Thursday, March 05, 2009

Smallpox, polio, and autism

A few days ago, Canada's senators were debating a law about autism. According to Senator Wilbert J. Keon, this proposed law, Bill S-210, would establish "World Autism Awareness Day in Canada, to be celebrated each year on April 2."

Senator Keon states:

Through the passage of this bill, we are showing that we truly respect Canadians with autism.
And what is the direction and purpose of this proposed Canadian law, a law to raise autism awareness, by which our government is to show that it truly respects autistic citizens? Senator Keon explains:

We must now do the necessary research to understand what autism is; then we must eliminate it as we did with smallpox and polio.
So parliament's power will be used to spread awareness--to inform schools, families, employers, communities, landlords, governments, and so on--that autism is as frightening and harmful, as dangerous to society and the public good, as smallpox and polio. And just like smallpox and polio, autism must be eliminated--regardless of science and ethics, regardless of the wishes of autistics and/or parents of autistics. According to Senator Keon, who demands a Canada free of autistic people, this is the kind of awareness Bill S-210 is all about.


codeman38 said...

To paraphrase Douglas Adams, this must be some new definition of the term "respect" that I wasn't previously aware of.

Clay said...

Better we should eliminate rampant ignorance and utter gormlessness.

Chris MacDonald said...

Just FYI, for those who don't know his biography, Senator Keon is also a heart surgeon.

(Not saying that justifies his wording...just saying that he's not a random politician...he's a physician too.)

Michelle Dawson said...

For those who are interested, Senator Keon has a Wikipedia entry here.

In his speech, Senator Keon gives figures for total number of autistic children and adults in Canada. These figures (they are slightly out of date) assume the same high, stable rate of autism across all birth cohorts.

But Senator Keon also claims "the prevalence of autism has increased greatly in recent years." He is contradicting himself.

Either there is a high, stable rate of autism, in which case his figures for total number of autistics are not too far from accurate; or the prevalence of autism has recently increased ("greatly"), in which case there would have to be many fewer autistics than he claims--and particularly, many fewer older autistics.

Gonzo said...

Yeah, everytime I mention, that Autism doesn't need to be cured, someone makes a snide remark, that I probably oppose a cure for Cancer/Smallpox/____________(insert any horrible disease here)
They always think they're clever and witty, and never assume, that I might say that, because I'm Autistic.

Michelle Dawson said...

In response to Miss Gonzo Galore, while I'd seen autism equated with polio before (and with leprosy, syphilis and tuberculosis--and of course, cancer and AIDS), Senator Keon's equating of autism with smallpox was new to me...

daedalus2u said...

I was at a talk on autism at MIT this past week where a researcher with the initials MB presented. His talk was ok, related to fMRI BOLD measurements mostly. At the end he talked about wanting to find a "cure" for autism, but (being the sensitive and caring individual that he perceives himself to be [/sarcasm]) a "cure" that would only improve the ability of people on the spectrum to communicate, not a "cure" that would take anything away from them, not a "cure" that would eradicate autistic ways of thinking.

I have tried to communicate with him multiple times in multiple different ways but he is simply unwilling to even try to understand what I have to say (even though it is very relevant to his work on functional connectivity) and I have offered multiple times to spend the time to bring him up to speed.

I raised my hand to make a comment and was chosen last. There was also a question about how oxidative stress affected fMRI BOLD measurements. I made a comment about how what the fMRI BOLD technique is really measuring is the level of NO in the brain where the NO level reaches the concentration where it activates soluble guanylyl cyclase, generates cGMP and so causes the vasodilation that brings the oxyhemoglobin into that brain volume element which perturbs the background magnetic susceptibility (deoxyhemoglobin is paramagnetic, oxyhemoglobin is not) and produces the fMRI BOLD signal. This exactly explained the behavior of the fMRI BOLD signal differences that he reported between ASDs and NTs. Oxidative stress lowers the NO level via consuming NO with superoxide, and so would reduce the fMRI BOLD signal (as is observed in people with autism, who have brains that are characterized by oxidative stress). The fMRI and the oxidative stress results thus support each other.

He made a snarky reply, said that no, the fMRI BOLD technique was only measuring hemoglobin and my statement about NO was characteristic of people trying to fit every observation about autism into their own narrow pet theory. Then the moderator immediately cut off further questions.

I spoke with him later during the reception following and asked if all the fMRI BOLD technique was measuring was hemoglobin, on what basis was he inferring neuronal activity or functional connectivity? (The mechanism for how that apparent neuronal activity couples to the observed vasodilation remains undescribed in the literature although it must be NO.) I pointed out that NO was the fundamental regulator of vasodilation, and that this was very well known. He mumbled something about CO2, (which plays essentially no role in the acute regulation of vasodilation under normal conditions and couldn't be the basis of the vasodilation associated with BOLD), told me I was wrong but offered no explanation as to why and then walked away. I had been discussing some of this with another person, who was standing there and observed the interaction and reported being flabbergasted at this unscientific and essentially content-free response (this was at MIT, where people expect scientific discourse to be at a certain level).

It is quite clear to me that the inability of some NTs to communicate with ASDs is about the NTs. I discuss this a great deal in my recent blog on "theory of mind".

My hypothesis is that most NTs develop their "theory of mind" from the top down, that is they learn about the world and how to interact in it from other NTs. This results in neuronal structures that translate what the NTs observe into mental concepts they understand. That primary translation is in terms of human languages, body language, emotions, human feelings and interactions. That is why NTs anthropomorphize so much. Uta Frith's moving and emoting triangles don't have a "real theory of mind" for someone to detect. Triangles are inanimate objects. A triangle only has an emotional state if an emotional state is imputed to it. That imputation is a type 1 error, a false positive. Falsely "seeing" an emotional state that is not there. Being unable to impute an emotional state to a moving triangle is not a deficit. It is an improved resistance to type 1 errors.

There will never be a "cure" for autism. There will never be a method to change the neuroanatomy of people with autism such that it corresponds to an NT-type neuroanatomy that has a top-down theory of mind. That neuroanatomy starts to be configured in an ASD pattern in the first trimester. The number of minicolumns is determined at 6 weeks post conception. That is when the ASD phenotype occurs.

Changing the ASD neuroanatomy such that they can impute emotional states that are not there to triangles will be to destroy their ability to observe moving triangles without imputing anthropomorphic motivations to them. The NT and ASD ways of conceptualizing reality are fundamentally different. There is essentially 1 NT way, the top-down theory of mind developed during childhood by interaction with the larger community of NT children. The ASD way of conceptualizing reality is unique to each ASD individual. It is a bottom-up conceptualization. A bottom-up conceptualization can't be forced into a top-down conceptualization without destroying it.

Anonymous said...

Dear Mr Whitlock

I don't usually read blogs (I haven't the time, unfortunately), but a friend pointed me specifically to your comment here.

Your summary of my view on a cure for autism, minus the sarcasm, is an accurate one. I do hope and believe that it will be possible to preserve autism's unique cognitive style but to augment it with social and communicative skills that allow people with autism to "meet halfway" with the broader social world, if they so wish. It's one thing to perceive the world "bottom-up" (to quote your mot juste), and it's quite another not to be able to communicate that perception flexibly and socially. I do suspect that this latter capacity can be augmented without destroying the former. This ambition of mine is guided by the experience of my autistic brother who, unlike all those who comment in this forum, is severely impaired at even typed communication, and whose current lack of ability to type independently leaves his every laboured word open to doubt and second-guessing. He wants to type independently, and he would love to be able to speak -- he has made these facts clear not only through typing but also through behaviour in general -- and I want him and people like him to have those options.

Note that I do not speak of "curing" Asperger syndrome. Many people use "autism" as a shorthand referring to all autism spectrum conditions (or all "autism spectrum disorders" -- an unfortunate term to which I used to subscribe before my postdoctoral mentor Simon Baron-Cohen taught me better). I refer to autism specifically, and I'm concerned with those cases in which people with autism lack the ability to communicate their needs, desires and ideas. I had a nice chat with Temple Grandin when she was here at Cornell this past fall -- she visits periodically as a Rhodes Professor -- and she and I are on the same page with this view.

Towards the end of the colloquium that you attended I cited Jacques Lacan's observation << Le symbole se manifeste d'abord comme meurtre de la chose >> (the symbol manifests firstly as the killing of the thing -- by which "thing" Lacan means the veridical percept). Lacan saw the concrete reality of sensation and the abstract representation of language as fundamentally opposed -- so he might have agreed with your view that it's impossible to have one without sacrificing the other. An alternative view, though, is that despite the inherent tension between symbolic communications and veridical perceptions, it is possible to have some of one without entirely losing the other. Whether you accept the possibility of this halfway view depends (somewhat self-referentially!) on whether you see the world and its logic as an affair of black and white or one of shades of grey.

These autism colloquia always are very busy events, and there always are many individuals and groups of people with whom I want to chat or who want to chat with me. This was particularly true this past Wednesday, because I was the speaker. So though I might feel a responsibility to dwell further with particular people or conversations, I'm often diverted. You may recall that some time ago, at a reception following another autism colloquium at MIT, I did sit down with you to hear what you had to say. (If I recall correctly, at the time you were propounding a bacterial culture to be applied to the skin to increase levels of nitric oxide.) Is oxidative stress a possible contributor to autism? Quite possibly. Is *every* aspect of autism connected through nitric oxide as some single unifying principle? I very much doubt it.

As I said in response to your comment during the colloquium, in any biological system, at some level everything is connected to everything else. (In your case of nitric oxide in particular, yes, nitric oxide mediates vasodilation and can therefore be said to underlie blood-oxygenation-level-dependent contrast in fMRI, but this would be like saying that an automobile accident was caused by fuel because it's the fuel that caused the car to accelerate into the tree. The fuel is a necessary component in the causal chain, but is not usually the component that varies.) In this sense, your comment highlighted an important issue in autism research: We need to sort out which connections within this thicket of relationships are meaningful, and in order to do that we need to avoid falling into the trap of projecting all our observations into our own narrow theoretical apertures. We are all guilty of such projection: For instance, as I said during the colloquium, when I was a graduate student I believed (with Courchesne at the time) that attention was autism's be-all and end-all, that slowed shifting of attention lay at the root of the developmental process that produces autism. Attention is a piece of it but not all of it. If what we're after is an integrative and comprehensive science of autism, we can't become stuck in these ruts. This imperative is what I was trying to enunciate in response to your comment, and I regret that that response came across to you as "snarky."

It is true that I avoided calling on you during the question-and-answer period. I did all along intend to call on you at the very end, but my host Professor Sur beat me to it. The reason that I wanted to sidestep dealing with your comment in the middle of the session (versus at the end of the session) is, frankly, that I knew that it would be some non sequitur about nitric oxide -- because that's what it always is, almost every time you make a comment at one of these colloquia. When the very same relationship is drawn, with the very same professed certitude, in response to nearly every presentation in this colloquium series, the situation becomes a bit like the story of the boy who cried "Wolf!"

Regarding your view that oxidative stress would decrease fMRI BOLD signal by depletion of nitric oxide, it isn't immediately clear how such a mechanism would explain (1) the *above*-normal signal in the clinically unaffected siblings, who might be expected either not to differ from the normal sample or else to share some familial liability to oxidative stress, and (2) the regionally specific pattern in which signal is below normal in frontal cortex but above normal in posterior cortex.

Regarding your comments on pCO2 and vasodilation, I readily admit ignorance of the minutiae of the relationship between blood gases and smooth muscle responses, and know the situation only in the broad outlines provided by studies of hyper- and hypocapnoea on cerebral blood flow. I would be interested to receive one or a small number of citations to the literature on this topic that you feel would be informative.

Kind regards
Matthew Belmonte

Michelle Dawson said...

I'm not going to delete (or respond to) deadalus2u's and Dr Belmonte's extremely off-topic and very lengthy comments, which are addressed mostly to and are mostly about each other.

But I suggest that if deadalus2u wants to write at length about Dr Belmonte, etc., that is totally fine--but he should do so somewhere other rather than in the comments of a totally unrelated post on someone else's blog.

daedalus2u said...

Ms Dawson, I apologize for posting a comment you consider to be off topic on your blog. I will post my reply to Dr Belmonte on my blog. Just so no one misconstrues my statements, I consider Dr. Belmonte one of the more enlightened autism researchers; in that he acknowledges there are some cognitive tasks at which ASDs have superior performance. The sarcasm I used was my own, and was about my statement and derives from my own frustration at my inability to communicate my ideas in ways that can be understood. I have no reason to doubt that Dr Belmonte is completely sincere in his statements about wanting to find a cure and what he considers a cure to mean. I don't consider Dr Belmonte to be a curebie as I understand the term, simply wrong about what neurological changes would be necessary to achieve NT-type communication skills and if those changes were possible (they are not) what those changes would mean for other ASD cognition skills.

Michelle Dawson said...

In case there's any confusion about what the topic is, I suggest reading the original post. This one doesn't mention Dr Belmonte, fMRI, etc.

Sometimes short off-topic comments are fine, as are comments that are related but not exactly on-topic. Lengthy comments that totally ignore the topic of the original post are a problem.

RAJ said...

Senator Kean was talking about 'preventing' autism not eliminating it. His reference to smallpox and polio is relevant.
After the great rubella pandemic of 1964 thousands of babies were damaged due to prental exposure to rubella.

The development of an effective rubella vaccine has 'prevented' thousands of new cases of 'autism' and other devlopmental disorders.

Are you against preventing autism?

RAJ said...

You said "But Senator Keon also claims "the prevalence of autism has increased greatly in recent years." He is contradicting himself".

Not so, the rate of autism prevelance has remained stable since 1994, the year Kanner's definition 'A pervasive lack of responsiveness to other people - autism' and replaced by the vague and ambigous 'Qualitative impairment in social reciprocity'.

Prior to 1994, the prevelance of autism was low 4-6 cases per 10,000. Fombonne hsa published an excellent study that showed that prevelance rates are stable, since 2000, with a prevelance of 60 -70 per 10,000.

Fombonne also states that the prevelance rates of 60-70 per thousand are stable over the decade but are significantly higher compared to pre-1994 prevelance rates, the year diagnostic criteria was not broadened, but rather abandoned with the removal of Kanner's criteria that was firstintroduced in 1980 (DSM-III).

Michelle Dawson said...

Continuing the off-topic theme, RAJ's comment re autism prevalence has nothing whatsoever to do with (my comment about Senator Keon's claims.

Similarly, re autism, smallpox and polio, in the original post, I report what Senator Keon stated in his recent speech. This can be verified through the source I provided.

RAJ takes the position that indeed autism should be equated with smallpox and polio. I disagree.

Rubella, which can cause miscarriages and stillbirths, is an infectious disease that can be prevented through vaccination. Vaccinating against rubella, an infectious disease, does not "eliminate [autism] as we did with smallpox and polio," as is Senator Keon's stated goal.

RAJ said...


Your statement on the consequences of congenital rubella are disingenuous to say the least.
Congenital rubella is one of the many known causes of 'Autism'. An epidemiological survey
published by Eric Fombonne (who you constantly reference) found rubella autism is one
of the many known causes of 'autism'.

Fombonne et al 1997 (Here )

Stella Chess was the first to recognize congenital rubella as a cause of autism:

Chess 1971 ( Here )

If you are truly against prevention, I would suggest you join the mercury militia in
their campaign against vaccinating children against rubella.

Michelle Dawson said...

In response to RAJ, Fombonne et al. (1997) report that in their study:

"congenital rubella was found in fewer than 1% of children, a rate not exceeding that in the nonautistic controls."

Fombonne et al. (1997) go on to state that this finding, indicating a lack of association between congenital rubella and autism, is consistent with numerous other studies. In addition, Fombonne et al. (1997) write:

"A recent Japanese survey of autism conducted in the aftermath of a rubella epidemic also failed to document any single case of autism associated with congenital rubella (Honda et al., 1996)."

I continue to disagree with RAJ that autism is the same as smallpox and polio, or that using vaccination to prevent rubella, an infectious disease, will "eliminate [autism] as we did with smallpox and polio," the goal stated by Senator Keon.

daedalus2u said...

Ms Dawson, you are correct, your post did have nothing to do with fMRI, but it did have to do with the concept of "cure" and prevention and what that means to different stake holders. I completely agree that language and actions equating autism with contagious and fatal diseases is inflammatory and understandably frightening; to people on the spectrum, their families, to people ignorant of what autism is and of what autism is not, and to people (such as myself) who are (naturally) worried about what misinformed people might do in their ignorance. Autism is not, never has been and never will be contagious.

To many, eliminating autism is equivalent to eliminating people with autism. At least one so called autism advocacy group has said (or at least strongly implied) that a dead child is preferable to a child with autism. Portraying autism (or people with autism) as monstrous or contagious is a standard and common marketing ploy to attempt to increase donations. The case you cited is an attempt by a politician to make political gains by exploiting animosity toward a vulnerable minority and whipping up hysteria.

Dr Belmonte did mention "cure" in his talk, which is rare for talks on autism research. What is very rare is that he also acknowledged that there are some aspects of the cognition of people with autism which is worth preserving, and that eliminating those autistic cognitive features should not be a goal of "cure", and is not part of his goal.

Most scientific talks on autism that I have been to relate to genetics, and the idea of prenatal diagnosis and the "prevention" of autism by preventing the birth of individuals who might express the autism phenotype. I happen to think that this approach will not work. In my opinion any and every human genotype will support an autism phenotype. I appreciate that in the autism research community that is a minority view, that the vast majority of researchers (who also happen to be NT and working on autism genetics) do not share. I think this is because they are unable to abandon their hypothesis that genetics must be all-important even when their data doesn't support it. There is no "smoking gun" of autism genetics, no likely candidate genes, there are a few single gene or few gene mutations that in some cases appear to sometimes cause some cases of autism. For the vast majority of ASDs, there is no clue as to what genes may be involved even though there have been many scans for such genes in many such individuals.

Exposure to certain things in utero does lead to an increased incidence of ASDs (which increase can't be due to "genetics"). Thalidomide and stress for example. No one in the ND community who is opposed to "prevention" advocates giving any pregnant woman thalidomide to cause her infant to have autism. Similarly, no one in the ND community advocates subjecting pregnant women to stress to increase the incidence of autism in their children. Reducing the bullying inflicted on pregnant women will reduce the incidence of autism. The ND community is opposed to bullying in all circumstances. The curebie community is not. Good prenatal care for all pregnant women will (likely) reduce the incidence of autism. Does the ND community oppose good prenatal care for all women? The answer is no.

My opposition to "prevention" is that as I understand attempts to do so via genetic screening, it won't work and will cause much heart-ache among women and their partners trying to implement it. I see prenatal genetic screening for autism as the next snake-oil that quacks will push. If it is implemented with as much testing, rigor, informed consent and care as was used (i.e. none at all) before anti-vax, supplements, chelation and hyperbaric O2 were implemented we will see similar results. The quacks will get rich and people will be exploited and injured.

Michelle Dawson said...

I suggest (again) that if daedalus2u wants to expound at length about his views of autism (to which I am not going to respond here), and his views of and experiences with another researcher (ditto), that is fine.

But using someone else's blog post--one which has a specific and unrelated topic--to do this is not okay.

If daedalus2u wants to disregard the topic and instead wishes to inform readers here, at length, about his views of autism and/or Dr Belmonte (etc.), I suggest that daedalus2u should briefly provide links here to daedalus2u's own blog, rather than writing very extensive blog posts (essays?) in the comments here.

RAJ said...

Don't know why hyperlinks do not work on this blog. To say that congenital rubella is not associated with the development of 'autism' is complete nonsense.

Here's Chess abstact:

Stella Chess1

(1) New York University Medical Center, New York

Abstract In the course of studying the behavioral characteristics of 243 preschool children with congenital rubella, we identified the syndrome of autism in 10 children and a partial syndrome of autism in an additional 8. These findings are discussed against the background of the behavioral investigations of rubella children. The methodology of our psychiatric study and the criteria for a diagnosis of autism are presented. The incidence of autism is considered with regard to the prevalence of other psychiatric disorders in this group and the physical status of the children. Two case histories of autistic rubella children are given and their behavioral characteristics are contrasted with nonautistic rubella children with matching sensory and other defects. The prevalence rate is compared with that found in two epidemiological studies and also with the rate indicated by other centers studying rubella children. Etiological implications of these findings are discussed. It is argued that these data support the concept of organic causation of the syndrome of autism.
This study was done under a grant from the Children's Bureau, HEW No. H-220 (C2).

If you read Chess's paper her detailed description of the functioning of two of the boys in her study are indistinguishable from the description of Kanner's 11 children in his seminal paper published in 1943.

Michelle Dawson said...

In response to RAJ, I suggest reading Fombonne et al. (1997), which in fact RAJ highly recommended, just recently.

I quote from this paper here. The authors found no association between autism and congenital rubella in a large population-based sample.

As I pointed out above, and as can be confirmed by reading the paper, Fombonne et al. (1997) state that their findings in this respect are consistent with many other population-based studies of autism.

In an impressive about face, RAJ is now calling Fombonne et al. (1997) "complete nonsense."