Remember this old Bhuddist parable?
Five blind men of Savatthi are all describing an elephant. The problem is that one grabs the tail, the other a leg, the other the side, the other an ear and the fifth, the tusk. Each, remaining blindfolded, seeks to articulate the attributes of an elephant. The one who grabbed the tail insisted that the elephant was like a rope. The one who grabbed the leg was as certain that an elephant was not like a rope, but a tree. The one who was feeling the side of the elephant was convinced that an elephant was like a mud baked wall. The fourth blind man, feeling the ear, was shocked that the others could not understand that the elephant was like a banana leaf. The fifth denounced them all as he held to the tusk, insisting that an elephant was most like a brandished sword.
Every time I hear talk about the ‘autism epidemic’ I remember this parable.
The only way we can _definitively_ establish if thiomersal (or any other vaccine ingredient) causes autism is to take a hundred kids and do a double blind study involving injecting them with either an applicable amount of thiomersal containing vaccines or a control over an established time period.
Obviously, thats never going to happen. Firstly there are the obvious ethics of such a thing – with the prevailing beliefs about what autism is, no parent is going to risk ‘causing’ autism. Secondly there is the more practical reason that there aren’t really any thiomersal containing vaccines left in the West anymore – hence Burbacher’s need to get vaccines and then _add_ thiomersal to them. I suppose our ficticious study could do that but nobody really knows what confounders there may be in such an action. Burbacher certainly didn’t control for them.
So, what else can we do to try and establish if thiomersal (or whatever) can cause autism?
We can examine the symptoms of mercury poisoning (in the case of thiomersal) and see if there seems to be a relationship with autism. This is in essence what the Bernard et al paper tried to do. They concluded there _was_ a link but a closer examination of the paper shows that there is _not one_ common symptom between the diagnstic symptoms of mercury poisoning and the DSM(IV) diagnostic criteria for autism. This fact usually results in two counter-claims. Firstly that the DSM(IV) is not ‘up to the job’ of reflecting the current state of knowledge about autism. Secondly, that autism is such a novel form of mercury poisoning that autism is totally different from all other forms of mercury poisoning.
The first objection is essentially a call to retro-fit the DSM(IV) to fit one persons own beliefs about autism and thiomersal. This is pointless. The DSM criteria (which _are_ periodically adjusted) reflect the symptoms it requires to fulfil a diagnosis of ASD. This means the symptoms are common to _all_ autistic people. People have quoted gut issues, constipation and various other issues to me as ‘evidence’ of the damage resulting in autism, that thiomersal can do. Trouble is, none of the things that get quoted at me are common to all autistic people. These things may be comorbidities. If people have found ways to treat debilitating comorbidities then more power to them I say. I do exactly the same every time I administer a puff of a ventolin inhaler to my daughter. People then go on to say, well, maybe we should start sub-dividing autism into different ‘types’. However, we have no idea what prevalence these ‘sub-types’ might have. As far as we know they might only exist in statistically insignificant numbers that wouldn’t justify a sub-type categorisation. One of the biggest comorbidities is epilepsy. Should we create a sub-category of ‘epileptic autism’. Why? The underlying autism would be just the same. No – this is the very reason why secondary conditions are called comorbidities and not subtypes.
The second theory – that autism is so unique it doesn’t resemble any other form of mercury poisoning – is very hard to take seriously. Anorexia appears to be common across all types of mercury poisoning (its mentioned in Mad Hatters Disease, Pinks Disease and typical mercury poisoning) – why would it skip autism? Occams Razor applies here. The simplest explanation is one which requires no mangling/disappearing/ignoring of known facts – autism doesn’t really resemble mercury poisoning.
So whats next? Epidemiology. We’re left with looking at the numbers.
The ‘autism epidemic’ is central to the thiomersal hypothesis. The argument goes that as thiomersal useage increased both temporaly (vaccines were administered in shorter time frames) and in amount (maximum body burden in the US was 187.5 ug of Hg) that the number of autism diagnosis increased.
The main problem with the epidemic idea is that this chain of events is _far_ from established. The reason is mainly the quality of the underlying data.
There are three main US sources for prevalence data – the Dept of Education, VAERS and CDDS.
Many autism advocacy groups use the data collected by the US Department of Education (USDE) to show a rapidly increasing prevalence of autism. Closer examination of these data to follow each birth-year cohort reveals anomalies within the USDE data on autism. The USDE data show not only a rise in overall autism prevalence with time but also a significant and nearly linear rise in autism prevalence within a birth-year cohort as it ages, with significant numbers of new cases as late as 17 years of age. In addition, an unexpected reduction in the rise of autism prevalence occurs in most cohorts at 12 years of age, the age when most children would be entering middle school. These anomalies point to internal problems in the USDE data that make them *unsuitable for tracking autism prevalence*.
This is a shame but Jim Laidler is absolutely correct that we must use good, accurate data – USDE data clearly isn’t.
VAERS has massive problems. It allows anyone to enter any data at any time. I recently demonstrated this when I, a UK citizen, managed to submit a VAERS entry stating that a vaccine had turned my daughter into Wonder Woman. Clearly, this is not an acceptable source.
CDDS is the most contraversial. Rick Rollens has toally misintrpretted the data time after time. CDDS themselves state that their data should not be used for tracking autism prevalence. However, if it is insisted that we _do_ use CDDS data then we need to be clear about its use. Rick Rollens lumped all stats from all age groups together – quite obviously this results in meaningless data. As David Kirby conceeded:
…total cases among 3-5 year olds, not changes in the rate of increase is the right measure.
When one does isolate this cohort things are very different. In this cohort, nnot only are autism cases still rising, in the last quarter, the increase in the rate of increase is climbing.In other words, when one uses the correct group of cases to examine, data that David Kirby has referred to as ‘the Gold Standard’ for testing prevalence, shows that autism cases are still rising despite his statement in the New York Times in *2005* that:
Because autism is usually diagnosed sometime between a child’s third and fourth birthdays and thimerosal was largely removed from childhood vaccines in 2001, the incidence of autism should fall this year.
However, despite all this, we need to rememember that CDDS disclaimers appply to our interpretation of the data as well as Rollen’s or Kirby’s. However, ours are more accurate and at least are preformed on the right section of the data.
Make sure to read Joseph’s first comment in this thread which addresses another failing of this data I forgot to address.
So there are very large problems with the epidemiology as well. This is vexing and means, as Paul Shattuck recently concluded, that the true growth of autism cannot be realistically determined. So we’re left with the opinions and research of experts – people who study autism. What do they say?
Almost to a man they say that the idea of an epidemic is questionable. They state there may well have been a rise in _numbers_ but not necessarily a rise in _prevalence_. The distinction is important.
What they say is that improved tests and more recognition adds up to more diagnosis. This is simple common sense. If you know what you’re looking for, you’ll find more of it than you would if you _didn’t_ know what you were looking for.
What do we know that might support this opinion? Here are a few ideas from my neck of the woods.
In 2004, an ‘autism audit‘ was performed in Scotland. One of the questions the audit asked was how accurate they thought the prevalence rate estimates were for their area. 45% of authorities who responded made a point of noting that they felt diagnosis for adults was very underrepresented. For example, Perth and Kinross council stated
Figures for adults reflect the national findings that the numbers known to services/diagnosed represent a significant underestimate of those individuals likely to be affected. For example day centre managers locally consider a number of people to be on the spectrum who have had no formal diagnosis.
Also, in a New Scientist piece last year, the findings of the University of Nottingham were reported. The team reexamined data from the 1970’s which resulted in five diagnosis. Using modern diagnostic criteria, the team found 56 cases, a ten-fold increase.
Lastly, earlier this year, Health Minister Liam Byrne reported figures that demonstrated autism diagnoses for children have nearly doubled in 8 years from 3100 to 6170. Meanwhile adult diagnoses have nearly tripled in the same period from 1120 to 3000.
That seems to pretty firmly establish the idea of widescale underdiagnosis. What about misdiagnosis? From its very start as a categorised diagnosis, autism has been misdiagnosed. Kanner mentioned several of his patients were diagnosed with schizophrenia. However, as Shattuck _also_ concluded, its not possible to ascertain to what degree diagnostic substitution in the past has resulted in more cases now we know better.
A fascinating news article caught my eye this morning and led to this post. It seems that even _after_ we factor in more availability of diagnosis and better tests for it, most doctors still don’t screen for autism because a lot don’t know how.
The study of 255 Maryland and Delaware pediatricians found that 209 (82 percent) said they regularly screen their patients for general developmental delays, but only 20 (8 percent) of them said they regularly screen for ASD. Of the pediatricians who said they do not routinely screen for ASD, 62 percent said they didn’t do it because they weren’t familiar with the screening tools.
Remember that this is in a time when awareness and screening tools are better than they’ve ever been – if they’re like this now, just imagine how bad they must’ve been 10, 15 or 20 years ago.
Do you see a rope? A tree? A wall? A leaf? Maybe a sword? Or do you put these things together and percieve an elephant?
Left Brain Right Brain 
Hi Kev. A common argument from the mercury causes autism proponents is that there is a missing elephant. Because I don’t have sources to cite (I haven’t looked in to this yet) I’ll hypothesize only that a substantial portion of this missing elephant can be found within the U.S. homeless population. I think the U.S. homeless population has been estimated to be somewhere between 500,000 and 2 million (based on use of shelters), and it has also been estimated (NYPIRG statistics) that 20-25% of the single adult portion of that population suffers from some form of severe and persistent mental illness [that’s the extent of their definition]. I had some first hand experience with this population on a regular basis in the 1990’s in southern California, and I plan to look into this further.
Good post Kev, but allow me to address some of the points:
The only way we can definitively establish if thiomersal (or any other vaccine ingredient) causes autism is to take a hundred kids and do a double blind study involving injecting them with either an applicable amount of thiomersal containing vaccines or a control over an established time period.
A hundred wouldn’t do because of the prevalence of autism. It would have to be at least 5,000. Also, MarÃa will chime in anytime now and point out that they would need to do this with autistic kids.
People have quoted gut issues, constipation and various other issues to me as ‘evidence’ of the damage resulting in autism, that thiomersal can do. Trouble is, none of the things that get quoted at me are common to all autistic people.
There are a couple contradictory studies on this. One says gut issues are more common, the other says they are as common as in the general population.
The ‘autism epidemic’ is central to the thiomersal hypothesis. The argument goes that as thiomersal useage increased both temporaly (vaccines were administered in shorter time frames) and in amount (maximum body burden in the US was 187.5 ug of Hg) that the number of autism diagnosis increased.
I believe there’s only one paper that tries to correlate thimerosal dose per child with autism prevalence, Geier & Geier (2004). I’ve demonstrated this paper is not only flawed, but also suspect.
The USDE data show not only a rise in overall autism prevalence with time but also a significant and nearly linear rise in autism prevalence within a birth-year cohort as it ages, with significant numbers of new cases as late as 17 years of age. In addition, an unexpected reduction in the rise of autism prevalence occurs in most cohorts at 12 years of age, the age when most children would be entering middle school. These anomalies point to internal problems in the USDE data that make them unsuitable for tracking autism prevalence.
I think this is because kids keep getting diagnosed until they are quite a bit older. That is, increasing recognition happens at all ages. Not all kids are diagnosed at 2 or 3. And then there’s loss of diagnosis in the teenage years. Perhaps 15% of autistic kids lose their diagnosis? (I understand some teenagers ask to be undiagnosed). I have a graph of prevalence by birth year cohort here.
Rick Rollens lumped all stats from all age groups together – quite obviously this results in meaningless data.
Well, the total caseload does give a rough idea of the total administrative prevalence of autism in California. But yes, it’s much better to look at the prevalene in the 3-5 cohort, which is the one that would change more quickly if something happens.
The more serious error Rollens and others frequently make is ignoring that caseload represents only active clients. Substracting caseload one quarter minus that of the previous quarter is not the number of newly diagnosed cases.
In this cohort, nnot only are autism cases still rising, in the last quarter, the increase in the rate of increase is climbing.
I’m not sure that last part is correct. It’s not important if it is anyway. Looking for decreases in the increase is really grasping at straws. Caseload is growing at 10% annually. It can’t possible keep growing this quickly. Growth has to drop necessarily.
I am aware of one practicing doctor who ‘does not believe’ in Aspergers, DCD etc – any of the ‘milder’ end of neurodevelopmental gubbins.
I had to explain trainspotters to a European friend a couple of months ago when we were travelling around London. Her mum works in special education, and she said “they are all autistic, right?”. The UK’s ‘Hidden Horde’ is hidden in plain sight, on the ends of railway platforms and preserved steam railways.
(Declaration of interest: my family like preserved steam railwways too)
An elephant is pretty darned hard to misplace.
The Horde has never been hidden. It just wore clever disguises.
Hi Joseph
You said
Also, MarÃa will chime in anytime now and point out that they would need to do this with autistic kids.
I would not consider adequate any study of this kind because I think that there is potential of real harm. The problem, as I always tell you, is that we do not know since birth because there is not biomarker known for all ASD population about immune weakness that could be related to negative effect of vaccines in autistic population. What I have tried to say is that biochemistry of ASD should be studied carefully – from the diagnosis because we do not know going back- to know about the potential effects that vaccines could do and what subset can be more susceptible to potential of negative effects.
Joseph, this was not fair. Ethics is a main concern for me and I hope that any study involving autistic children teens and adults consider it carefully.
Again, I think that to consider risks is the main issue in any study involving autistic children, because of their different biochemistry.
Sincerely
MarÃa Luján
You can find a piece of the Hidden Horde at Sci Fi conventions, too. There are at least 2 of the adults on the Autistic Adult Picture Project who are in their late 30’s to late 40’s and who have been big Star Trek Fans. Parrish is wearing a star-trek uniform if I remember right. There’s a photo of another man relaxing in a hotel lounge or something during a treker convention. I think they are also to be found at “society for creative anachronism” events.
Bird watchers? Those guys who hand grind their own telescope lenses? Chess clubs. Linux users clubs.
And certainly among the records of suicides and in prisons (homeless people end up in jail alot) and living under bridges, etc.
Great post, Kev. Each specialist sees autism through his own specialty which is why to Wakefield autism is almost purely a gut disorder you don’t hear him talking about the cingulate cortex or the amygdala. To Dr. Pessah autism is about ranatadine (sp?) receptors because that’s his specialty. It used to be that JB Handley said all autism was mercury poisoning, but now he seems to be saying that it’s a viral thing and can be cured with valtrex. Maybe JB will correct me here if I got that wrong.
I would add, though, that the kind of study you propose ought to be doable in poor countries where the kids are getting vaccinated with TCVs right now. Just send lots of thimerosal preserved vaccines to half a nation and thimerosal free vaccines to the other half of the nation for a year or two and follow autism rates between the two halves.
That would give you the large N you need. The WHO is not freaking out about thimerosal in vaccines. Why? Oh, yeah, the mercury phobes will say that the WHO is part of that worldwide conspiracy…
On ASD and the homeless-
When I was at U of Mich, the organic department had seminar every Wednesday, 4 pm with coffee and dough nuts. One day an obviously homeless man came in, got a cup of coffee and sat down. He listened politely, and during Q&A asked a question that demonstrated a background in quantum mechanics. I had never heard of autism then, but I wonder about him sometimes. Was he an Aspie who could understand physics but not function at a job? How many are there like him?
Joseph, this was not fair. Ethics is a main concern for me and I hope that any study involving autistic children teens and adults consider it carefully.
I did not imply that you would send autistic kids to be harmed. I was only referring to proper study design. (I don’t believe they’d be harmed anyway).
Much of the hidden horde has an ADHD diagnosis. About 4.4% of the adult population is ADHD. One study in Europe screened ADHD adults for an ASD comorbidity and found that 30% had ASD as well. Do the math. There are plenty of findings of this nature.
The only way we can definitively establish if thiomersal (or any other vaccine ingredient) causes autism is to take a hundred kids and do a double blind study involving injecting them with either an applicable amount of thiomersal containing vaccines or a control over an established time period.
Obviously, thats never going to happen.
What about this CDC study?
The thimerosal follow-up study compares performance on a number of neurodevelopmental measures (such as speech and language skills, attention, coordination, tics, and hearing) among children who were exposed to different amounts of thimerosal through vaccination and other exposures. This study was designed to look more closely at inconsistent findings from the earlier, 2003 VSD study listed above. It does not assess autism or Autism Spectrum Disorders (ASD) as possible outcomes of thimerosal exposure through vaccination. The study includes over 1,000 children 7 to 10 years of age. The researchers collected information from the children’s medical records, gave them standardized tests, and interviewed their parents about things that could influence the results of the study (such as a mother’s diet during pregnancy and parental health seeking behavior). Although CDC funded this study, 13 non-CDC expert consultants gave input on the study design, conduct, and analysis. All of the information (data) needed for this study has been collected. Initial preliminary results are being reviewed by the expert consultants and the CDC study investigators. Researchers will continue to analyze the data and final results are expected to be published in 2006.
The thimerosal and autism case-control study. The possibility that exposure to mercury may cause autism has probably caused the greatest concern about exposure to thimerosal as a preservative in childhood vaccines. Although the weight of scientific evidence, including results from the VSD study, do not support this association, autism can be difficult to diagnose and study data based on autism diagnosis from medical computerized databases can be difficult to verify. This study is designed to address these issues.
The Thimerosal and Autism Study.
CDC is conducting a study through the Vaccine Safety DataLink in which thimerosal exposure in children with autism is being compared with children who do not have autism. The cases of children with autism are being evaluated in-person by certified specialists using the most up-to-date standardized diagnostic assessments. Researchers also are reviewing medical records and interviewing children’s parents to assess any factors that could influence the study’s findings. The study is anticipated to be completed in September 2008.
The study includes over 1,000 children 7 to 10 years of age.
Unfortunately, I don’t think this addresses concerns. Let’s suppose that thimerosal affects 5 of 10,000 children aged 1-2.
That said, it appears to be very difficult to design a study that will make everyone happy once and for all.
Kev wrote: “This fact usually results in two counter-claims. Firstly that the DSM is not ‘up to the job’ of reflecting the current state of knowledge about autism.â€
And
“The first objection is essentially a call to retro-fit the DSM to fit one persons own beliefs about autism and thiomersal. This is pointless. The DSM criteria (which are periodically adjusted) reflect the symptoms it requires to fulfil a diagnosis of ASD. This means the symptoms are common to all autistic people. People have quoted gut issues, constipation and various other issues to me as ‘evidence’ of the damage resulting in autism, that thiomersal can do. Trouble is, none of the things that get quoted at me are common to all autistic people. These things may be comorbidities. If people have found ways to treat debilitating comorbidities then more power to them I say. I do exactly the same every time I administer a puff of a ventolin inhaler to my daughter. People then go on to say, well, maybe we should start sub-dividing autism into different ‘types’. However, we have no idea what prevalence these ‘sub-types’ might have. As far as we know they might only exist in statistically insignificant numbers that wouldn’t justify a sub-type categorisation. One of the biggest comorbidities is epilepsy. Should we create a sub-category of ‘epileptic autism’. Why? The underlying autism would be just the same. No – this is the very reason why secondary conditions are called comorbidities and not subtypes.â€
I don’t agree. The DSM-IV is loose enough that two people can have an autism diagnosis without a single criterion (as distinct from broad category) in common. Are we really sure that there is only one idiopathic autism? If so, based on what scientific evidence? Those searching for the underlying genetic explanation suspect that there may be as many as 15 or more genes involved in several potential combinations. If so, then the potential for more than one type of autism based on genetics alone is not far fetched. How many autistics have SI issues? Are they a comorbidity, or do they drive much of the autistic presentation? Are SI issues part of the DSM-IV?
You seem to be ruling out ‘sub-types’ on the basis that they may be statistically insignificant numbers, but what if they are not? Until someone makes the effort to at least properly list and quantify the comorbidities, you cannot say that they are comorbidities and not essential to certain sub-types. You can only assume. I’d suggest that saying that we don’t understand them and then using our lack of knowledge as a basis for not exploring them is an interesting bit of circular reasoning.
So if a potential characteristic of autism is not currently part of the DSM-IV then should it be assumed to be merely a comorbidity? GI issues are not part of the DSM-IV. Neither are SI issues. But neither is autistic intelligence, as explored by Mottron and Michelle Dawson. Is autistic intelligence then merely a comorbidity? Does its absence from the DSM-IV mean that it is not real, or that only some autistics possess ‘autistic intelligence’ or ‘autistic cognition’? Of course not. But then do we only allow for the possibility of counting currently non-DSM-IV criteria that we like, or that cast autism in a favorable light?
Unfortunately, any potential non-behavioral characteristic of autism – especially those that might be medical in nature – seems to get caught up in the thimerosal argument. The potential existence of medical – as distinct from behavioral – characteristics of autism does not automatically support or refute a thimerosal argument or suggest that autism is or is not a valid state of ‘being’. If these medical conditions are properly investigated, this may one day allow for the treatment of what are today considered comorbidities, without negatively impacting autistic intelligence but instead improving the quality of life of those who wish to pursue treatment. What if autistic epilepsy is treatable without compromising autistic thought? Is this not worth exploring? Or should epilepsy research be limited only to those who are non-autistic, even if epilepsy turns out to be much more common in autistics than in the general population? Investigation may even definitively disprove the thimerosal hypothesis by finding provable alternative causation. But if we close the door to this possibility, we’ll never know. And how does that help anyone?
An elephant is pretty darned hard to misplace.
The Horde has never been hidden. It just wore clever disguises.
So THAT’S why an elephant wears green sneakers (or paints their toenails red). 🙂
IP: “The DSM-IV is loose enough that two people can have an autism diagnosis without a single criterion (as distinct from broad category) in common.”
What? Ridiculous!
The categories *are* the criteria! If you were to narrow the diagnosis down to exact-same behaviours, hardly any dx would be made!
David Andrews writes:
“What? Ridiculous!
“The categories are the criteria! If you were to narrow the diagnosis down to exact-same behaviours, hardly any dx would be made!”
Jonathan has listed the DSM-IV criteria here.
“A total of six (or more) items from (1), (2), and (3), with at least two from (1), and one each from (2) and (3):”
Is it not possible for person A to have 1 a & b, 2 a & b, 3 a & b and another to have 1 c & d, 2 c & d, 3 c & d? Is there any overlap there?
Ms Clark writes: “At any rate, no one, to my knowledge is arguing that seizures should go untreated.”
Agreed. I’m just suggesting that for comorbidities in which autistics have a higher rate than the rest of the population, there may be some justification to researching them in relation to autism rather than just assuming that there is no link without evidence to support this position. Epilepsy was Kev’s example, so I went with it. I’m just as content to discuss SI instead.
Regarding thimerosal, I’m not arguing for or against, but rather that there may be merit in investigating comorbidities in relation to autism rather than just assuming that there is no link or sub-types. I’d suggest the same even if thimerosal never existed – I’m probably one of the few who isn’t hung up on it, either for or against.
Mr Parker,
Are you familiar with Dr Amaral’s Autism Ahenome Project (APP)? They are already gathering data on blood proteins and various measurements of behavior and head size, maybe shoe size, for all I know, but they are getting a massive amount of information on kids, starting as young as possible, 2-4 with 2 being better than 4… they are doing intensive screening for all kinds of chemicals that the kids may have been exposed to, including their vaccinations… Dr. Amaral’s scientists have already found major differences in chemicals in the blood of babies who are later dxd with autism.
The thing is that they are trying to get this big batch of data to see if, for instance, the kids with a certain allelle of a certain gene, all stop talking at age X and all have moms who dye their hair or use bug spray or all the ones with big heads also teach themselves to read at age 3… to see if they can find these legendary, subtypes, of course, they should be able to turn up a few kids who enter the California DDS system as your basic “autistic” but who have Fragile X, Angelman’s, mitochondrial disorders, the MeCP2 (Rett) gene, or some other missing chunks of chromosome or whatever…
Dr. Hertz-Picciotto has been running the CHARGE study for a while now and has found nothing to indicate an influence of mercury on autism prevalence in California.
Speaking of “CHARGE”, some people have commented to me that they thought the CHARGE acronym was confusing because there is a disorder called CHARGE association, which I knew about back in 1981 or so, because I met a mom who’s son had it… anyway, I was talking to a gray-haired mom of a young man with an ASD diagnosis and some serious physical problems… she was telling someone at the MIND how sweet her son was and how much she enjoyed him… etc, she said the doctors thought he might have the CHARGE Association, but he wasn’t an obvious example of it.
—
update, I’ll be getting a DTaP vaccination tomorrow because pertussis is going around at the high-school I go to to observe 3 hours a week, and if I get it my child could die if xe caught it from me. The potential death of my child and others being one of those little minor annoyances caused by not enough people getting vaccinated to keep the outbreaks down.
Ooops, I was changing lower case letters to capitals and got and “A” where I wanted a “P” it’s “Autism Phenome Project.”
Hi Ms Clark,
Is Dr Amaral’s Autism Phenome Project (APP) the one recently announced that is being conducted by UC Davis? If so, I have heard of it and think that it is a great idea. If not then I haven’t heard of it and would welcome more info.
As I’ve said elsewhere (and I don’t expect everyone to agree with me on this view), I have no issues with autistic thought and think that there is nothing to ‘cure’. My concern is with the issues that come with autism, esp. SI issues. I’m probably closest to a ‘genetic vulnerability linked to immune/autoimmune causation’ viewpoint, believing that this may be driving the SI issues. I don’t “know” this, but it strikes me as a reasonable hypothesis, and I support research in this area (not that anyone conducting this research is asking for my support or opinion).
I also believe that there is more than one cause of autism, and other people who lean close to the neurodiversity POV have said the same thing. Strangely though, it only seems to be a controversial statement if it comes from me. It may be because the battle lines between the mercury and non-mercury causation groups are so sharply drawn that people have a hard time believing that someone could have an alternate POV, and therefore must be hiding their ‘real’ opinion. Anyway, by identifying, categorizing and quantifying the various ‘comorbidities’ it may be possible to isolate subtypes. This research may also find that subtypes don’t exist, but without investigating we’ll never know.
Mr. Parker asked,
_Is it not possible for person A to have 1 a & b, 2 a & b, 3 a & b and another to have 1 c & d, 2 c & d, 3 c & d? Is there any overlap there?_
The answer is, “No.”
If you have A 2 a you can’t simultaneously have A 2 b, they are mutually exclusive.
—– also:
If a person has A 1 a, he’s probably going to have A 1 b as a natural consequence,
and if he gets A 1 c, he’ll likely get A 1 b also, as a natural consequence.
likewise if he gets A 1 d, he’ll likely have A 1 b …
Though your point is almost correct, there is wide variation of what autism looks like, and we haven’t even thrown in the other PDDs. My child mostly fits PDD,nos, but with a tiny bit of squinting xe really could fit in Autistic Disorder quite well. Basically, if it’s applied as is in the DSM everyone who fits Asperger’s also fits autism.
—
A
(1) qualitative impairment in social interaction, as manifested by at least two of the following:
(a) marked impairment in the use of multiple nonverbal behaviors, such as eye-to- eye gaze, facial expression, body postures, and gestures to regulate social interaction
(b) failure to develop peer relationships appropriate to developmental level
(c) a lack of spontaneous seeking to share enjoyment, interests, or achievements with other people (e.g., by a lack of showing, bringing, or pointing out objects of interest)
(d) lack of social or emotional reciprocity
(2) qualitative impairments in communication, as manifested by at least one of the following:
(a) delay in, or total lack of, the development of spoken language (not accompanied by an attempt to compensate through alternative modes of communication such as gesture or mime)
(b) in individuals with adequate speech, marked impairment in the ability to initiate or sustain a conversation with others
(c) stereotyped and repetitive use of language or idiosyncratic language
(d) lack of varied, spontaneous make-believe play or social imitative play appropriate to developmental level
(3) restricted, repetitive, and stereotyped patterns of behavior, interests, and activities as manifested by at least one of the following:
(a) encompassing preoccupation with one or more stereotyped and restricted patterns of interest that is abnormal either in intensity or focus
(b) apparently inflexible adherence to specific, nonfunctional routines or rituals
(c) stereotyped and repetitive motor mannerisms (e.g., hand or finger flapping or twisting or complex whole-body movements)
(d) persistent precoccupation with parts of objects
B. Delays or abnormal functioning in at least one of the following areas, with onset prior to age 3 years: (1) social interaction, (2) language as used in social communication, or (3) symbolic or imaginative play.
C. The disturbance is not better accounted for by Rett’s disorder or childhood disintegrative disorder.
_”You seem to be ruling out ‘sub-types’ on the basis that they may be statistically insignificant numbers, but what if they are not? Until someone makes the effort to at least properly list and quantify the comorbidities, you cannot say that they are comorbidities and not essential to certain sub-types. You can only assume. I’d suggest that saying that we don’t understand them and then using our lack of knowledge as a basis for not exploring them is an interesting bit of circular reasoning.”_
But I’m _not_ saying that Ian. You correctly say that I said that they _’may’_ be statistically insignificant. I certainly don’t claim they _are_ at insignificant occurrence. I was attempting to make the same point as you – we just don’t know. I also would never say we shouldn’t investigate further. We should.
A lot of the issues that arise come about due to our state of total knowledge. Its pretty paltry. We are really nowhere near understanding a cause (Rett excepted) except that it obviously has a genetic aspect (autism has 60% hereditary levels), but what that exact genetic aspect may be is still largely conjecture. We also may strongly suspect some environmental trigger for some people (immune disorder etc) may play a role but this is even more in the dark than the genetic variables.
If I may drop the elephant analogy and move onto a ‘darkroom’ analogy? We’re all like people in a pitch black room trying to find the door ‘out’ into the light of understanding (if you’ll forgive the overly flowery phrase). All we have to find that door is what we know for certain about where we are and our knowledge of rooms and doors. However, when we try and move forward we still need to wave our hands about to make sure we don’t crash into anything.
In this analogy, the ‘knowledge of rooms and doors’ is the DSM criteria. These are things _we know_ about autism. I’d hazard an opinion that in scientific (and definitely diagnostic) terms, we _know_ nothing else. We should play around with that knowledge at our peril. If we want to shape it, or adjust it, or throw it aside then we need to have _knowledge_ to make that action. We cannot afford to reply on guesswork or ‘maybes’. Even if we strongly suspect that X (using X to avoid naming controversial subjects) is a good candidate for an environmental trigger, until we _know_ with the same certainty that we _know_ of the accuracy of the existing DSM, then we should not tinker with it. If we do, we tinker with the only solid bit of scientific knowledge we really have.
_”So if a potential characteristic of autism is not currently part of the DSM-IV then should it be assumed to be merely a comorbidity? GI issues are not part of the DSM-IV. Neither are SI issues. But neither is autistic intelligence, as explored by Mottron and Michelle Dawson. Is autistic intelligence then merely a comorbidity?”_
Well, I’d hesitate to use the word ‘merely’ about anything to do with autism. I’d also suggest that the idea of comorbidity relates to secondary medical _conditions_ which I think is not really how we can think of any type of intelligence. Further, I think one would be very hard pressed to make a case for intelligence forming a part of a diagnostic criteria. Maybe an interesting offshoot would be to look at methods of thinking and/or processing information but intelligence itself? I don’t see how it could work as you posit it.
_”Does its absence from the DSM-IV mean that it is not real, or that only some autistics possess ‘autistic intelligence’ or ‘autistic cognition’? Of course not.”_
A secondary conditions absence from the diagnostic criteria does not in any way mean that that secondary condition is not real. What I think it means is that we cannot use that secondary condition to make a diagnosis of ASD.
_”But then do we only allow for the possibility of counting currently non-DSM-IV criteria that we like, or that cast autism in a favorable light?”_
No. I think we should only allow for the possibility of counting things that apply universally.
I agree with Ian that children with ASD can be totally different from one another, particularly when you include PDD-NOS where a minimum number of characteristics is NOT specified. In particular, you can have a child with a simple language delay and some sterotypical behavior (hand flapping, for example), and that alone can get them a PDD-NOS diagnosis. These children can be perfectly sociable, exhibit no obsessions, and still be PDD-NOS. Don’t forget that the 1 in 166 includes PDD-NOS, and in fact PDD-NOS can be a majority (or very large fraction) of the total, depending on which study you are looking at.
FAO All: I’ve added in the ability to edit one’s own comments. Its only applicable for 30 minutes after the comment is posted and you must be using the same IP address as the one you posted with (if you haven’t shut down your internet connection since commenting it won’t have changed).
This is to help with the odd spelling error/typo/brain fart.
If you click the ‘edit this’ link in the head of your comment, it will reload the page with your existing comment in the comment form. make your adjustments and repost :o)
Ian said: I also believe that there is more than one cause of autism, and other people who lean close to the neurodiversity POV have said the same thing. Strangely though, it only seems to be a controversial statement if it comes from me.
Not in my book Ian. Though I may not agree with all you say, I don’t find your words to be controversial in the least. Thoughtful, honest and intelligent commentary should always be welcome.
Hi Ms Clark,
You got me. I was being intellectually (if I may use that word in relation to my thoughts) lazy and threw down a couple of profiles without considering either/or criteria. I should probably have gone with 2 a & d vs. 2 b & c. But I think we agree that there is a wide variation in autistic presentation, and I agree with your thoughts re: similarities with the other PDDs.
Regarding 1b, I have some issues with this one, in that I agree with Dr. Gernsbacher (if I’m interpreting her correctly) that this may be categorizing the ASD child on the basis of what is in fact an issue of reciprocity (i.e. it takes two to tango). But that’s another discussion.
Hi Kev,
I know you ‘got there’ by “This fact usually results in two counter-claims. Firstly that the DSM is not ‘up to the job’ of reflecting the current state of knowledge about autism.â€, but I interpreted (over-interpreted?) what followed – i.e. your thoughts on changes to the DSM-IV – as ‘should we ever’ as distinct from ‘should we today’ allow for the possibility of sub-types.
As long as you’re not opposing researching further (and you clearly indicate above that you are not in opposition), and are open to the possibility of future changes as the state of knowledge evolves, then we are not in disagreement. I agree with you that we should not change the DSM-IV on the basis of what ‘might be’, but need knowledge to do so. I like your statement, “If we want to shape it, or adjust it, or throw it aside then we need to have knowledge to make that action. We cannot afford to reply on guesswork or ‘maybes’.â€
I do get stuck on “I think we should only allow for the possibility of counting things that apply universally.†As above, I’d suggest that there is a lot in the DSM-IV today that does not apply universally. But that is semantics if the prior identification of sub-types allows for their inclusion in future criteria, if and only after the knowledge exists to justify them.
Hi Clone3G,
Thank you. I really appreciate your comment.
Ian,
I appreciate your contributions as well. I tend to agree with your basic premise – that autism may have various sub-types influenced by different things…or it may not.
My objection to the mercury folks has never been so much that they’re wrong as that they’re premature and simply speculating. Based on the amount of research they’ve brought to the table to date as well as the prevailing data wrt autism, there is no plausible way they can even suggest that thimerosal has anything to do with neurodevelopmental disorders. In ten or twenty years, may we know differently? Sure, if we have a better understanding of the etiology of autism.
My gut feeling is that there is some kind of environmental component to at least some “flavors” of autism, but I readily admit that is little more than my gut feeling. I am also inclined to believe that post-natal heavy metal exposure is unlikely to be one of those components. But I am more than willing to admit I’m wrong if provided reasonably compelling evidence to the contrary.
GI issues are not part of the DSM-IV. Neither are SI issues. But neither is autistic intelligence, as explored by Mottron and Michelle Dawson. Is autistic intelligence then merely a comorbidity?
Yes, actually. These are not diagnostic characteristics. Their prevalence (presumably) is simply higher than that found in the general population.
If these medical conditions are properly investigated, this may one day allow for the treatment of what are today considered comorbidities, without negatively impacting autistic intelligence but instead improving the quality of life of those who wish to pursue treatment.
I tend to agree with you, Ian. And it applies to any blanket term for a phenotype. If we continue to investigate the causes of mental retardation, we might find some types which are treatable (and some have been found which are treatable). But at the end of the day, 3% of the population will always score in the 3 percentile in IQ tests. Hence, mental retardation as a whole is inherently non-curable.
Ian said: Unfortunately, any potential non-behavioral characteristic of autism – especially those that might be medical in nature – seems to get caught up in the thimerosal argument.
Which is one reason why it becomes difficult to adopt a neutral position regarding the thimerosal hypothesis.
Whether you realize it or not, attempting to roll up any and all research in with the grande thimerosal burrito makes it harder to swallow the individual side dishes.
If you truly support unimpeded and objective scientific investigation, the thimerosal issue should bother you immensely.
If, for example, GI issues are more common in autistic individuals, why should that be held up as evidence of persistent measles infection which is evidence of a thimerosal weakened immune system?
Communication between the brain, the gut, and the immune system, is multiplex. Who is to say which symptom precedes or causes the other? It would be nice to find out and perhaps treat related or independent health issues but the thimerosal-did-it mentality does not create a researcher friendly environment. Unless of course the researcher supports the hypothesis and is willing to play ball with the major autism orgs.
I wish I could sit back and say, “Oh well. That doesn’t sound right but it doesn’t concern me.” but it does concern me. Bad science and bad science policies should concern us all whether they come from the current US administration or the mercury militia.
There is recent news story about surgical correction of epilepsy for Tuberous Sclerosis patients. TSC can cause seizures and autism. I won’t comment on the article but it may be relevant to this discussion.
http://www.medpagetoday.com/Neurology/Seizures/tb/3259
Anonimouse, thank you for your kind words.
Clone3g, I’ll try to respond later this afternoon, but I have to take my daughter to PECS soon, and don’t have time to give a proper reply. Thanks.
IP: ““A total of six (or more) items from (1), (2), and (3), with at least two from (1), and one each from (2) and (3):â€
Is it not possible for person A to have 1 a & b, 2 a & b, 3 a & b and another to have 1 c & d, 2 c & d, 3 c & d? Is there any overlap there?”
I am trained to make this diagnosis, although we don’t use DSM in Europe… in fact, in Finland we use either the ICD 10 criteria or (if we suspect an AS dx) the Gillberg & Gillberg criteria (which were actually operationalised from Asperger’s own work).
My colleague has pointed out in her post the mutual exclusivity of 2a and 2b.
Regarding the notion of possibility for dx to be confirmed in any two individuals without either having a single criterion in common, my point is that the broad categories themselves are the criteria.
In your example, you list combinations of elements from the sets of issues forming the criteria themselves… and when those elements are combined in the ways which fulfil the criteria, the diagnosis is confirmed; it doesn’t matter what elements they are, as long as the criteria are confirmed. In either case you state (if we agree to the 2a/2b thing maybe being resolved as either of those and one other non-exlusive element from the set), the diagnosis is confirmed on the basis of the criteria which are fulfilled, rather than one the basis of elements from the sets themselves.
To use your terms, yes, the overlap is there: subject to my amendment above, the criteria are fulfilled and they are identical criteria (as they need to be for the dx to be made). There may be no appreciable overlap between the elements of the sets that would signify differing *presentations* of the syndrome, but the criteria do – by definition – overlap.
_My colleague has pointed out in her post the mutual exclusivity of 2a and 2b._
(blows a kiss to David Andrews) 🙂
Thank you all for a very interesting exchange of ideas to read. I think that you have pointed very important aspects about autism diagnosis and perspectives of approach to the limitations and problems with DSMIV criteria and what comorbidities serious research can/ can not imply.
Ian , when you say
If these medical conditions are properly investigated, this may one day allow for the treatment of what are today considered comorbidities, without negatively impacting autistic intelligence but instead improving the quality of life of those who wish to pursue treatment.
I agree completely.
MarÃa Luján
There is recent news story about surgical correction of epilepsy for Tuberous Sclerosis patients. TSC can cause seizures and autism. I won’t comment on the article but it may be relevant to this discussion.
Shoot, *I* want that surgury protocol. Keep electrodes in my head for a month if you have to…the medgoround with NO RESULTS sucks.
Incidentally, epilepsy can kill you, either via SUDEP or status epilepticus…good reason to aim for seizure-free-ness.
*no TSC, just mecp2 related autism & epilepsy that won’t quit*
(sorry, slightly off topic here)
Hi Clone3g,
You state based on my quote that unfortunately any potential non-behavioral aspects of autism get caught up in the thimerosal argument that: â€Which is one reason why it becomes difficult to adopt a neutral position regarding the thimerosal hypothesis.â€
And
â€If you truly support unimpeded and objective scientific investigation, the thimerosal issue should bother you immensely.â€
I stated that: â€Regarding thimerosal, I’m not arguing for or against, but rather that there may be merit in investigating comorbidities in relation to autism rather than just assuming that there is no link or sub-types. I’d suggest the same even if thimerosal never existed – I’m probably one of the few who isn’t hung up on it, either for or against.
By that I mean that my view of autism does not live or die based on whether thimerosal as an agent of causation is proven or refuted. My thoughts on causation stray much further than thimerosal
To me there are two thimerosal hypotheses: a) thimerosal may be a (not the) causative agent in some (not all) cases of autism, and b) all autism = mercury. My thoughts regarding the first hypothesis are substantially different from my thoughts on the second and my opinion of the conduct of the debate (which I’d suggest has become an ideological crusade).
I support legitimate peer-reviewed scientific research into the role – if any – of thimerosal in autism causation (hypothesis a), just as I support other lines of inquiry, including genetic, environmental, and immunological research. But I reject the ‘all autism = mercury’ hypothesis (i.e. hypothesis b), I dislike the poor science that has been conducted and put forward as ‘proof’ of a mercury-autism link, I am disappointed in the DAN! Doctors who claim to have methods to potentially ‘cure’ autism but conduct either no research or poor quality research, I oppose the support of the thimerosal hypotheses using research that has been effectively refuted, I oppose the misuse of data and the drawing of clearly erroneous conclusions to garner public support, I agree with Kev’s ‘Enough’ post, I am angry at the environment created when legitimate non-thimerosal research and researchers are challenged by those who think we should take a one track only approach, I object to the language used by some of the autism = mercury crowd (‘train wreck’ really bugs me, as does the depiction of our children’s souls as being kidnapped, and I really wish that all concerned would learn how to spell cuckoo.
But, on the other side, I also think that some are so unwilling to give any credence whatsoever to the idea that thimerosal could have any impact that they object to any view on idiopathic autism beyond genetics, because it may open the door to a new paradigm. The anti-‘thimerosal as causation’ view has widened to oppose a lot more than just the core autism does not equal mercury viewpoint. I don’t see many posts or comments publicly supporting non-thimerosal autism causation research these days. Even genetic research is causing alarm.
My view is that there is a lot more to talk about than just thimerosal. I try to stay away from the topic as much as I can (I think everyone else has it just about covered), jumping in occasionally to attempt to support research beyond pure genetics as well as moderate interventions that can potentially improve my daughter’s quality of life, including some that many consider quite mainstream. This is the direction that I am also trying to take in my blog, unsuccessfully.
David Andrews writes:
“Regarding the notion of possibility for dx to be confirmed in any two individuals without either having a single criterion in common, my point is that the broad categories themselves are the criteria.â€
Okay. If it is a terminology issue then I’ll gladly switch the word category to item and make the same statement: The DSM-IV is loose enough that two people can have an autism diagnosis without a single item (as distinct from broad criteria) in common. My point is still the same.
From Ms Clark (above):
(3) restricted, repetitive, and stereotyped patterns of behavior, interests, and activities as manifested by at least one of the following:
(a) encompassing preoccupation with one or more stereotyped and restricted patterns of interest that is abnormal either in intensity or focus
(b) apparently inflexible adherence to specific, nonfunctional routines or rituals
(c) stereotyped and repetitive motor mannerisms (e.g., hand or finger flapping or twisting or complex whole-body movements)
(d) persistent precoccupation with parts of objects
My daughter meets 3 c. She does not qualify under 3 a and 3 d, and she is about as opposite from 3 b as one can be. If you consider her qualification under ‘criteria’ 3 as the same as a child who qualifies under 3a, b and/or d then I guess I should accept your appeal to authority. I’ll leave it up to those reading this to determine if they agree that my daughter’s and this ‘other’ child’s autism are the same or if they think that there is a difference between the two based on the qualifying items.
Ian, first and foremost, I have to say that your discussion seems refreshingly welcome and open-minded. I chatted briefly at another blog with you elsewhere and thought the same. Bravo for not taking a black and white approach in general. Although I don’t necessarily agree with everything you’ve written, I’ve enjoyed reading the portions of your blog that I have read.
But, on the other side, I also think that some are so unwilling to give any credence whatsoever to the idea that thimerosal could have any impact that they object to any view on idiopathic autism beyond genetics, because it may open the door to a new paradigm.
I think the truly scientific would not be as quick to adopt a 100%-genetic view as could be inferred from this statement. The scientific realtity today is that the unknowns greatly outweigh the knowns of autism. Although I see heritability as likelihood as a major influence, there are circumstances with my own son (involving pregnancy, delivery, prematurity and first weeks of life complications compared to typcical) that lead me to remain open-minded. As far as unwillingness to open a door to a new paradigm with respect specifically to thimerosal, I’m not convinced there’s scientific evidence to suggest that there is anything to it. I’m open-minded to the idea, but scientific evidence is required. I also think Maria provides some very valid input in this respect, in that she is open-minded and in pursuit of additional knowledge, yet she also insists on valid science.
The anti-‘thimerosal as causation’ view has widened to oppose a lot more than just the core autism does not equal mercury viewpoint. I don’t see many posts or comments publicly supporting non-thimerosal autism causation research these days. Even genetic research is causing alarm.
That’s a good point. I think even the genetic research is concerning because it appears so strongly supported by many who are quick to demonize autism, discuss burden on society, and play in to fear and misunderstanding in general. I would speculate that there are many who consider themselves most closely aligned with Neurodiversity, who are not opposed to reasearch at all, with understanding etiologies as the primary goal. Understanding etiology and wanting to prevent or ‘cure’ autism are two very different things.
I’ll leave it up to those reading this to determine if they agree that my daughter’s and this ‘other’ child’s autism are the same or if they think that there is a difference between the two based on the qualifying items.
I think the answer is “currently unknown” as to whether there is a difference between the two based on the qualifying items. It looks like your asking about etiology, which the DSM does not.
Kassiane said: “Incidentally, epilepsy can kill you, either via SUDEP or status epilepticus…good reason to aim for seizure-free-ness.”
Exactly. Which is why my son’s seizures that were becoming non-stop when he was two days old was a very big concern. Fortunately the first dose of phenobarbitol stopped them, and he was weaned from it when he was one year old (he had one other seizure while dehydrated due to a gastro infection).
Not so fortunate was a younger classmate in his special ed. preschool. When that boy was in 2nd grade he had is first seizure in school… one that caused him to stop breathing. Fortunately the staff there kept him alive, the ambulance came quickly… as did his mom (who almost ran me over in the hallway… I also had gotten out of the way of the ambulance in front of the school).
Until his seizures were controlled by the time he was in middle school, his mom only ever let him out of her sight when she let him off in his classroom in the morning. (he did start having seizures on a semi-regular basis, about once every few months…. each time he stopped breathing).
Then it turns our that his little brother had a worse time learning to speak. Turns out he had Landau-Kleffner Syndrome. He was also having seizures, but they were only noticed with an EEG… and with an MRI. The little brother got surgery to stop the seizures, but he still has some serious neuro-impacts. I haven’t seen him since he was six years old, and he was still not speaking. (the older brother was doing well, though still in a self-contained education program).
There were some definite genetic factors in that family. But then again… in our family it seems that the seizure tendency is related to a strong history of migraine headaches (not my family… the other side, my family contributed the genetic heart condition).
A silly aside… One of the last times I spoke to the mom of these two boys was at the pool when they were getting “special pop” swim lessons. About the same time during my kids’ regular swim lessons I was talking to another mom whose younger boy was NOT going to get swimming lessons until he grew out of a uncommon but known bit of neuro bizarreness. Every time this child’s face got covered in water he stopped breathing. She found this out when she tried giving him a bath as a toddler. She had a name for it, but I can’t remember it. This was a long time ago (the interesting things you learn while conversing during kid swim lessons!).
_”I really wish that all concerned would learn how to spell cuckoo.”_
/penny drops
Ahhh – is _that_ what he meant?
How nice it is by the way to have a thread on here without the usual dumbing down and ranting from certain absent people. Long may it remain so.
HN: Your son was lucky that the pheno. worked and that he’s been basically seizure free since.
The classmate is relatively lucky too. I met a girl who needed a helmet because of Lennox-Gastaut, which includes loads and loads of drop seizures. Landau-Kleffner can be pretty narly toom but in a different way…a sibling of one of my former tumbling students had it, and his seizures were controlled, but the aphasia was BAD. Poor kid, his teachers didn’t understand what he was trying to say, and he didn’t understand what THEY were saying if they used new words…I don’t know how he was as mellow about it all as he was. Especially since he went through four dx’s before anyone saw fit to do an eeg *eyeroll*
I liked him. Good kid. Hard worker. Took being different in stride. And he does a mean somersault.
-Miss Off Topic
who’s met way too many kids…-giggle-
IP: “If you consider her qualification under ‘criteria’ 3 as the same as a child who qualifies under 3a, b and/or d then I guess I should accept your appeal to authority.”
Appeal to authority? Are you serious? The DSM may well be atheoretical, but it is not based purely on appeal to authority. The topics in it are at least discussed on the basis of available clinical research. Ms Clark knows her stuff… and so do I. This is not ‘appeal to authority’, or any other logical fallacy.
IP: “The DSM-IV is loose enough that two people can have an autism diagnosis without a single item (as distinct from broad criteria) in common. My point is still the same.”
Not really… The elements in the criteron sets represent behavioural characteristics observed as falling within the scope of the criterion set in which they are listed. Since it is the criteria and their fulfilment which gets the diagnosis, not merely the presence of elements, essentially the overlap (as you call it) is always present since it is demanded in the rubric for making the diagnosis. The reason for this so-called “looseness” is that – even if all variables on the ‘outside’ of a person (or on the ‘inside’, for that matter) are the same for any two people – no two people behaviour in exactly the same way. My appreciation of Lewin’s work – the whole B=f(P,E) thing – is not logical fallacy (as ‘appeal to authority’ would suggest it to be); my understanding of how Kelly’s work on Personal Constructs fits in is not appeal to authority; and nor is my understanding of Vygotksy’s work on the way in which local culture influences individual knowledge as part of an overall socially constructed knowledge such an appeal; and I could go on. Ms Clark and I have studied these issues.
Ms Clark: “(blows a kiss to David Andrews) :-)”
*blushes bright red* (except it appears bold black here)
one thing that i think people are overlooking is the fact that the california DDS data showing that the prevalence of autism doubled between the birth years 1970 and 1987 yet the DTP vaccine was the only thimerosal containing vaccine at this time and I don’t think there were any changes in the number of DTP shots given at this time. One possibility is that the rate of vaccination gradually increased in this 16 year period, but i don’t have any data to check this. I wonder why SAFE MINDS and other organizations have never provided date on rates of compliacne with the DVT vaccine between 1970 and 1986 or shown that a much higher percentage of people born in 1986 were vaccinated as opposed to people born in 1970 food for thought.
Comments?
Interesting points to ponder Jon. I’m sure Joseph or Jon S will be interested in that too.
Hi jon
You can find here some information
“Changes in vaccination schedule in USA”:http://www.cdc.gov/nip/publications/mmwrpubs.htm#4
Also I have looked about the changes in vaccination schedule in UK since 1950.
Jon, if you are interested in the analysis I have done, please e-mail me.
Kev, are you interested that I comment about the analysis I have done?
The problem, as always, are the data, because we only have educational data or epidemiological data that are known are affected by a lot of confounding facts such as changes in diagnosis criteria and social changes in the parental attitude and medical attitude about the condition-broadening awareness and so on-, therefore I consider it an exercise :the comparison between changes in vaccination schedule and autism data, that can be interesting to find some clues but that can not be used to obtain definite conclussions in taxative ways, in my opinion. However, I found no published study about the topic of changes of vaccination schedule in time and changes in autism prevalence data.
MarÃa Luján
_”Kev, are you interested that I comment about the analysis I have done?”_
Of course MarÃa :o)