Which autism causation theory has the most evidence?

Discuss autism theories, media stories, and efforts to put ASD on the government agenda here.

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MCA
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Which autism causation theory has the most evidence?

Postby MCA » Sun Apr 30, 2006 12:43 am

Posting this on the HOT board... whoo hoo! Don't even know if it belongs here or not

Traditional medicine says the brain is short circuiting or not functioning correctly... has anyone observed this on an MRI or something like that without there being a secondary diagnosis such as seizure disorder? Is there any evidence aside from assumption that the neurons are not firing correctly, or is that just assumed from what we see in their behavior?

The GFCF gut thing is really interesting... is it actually possible to SEE the diseased gut via a colonoscopy or something? When Krigsman scopes, does he see a permeated gut? Or are we assuming it by what we see happens when the kids eat gluten or casein, coupled with the heroin similarities at the molecular level?

The metals toxicity testing is interesting and provable but I really don't get why you have to send the tests to very specific, out-of-state (for me) labs if the metal levels are that clearly inflated. Why wouldn't every single lab want a piece of the $$$ action?

Has anybody seen indisputable physical evidence of an autism cause? Like a kid having an MRI on a bad day, then on a good day, and seeing different patterns in brain activity?

Winnie
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Postby Winnie » Sun Apr 30, 2006 1:12 am

I don't think anyone in the traditional medicine/treatment realm claims to know the cause of autism or to have indisputable evidence -- though certainly there are many theories. I thought the following was a fascinating site -- it is the 5th Annual Meeting for Autism Research (IMFAR) in Montreal -- you could literally spend a day reading over the number of studies just being presented at this convention. These appear to be new studies -- pre-publication (presumably pending peer review and such). Check out the list of abstracts (includes entries in just about every imaginable category):

http://www.cevs.ucdavis.edu/Cofred/Publ ... webid=1245


As far as MRI examining the brains of people with autism, I noticed this study found anatomical differences even between the brains of study participants with autism v asperger's (and NT controls):


Royal College of Suregons, Dublin
Abstract Title
THE RELATIONSHIP BETWEEN CLINICAL PHENOTYPE AND BRAIN ANATOMY IN AUTISTIC SPECTRUM DISORDER : AN sMRI STUDY.
List of Authors
F. Toal, E. Daly, L. Page, B. Cutter, Q. Deeley, B. Hallaghan, S. Curran, D. Robertson, C. Murphy, F. Happe, P. Bolton, K. C. Murphy, D. G. Murphy
Enter your abstract here
Background: It is unknown if differences in the clinical phenotype of Autistic spectrum disorder (ASD) are associated with differences in brain structure.
Methods: We investigated, as part of the MRC UK A.I.M.S. program, brain anatomy in 87 adults with ASD (58 people with Asperger syndrome, 18 with High Functioning Autism , 11 with Classical autism) and 46 controls using volumetric magnetic resonance imaging.
Results: People with ASD had significant reduction in white matter in cerebellar brainstem and parahippocampal regions; . Further, we found significant differences within people with ASD according to clinical phenotype. Those with Asperger syndrome had reduction in grey matter in both cerebellum and social brain regions including medial temporal and fusiform gyrus; whereas those with High functioning autism and Classical autism had an increase in grey matter in fronto-striatal and tempo-parietal regions. Finally when we compared people with High functioning autism and Classical autism to Asperger syndrome we found excesses in grey matter in language specific regions.

Interpretation: People with ASD have significant differences from controls in the anatomy of brain regions implicated in behaviours characterizing the disorder. These may arise from abnormalities in at least two neurodevelopmental processes, one associated with a regionally specific excess of grey matter, and another with deficits in both grey and white matter. Further, variation in the behavioural phenotype of ASD is associated with differences in brain anatomy. Our findings may also partially explain the variable results from prior studies of ASD; because many studied people from different parts of the autistic spectrum


There is a vast planet of avenues being explored and those yet to be explored -- I am awed by how much we still don't know.
Winnie
"Make it a powerful memory, the happiest you can remember."

rlneub
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Postby rlneub » Sun Apr 30, 2006 7:36 am

One interesting brain observation is in the spec scans. Not sure if all/most/some kids with autism have this type of spec scan, just found it interesting that Dr. Buckley has a before and after HBOT spec scan that I as a non doc can see there is a big difference.

I posted these scans on the mHBOT tab of our website. I think is is page 8 of the pressure point magazine.

Is this proof, no more than any of the other "proofs" out there. Its just another "hmmm, aint that interesting".

kelly
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Postby kelly » Sun Apr 30, 2006 12:09 pm

our son's MRI showed delayed myelination which means the circuits that carry messages are not moving as fast as they could be.
Mom to Ryan 5yr PDD-NOS,ADHD

Mary
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Opinion

Postby Mary » Sun Apr 30, 2006 12:41 pm

It may be decades from now before anything is known, but I personally believe, from talking to scores of parents whose children's autism progressed and developed differently and who have different symptoms, that there is no one "autism."

Autism is a description of a collection of symptoms that have different causes, in my opinion. Some kids have autism caused by Fragile X Syndrome (X chromosome), a genetic condition, but most kids with autism don't have this genetic anomaly. Some girls with Turner Syndrome (X chromosome) have autistic characteristics, but most girls with autism do not have Turner Syndrome. Some children with Down Syndrome (Chromosome 21) have autism, but most people with autism don't have Down Syndrome.

Some kids were autistic from birth and others developed normally and had a major, sudden regression. Some kids were in between those two extremes. Some kids have gut problems, some don't. Some kids had vaccine reactions, some didn't. A few kids with autism never got vaccines. In some families, there are multiple people diagnosed with autism. In others, the person with autism is the only one in the family with anything resembling an ASD. There is no "history" of autism that would point to genetics for those families. Right now, there is no gene for autism that has been discovered.

In the meantime, we all will have to do the best we can to figure out the best way of helping our kids achieve their potentials.

Alex's mom
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Postby Alex's mom » Sun Apr 30, 2006 1:27 pm

I have the exact same understanding and take on this as Mary. I too believe that autism is the final expression and common denominator of a variety of disease mechanisms.
There are studies to show increased intestinal permeability in some autistic children, as well as intestinal abnormalities by scope. Also studies that show abnormal SPECT scans in ASD. Also autopsy studies confirming that there are abnormalities in the autistic brain.
Studies using lumbar punctures to show increased inflammatory markers in the spinal fluid. Problem is, all of these studies are very small, low double digit patient numbers at best. No unifying thread.
Also some data in rats or cell cultures (like the ones about mercury toxicity). VERY little. Not really evidence based medicine.
That's what I remember off hand. You can plug in your search into www.pubmed.com and see what comes up.
As far as the heavy metal theory- I'm not sure if I would call it "provable" at this point. You are bringing up a great point about lab testing. Remember that the metal tests our DAN!'s order usually compare challenged samples (urine) with non-challenged "normal" values. So then when stuff comes back off the charts, I don't really know what that means. I think there is a huge lack of standardization of these tests, as well as a lack of a clear chelation protocol (look at how many protocols are used only on this board alone) as well as a lack of clear understanding of what these chelators actually do so far out of the presumed insult.
I don't know of any indisputable evidence either way. I'm not sure how up to date I am any more, lately I've concentrated my efforts much more toward interventions that have more practical relevance for my son, and for some reason these appear to be more educational than medical in nature.
Alex's mom

KristenP
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Postby KristenP » Sun Apr 30, 2006 3:44 pm

hi all. So much info. it is hard to know what is right. Most researchers are saying that there is definitely a genetic predisposition to autism that is brought out by the accumulation of environmantal factors. Unfortunately the actual cause is still hard to pinpoint. I think that there are numerous causes depending on the child. Autistic children may either lack the ability to process and excrete toxins or this process may be inefficient, causing toxic elements to accumulate and deposit in the tissue. These environmental factors could include, and not limited to,
Heavy Metals-including mercury...can be in the air we breathe, the fish we eat, and of course vaccinations.
Pesticides-in our food, ground water, and lawns
Chemicals- carpets, plastics, cleaning agents, etc.
Natural elements-aresnic, radon etc. getting into food and water supplies.
The list goes on.
So, here is my question....We are thinking of having another child...what do I do different to prevent my second from developing autism???
Eat only organic, no fish, test well water often, don't vaccinate, and pray? I get nervous when I hear of cluster situations. Why does this happen? there has got to be more to this environmental effect than meets the eye.
Kristen

LM
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Postby LM » Sun Apr 30, 2006 6:39 pm

We too talk about having more kids in the distant future - I hear the 3rd time's a charm :wink:

We sort of got a surprise with both kids in which for the majority of their development we thought they were pretty normal, and then, surprise!: Quirky ='d autistic, and funny looking delayed baby ='d possible genetic condition.

I'm constantly beating myself up over what could've caused both kids to have developmental issues. Since geneticists could not find a specific condition for #2, I wonder how much of both kids' issues are related. I wonder if it was the sinus medication I took when I was 8 weeks pregnant w/#2, was it because we lived in a 100+yr old flat, was it because we lived in the city, was it because I was working in a stressful job (trading) - I have no clue.

All I know is that there are a number of times I can't help myself from feeling that life just isn't fair - and I know that's a pretty self-centered thing to say. I know there are those who endure bigger problems, tougher decisions, and I can't imagine what it must be like to be in their shoes. At the same time I can't help but feel my heart being ripped out every time I see children the same age as my own, doing and saying so much more.
I wish there were more answers to the why's, and just as important, what happens next?

I guess that until we find out the whys, you just have to be wide open about the future.

SDYLADY
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Postby SDYLADY » Sun Apr 30, 2006 8:55 pm

I got my tubes tied after finding out my second child had Autism. I don't have the time or energy a third child would deserve with or without the threat of Autism. One thing I have learned from this board is there are so many of you working as hard or even harder than I do, and at least I don't feel alone. I wish none of us had to make any of these decisions. I always keep in mind there are many people worse off than we are, and I should be thankful everyday for what we have.

TamiW
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Postby TamiW » Sun Apr 30, 2006 9:07 pm

One interesting brain observation is in the spec scans. Not sure if all/most/some kids with autism have this type of spec scan, just found it interesting that Dr. Buckley has a before and after HBOT spec scan that I as a non doc can see there is a big difference.

I posted these scans on the mHBOT tab of our website. I think is is page 8 of the pressure point magazine.

Is this proof, no more than any of the other "proofs" out there. Its just another "hmmm, aint that interesting".


Can you get a spec scan pretty easily? Or does it take a miracle for this to be given? We are doing HBOT in a month and I would love to see before and after. I would even post the results, if possible.
Tami

give a mouse a cookie
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Postby give a mouse a cookie » Sun Apr 30, 2006 9:45 pm

Wow. I think it all depends on who you ask, doesn't it? There are SO many theories out there; some with evidence, some without, some with tenuous evidence--fair enough?
Everyone's got their own feelings on this topic.
My feelings, not scientific evidence, mind you, are that genetics play a large role, and that there may be environmental factors that exacerbate symptoms or behave as a catalyst for a lot of kids.
When I Googled "Autism Causation Theory", there were more genetics studies than any other type on the first page of results, but that doesn't mean much, really.

TamiW
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Re: Which autism causation theory has the most evidence?

Postby TamiW » Sun Apr 30, 2006 10:09 pm

Traditional medicine says the brain is short circuiting or not functioning correctly... has anyone observed this on an MRI or something like that without there being a secondary diagnosis such as seizure disorder? Is there any evidence aside from assumption that the neurons are not firing correctly, or is that just assumed from what we see in their behavior?


Gavin got an MRI at 9 months old cause he slipped and lost consciousness. They said his brain was looking pretty darn good!

The GFCF gut thing is really interesting... is it actually possible to SEE the diseased gut via a colonoscopy or something? When Krigsman scopes, does he see a permeated gut? Or are we assuming it by what we see happens when the kids eat gluten or casein, coupled with the heroin similarities at the molecular level?


Gavin had a colonoscopy at 18 months old to test for celiacs disease (came back negative). But his intestines were very inflamed. He had polyps and lesions on his colon.

The metals toxicity testing is interesting and provable but I really don't get why you have to send the tests to very specific, out-of-state (for me) labs if the metal levels are that clearly inflated. Why wouldn't every single lab want a piece of the $$$ action?


We've used different labs. All of them indicated that his metals (or specific ones, not all at the same time) were at toxic levels. We did hair analysis too.

Has anybody seen indisputable physical evidence of an autism cause? Like a kid having an MRI on a bad day, then on a good day, and seeing different patterns in brain activity?

Nope, never did that. I think it would be hard to have a ped order that sort of test, just to see. I wouldn't do it anyways since, to me, his getting better indicates we are on the right track. Good questions though.
Tami

rlneub
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Postby rlneub » Sun Apr 30, 2006 10:32 pm

Can you get a spec scan pretty easily? Or does it take a miracle for this to be given? We are doing HBOT in a month and I would love to see before and after. I would even post the results, if possible.


Yes but VERY pricey.

TamiW
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Postby TamiW » Sun Apr 30, 2006 10:33 pm

Figures! :(
Tami

Ty's Mom
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Which autism causation theory has the most evidence?

Postby Ty's Mom » Mon May 01, 2006 12:59 am

LM - Your comment about thinking that life just isn't fair -- isn't self-centered. I think about this often and am also torn when another child my son's age is talking up a storm or just enjoying playing with other children.

I'm saddened that my son has such hurdles to overcome, many of which are "typical" and come naturally to NT children. I would agree that life is unfair for the children that are diagnosed on the spectrum. They have a lot to learn and yet are faced with so many biomedical challenges.

In reading another post on this website under rate of recovery, I was really saddened to read that Rick mentioned that none of their patients have been cured at the point of NT. This is my biggest fear to think that my son will always have hurdles to overcome and I wonder if he will reach the point of learning from his environment rather than being taught everything via ABA.

He has made some nice gains but has so far to go....

MCA
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Postby MCA » Mon May 01, 2006 1:54 am

Thanks you guys. I appreciate your replies and understand the feeling behind them. I know we all have to look forward and do our best to help our kids. I am just trying better to understand exactly where we are in getting a true picture. So I made this list of things to research: delayed myelination, hbot results, chromosomal abnormalities, visible intestinal permeability and/or inflammation, SPECT scans, markers in lumbar fluid (I remember learning about that one a while ago here, thanks you guys.)

Luckily, I do know well the toxicity theories because they are discussed so articulately here on this board. Please understand I am not trying to prove or disprove any theories, alternative or mainstream. I'm just trying to figure out what we know for sure, because as I keep fighting I still want to know what the hell happened.

I agree too that there are different types of autism just as there are different types of brain damage, and our kids came here travelling different roads. Winnie, thank you tremendously for your post about the conference and the ASD/Aspergers brain studies. That is the kind of thing I am wondering about.

I found this on the media board, it's part of the research study results posted in the "MERCURY IN YOUNG CHILDREN WITH AUTISM USING HAIR SAMPLES" thread...
While autism has a known association with some environmental factors such as rubella and valproic acid exposure in utero,
Anyone know anything about this?

There is a vast planet of avenues being explored and those yet to be explored -- I am awed by how much we still don't know

Me too. And I am equally awed and terrified by how little the people who should know actually do.

I appreciate it everyone. Thank you for replying.

An unrelated side note... Jana, tubal ligation has a somewhat significant failure rate. If having another child is out of the question you should use a secondary method. Sorry to post this on a public board but I thought you should know.

rlneub
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Postby rlneub » Mon May 01, 2006 6:49 am

reading another post on this website under rate of recovery, I was really saddened to read that Rick mentioned that none of their patients have been cured at the point of NT.


I think you read this incorrectly. We have many who are completely indistinguishable from their NT peers as long as they are being treated. Not one of our patients hold all gains should treatment stop. If cured, then stopping treatment without regression would happen.

BTDT
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Postby BTDT » Mon May 01, 2006 9:48 am

Traditional medicine says the brain is short circuiting or not functioning correctly... has anyone observed this on an MRI or something like that without there being a secondary diagnosis such as seizure disorder? Is there any evidence aside from assumption that the neurons are not firing correctly, or is that just assumed from what we see in their behavior?


Well, from what I have heard and read, MRI's are not usually able to detect significant anatomical differences in the brains of those with autism, except there does seem to be a certain (small) percentage of kids who have a Chiari malformation. I think the thought is that if there are anatomical differences they are at a smaller level than MRI would be able to visualize.

I think the research about the differences in the minicolumns in the autistic brain is intriguing. Here is a link describing this research. MCA I put in bold some of the text that speaks to your question about in utero exposure to rubella and certain drugs that are known to predispose autism.

http://www.awares.org/conferences/show_ ... ll_paper=1

AUTISM AND MINICOLUMNS

Autism is a medical condition whose core features include both language and brain size abnormalities. Autopsy, head circumference, and structural imaging studies all suggest that the brains of autistic individuals are, on average, larger than normal. Furthermore, a significant percentage of autistic patients have delayed and deviant language development.

Some patients remain mute throughout their lifetime. Furthermore approximately one third of autistic individuals suffer from seizures, a phenomenon that usually localizes to the neocortex. The available facts from both clinical and structural imaging emphasized the need of studies focusing on the neocortex and its modular organization.

Our first study of autism involved nine patients and an equal number of controls. Three brain regions were examined, including a specific portion of the language regions of the brain. Striking disturbances in minicolumnar morphometry were found in autistic individuals. More specifically, minicolumns in the brains of autistic individuals were smaller in size and more numerous in all three areas examined. These results were soon corroborated using a different technique called the gray level index (GLI).

Furthermore the results were not a confound of other superimposed conditions like mental retardation. Down syndrome patients have normal sized minicolumns despite having smaller brains. If anything, they acquire their mature size sooner than normal individuals. This has been seen, in the context of Down syndrome, as suggestive of accelerated aging.

Our findings, smaller minicolumns in the brains of autistic individuals, have been replicated as part of an international study in collaboration with Dr. Christoph Schmitz of the University of Maastricht, the Netherlands. This new and independent sample examined the brains of six autistic patients and an equal number of controls. All facets of the study, including the identification of brain regions, analysis of minicolumns, were done blind to diagnosis.

In autism, smaller minicolumns in brains that are, on average, larger than normal suggests their total increase in numbers. The total number of minicolumns is defined during the first forty days of fetal development. This window of vulnerability coincides with reports of autistic behaviors in fetal/developmental conditions such as rubella babies, infants exposed to thalidomide, tuberous sclerosis.

What is the meaning of smaller minicolumns? First, this question has been approached from the standpoint of computer modeling by a group in Switzerland (Dr. Gustafson’s). Results suggest that smaller minicolumns tweak information processing in favor of the signal. By comparison other conditions characterized by larger minicolumns (e.g., dyslexia) tweak information processing in favor of noise. This means that autistic individuals usually do well in processing stimuli that requires discrimination while dyslexics are better at generalizing the salience of a particular stimulus.

Second, minicolumns are compartmentalized. Information is transmitted through the core of the minicolumn and is prevented from suffusing into neighboring units by surrounding inhibitory fibers. The inhibitory fibers act in analogous fashion to a shower curtain. When working properly and fully draping the bathtub the shower curtain prevents water from spilling to the floor. In autism minicolumnar size reduction involves primarily the peripheral compartment that provides the inhibitory surround.

This means that stimuli are no longer contained within specific minicolumns. Stimuli overflow to adjacent minicolumns thus providing an amplifier effect. This may explain the hypersensitivity of some autistic patients as well as their seizures. Third, most environmental information is transmitted to the brain via a structure called the thalamus, a salient exception being olfactory information. The thalamus sends projections which span a finite distance within the cortex. It is believed, but not proven, that thalamic innervation is a way of binding minicolumns into larger modules called macrocolumns.

If the terminal field of thalamic innervation remains the same size while minicolumns are smaller, the end result would be many more minicolumns per macrocolumns. Again, this change similar to the previously described on loss of peripheral inhibition, would help make the brains of autistic individuals behave as an amplifier system. Finally, comparisons of minicolumnar parameters across many species suggests that smaller minicolumns (and more of them per given area) provide complexity in terms of information processing.

A visual cortex constructed of smaller minicolumns may provide for added aspects of functionality, e.g., depth or color perception. Researchers believe that this complexity is due, in part, to the overlap of neuronal projections between different minicolumns. That is, dendrites and axons of neurons that remain the same size in autism may have more of an opportunity to overlap when their constituent minicolumns become smaller.

Minicolumnar size is not the only abnormality observed in the neocortex of autistic patients. It appears that cells (neurons) within individual minicolumns are also reduced in size. This has important consequences in terms of connectivity. Long connections require the metabolic sustenance of large cell bodies. A neuron in the brain that connects all the way to the lower spinal chord requires a fairly large cell body. By way of contrast, a neuron whose projection remains within the cortex, contacting a closely adjacent cell, can manage its metabolic demands with a small cell body.

The small cell bodies in the brains of autistic patients favor information processing through short intra regional pathways, e.g., mathematical calculations, visual processing. Similarly, cognitive functions that require long inter regional connections would prove metabolically inefficient, e.g., language, face recognition, joint attention.

In this regard, the less affected region of the brain should be the striate cortex which is composed of a majority of small granule cells having short connections between closely adjacent areas. It is no wonder that in terms of information processing autistic patients use coping strategies in day to day activities that play to their strength. This is one of the main themes of the popular book “Thinking in Pictures” by Temple Grandin.

At present we are hoping to translate our basic research findings into clinical trials, diagnostics, training, and education. First and foremost we would like to explore ways that could increase the inhibitory surround of the minicolumn. Another of our main preoccupations is to define the genetic and environmental influences that account for minicolumnar organization in both health and disease. I am summarizing two of the projects that I would like to finalize in the near future, one relates to epidemiology (the rising incidence of autism) and the other to a potential therapeutic intervention.

srinath
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Re: Which autism causation theory has the most evidence?

Postby srinath » Mon May 01, 2006 10:30 am

TamiW wrote:<snip>
We've used different labs. All of them indicated that his metals (or specific ones, not all at the same time) were at toxic levels. We did hair analysis too.
<snip>


The labs basically reference it against their data. If it falls in their 80% ... that is 80%. The irony is ... I drew my son's testosterone test to Presbyterian hospital who sent it to quest. They tested it and said it was like 16 and that was low (under 25 is low ... for an adult male as the desk reference manual says). They also said it was average in their sample database. I looked at their reference sample size (and its harder to find than you'd think) and that was 1. Hence the contradiction. Its somehting like saying the doctors say it should be 25 for an adult male, for a 3 year old we dont know. We have determined that its average for 3 year olds and we have picked that average from 1 3 year old (aka he set his own reference mark and he was equal to it). With labcorp I saw that they said he was high for a 3 year old inspite of being the same 16 since for 3 year olds the reference ranges are 2-5 ppm. Great plains or DDI probably maintain the largest databases of anyone in the industry. Lets say I went around and bought copies of every lab's results data and complied it into one massive data repository ... I will then have 10000's of kids in every category in that database. Maybe DDI and Great plains did that a few years ago and have the ability to now sift through piles of data to determine what is their average and also what the desk reference manual says. BTW labcorp was what Dr G uses, and the general DAN community uses GP and DDI.
Cool.
Srinath.

brooke
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Postby brooke » Mon May 01, 2006 4:56 pm

I think the gut/immune issue and ASD has the most published research in peer related journals but people would still have to follow the trail. It has been piece by piece in the literature world and since it is relatively new like in the last five years and it takes on average 10 years for the latest research to become part of public policy, we should expect mainstream exceptance in the next 10 years or so. This is why I respect research but I am not willing to wait for it when it comes to treatment for my child. Clinicians have always been light years ahead of research facilities since they see it day in and day out and are in the trenches so to speak. It is going to be an exciting year in our world, wait and see.

Brooke


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