If Not Mercury, Then What?
If Not Mercury Than What?
Here's a question I've heard far too many times, in one form or another. When I've questioned the validity of the underlying science to the mercury hypothesis, I've heard "Well, what do you think causes autism?" or "It's the best theory we have so we're going with this until something better comes along" I've even heard a few antivaxers say "We know it's not all about the mercury but it's a way to get our foot in the door." Oh, and "The public understands why injecting a known neurotoxin into a baby is a bad idea. It's a no brainer!"
Indeed it is. ....
Let's take a look at the arguments for and against the teaching of "Intelligent Design" in our schools. ID is presented as a valid alternative hypothesis because the theory of evolution is unable to completely explain our world and our existence. Kind of like saying "If not ID than what?"
Here's what Judge John E. Jones III had to say about it:
To be sure, Darwin's theory of evolution is imperfect. However, the fact that a scientific theory cannot yet render an explanation on every point should not be used as a pretext to thrust an untestable alternative hypothesis grounded in religion into the science classroom or to misrepresent well-established scientific propositions.
Sounds like a good response to the "If Not Mercury, Than What?" argument too. Of course it can be argued that the mercury hypothesis is testable and some claim the science proves it but no one is able to present that science upon request. "It's there, just read this website or the other."
Well I'm willing to listen and consider the science so here's my challenge: Show me your science not your faith.
The mercury hypothesis has taken on many of the appearances of a false religion or cult and to some degree it serves them well. Take a substance that we all know to be dangerous and it makes it easy to divide the world into two groups, good and evil, pro-mercury or anti-mercury. The anti-mercury underdogs are persecuted by the government and pharmaceutical companies and a few rogue scientists, willing to step up and speak out against the establishment and the evils of mercury, are brought to the pulpit to preach.
There are few doomsday religions who have predicted the world will end on specific dates. Of course when the dates arrive and civilization as we know it remains intact, they are forced to revise their predictions and calculations. For some reason very few of their followers question the elders while they robotically recite the new deadline.
Who can dispute that mercury is toxic and thimerosal shouldn't be in vaccines. After all, it doesn't need to be there if the only reason is affordability so let's err on the side of caution and let's remove it. Why would anybody say mercury is a good thing and babies should be injected with thimerosal?
At some point we will be forced to admit that removing thimerosal from vaccines had no impact on autism rates but the focus on mercury, which started with vaccines and thimerosal, will not end there. Already the focus is shifting over to environmental mercury so as long as mercury remains the embodiment of all evil and a major cause of autism, the religion will thrive.
But the question remains, If it turns out it's Not Mercury, then what?
posted by notmercury @ 5:31 AM
61 comments
61 Comments:
I am not sure that the incidence of autism is really rising. But, for the sake of argument, let's say it is. Under that assumption, since it could not be "just" genetic, then what could it be?
Most parents on-line would still argue that it must still be vaccines (too many, too soon). But, vaccines are one of the potential triggers that has at least been investigated, and found to be unlikely. There are a myriad of other possible triggers. Thousands, if not millions of man-made chemicals have been introduced in the last century. Any one of those could be responsible.
How about phthalates, which are known to produce developmental and/or reproductive effects in rodents?
Polybrominated flame retardants (endocrine-active compounds that interfere with sexual development and give sexually dimorphic behavior)?
Trans fats (which interfere with the absorption of essential fatty acids in the body - and essential fatty acids are essential for normal brain functioning)?
Smog (there is a much higher prevalence of autism in urban environments)?
To me, all of these meet the biological plausiblity argument that is touted by the mercury advocates.
Has there ever been a study on defective sperm in fathers of autistic children? I watched a facinating Discovery show last night that was about Cheetah's and the fact that almost all male Cheetah's carry defective sperm as a result of inbreeding during the ice age. I don't know where I come down on the "pro-mercury" vs. "anti-mercury" debate. It seems to me that neither side has proven anything. Therefore, anyone who pretends to know the answer is to me just speculating.
Rather than the analogy with to the "Intelligent Design" theory, perhaps a more apt analogy might be with ALD and the work of one set of parents to push scientists and researchers. Augusto Odone's fight to find a cure for his son's ALD led to a discovery that has helped thousands of ALD children around the world. In the beginning, many thought it was "junk" science as well. You should take some time and read about the Odones and what their work produced.
I don't chelate my child as I think it has to do with genetics in our case. However, we are likely to find that autism will have several etiologies. Science really hasn't focused on this disorder until recently and that is because parents and some wealthy and powerful people have been effected.
The sperm thing would be an interesting study, as it's known that a child can be born with FAS if the father is a heavy drinker and the mother doesn't touch liquor at all.
I also like the damaged sperm argument. Here is an interesting medline abstract. Autism is indeed correlated with increasing paternal age. {Could someone please tell me how to do these links properly?}
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16108999&query_hl=32&itool=pubmed_docsum
J Child Psychol Psychiatry. 2005 Sep;46(9):963-71. Related Articles, Links
Effects of familial risk factors and place of birth on the risk of autism: a nationwide register-based study.
Lauritsen MB, Pedersen CB, Mortensen PB.
Centre for Basic Psychiatric Research, Psychiatric Hospital in Aarhus, Aarhus University Hospital, Denmark. mbl@psykiatri.aaa.dk
BACKGROUND: The etiology of autism is unknown. A strong genetic component has been detected but non-genetic factors may also be involved in the etiology. METHODS: We used data from the Danish Psychiatric Central Register and the Danish Civil Registration System to study some risk factors of autism, including place of birth, parental place of birth, parental age, family history of psychiatric disorders, and paternal identity. RESULTS: A total of 943,664 children younger than ten years were followed from 1994 to 2001; of those, 818 children developed autism. The highest risks of autism were found in siblings of children with autism, or Asperger's syndrome and other pervasive developmental disorders (PDDs), with relative risks of 22 and 13, respectively. The relative risk of autism in the child was about twice as high if the mother had been diagnosed with a psychiatric disorder. The risk of autism was associated with increasing degree of urbanisation of the child's place of birth and with increasing paternal, but not maternal, age. An increased relative risk of 1.4 was found if the mother was born outside Europe, and in children of parents who were born in different countries. CONCLUSIONS: The highest risk of autism was found in families with a history of autism, or Asperger's syndrome and other PDDs in siblings, supporting the commonly accepted knowledge that genetic factors are involved in the etiology of autism.
Great discussion NM!
Good luck on finding that science you are looking for, you're going to need it (if you do find some, don't be surprised if related labs came from Doctor's Data). I think you're indirectly onto the whole lack of patience for good science thing here.
Hiya Jennifer,
You know, you have some of the most constructive and evidenced-based comments I have seen (on my blog included) - I wish you had a blog! E-mail me at comments at autismstreet dot com, and I'll get you set up with how to do links in the comments. You need this, because it seems you always have relevant studies and comment to provide.
I don't agree with the "defective sperm" theory at all, because my two Autistic Spectrum children have two different fathers, neither of whom are drinkers or drug users. I also have three nephews on the Spectrum- they are my brother's sons- which would suggest that any "autism genes" my children have came from my side of the family, and were passed down through me (the mother) to my children.
I think there's plenty of evidence to suggest that there is not really an increase of autism- what we're seeing is an increase of autism diagnosis, while at the same time, the rates of "idiopathic mental retardation" - meaning MR with no known cause- are dropping. In other words, kids that once would have been simply called "retarded" are now diagnosed properly as being autistic.
(It's also become more recognized that autistics are usually not retarded, even those who can't pass a standard IQ test, but that's drifting off topic.)
If there is an increase in autism at all, I think the best theory isautism researcher Simon Baron-Cohen's Assortive Mating theory, which you can read about here:
http://edge.org/documents/archive/edge158.html
Bascially, the gist of it is that in our modern world, more people who are "Systemizers" (i.e. typical "computer geeks", or engineers, or scientists, or whatever) are meeting each other and marrying, and thus many kids are getting a double dose of the "geek" gene. Since I met my current husband online, and we're both very much "geeky", that theory makes sense to me.
Alexander's Daddy said...
It seems to me that neither side has proven anything. Therefore, anyone who pretends to know the answer is to me just speculating.
That's exactly right, thanks for your comments by the way. Neither side has proven anything but I also don't see this as a two sided debate.
On one hand you have a group of people saying that all autism is mercury poisoning, along with others saying that it may cause autism in some people, and on the other hand are many, many, different groups of people from different backgrounds and interests saying that it hasn't been proven and there is very little evidence to support the claim. OK, we've run out of hands, haven't we?
One thing that is important to remember, the responsibility of proving a connection belongs to those making the claims. No one has an obligation to prove autism can't be caused by mercury. I don't think that would be possible short of finding a major cause.
I am familiar with the Odone's story and though I don't think my ID analogy is completely accurate, I also fail to see the parallels between addressing a heritable defect in VLCFA oxidation through dietary fatty acid intake modifications and the use of chelation agents, that may or may not bind mercury, to remove a metal that may or may not be present.
If the parallel is the pioneering spirit of the parents in both circumstances, I see your point, but the Odones could probably teach us all a thing or two about the science of Lorenzo's Oil. I'm not sure the same would apply to even the best informed chelation parents.
Lili,
I think one day it will be discovered that there are at least four etiologies of autism. Simon Baron-Cohen's thesis is very interesting and I think there is some anecdotal evidence to support it. I took his autism quotient test and scored very high (38). I had my wife take the test for me as well and her answers scored me at a 36. I'm sure my nephew has Asperger's, although he is undiagnosed. However, he would be clearly AS to anyone that had a cursory knowledge of AS.
I however, don't buy the "retarded" relabeling theory. If I was my son's age today, I would have surely been diagnosed as autistic. However, I do think that many HFA kids are being caught by the change in DSM. I have video from Lovaas study from the 60's and 70's and those kids that were labeled autistic then are what we might label today as severely autistic. I don't think HFA was in the lexicon at that time. In addition, did you know the first draft of the DSM IV contained language that some HFA kids will loose much of their traits as they become older? I don't know why that didn't make the final draft, but I understand there was a lot of argument over inclusion. I was probably one of those children
I do those AQ tests and other such surveys, and I tend to come out AS. Except that AS doesn't describe me the way ADHD does (unless you count the days when my anxiety is over the top and I just want to hide in my room and have no contact with anyone while I stim on a bookmark), and ADHD meds help me tremendously. (And I do own - but haven't yet read - The Autism-ADHD Connection.)
Most of those tests, it seems to me, are basing things off a person's social ability. Thing is, it can be just as impaired (if not moreso) in a person who has ADHD, because we tend to miss information and don't learn things when other people do.
I often feel like a 15yo girl in the way I interact with others, for precisely this reason. (At other times, of course, I feel 50 years old and want to strangle the 17yo girls I know.)
NM,
When you've used "on the one hand" and "on the other hand", and still need yet another hand, remember the SF race that had a third hand that was just to grip stuff so the other two could manipulate it, and say "on the gripping hand".
At least, that works with SF freaks. :) (And sometimes it does work out that you need to enumerate three things like that. So it can come in handy. No pun intended.)
Thanks Julia,
A motes helpful reminder.
alexander's daddy- you might not buy the "relabeling" theory, but I've seen it in my own family (with both a great-uncle and an aunt- one who was labeled "retarded" and the other "brain-damaged" by a difficult birth, but- on looking back- it's quite clear that they were both non-verbal autistics.
I also have a friend whose older brother was labeled "mentally disabled" here in Ireland in the 1970's, who is also clearly autistic. I wouldn't "buy" this theory either, if I hadn't seen proof of it with my own eyes.
Also, my father and my grandmother are classic Asperger's, but neither has had a diagnosis of any kind- they're just thought of as "eccentric". It's only in the past 15 years that there's been a name for Aspies and HFAs- anyone who was high-functioning enough to survive in the world didn't get a diagnosis at all (which may or may not be a good thing!).
as a trained geneticist, i'm puzzled about the oft-made assertion that "it's not just genetics" ... i'm not convinced that genetics alone is insufficient to explain the prevalence or the diversity of autism spectrum disorders.
i suspect that autistic disorders are the result of a matrix of genes and the interactions between their products. i don't discount the possibility that environmental factors may be involved, but i've seen no consistent evidence that links anything but genetics to 'causing' asd.
rather than asking "if not mercury, then what" we ought to be asking "what does the evidence we have tell us?". conan doyle's sherlock holmes was the consumate scientist. look at what you have, not what you haven't, to formulate hypotheses to be tested.
i should point out that i'm an aspie. i have degrees in genetics and law, postgrad education in law, computer science and education, and undertaken postgraduate research in genetics, computer science, and law.
i can point to several people in my near genealogy who exibit autistic traits.
maelorin: I think it's probably going to turn out to be genetics. It's just not simple genetics, like eye colour and hair colour, so we laypeople just can't wrap our brains around the hows and whys of it.
In my own immediate family, I have diagnosed ADHD and I am pretty sure that one of my brothers is AS and another is ADHD; the third definitely has some Sensory Processing Dysfunction. My parents both demonstrate many of the behaviours of ADHD, and one of my mother's brothers is likely AS (more severe than my own brother). One of my cousins on my mother's side has diagnosed ADHD, and my mother's father was very likely mildly affected by Asperger Syndrome himself. On Dad's side, it's a family of packrats and chronic lateness, not to mention the tangential story-telling that is so characteristic of ADHD.
I say I come by my "insanity" honestly; just look at my family. Honestly, I think it's proof that ADHD and ASD are very much genetically based and genetically related to each other.
Thanks maelorin,
I'd also like to point out that traits that appear non-Mendelian don't have to rely on an external factor other than genes. To complicate matters, people have a choice about their potential mate. The courting/selection process is a bit different than that for pea plants and lab mice.
An example (SFW) - is a some woman with this t-shirt going to hook up with a geek who likes to listen to the same led zeppelin song repeat for a hour or two? No, but a brainy woman just might.
/notice the port-o-potty background - so classy
BC said is a some woman with this t-shirt going to hook up with a geek who likes to listen to the same led zeppelin song repeat for a hour or two?
Are we talkin' Kashmir or the Lemon Song?
Hi "Alexander's Daddy"... please get yourself included on the Autism Hub ...
Oh, and my response to all of this (tongue in cheek) is "apple juice is to blame".
"If the parallel is the pioneering spirit of the parents in both circumstances, I see your point, but the Odones could probably teach us all a thing or two about the science of Lorenzo's Oil. I'm not sure the same would apply to even the best informed chelation parents.
Methinks your have a great point NM!
I agree it's the genetics. The APO's show us the kids who can't excrete mercury. Chelation shows us cured children. What else do you need to know?
fore anon, is that APO-AE? btw, you might check out the current state of the US military: Army of One != team. Does a DD214 give me street cred? I didn't think so.
/cross post threadjack
I'd post on your blog but not feeding trolls is one of my new year's resolutions.
HatingBigots.com
anon (non-jerk version):
In My Time of Dying. Which, at like 20 minutes long, is a bit worse. I guess I'm lucky I conned her into the deal.
Conrad Gilliam the genetecist from the University of Chicago or some place like that who spoke at the MIND institute pointed to the graph of the increase in autism DIAGNOSES (not cases) that everyone loves to point to and cry "epidemic!" and said words to the effect of, "I've heard people say that you can't have a genetic epidemic, but genes alone can definitely account for this kind of increase."
I, for one. am sick of this "no genetic epidemic" garbazh. No one ever gives a citation for it and there's been no epidemic just a pathetic reworking of some numbers from the IDEA stats and the DDS stats.
The epidemic never happened! If it had happened the mercury parents wouldn't have had to push push push push scream and eviscerate themselves in the media in order to convince people that there had been an epidemic.
Even Imus (the weirdo) said in one of his interviews with the PR master, David Kirby, that it was all news to him, he never knew there was an epidemic before Kirby came and whispered it in his ear.
Well, Imus didn't say "whispered" but he did say that he didn't know there was an epidemic.
How could that be if by the time Kirby (ick) showed up the rate of autism was one in 166????
How many people do you have to know to know one who is related to a 1 in 166 kid? Even if it was "blue eyes" that was 1 in 166, everyone should know someone who has a kid with "blue eyes". Then they like to say it's 1 in 50 boys or something. Like Imus wouldn't know of 50 parents of boys?
The whole thing is a bogus campaign to get the mercury parents compensation from whomever they can get it. It might have started out with people sincerely believing it, but once the lawyers got involved... I think the lies, smear techniques and propanganda just multiplied, much aided by the historically entrenched and paranoid antivaxers.
Seems like one enterprising dad has figured it all out anyway.... at
autismfries.com
Anonymous said...
I agree it's the genetics. The APO's show us the kids who can't excrete mercury. Chelation shows us cured children. What else do you need to know?
Hmm, what more do I need to know....Maybe we could start with who or what are the APO's and how do they show us what you've said? If you meant apolipoproteins, how or what are they showing you that the rest of the world has somehow missed? Please tell us more.
Bartholomew Cubbins said...
anon (non-jerk version):
In My Time of Dying. Which, at like 20 minutes long, is a bit worse.
Page isn't the best slide player around, but it was enough to hold my attention for the full 20 more than once. Of course my ability to pay attention was legendary back then. [cough]
Hi Not mercury
As a mom of a child with ASD I have read your blog with interest. Although I can disagree in some aspects, I also think you pointed out several important topics. I wonder if you are interested to contact me off Internet to share thoughts. Please, if you are you can read some of my thoughts in Kevin´s forum.
Thank you in advance and sorry if I disturbed you
María Luján
Hello Maria,
You haven't distrubed me at all -- nice to meet you.
I'm glad you disagree with me on some things. The world would be kind of boring if we all agreed, don't you agree? Where is Kevin's Forum?
Hi not mercury
Nice to meet you too.
The Kevin´s Leitch forum is in
http://www.kevinleitch.co.uk/forum/index.php
I signed all my post there as María Luján. Please contact me when you want.Thank you very much for your answer.
María Luján
I am not sure that the incidence of autism is really rising. But, for the sake of argument, let's say it is. Under that assumption, since it could not be "just" genetic, then what could it be?
Well, it's not rising. But if it is, why discount genetics? People assume that the frequency of alleles cannot increase noticeably in a couple generations. There's no mathematical reason to believe this.
-Joseph
Smog (there is a much higher prevalence of autism in urban environments)?
Yes, I noticed that in the California DDS data. What you have to realize is that a diagnosis of autism is inherently subjective. There's no objective test for autism. So our conception of what autism is can change with time. Just considering Asperger's syndrome, it's clear that it has, but the shift has likely occurred across the spectrum. And if it shifts through time, it's not surprising that it shifts regionally as well. Higher degree of urbanization is probably well correlated with pediatrician and parent awareness.
-Joseph
Ah, and also, if you look at the California data, you'll see that in places of high degree of urbanization and high autism prevalence, the increase in prevalence is starting to level off. Meanwhile, in places with low population density, prevalence is still increasing rapidly. They are basically catching up. At some point it should even out. This is all quite consistent with increased parent/pediatrician awareness and concensus of conventions.
-Joseph
I agree it's the genetics. The APO's show us the kids who can't excrete mercury. Chelation shows us cured children. What else do you need to know?
I need to know where the double-blind effectiveness studies on chelation are.
-Joseph
I don't know where I come down on the "pro-mercury" vs. "anti-mercury" debate. It seems to me that neither side has proven anything. Therefore, anyone who pretends to know the answer is to me just speculating.
The burden of proof is always on the side that makes the extraordinary claim. Mercury poisoning is inconsistent with most of the science done on autism to date.
-Joseph
Hi Joseph
Are you interested on the analysis of another point of view about? If you are please contact me. I think that many of your points deserve consideration and analysis.
Sorry if you are not interested.
You can see part of my opinion in Kev´s forum
http://www.kevinleitch.co.uk/forum/index.php
Sincerely
MAría Luján
You can see part of my opinion in Kev´s forum
http://www.kevinleitch.co.uk/forum/index.php
You mean the encephalatis stuff?
The first thing I noticed is the article author:
"Abnormal Measles Mumps Rubella Antibodies and CNS autoimmunity in Children with autism" Journal of Biomedical Science V. Singh, S. X. Lin, E. Newell, C. Nelson J. Biomed. Sci. 2002, 9, 359-364.
Dr. Singh has made the following claim: Only 10% of autism cases are genetic in origin. The pro-mercury camp has been known to cite this claim. Has Dr. Singh ever justified that claim or backed it up? No. He just blurted it out. Based on that, I don't think it would be appropriate to refer to him as a scientist.
-Joseph
Hi Joseph
I am sorry if you consider this. I think that the overall study must be analyzed with care and scientific method, beyond the interpretation or use that after this is done.
I propose you to follow an explanation/discussion of Dr Singh work and other authors by e-mail. -I have recopiled several material on the issue that perhaps you can be interested to read about.
The encephalitis has been linked to the development of autistic traits.
I do think that the ASD has a strong genetic component in the generality of the children affected.
I do think that every paper published in the field has useful, less useful and not useful prompts as a personal analysis. There is no perfect paper in this area and there are a lot of controversy today about what is the relative proportion of regresive/stagnant autism and the Kannerian autism. I have several papers that mention different relative proportions.
María Luján
Hi Joseph
Sorry, I mentioned the Kev´s forum because I am interested on several areas of science in autism(Genetics/Epigenetics/Immune/General/MMR/Epidemics) and I tried to learn as much as possible in each field, beyond the controversy.
María Luján
María Luján,
One thing you should realize is that any environmental hypothesis, be it toxins or whatever, requires genetics. This is obvious since the prevalence of autism is 0.08%, not 100%. Since nearly everyone has been vaccinated, there has to be something about this minority of kids that makes them vulnerable, and that something would either need to be genetic or some other environmental factor that's totally random. (The latter does not make sense - that random factor would be your enviornmental trigger - and genetics is consistent with twin study results).
So now that it has been established that genetics has to play a significant role, there would need to be a model that explains observations. A single-gene model cannot explain the difference in concordance between identical twins and fraternal ones. There would need to be 3 or 4 genes.
But it would seem odd to me that 3 or 4 genes are required to create a genetic suceptibility to an enviornmental trigger. You'd think a single gene might be sufficient.
In reality, the genetic picture is a lot less clear. There are about a dozen different alleles that have been investigated, and some show pretty good linkage to autism, but none are required for autism. Obviously, autism is very heterogeneous and is not something that can be tested objectively, like Down's syndrome.
Some of the alleles are prevalent in the general population, and it would seem that no combination of alleles guarantees autism.
The functions of these alleles are understood to some extent, and none of them have to do with mercury toxicity or anything of the sort.
So the problem with the environmental theories is that they are mostly inconsistent with scientific findings, not only genetics, but other documented neurobiological differences and cognitive style differences.
For example, how does an environmental theory explain the male vs. female ratio? A model based on empathizing vs. systematizing explains it quite nicely.
-Joseph
I don't doubt that if, say, you take a group of autistic children, and test for encephalitis against a group of non-autistic children, you might find that the autistic children are more prone to encephalatis, in average. I'm sure encephalatis can amplify the perceived symptoms of autism.
But is autism encephalatis? No, there's no evidence of that.
-Joseph
Hi
Joseph
Thank you for your answer and comment.
Please see that I maintain I think that 100 % there is genetics involved: or a real deletion/chromosomic problem or a combination of polymorphims of individual presentation. Considering overall for me is the 100 %. Even more , I think that more than 4 genes, but up to 16 has been considered/mentioned linked to autism.
The problem for me here is the lack of knowledge of the proteoma we have and how epigenetics affects us. In this sense, epigenetics for me is very important.
You are right. If you see, In the section of genetics, I included several manuscripts on the potential genes / linked genes to autism based on research.
Please, do you agree to contact me by e-mail? I have prepared some comments/manuscripts to share with interested people to discuss. However, you can read some of my opinions in the different sections of the forum and I will be glad to share thoughts with you there or by e-mail.
For me the male vs female ratio could be understood by different biochemical/enzymatic/nutritional requirements in the development of brain and systemic, considering always the different genetics at an individual level in ASD and how environmental insult can play a role. The role of testosterone can not be ruled out. There are published manuscripts about the role of testosterone/ and also how thyroid dysfunction in the mother can affect differentially girls and boys.
María Luján
Hi
Joseph
I agree with you. Please do not understand me when I am analyzing some aspect that my idea is to point something as THE CAUSE. for me ASD is multicausal in nature (Including genetics) and of individual presentation and therefore extremely complex. For me there are so many autism as autistics. It would be extremely over simplistic to consider ONE CAUSE .
The fact that encephalitis has been found as a trigger for autistic traits in some patients implies for me that this medical condition can be considered important for these individuals. the same with the case of PANDAS, or autoimmune diseases found in SOME subgroups of ASD children, beyond always the genetics.
Thank you
María Luján
I was searching for Dr. Singh's papers in PubMed, and found this from 2004: "This finding suggests that the mercury as in thimerosal-containing vaccines is likely not related to autoimmune phenomenon in autism."
Perhaps he's changing his tune.
-Joseph
Hi Joseph
At my understanding, he considered that viruses could play a role.
http://vacinfo.org/vijendra_singh.htm
María Luján
a real deletion/chromosomic problem
Why? Any rare mutation or chromosomic damage is highly unlikely to account for a majority of cases. The prevalence of autism is quite high, and the number of genes involved have to be many. It's clear that each allele is not pathogenic, i.e. you can have it and be perceived as perfectly normal. In fact, some of those alleles probably have a high frequency for a reason.
-Joseph
REferences I found related to the possibility of immunosuppresion by measles and concomitant gut problems.
1- Measles virus infection in a transgenic model: virus induced immunosuppresion and central nervous system disease Cell 1999,Sep 3. 98 (5), 629-640.
2-Measles virus infection causes transient depletion of activated T cells from peripheral circulation J. Clin, Virol. 1999, 12 (3), 201: 10 Nanan R, Chittka B, Kreth H. W
3-Changes within T cell receptor B subsets in infants following measles vaccination Clin. Immunol Immunopathol 1996 May 79 (2) 163-170. Auwaerter PG, Hussey GD, Hughes J. Goddard EA, Ryon JJ, Strebel PM, Beatty D, Griffin DE-from John Hopkins
4-Pathogenesis of measles virus infection: an hypothesis for altered immune responses J Infect Dis 1994 Nov 170 Suppl 1 S 24-31. Griffin DE, Ward BJ, Esolen L. M: John Hopkins
The immune response that is effective in clearing virus and in establishing long term resistance to reinfection.. “ is associated with immune suppression, autoimmune encephalomyelitis and increased susceptibility to secondary infections”. This apparent paradox may be explained in part by preferential long term activation of type 2 CD4+Tcells by measles virus infection. Preferential stumulation of type 1CD4+Tcells by inactivated virus vaccines is hypothesized to play a role in subsequent development of atypical measles,
5-Measles virus induced immunosuppresion in vitro is associated with deregulation of GI cell cycle control proteins J Gen Virol 1999, Jul 80 (7), 1599-1608 Engelking O, Fedorov LM. Lilischkis R, ter Meulen V, Schneider-Schaulies S
6-Measles virus infects human dendritic cells and blocks their allostimulatory properties of CD4+Tcells J Exp Med 1997, Sept 15; 186 (6) 801-812.
7- The pathogenesis of Crohn´s disease J Gastroenterol 1994, Jul 29 Suppl 7 11-15.Pounder R. E
The author considers that the main problem is the mesenteric blood supply
“Viral particles have been identified within the vascular endothelium, with the appeareance of para myxoviridae. In situ hybridization and other studies suggests that these particles are measles virus”
8-Colonic CD8 and gamma delta T cell infiltration with epithelial damage in children with autism LJ Pediatrics 2001 Mar 138 (3) 366-372 Furlano e al.
9-Early measles virus infection is associated with the development of inflammatory bowel disease Am J Gastroenterol 2000 Jun 95 (6) 1480-1485
Pardi DS, Treamine WJ, Sandborn WJ, Loftus EV Jr, Poland GA. Harmsen WS, Zinsmeister AR, Melton LJ 3rd, Mayo Clinic and Mayo Foundation
And recently from an Italian Group
Autistic enterocolitis confirmation of a new inflammatory bowel disease in an Italian cohort of patients Federico Balzola et al American Gastroenterological Association 2005
"Autistic Enterocolitis: Confirmation of a New Inflammatory Bowel Disease in an Italian Cohort of Patients." Digestive Diseases Week, Chicago, May 2005 and "Panenteric IBD-Like Disease in a Patient with Regressive Autism Shown for the First Time by the Wireless Capsule Enteroscopy: Another Piece in the Jigsaw of this Gut-brain Syndrome." Balzola F, et al. American Journal of Gastroenterology, April, 2005, pag 979:
Obviously, this was one patient.
María Luján
Hi Joseph
There are a lot of genetic conditions linked to autism, I am mentioning here 10
1-Phosphoribosylpyrophosphate (PRPP) synthetase superactivity (very rare), an Xq chromosomal fault exacerbated by impaired proline metabolism. PRPP is the sugar template on which purine and pyrimidine nucleotides are assembled, and superactivity of the synthase imbalances nucleosides/nucleotides.
2-Adenylosuccinate lyase deficiency is a 22q 13.1 chromosomal fault which impairs purine formation before inosine monophosphate formation and after adenylosuccinate formation. Elevated “succinylpurines” occur, adenosine, AMP, ADP, ATP imbalances occur and immune dysregulation is likely.
3-Histidinemia is a chromosomal fault at 12q22-23 which causes deficiency of formiminoglutamate (“FIGlu”) and consequently, limited amounts of special folate forms needed for purine synthesis. Occurrence is about one in 10,000 and victims may have poor auditory memory and poor response to verbal input.
4-Lesch-Nyhan disease, a fault at Xq26-27 with mutant activity of hypoxanthine-guanine-phosphoribosyltransferase. Occurrence is about one in 10,000 male births; purines are wasted as urate, and formation of cytidine triphosphate, CTP, is deficient in certain cells. Victims are typically self-destructive.
5-Fragile X syndrome has faults at Xq27-28. The problem was originally considered to be deficiency of 5,10-methylene THF which is required in pyrimidine metabolism to form thymidine from uridine. Fragile X is a leading genetic cause for mental retardation in males; some become autistic.
6-Rett Syndrome, a fault at Xq28 seen in females (males do not survive), with 21 different possible genetic mutations. Incidence is about one in 12,000 females. Gene binding of methylated cytosine and guanine is disordered, and progressive regression occurs starting at 6 to 18 months.
7-Dihydropyrimidine dehydrogenase (DPD) deficiency, a chromosomal fault at 1p22, results in uracil not forming enough dihydrouracil and thymine not forming enough dihydrothymine. Elevated uracil/thymine occurs in urine. Mild heterozygous DPD is common; severe cases with autism are uncommon.
8-Tuberous sclerosis, a fault at 16p13.3, results in formation of a protein called “tuberin”. Tuberin has homology for GTPase activating protein, and it can deplete guanosine as GTP, GDP, GMP by dephosphorylation. Incidence is one in 10,000 births with 25 to 60% featuring autistic traits.
9-Superactivity of pyrimidine 5’-nucleotidase (P5N) with several chromosomal links (4q26 cytosolic, 17p11.2 mitochondrial). This causes accelerated depletion of uridine monophosphate (UMP) and cytidine monophosphate (CMP); urate is typically subnormal. Incidence is unknown.
10-Phenylketonuria with possible faults at 12q22-24 and at 4q15.1-16.1 (biopterin), which is now a rare autism condition due to diagnosis and treatment in early infancy. Without treatment, as many as 40% of PKUs could become autistic. In PKU there is futile use (wasting) of GTP to form biopterin.
From J. Pangborn presentation
... and there are more. I think that the actual controversy is how much of these "pure "genetic presentations are actually present versus the stagnant autism or regressive autism, when these conditions are not found.
MAría Luján
for me ASD is multicausal in nature (Including genetics) and of individual presentation and therefore extremely complex. For me there are so many autism as autistics. It would be extremely over simplistic to consider ONE CAUSE.
I definitely agree with that, but I go even further. There's a continuous spectrum of behavior. It's possible for someone to be 'just a little' autistic and for someone to be 'not quite' autistic. The boundary between the two is really subjective and arbitrary. There's no objective test for autism, nor will there ever be one IMHO.
It's true that some person's autism might have a cause that is pathological in nature. That's true of any human variation. For example, if someone is too short, this might be caused by a tumor or a thyroid disease. But it would be wrong to claim that short stature always has a pathological cause. (And it doesn't matter how short, mind you). Similary, in many cases autism is just a 'way of being'.
-Joseph
Hi Joseph
The problem I see is that under the DSMIV- an enormous and for me problematic umbrella- ALL the conditions are included, since the otherwise clinically normal ( in labs analysis and without detected biochemical/enzymatic/immune/autoimmune/other imbalances)-but under the DSMIV with autistic traits by behavior consideration only- to the physically very ill, with a lot of comorbilities. In this sense, for me the problem is the tool for diagnosis. Also, there are things we do not know about roots of autistic traits so perhaps what we do not detect today it will be detected as a comorbility tomorrow.
I hope that in the future the better differential diagnosis and the clear separation in subgroups will order the confusion.
María Luján
About the identified conditions that look like autism, I'd note a couple things:
1) Isn't it odd that all of them are caused by genes and are not environmental?
2) On their own they have low prevalence and are caused by a single deletion or mutation. This obviously can't be true of most autism cases.
3) It's possible to objectively test for them. This will not be true of all autism cases, IMHO.
4) Autistic kids in general have an unremarkable appearance. Individuals with these conditions have identifiable features.
Granted, there are probably more of these conditions that are yet to be identified. But the bulk of autism is not going to be clear-cut. Genome-wide scans are suggestive of this.
-Joseph
Hi Joseph
Your points are good. I think that they are not against the idea of a lot of different conditions that are considered "Autism". As you say, many times there must be awareness to search for this (including for example Angelman or Prader Willi that also present characteristics).
What I have read, SOME clues and some published evidence present that now near 80 % is not Kannerian autism, but regressive or stagnant autism, focusing to the point.
For me it is not odd, if I consider that the whole picture includes genetics AND environmental insult with an enormous variation at an individual level. In some children the genetics can be more important, in others the multiple combination of genetics+environments-and epigenetics.
María Luján
MAría Luján
Hi Joseph
Perhaps you can be interested on a manuscript
Comparative genomics of Autism, Tourette syndrome and autoimmune/inflammatory disorders
Simon et al.
María Luján
This thread is good stuff.
"It's possible for someone to be 'just a little' autistic and for someone to be 'not quite' autistic. The boundary between the two is really subjective and arbitrary. There's no objective test for autism, nor will there ever be one IMHO."
I began thinking about autism some years ago right after our boy's diagnosis and I was gunning for a cure for the single disorder. I'm now of the mindset that nothing needs curing, rather understanding is needed. Also, I'm now firmly wedded to the idea that a spectrum of issues at the molecular level can manifest into a single class of behavioral traits. Sometimes that's depressing because then I wonder if I'm wasting my time researching the science behind autism. I've come to the conclusion that as long as I'm enjoying learining about the brain then it's all good.
Hi Maria, you're back!
anon - I'm not prepared to rank order slide guitarists as I'm a fan of Allman, Page and Elmore James, among others. In short, anyone better than me is worth listening to, but I tend to perseverate on Page's work.
Hi Bart
In weekends I can participate a bit in exchange of opinions. Otherwise, is very difficult through the week. I found some little time this weekend.:)
For me also was an evolution. I am overwhelmed because of the complexity of Autism. However, I think that if I learn as much as I can I will have more information to do the best elections for my son in terms of search/treat comorbilities.
María Luján
Not only what I mentioned, but also I am interested in the understanding -at least at the best of my effort-of what autism is in general and in particular for my son, at all the levels.
María Luján
Cubbins: I basically agree with your conclusions (except in re: Page - please re-think that).
What I'm interested in is what physical maladies might cluster with those on the spectrum and if there are sub-types, then how many? We know that certain physical issues are inherent in Down's. Maybe it's my own peculiar view, but I see something of a "Princess in the Pea" syndrome (don't like using "syndrome", but can't think of the better word now). And by PITP, I am NOT referring to vaccines. In fact, I think those on the spectrum need bascially need vaccines.
I'll elaborate more later on PITP (as if anyone is really interested, lol), as I've been pondering it for well over two years, but have never posted about it -- because obviously it sounds kinda woo-woo without my really explaining it further and backing it up with some approximation of science.
Hi HJ - PITP meaning perseveration/stimming/order requirement?
Hi HJ
I would need clarification about PITP, but I am interested on your ideas, even if you consider are not enough backuped by science. If you want, please contact me by e-mail. In weekends I can have some time to read about ASD.
María Luján
Hey, Cubby:
Um, ya, I missed that whole order thing in the story ... gawd. For me the story is all about the pea, but I suppose Anderson had a more pedestrian meaning to it all. So, it's really, to me, about increased sensitivity and in that regard, I mean a more highly particular kind of immune system.
Of course I am dancing around words because I don't want to employ the terms used by many of the 'usual suspects', as I feel they've diminished their actual meanings.
My interest is in epigenetics (which I am not at all well-versed in); increased cytokine activation; maternal-fetal transmission and the like.
Lately, as hobby I suppose, I have been trying to disprove some of the theories that have held my interest.
/disregard my Page comment; he rulz
Hi, Maria:
Thank-you for your response and for the great collection of abstracts which you sent previously. I apologize for not yet following up. I am not really competent enough to engage in a verbal discussion about most of the science in this area. I have good visual skills and can see a lot more in my mind than I can put into words -- so I mainly argue with myself, lol.
Let me go over the things you've already sent to see if there are discrete areas for discussion. Also, we can go to the Autism-Science board and restart our epigenetics discussion, but again, I am not very knowlegable in this area ... just interested.
Hi HJ
Do not worry about. Do the discussion the way you want or feel confortable.I understand.
Remember please that english is my second language. With the complexity of ASD, sometimes language is a problem, but I do my best. KEv´s forum is OK. Do not think please that I am knowlegable in epigenetics. As I always say I study a lot but this does not mean that I know a lot :). As a researcher ( my profession) this attitude is a permanent assurement that I am - and will be-a perpetual student in science, perhaps a different level of student, but always one.
Now, I returned to work so I can only return posts on weekends. Please if I do not answer do not think I am not interested. REally through the week I am now awfully busy.
Thank you for your answer.
María Luján
Maria ... a Post Script here:
First, I have been meaning since my first post here to make a correction (grammatical) -- especially since I don't want to make my English even more confusing than it is even to native speakers ; ] The acronym I employed is incorrect, and I want to point that out lest I confuse you, it should be: TPATP {/warning: dyslexia may still not be turned off}
Second, don't put too much stock in my ramblings. My little Princess/Pea theory came about really in reaction to the whole use the "changeling" (sp) story idea AND the "canary in the coal mine" premise that has gotten so bandied about for some years. Some seem to forget what really happened to the canaries.
The upshot is that the Princess, sensitive as she may be, proves victorious ... or at least "lives happily ever after."
But back to Science. I'll see you on the Aut-Sci board. The results of the St Louis meeting this past week-end (see Diva's blog) and the studies just out today from Harvard and Boston's Childrens Hosp. about myocyte enhancer factor 2 (MEF2) have really piqued my interest.
Later!
I do believe from my experience and reading the research going way back that non-familial autism is related to advancing paternal age. I also believe that an entirely separate risk factor is having relatives and/or siblings who are on the spectrum. There are many disorders of the nervous system that increase in non-familial cases such as Alzheimer's, up to 1/3 of all schizophrenia and some cases of mental retardation. http://www.schizophreniaforum.org/for/curr/Malaspina/default.asp
I don't think there are environmental triggers with these two risk factors except the environment in the womb. I think genetics alone are enough to cause autism. That doesn't mean that there is not environmentally caused autism that is not from paternal age over 35 or familial history of people on the spectrum In many familial cases it seems that the mother might be the carrier of the genes. Maybe the X chromosome is involved. Please try to look at the risk factors for autism with a broad brush familial autism and paternal age de novo autism are not the same. In Reichenberg's study the ratio of boys to girls was close to 1:1.
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