiveness of Na2EDTA in pediatric patients has not been established, and its use is not recommended because it induces hypocalcemia and possibly fatal tetany (1).
In 2005, the Texas Department of Health childhood lead poisoning surveillance program reported a death attributable to chelation-associated hypocalcemia to CDC. Subsequently, CDC queried state and local lead-surveillance programs regarding chelation-related fatalities; additional deaths were identified in Pennsylvania and Oregon. ”
Further, there are several decades of experience as to chelation therapy, since chelation therapy has been proposed to treat existing atherosclerosis and to prevent it from forming. Still, the American Heart Association concluded:
“After carefully reviewing all the available scientific literature on this subject, the American Heart Association has concluded that the benefits claimed for this form of therapy aren’t scientifically proven. That’s why we don’t recommend this type of treatment.” See http://americanheart.org/presenter.jhtml?identifier=3000843
And, I am qualified to draw the comparison to human experimentation. I’m an attorney, retired from the military. I not only took the law of war courses, I have taught them. I have also several of the war crimes trials against Nazi and Japanese doctors who engaged in human experimentation.
It is true that a huge amount of medical knowledge resulted from that human experimentation. However, the approach of those doctors is that since the subjects were persons of “unworthy life”, it was a let’s try this and see what happens approach. The medical knowledge gained did not justify what was done, and they were rightly punished for crimes against humanity.
Gracie — since you’re the proponent of chelation “therapy” for persons diagnosed ASD, you have the burden of using good scientific reasons to identify the particular chelation “therapy” you support and showing its expected benefits exceed the known, substantial risks and cost. As Prometheus said “Now, if you are in possession of data showing that chelation is more effective than placebo, then I am all ears.”
Otherwise is looks a lot like human experimentation where the consequences can be fatal.
September 18th, 2007 at 6:44 pm
wfjag,
You say “human experimentation” like it’s a bad thing.
There are thousands of human research projects going on in the US, UK and Europe today. Without them, medical research would be nearly impossible.
However, there are rules for human research that must be followed. The Nuremburg Code and the Declaration of Helsinki provide the basis for most of our current laws and rules regarding human experimentation.
On the other hand, a number of practitioners, impatient with the progress of medical research, have taken matters into their own hands and are, essentially, conducting unmonitored human research.
They usually don’t refer to it as “research”, preferring (for legal reasons) to call it “cutting edge medical treatment” or some such tripe. They are using FDA-approved (or the UK and EU equivalents) drugs in “off-label” fashion or - worse yet - they are administering un-approved substances that have never been properly studied in humans.
As Grace mentioned, “off-label” use of drugs, including chelating agents, is legal, even where it cannot be supported by data.
Does the use of drugs “off label” constitute “human experimentation”? Perhaps. Perhaps not. Many “off-label” uses have been researched as thoroughly as the “on-label” uses. Sometimes even more.
Grace comments:
“You never get all the lead out and you cannot reverse all of the effects of the exposure - it gets stored in the bones and it damages the brain.”
Technically, she is correct - even if no new lead were imbibed, the chelating agent would never get all of the lead out, even if it were given for an infinitely long period of time. The removal of lead - or, for that matter, any substance - from the body follows an exponential decay curve and so - technically - continues indefinitely.
However, large human studies have shown that two to three months of chelation with DMSA (or even IV EDTA - no longer a front-line drug) will reduce the lead level to “baseline”.
Grace goes on to state:
“Yet they do use chelation therapy for lead poisoning and do typically but not always see improvements.”
A study of the long-term benefits of chelation for lead poisoning (in over 600 children) was published in 2004. They found no difference in neurodevelopmental scores between the group treated with chelation and the group not treated.
(see: http://pediatrics.aappublications.org/cgi/content/full/114/1/19 )
This suggests that the putative benefits of chelation in autism are not due to any effects on heavy metals. Or that they are illusory (”placebo effect”).
PassionlessDrone states:
“Most certainly risperdal would fail the tests that you have described above, and it certainly has it’s share of potentially scary side effects…”
As of today, risperidone has undergone 5 placebo-controlled, double-blind studies and 9 open-label studies in autism. All have shown it to be beneficial in a number of behavioral problems commonly encountered in autistic children.
These studies were done with approval of IRB’s and full parental consent - all in accordance with the Nuremburg Code and the Declaration of Helsinki. They were all “human experimentation”, but they were all done according to the rules.
The difference between risperidone and chelation, from a research point of view, is that only one “real” study on chelation has been done (and the results, curiously, have not been released yet).
Prometheus
September 18th, 2007 at 6:57 pm
WFJAG,
I think I see the cause of some confusion.
Chelation with EDTA - especially if the incorrect form is used - is hazardous and has resulted in a number of deaths. EDTA is not the first-line drug for lead, mercury or arsenic poisoning (it also isn’t particularly effective in chelating mercury).
Chelation with the oral agent DMSA is very safe, with no deaths attributed to its use - even in the case of an accidental overdose. Interestingly, DMSA is not FDA-approved for mercury (or arsenic) poisoning, even though it is far better and safer than the approved drug (BAL).
However, no matter how low a risk might be, if the probability of benefit is lower (say, zero), it is an unacceptable risk.
I defer to the legal expert in matters of the law, but it seems to me that practitioners who treat autism with chelation run the risk of being accused of performing research without a consent.
Prometheus
September 18th, 2007 at 11:28 pm
Hi wfjag -
“Risperdahl (not “risperdol”) is FDA approved as a treatment for ASD, and used for treatment of symptoms related to lack of sociability. Sorry, your assertion is completely in error. The risks and side-effects of risperdahl are known. That is why, among other symptoms a treating physician will monitor for, complete blood testing is done every year to 18 months. So, “No”, risperdahl does not fail the tests I stated. Its expected benefits have been shown to exceed its risks and cost.”
Your tests have nothing to do with risks or costs.
“1. That ASD (or some identifiable sub-set of ASD) is caused by mercury or other heavy metal exposure; and”
Is ASD or some identifiable subset of ASD caused by what risperdahl treats? No.
“2. That even after the mercury or other heavy metal has been excreted or is no longer present in amounts sufficient to cause symptoms, that chelation will reverse, in whole or in substantial part, the effects of the exposure.””
Can you stop taking risperdahl and have the symptoms you were treating not return? No.
How can we conclude that risperdahl passes either the test of treating a cause of autism, or reversing the effects of autism?
- pD
- pD
September 19th, 2007 at 11:24 am
Yes, I do consider “human experimentation” — as I use the term, which is as it is used in the context of crimes against humanity — to be a “bad thing.”
That is not anywhere close to human subjects enrolled in studies conducted in accordance with established medical and ethical protocals. It would be exceedingly unwise to approve new treatments or therapies without first doing such controlled studies — which include obtaining the informed consent of the subjects.
However, so called “cutting edge medical treatment” is far different and resembles “human experimentation” as I use the phrase. Since such “cutting edge medical treatment” is experimental, there are no applicable standards of care. Further, any warnings of potential adverse consequences almost surely will be deficient since data is lacking on which to base such warnings. These problems are compounded by at least 2 additional factors. One I call “desperate parents symdrome”. By that I mean that there is a noticable tendency of the parents of a child diagnosed as ASD to go looking for a miracle cure — of which there are many touted on internet sites. Second is the fact that typical symptoms of ASD include disruption of communication abilities and inability to express internal states (including emotions and pain). So, such “cutting edge medical treatment” is performed on those least able to protect themselves or tell others how they feel or if the “treatment” is causing them to feel worse or experience pain.
And, yes, I am familiar with curvilinear relationships, and that at some point the test results for mercury, lead or other heavy metal that allegedly causes ASD (or some subgroup) will go below either those established as levels of concern, or below detection levels. I included the qualification within my condition #2 “is no longer present in amounts sufficient to cause symptoms” for that reason.
However, that does not undercut the main point of my condition #2: “that chelation will reverse, in whole or in substantial part, the effects of the exposure.”
The advocates of chelation (of whatever type) not only have to establish using good science their theory that mercury (or lead, or whatever heavy metal they contend) causes ASD (or some subset), they also have to establish using good science that the chelation “therapy” proposed will reverse, in whole or in substantial part, the effects of the exposure. The advocates of chelation “therapy” fail on both points.
You also said “As Grace mentioned, “off-label” use of drugs, including chelating agents, is legal, even where it cannot be supported by data.”
That is only technically true as to criminal prosecution, in that it is not necessarily a crime to use drugs off-label. However, if there are adverse effects, since such use cannot be supported by data, that may meet the standards of a battery, or if death results, some form of negligent homicide or manslaughter.
Further, if the off-label use cann be supported by data, that easily will violate licensing standards (an administrative action) or negligence standards (a civil action).
You also said “Chelation with the oral agent DMSA is very safe, with no deaths attributed to its use”. While I’ll generally defer to your expertise as a scientist, I question whether DMSA can be considered “very safe” because no deaths have been attributed to its use. See “Commonly used therapy for lead poisoning might alter the immune system, Cornell animal study indicates” (Feb. 23, 1999)
http://www.news.cornell.edu/releases/Feb99/chelate.hrs.html
While Chelation with the oral agent DMSA appears to be the safest chelation “therapy”, it too can cause side effects, and, as the article from the Cornell News indicates, it may cause serious side effects that are not yet known. I do not know if this study has been replicated, but it illustrates that just because a treatment has not been linked to a death is far different from concluding that it is safe. Being “safer” than the other chelation “therapies” [which I am deliberately putting in quotes, since there is no known benefit when used for treatment of ASD symptoms] is far different than concluding that it is “safe.” I suspect we probably agree on this, since I recognize that no medical treatment, therapy or procedure has zero risk — rather, its risk and cost must be weighed against its expected benefits.
Still, perhaps DMSA is safe. However, as you know, the FDA and European protocals call for conducting animal studies before moving to studies with human subjects. That DSMA has only been FDA approved for treatment of lead poisoning indicates as to that use there has been a determination that the benefits exceed the risks and cost. That is very different from concluding that chelation using DSMA is safe for any other use or that its benefits exceed its risks and cost.
Thank you for the time and information you have put into your comments. They are most educational.
September 19th, 2007 at 11:29 am
I apologize for the typo. I meant:
“Further, if the off-label use cannot be supported by data, that easily will violate licensing standards (an administrative action) or negligence standards (a civil action).”
September 19th, 2007 at 12:06 pm
pD,
According to Jannsen Pharmaceutica, the correct spelling (for the trade name) is “Risperdal”. The generic name is “risperidone”.
wfjag,
I see that we were in agreement in principle and in conflict over terminology. As a scientist involved in clinical research, I see the “off-label” use of drugs as “legal” in that the FDA cannot prosecute a physician for “off-label” use.
Of course, if the patient comes to any harm, this will not protect the physician from civil or even criminal liability. A perfect example of this are the criminal charges filed against Dr. Roy Kerry, whose “off-label” (and “out-of-his-mind”) use of NaEDTA killed a 5-year-old boy.
Likewise, I see (and remember from my own time in the service) that “human experimentation” has a special legal (and historical) meaning. I would submit that “human subject research” (the current “buzz-word” in clinical research) is a better term for that subset of “human experimentation” that meets the criteria of the Nuremburg Code and the Declaration of Helsinki.
I also agree that some practitioners’ use of “off-label” drugs runs dangerously close to non-sanctioned human experimentation. In some cases, the practitioner may not realize this, but in a few situations it seems that the practitioner is fully aware that they are conducting an experiment.
A question to you, sir. Does “intent” factor into whether a person is conducting illegal human experimentation? Does it matter that the practitioner’s intent was to treat (as oppsed to research), using a therapy which was not supported by data?
Prometheus
September 19th, 2007 at 5:26 pm
Prometheus. I concur with your last posting.
As to “intent”, it generally depends on the charge. Generally speaking, “specific intent” offenses require that the defendant intend to commit the criminal act — e.g., murder is a specific intent crime, in that the person intended to commit an unlawful killing (vs. something like an accidental killing or justified killing in self-defense). Most crimes are “general intent” offenses. Essentially, did you intend to commit the act, not did you intend to cause the harm — e.g., while traveling 55 MPH in a school zone marked 20 MPH, the defendant hits and kills a child. That the defendant didn’t intend to cause harm but merely was in a hurry or not mindful of his surroundings, is not a defense to manslaughter or negligent homicide.
I’m not aware of any US federal or state laws prohibiting “conducting illegal human experimentation.” That doesn’t mean that the person is off the hook — since various criminal laws prohibiting the various types of homicide or battery (or, if the treatment is ineffective, fraud) still may be applied.
“Does it matter that the practitioner’s intent was to treat (as opposed to research), using a therapy which was not supported by data?”
If the person could establish reasonable good faith — which appears hard without support by data to show that the good faith had an objective basis — that could be a possible defense, particularly to a specific intent offense.
Or, even without being able to show that the good faith was reasonable as having an objective basis, proving that the person had a sincere belief that he/she was providing a treatment whose expected benefits outweighted the risks and cost, could be used to argue in mitigation on sentencing.
Of course, the problem with any good faith argument is that it is brought up after a harm has occurred, and so tends to sound like a post hoc rationalization.
And, in the chelation situation, any argument about the defendant’s “intent” is faced with the counter argument that the person providing the “treatment” was mainly motivated by profit. The typical charge for a single chelation treatment appears to run in the $2,500 to $5,000 range. The costs of providing a single treatment aren’t all that high. I know of no insurance company that will pay for such a treatment, as it is classified no better than “experimental.” By not following the established medical and ethical protocals which can be done even in clinical trials (which are also treatment), but, instead, charging so much, I’d think that a defendant arguing that his/her “intent” was pure will be a hard defense to sell. (Not that, if I was defense counsel, I wouldn’t argue that if I didn’t have a better defense to argue. But, it strikes me as a classic “backfire defense” — one that likely will blow up in your face.)
In short, the established protocals — which exist for very good reasons that you understand very well — and the availability of providing a treatment as part of a clinical trial, and for chelation, the fact that a fairly large amount is charged and no insurer covers the cost, means that any provider who does so is gambling with his/her license and freedom, possibly in addition to with his/her patient’s health and life.
I came across a quote, but unfortunately don’t know where it came from:
“Being on the cutting edge usually means that the knife can cut both ways.”
September 20th, 2007 at 1:59 pm
Dear Prometheus:
FYI: Expect a new round of “thimerosal” causes autism. Jenny McCarthy — yes, that Jenny McCarthy, the blonde with big (well, let’s just say that she and they attract photographers) has written a book saying that caused her son’s autism, and Oprah (yes, that Oprah) gave her the chance to say that on TV. See, http://www.associatedcontent.com/article/385209/jenny_mccarthy_tells_oprah_that_autism.html
At least one of the commentators to the blog noted that the MMR vaccine that her son received didn’t contain thimerosal, but said it was contained in most flu vaccines.
Actually, it’s too bad about the thimerosal allegation. It appears that she’s working intensively with her son, and has gotten him the type of early, intensive intervention by qualified providers that can provide real benefits. However, it appears that the thimerosal allegation is getting more media play.
September 22nd, 2007 at 3:16 am
Well, before I mosey off into the sunset (no tears now), there are a few loose ends I’d like to tie up & a few questions I’d like to ask in this exchange:
~I am not a “proponent of chelation” nor do I play one on tv; I am a proponent of non-phlogiston thinking with a modicon of devil’s advocate. See the conclusion.
~Having checked my resources, I am still scratching my head at the assertion that chelation for acute lead poisoning is a one time dose with any of the indicated DOC’s.
~Disodium EDTA is never recommended for lead poisoning or heavy metal removal (outside of the noted hypercalcemia) so that really has no bearing on the subject of chelation therapy in general
~I had a small degree of sympathy for the doctor involved in the death of the boy (yes, my sympathy for the boy & his parents was far greater) who used disodium EDTA when I thought it was a medication error - it is a pharmacist’s worse nightmare. I had none upon learning that it was a deliberate choice; he is without excuse. The mfr. specifically states that it is not to be used as such.
~Exceptions do not make the rule, however. Why is it brought up as if it were a case in point? It’s not & never has been a DAN recommendation - check ARI. ARI & DAN are no more responsible for the individual decisions made by associated physicians than is the AMA or AAP. This case is hardly typical or we would not be able to count the yearly deaths from chelation on our fingers and have some left over. If we are going to judge drugs in that fashion, then it is well past time to remove aspirin (and just about everything else) from the OTC shelves.
~Speaking of exceptions to the rule, I question the asserted “typical” charge of $2500+ for chelation. Is that a national average? For DAN tx’s with DMSA? For cardiovascular treatments with EDTA? For all forms of chelation therapy? Who crunched those numbers and what is included with that price? (Face it, if that includes the necessary labs, then it is very normal & no more unreasonable than the typical lab fees of today)
~While DMSA is specifically indicated for lead, it does have a fairly well known effectiveness for removing mercury & arsenic as well. That chelation is controversial is hardly a revelation, but to speak of it as if the jury is not still out is disingenuous.
~In the referenced chelation study from Pediatrics: Not with the intent to single this study out as it appears to be typical, but I have to wonder
-Why do they chelate for such a short time & with so few courses when it is a known fact that
“patients should be monitored for rebound in blood lead concentrations after therapy, because, as with all chelating agents, elevated blood lead concentrations and associated symptoms may return rapidly after discontinuation of succimer due to redistribution of lead from bone stores to soft tissues.”
(DMSA is safe for chronic use barring the appearance of side effects & with monitoring of the appropriate labs.
Long-term outcome of repeated lead chelation therapy in progressive non-diabetic chronic kidney diseases.)
-Did the children fail to recover from the damage or did the lead that remained in their systems do additional damage as it redistributed?
~Chelation therapy for lead has been shown to improve motor skill impairment.
Effect of succimer chelation therapy on postural balance and gait outcomes in children with early exposure to environmental lead.
Are some improvements better than none? Admittedly, the studies on children have been more depressing than those with adults (And all the conclusions urge that exposure prevention be made primary, yet we still deliberately put heavy metals like mercury & aluminum into babies’ & pregnant women’s bodies - is this rational?)
-Even if the children did fail to recover or improve with chelation therapy, on what basis can it be assumed that leaving the toxic burden in the body (& brain) would not be a source of ongoing and worsening damage for the duration of their lives? Especially with recent studies showing that people with lead poisoning have experienced serious damage decades after their exposure:
Past adult lead exposure is associated with longitudinal decline in cognitive function. (Click on related links for a substantial number in this same vein)
~While noting the possible permanent damage to the immune system from the use of DMSA, how could the far greater damage from lead to the immune system escape one’s attention? Check out their abstract:
Persistent effect of in utero meso-2,3-dimercaptosuccinic acid (DMSA) on immune function and lead-induced immunotoxicity.
Their conclusion: “These results suggest that DMSA reverses some of the lead-induced immunotoxicity; however, this treatment itself during embryonic development produces subsequent adult immunomodulation.”
Essentially it is a trade-off - would you rather have a larger or a smaller number of things wrong with your immune system? (BTW, other studies indicate the possibility that appropriate supplementation may reduce or eliminate that risk but have not yet moved past rodent models)
The same immunotoxicologist who headed up that 1999 study, also published this one in 2006:
Lead and immune function.
What he published in this study is consistent with the DAN approach, at least since I have been looking it over the past two years.
The DAN theme brings us back to lead’s fraternal heavy metal twin - mercury.
It was stated that the symptoms of mercury poisoning & autism may sound similar but are not really. Since social withdrawal is the most consistent behavioral characteristic of ASD, what is the difference between the social withdrawal described in cases of mercury exposure and the social withdrawal in autism? (I truly want to know this information! Does it actually manifest differently or is it possibly degrees of severity which could be attributable to fetal vs adult exposure?)
Dr. Herbert Needleman - who suffered substantially for arguing (& proving) that even low levels of lead are neurologically damaging -”A no-effect level has not been found.”- indicates in his discussion on Behavioral toxicology that “The clearest data on the deleterious effects of prenatal exposure to toxicants comes from the study of two metals, lead and mercury”.
Interestingly while Needleman was being persecuted in America by vested interest groups, other countries were coming up with conclusions on low level lead exposure that corresponded with his own.
This is so similar to the current situation with mercury that it seems well beyond coincidence.
A German study was just completed that showed that
Higher mercury concentrations were found in brain regions and blood of some patients with Alzheimer’s disease (referred to by many as adult autism - my DH’s dad had it, including a form of social withdrawal, and I would wholeheartedly agree with them).
Given what is known about the damage that mercury can do inside the body & that, like lead, it has no known safe level & that the studies that would provide the hard data on the effectiveness of chelation therapy vs leaving the heavy metals there till death do they part have not been done - knowing that as we age our immune system becomes more vulnerable at a time when our bones tend to mobilize calcium & therefore stored lead too, as well as toxins like mercury stored in body fat which also tends to be mobilized as we age, (additionally similar mobilizations occur with pregnant women) - on what basis can one possibly argue with reliable certainty that leaving the toxic metals in the body is generally safer than trying to get them out?
Prometheus, you seem like a decent person & you sound sincere in your desire to seek out and share truth with others. And it may surprise you to hear that you have helped me substantially - for which I am grateful. I will leave you in peace - at least for a little while.
I remain perplexed, though, at how you can claim to be looking at these issues objectively and come to the conclusion that mercury is not likely to be a source of harm in low doses when lead has already proven that false. Too many unanswered questions remain. The level of research necessary to reach such a conclusion is simply not there yet.
September 24th, 2007 at 3:49 pm
Grace,
Nice straw men! How seasonal!
[1] I do not recall ever saying that you were a promoter of chelation. If I did, that was in error - I cannot recall you ever saying that chelation was a good idea, just that it shouldn’t be discounted.
[2] I also don’t recall ever saying that the appropriate treatment for lead poisoning was a single dose of a chelating agent. In fact, looking over my notes, it appears that - on several occasions - that I explicitly said that lead required a longer course of therapy than mercury.
That said, it doesn’t take years to treat even severe lead poisoning.
[3] You trot out the tired canard that chelation has killed (so far as we know) only a few people, while aspirin (to use your example) has killed thousands (or more).
The reason that this is a canard is that chelation is not an appropriate therapy for autism, atherosclerosis or most of the things it is used for. Chelation for real, documented heavy metal poisoning wouldn’t account for a tiny fraction of the Versenate, Endrate, DMSA or DMPS used in the US.
When chelation is used to treat atheroscleosis (for which it has been shown to be ineffective) or autism (for which it has not been shown to be effective), we have a situation where the risks - no matter how low - greatly exceed the potential benefit.
I think that you’d have to admit that even aspirin - which would never make it through the FDA approval process today - has done more good than harm, overall. And chelation for real, documented heavy metal poisoning has probably done more good than harm.
But chelation for atherosclerosis and autism - even though the death toll is less than that for aspirin - has not done any good (or, at least, hasn’t been shown to do any good, in the case of autism), so the deaths aren’t counterbalanced by people who have benefitted.
[4] You state that mercury and lead “have no known safe level” and cite Dr. Needleman’s work (and his alleged “persecution”) in support.
You are aware that lead and mercury have been present in the environment since before the origin of life, are you not? And that even before the advent of human industry there were areas (such as the Rio Tinto) which had what we would even today call dangerously high levels of heavy metals?
The argument that there is no “safe level” of mercury or lead is rather disingenuous. Did Dr. Needleman compare animals raised for generations in a lead-free environment? No. He is comparing the IQ testing of children with different blood lead levels.
As I read Dr. Needleman’s work, he seems to be advocating that the maximum allowable levels should be reduced, not that there is no “safe” level. I suppose one could extrapolate and say that there is some harm done at any level, even if the harm is too small to detect (or has merged with the baseline random fluctuation).
You seem to be making the erroneous assumption that I think lead, mercury, arsenic etc. are safe. Not at all. I make no such assertion (although the straw man you have constructed seems to).
[5] You also assert that I have “…come to the conclusion that mercury is not likely to be a source of harm in low doses …”. If you read back through my statements, you will see that assertion is false.
I have stated - on numerous occasions - that the currently available data does not support the assertion that mercury causes autism. You’ll note that I make no claim that mercury causes no harm - at high, medium or low doses.
Your statement that “Too many unanswered questions remain.” is absolutely true. For that reason, I implore people to not rush to conclusions.
Mercury has not been shown to cause autism.
Chelation has not been shown to cure or even substatially alter the course of autism.
These are the statements I have made. They are - so far as I know - true statements as I have yet to receive any data suggesting they are not.
There are a lot of unanswered questions, but the solution is not to simply make up the answers.
Prometheus
September 25th, 2007 at 3:26 am
Prometheus,
You make it difficult to fade out “grace”fully…
I was trying to wrap up multiple strands in this discussion in that last post and most of the ones at the beginning were in response to wfjag’s comments.
I promise I have no intention of continuing the debate as I have pretty much gotten what I came here for. But I do wish to clarify some of your doubts that are worthy of documenting.
[1] & [2] See wfjag’s comments
[3] “That said, it doesn’t take years to treat even severe lead poisoning.”
Well, that was (& is) my question! Why do they treat it for only a few courses when all the chelation studies I looked at mention the rebound & redistribution effect of lead? The chronic use for lead damaged kidneys shows that DMSA can be used long term so why do they seem to chelate enough to let the lead remobilize in these kids, probably cause new additional damage, & then resettle in the body for later trouble?
And where are the studies showing that the chelated fare no differently than the unchelated lead exposed children when they reach adulthood? If the unchelated develop Alzheimer’s at a higher rate than the chelated, for example, or die sooner then maybe it would be worth it after all? But we won’t know until somebody does the requisite studies - so how can we say chelation is useless until those questions are answered?
Alas, I have no clue about the answers to your chelation study questions - I would love to know the answers, too.
[4] I was directly quoting Needleman, but failed to attach the links.
Behavioral toxicology.
“The clearest data on the deleterious effects of prenatal exposure to toxicants comes from the study of two metals, lead and mercury, and from epidemiological investigations of the effects of alcohol taken during pregnancy. Less complete data are available for two other groups of agents, solvents and pesticides. What we do know about their effects on the fetal brain is convincing enough to make us demand caution in their distribution.”
The persistent threat of lead: medical and sociological issues.
“Biochemical and functional changes have been demonstrated in the heme biosynthetic pathway and in the renal, cardiovascular, endocrine, immune, and nervous systems. The threshold for effect depends on the sensitivity of the methods used. A no-effect level has not been found.”
Needleman’s subsequent studies found negative effects at even lower levels than this one.
This interview with Needleman that I came across was very helpful Standing Up to the Lead Industry: An Interview with Herbert Needleman - Whether his persecution appears alleged or real, I still found it quite interesting - especially his time working for Dupont & his comment at the end about the effects of lead at both ends of the distribution curve.
[5] You state: “You also assert that I have “…come to the conclusion that mercury is not likely to be a source of harm in low doses …”. If you read back through my statements, you will see that assertion is false.”
While in Part 1 of your series you stated: “In fact, it is most likely that mercury causes zero cases of autism. However, in order to be rigorously honest, I have to concede that a small number of cases could be caused by mercury and remain undetected by the current techniques employed to study autism.”
I suppose whether or not one finds these two statements at odds with each other brings us back to my other question. Do you remember when you said: “The symptoms of mercury poisoning - “high” or “low” level - do not replicate the symptoms of autism. There is some overlap in the words used and even in some of the symptoms, but the totality of the two look completely different. Influenza and heat stroke both cause a rise in body temperature, but the two conditions do not resemble each other.”
I was asking you to clarify at least some of the major distinctions. There are a number of symptoms that appear to the ignorant lay person to be quite similar, but since social impairment is the primary defining behavioral characteristic of autism, that seems to be the one worth focusing on. And of course, all this needs to be done with the recognition that we know that the effects of neurotoxins on children in the stages of early development & esp. in the womb can vary substantially from the effects on adults. (On the topic of social impairment in adults, this is where Needleman’s recollection about the “House of Butterflies” at Dupont seemed rather pertinent to me)
And FWIW, I was just telling someone today that it appears to me as if something has made this new generation more vulnerable to neurotoxic substances like heavy metal exposure than they were in the past. Judging from Needleman et al’s work, clearly the significant downturn in contemporary functional nutrition plays a serious part in it. Perhaps this is where epigenetics enters the picture - it’s not hard to see how we might have built things up to this point.
Speaking of natural vs unnatural selection, I’d be willing to bet that the areas you mention with naturally high levels of heavy metals are surrounded by populations that are highly efficient detoxifiers…
P.S. FYI - about the comment that you said hung up your filter because there were 5 copies in it. When I hit ‘Submit Comment’ as I would normally, the page refreshed without my comment and without the usual note saying that it was awaiting moderation. I tried several times & the same thing happened. I tried again the next day & ditto. That’s why I had assumed you had blocked me from posting. I don’t know what caused it, but I do know that it began with my first attempt rather than following successive attempts. FWIW.
March 18th, 2008 at 10:45 pm
DoC,
VERY enlightening and well-written blog. I’m impressed with what you have going on here.
I personally have no idea what caused my son’s autism. All I know is that he never “changed” after his vaccinations, he was always autistic. I don’t know if it was passed down from my genes, I don’t know if it came from his father’s side of the family. I mean, maybe I ate too many tuna fish sandwhiches when I was pregnant;) It seems to me the people most concerned with what causes autism are the people who don’t have it or who are bothered by it. Honestly, for the first 2 and a half years of my son’s life I thought he hated me. Finding out he had autism was like a little miracle, I was like, “Yesss! My kid DOESN’T hate me!!! I’m not an awful person!!” Now that I don’t perceive his lack of eye contact and alternative methods of communication as a rejection, we’re getting along really well. Autism I can deal with. Perspective makes all the difference.
March 30th, 2008 at 9:58 pm
“Education and social services criteria for “autism” are even looser than the medical criteria”
That strikes me as being an odd state of affairs. The criteria are the criteria, and - when I ever make a diagnosis - I use the criteria that fit the person who has the characteristics. By this I mean that - if someone meets the Asperger syndrome criteria, then that is the diagnosis. If they are more like the criteria for childhood autism (also listed in ICD 10 as Kanner syndrome), then that is what they get. If there is a presentation that does not meet exactly the criteria for either (many don’t) then there is a number of catch-other categories one can use in diagnosis, one of which is ‘atypical autism’… in DSM, that would be part of PDD-NOS, but ICD retains ‘atypical autism’ and some others that DSM subsumes into PDD-NOS.