Autism Mashup – Hypothyroidism, Reelin Expression, and Scary Chemicals
Posted on: July 27, 2010
- In: Autism | BDNF | Biological Plausibility | BPA | Brain | Epigenetics | Epigenome | Genetics | Impending Doom | Intriguing | PBDE | Pesticides | Prevalence | Purkinje | Reelin | Some Jerk On The Internet | Synthetics | The Fairytale | Uncategorized
- 33 Comments
Hello friends –
I ran into a few abstracts, read a few papers, and tried to get my way through one really dense paper in the past few weeks that got me thinking about this post. It’s all shook up, like pasta primavera in my head, but hopefully something cogent will come out the other end. (?)
Of the metabolic conditions known to be associated with having a child with autism, hypothyroidism is one that I keep on running into by way of the pubmed alert grapevine. By way of example, we have two studies that looked for autoimmune conditions in family members which found hypothyroidism to be one of many autoimmune diseases as a risk factor for autism, including, Familial clustering of autoimmune disorders and evaluation of medical risk factors in autism, and Increased prevalence of familial autoimmunity in probands with pervasive developmental disorders. This shouldn’t be too surprising, we know that, for example, perinatal hypothyroidism is a leading cause of mental retardation, with similar findings for the condition during pregnancy. It turns out, it appears that rates of hypothyroidism are slightly increasing, though at this time, the increases are of relatively small proportions, and as such, may be artifacts unrelated to an actual increase in classically recognized hypothyroidism. In any case, I think it is safe to say that interference with thyroid metabolism is something to be avoided at all costs when possible.
So after having read about that, this paper showed up in my inbox a while ago:
Thyroid hormones have long been known to play important roles in the development and functions of the central nervous system, however, the precise molecular mechanisms that regulate thyroid hormone-responsive gene expression are not well understood. The present study investigated the role of DNA methylaion and histone acetylation in the effects of perinatal hypothyroidism on regulation of reelin and brain-derived neurotrophic factor (BDNF) gene expression in rat hippocampus. The findings indicated that the activities of DNA methyltransferase (DNMT), methylated reelin and BDNF genes were up-regulated, whereas, the activities of histone acetylases (HAT), the levels of global acetylated histone 3 (H3) and global acetylated histone 4 (H4), and acetylated H3, acetylated H4 at reelin promoter and at BDNF gene promoter for exon II were down-regulated in the hippocampus at the developmental stage of the hypothyroid animals. These results suggest that epigenetic modification of chromatin might underlie the mechanisms of hypothyroidism-induced down-regulation of reelin and BDNF gene expression in developmental rat hippocampus
This gets interesting for autism because reelin, and bdnf levels have been found to be decreased in several studies in the autism population, with direct measurements, genetic expression, mouse knockout based models of autism , and genomic alterations all being implicated. There have been some negative genetic studies, but considering that it isn’t always the genes you have, but the genes you use, our other available evidence certainly points to BDNF and reelin involvement with some percentage of children with autism, and the association is such that a reduction in reelin or BDNF is a risk factor for developing autism. It would seem that the paper above might give some insight into the lower level details of the effects of hypothyroidism and subsequent developmental trajectories; modifications of reelin expression; through epigentic mechanisms, no less!. That’s pretty cool!
Then, I got my hands on a review paper that tries to go into detail as to the functional mechanism by which reelin deficiency could contribute to ASD, Neuroendocrine pathways altered in autism. Special role of reelin. It is a review that touches on a variety of ways that reelin contributes to neurodevelopment that have findings in the autism realm, including neuronal targeting and migration during brain formation, interactions with the serotonin and GABA systems, testosterone, and oxytocin. In short, there are plenty of ways that decreased reelin expression can impact development in ways that mirror our some of our observations in autism.
Of the many things that convince me that we are doomed, the proliferation of chemical compounds whose interactions within our bodies we scarcely understand is among them. In my readings on endocrine disruptors, one thing I found that seemed to be worrying lots of researchers was that some classes of these chemicals are capable of interfering with thyroid metabolism, and in some cases interfering with development of cells known to be associated with autism. Terrifyingly enough, since I read those papers, several others have come out, including Polybrominated Diphenylether (PBDE) Flame Retardants and Thyroid Hormone during Pregnancy and Mini-review: polybrominated diphenyl ether (PBDE) flame retardants as potential autism risk factors. At this point, it is important to point out that, as far as I know, there have not been any studies showing that non occupational exposure to PDBEs or other environmental pollutants can lead to classically defined hypothyroidism, at least none that I know of. (?) Be that as it may, I think it is realistic to assume any interference in thyroid metabolism is a bad thing, and while finding people in the outlier regions of hypo (or hyper) thyroidism gives us information on extreme environments, it would take someone with a lot of misplaced faith to assume that we can safely disturb thyroid metabolism just a little bit, and everything will come out in the wash.
I’ve had the argument made to me in the past that environmental pollutant driven increases in autism lacked biological plausible mechanisms; this argument is almost always made within a context of trying to defend the concept of a static rate of autism. While the papers I’ve linked to above do not provide conclusive proof that our changing environment is causing more children to be born with autism, they do provide increasing evidence of a pathway from pollutants to ASD, and indeed, the lack of biological plausibility becomes an increasingly flacid foundation on which to assume that our observations of an increased rate of autism are illusory. Unfortunately, in my opinion, the focus on vaccines has contributed to the mindset that a static rate of autism (or nowadays, maybe a tiny increase), must be protected at all costs, including some ideas on the application of a precautionary principle that seem outright insane to me (or at least, the exact opposite of what I would consider to be a precautionary path).
One thing is for certain, the number of child bearing women in developing countries with measurable concentrations of chemicals known to interferre with thyroid metabolism nears 100% in the industrialized nation as we eat , drink, breathe and bathe in the microscopic remnants of packaging materials, deteriorating carpet fibers, and baby clothes that are made to be fire resistant. This is an environment unambiguously different than that encountered by any other generation of infants in the history of mankind. To believe that we can modify our environment so drastically without having an impact seems incredibly naive to me, or on some days, just plain old stupid.
– pD
33 Responses to "Autism Mashup – Hypothyroidism, Reelin Expression, and Scary Chemicals"
August 1, 2010 at 4:05 pm
pD, Interesting (in a good way) post. To apply this to the real world, there has to be undiagnosed perinatal hypothyroidism correct? Isn’t thyroid testing part of the neonatal screen in every state? http://www.acmg.net/resources/policies/NBS/NBS_Main_Report_03-02.pdf
Yes, it is bizarre how vaccine protectionism results in convoluted arguments.
Yes, it is bizarre how anti-vaccinationism results in convoluted arguments. Fixed that for you.
This seems to me to also impact the area of dietary intervention — else why so much arguing against simple harmless dietary intervention which is worth a try and often has great results? And studies that seem oddly skewed towards denial of what so many parents and people with autism witness (see Judy Converse’s 7/22 letter at http://pediatrics.aappublications.org/cgi/eletters/peds.2009-2391v1 )
The more rigorous studies don’t support a sub-population benefit of GFCF diets:
http://www.ncbi.nlm.nih.gov/pubmed/19033217
http://www.ncbi.nlm.nih.gov/pubmed/18600441
http://www.ncbi.nlm.nih.gov/pubmed/16555138
http://www.ncbi.nlm.nih.gov/pubmed/18425890
http://www.urmc.rochester.edu/news/story/index.cfm?id=2860
http://photoninthedarkness.com/?p=145
While less rigorous and authors with vested interests in the outcome, i.e. also conflicts of interest, magically find some benefit: http://www.ncbi.nlm.nih.gov/sites/entrez/20406576
GFCF diets are not ‘harmless’ either and seem to be a ‘one size fits all’ approach by DAN!s. Another ‘throw it at the wall and see what sticks’ approach. GFCF diets do benefit those with actual allergies or intolerances but it is treated as a panacea, that is where the argument lay. You prefer to rely on anecdotes but never challenge groups like SafeMinds an ARI to fund or conduct proper studies to validate their claims. Why is that? Parental reporting is notoriously biased, so is practitioner reporting when they believe their methods.
That is what we have blinded trials for, to remove those biases and determine if the observational effects are real. Have you ignored the trials underway to examine such interventions on autism that are being funded by your evil government? How many of you have even inquired about participation? Put your money where your mouth is.
Clinical Trial for gfcf
http://www.clinicaltrials.gov/ct2/show/NCT01116388?term=gfcf&rank=1
Remitted Autsim Study’
http://www.clinicaltrials.gov/ct2/show/NCT00938054?term=gluten+casein+free&rank=4
It makes me wonder, why? Is positive response to dietary intervention evidence of vaccine causation? If not, why all the denial?
What?! This doesn’t even make any sense. How does a response to a restrictive diet provide evidence of vaccine causation? Do you even think about what you are saying or does it just fall out?
Just narrow-mindedness, or something else being protected, or do certain high-up people know that the immune system responds abnormally to foods such as wheat and milk because vaccines contain substance such as casein hydrolosate (used as substrate to grow microbes for vaccines such as DPT) and wheat germ oil (which rumor has it is used in some vaccines, but I’m not sure of this). Not to mention peanut oil.
You are really just off the rails here. There is no casein hydrosylate in vaccines, there are trace amounts of bovine casein from culture media in a few paediatric vaccines, in a quantity often too small to measure. If a child would react to that, then they would be in a whole lot more trouble if they even drank a few drops of milk. You are really grasping here.
Wheat germ oil and peanut oil? Yea, you’re just making that up too.
August 2, 2010 at 7:26 am
“Merck, Sharp and Dohme workers have developed a peanut oil preparation, Adjuvant 65…”
Click to access jhyg00071-0101.pdf
Heather Fraser’s 2010 book, “The History of the Peanut Allergy Epidemic” is reviewed here:
http://www.foodsmatter.com/allergy_intolerance/peanut_treenut/articles/history_peanut_allergy_epidemic.html
http://vactruth.com/2010/07/15/non-disclosed-hyper-allergenic-vaccine-adjuvant/
“Second is the matter of obtaining the highest antibody levels of longest duration and broadest coverage using the elast amount of antigen. Here, an adjuvant such as adjuvant 65 appears to afford a substantial contribution.” (from the Conclusion)
Click to access bulletin_1969_41(3-4-5)_623-628.pdf
August 2, 2010 at 1:05 pm
Hi Tywla –
I do not believe this adjuvant, or any adjuvant besides aluminum based salts; i.e., alum, are licensed for use in humans in the United States. In Europe, an oil based adjuvant, squalene, is in use in some vaccines if I remember correctly. There are a great number of potential adjuvants being investigated, but the regulatory hurdles are significant. That being said, I do find it illustrative that we are only beginning to understand how alum actually works, for decades, we just knew that it did.
– pD
August 2, 2010 at 3:34 pm
Pd, are you sure about that? A quick Google search seems to indicate that Adjuvant 65 has been used, and also that peanut oil does not necessarily have to be listed as a vaccine ingredient.
http://www.patentlens.net/daisy/adjuvants/notable_adjuvants.html
“Adjuvant 65 (in use since the 1960s)…”
This is inadequate info, but gotta go now…
August 2, 2010 at 6:30 pm
Hi Twyla –
There is a big difference between in use at one point in time in clinical trials, and actively being licensed for distribution to everyone.
http://www.cdc.gov/vaccinesafety/concerns/adjuvants.html
Aluminum gels or aluminum salts are the only vaccine adjuvants currently licensed for use in the United States.
That being said, there are a lot of different compounds being tested, usually on animals, but sometimes in humans, for a new generation of adjuvants. The studies I saw regarding Adjuvant 65 in humans were all from 1970 or earlier, and looked like trials to test the adequacy of the immune response. It would seem that either effictiveness, changes to regulatory procedures, safety, or some combination of those has kept adjuvant 65 from being licensed in the United States.
Regarding the necessity of listing peanut oil as an ingredient, while this may be true, I think we need a stronger basis of evidence before we can do more than engage in very difficult to defend speculation towards an association with food allergies. I’m not saying it isn’t possible, but I am of the opinion that we need to be very cautious in these types of things.
– pD
August 3, 2010 at 5:12 am
Pd, I appreciate that you are “of the opinion that we need to be very cautious in these types of things”. I also really appreciate that you discuss things in a civil, thoughtful, intelligent, knowledgeable manner.
I have the impression that peanut oil may also be used for other purposes, such as emulsion. But I don’t have hard proof.
http://barbfeick.com/vaccinations/allergy/610-patents.htm
At any rate, this is off the main point of your article. There is a recent book on peanut allergies and vaccines, which will be interesting to read. In the meantime, I’m just wondering.
I like how you put it that, “The reasoning behind such a vigorous contempt over dietary interventions confuses me as well.” It is indeed odd.
August 3, 2010 at 10:16 pm
Hi Science Mom –
Lets try discussing the diet stuff for a while. It’s a tricky area, but an important one for some children in my opinion. I’m also a bit torn about derailing the thread versus having actual traffic on my blog. Hah.
In any case,
The more rigorous studies don’t support a sub-population benefit of GFCF diets:
http://www.ncbi.nlm.nih.gov/pubmed/19033217
http://www.ncbi.nlm.nih.gov/pubmed/18600441
http://www.ncbi.nlm.nih.gov/pubmed/16555138
http://www.ncbi.nlm.nih.gov/pubmed/18425890
http://www.urmc.rochester.edu/news/story/index.cfm?id=2860
http://photoninthedarkness.com/?p=145
The links you provide do not seem to support your statement. In order:
http://www.ncbi.nlm.nih.gov/pubmed/19033217 — This is a review paper and not a study.
http://www.ncbi.nlm.nih.gov/pubmed/18600441 — This paper was on nutrient consumption, and not a study of GFCF per se.
http://www.ncbi.nlm.nih.gov/pubmed/16555138 — The very first attempt at a blinded GF trial. In this paper, the authors specifically state that some individual children did show benifits, but that at a group level these results were not significant. From Elder:
It is also interesting that even though grouped data were nonsignificant for each of the dependent variables, behavioral and language improvement could be seen in individual children
Also interesting were the unsolicited reports of one teacher and one respite worker who claimed to observe language and behavioral improvements in two of the children
A common problem in the study of children with autism is the wide variability among the children regarding behavioral and developmental traits and levels. Clearly this was a heterogeneous sample in reference to age, severity of autism, and cognitive abilities and thus it was difficult to draw meaningful conclusions about the group as a whole.
Finally:
Also, even though most parents were conscientious regarding the dietary restrictions, there were several reports of children ‘‘sneaking food’’ from siblings or classmates
If I had a pill for autism, and I ran a study with thirteen children in it, and the placebo group “snuck” actual medicine, would you consider that a rigorous study?
http://www.ncbi.nlm.nih.gov/pubmed/18425890 — Another review that states that while existing evidence supporting the diet is poor, what we need are good trials.
Large scale, good quality randomised controlled trials are needed.
[Note this was performed after Elder 2006, and the reviewers still felt the quality trials were lacking.]
http://www.urmc.rochester.edu/news/story/index.cfm?id=2860 — The authors of the study specifically state that there may be subgroups of children who would benifit from such a diet that their study would not be able to discern. From the link:
However, the study didn’t include children with significant gastrointestinal disease. It’s possible those children and other specific groups might see a benefit
And this being the ‘best’ study available, only 18 participants completed the study.
Of your listings, we have two reviews, one paper on nutritional intake, two actual studies, and one blog posting that seems to assume that the only mechanism by which dietary restriction could be having an effect is opiods; a study on permiability, as opposed to diet. Of the actual studies that addressed GFCF specifically, we have a total of 31 children who completed trials of diets.
If this is your idea of ‘rigorous studies’, I’m starting to understand why we have such different ideas concerning the strength of our vaccine analysis. Considering the author acknowledged lack of attention towards children with gastro intestinal problems, the idea that our existing research suite appropriately begins to address the question of subgroups of children is one that you have failed to defend.
Of potential salience in understanding if subgroups of children should be evaluated, this abstract from the last IMFAR, which tells us children with autism and GI disturbances are qualitatively different than children without autism and GI disturbances.
Microarray and pathway analysis revealed significant changes in genes involved in carbohydrate metabolism and transport and inflammation in ileal biopsies from AUT-GI as compared to Control-GI subjects. Real-time PCR confirmed significant decreases in the AUT-GI group in the primary brush border disaccharidases, sucrase isomaltase (p=0.0013), maltase glucoamylase (p=0.0027), and lactase (p=0.0316) as well as in two enterocyte hexose transporters, sodium glucose co-transporter 1 (p=0.0082) and glucose transporter 2 (p=0.0101). In contrast, increases were confirmed for inflammation-related genes in AUT-GI subjects: complement component 1, q subcomponent, A chain (p=0.0022), resistin (p=0.0316), CD163 (p=0.0150), tumor necrosis factor-like weak inducer of apoptosis (p=0.015), and interleukin 17F (p=0.0220). No significant group differences were observed for the enterocyte-specific marker, villin. In conjunction with changes in intestinal gene expression, bacterial content differed between the AUT-GI and Control-GI groups: pyrosequencing and real-time PCR revealed lower levels of Bacteroidetes (ileum: 50% reduction, p=0.0027; cecum: 25% reduction, p=0.0220, and higher Firmicute/Bacteroidete ratios in AUT-GI children (ileum: p=0.0006; cecum: p=0.0220). High levels of Sutterella species were found in 47% of AUT-GI biopsies (7/15), whereas Sutterella was not detected in any Control-GI biopsies (0/7; ileum: p = 0.0220; cecum: p = 0.0368).
We describe a distinctive syndrome in autistic children wherein gastrointestinal dysfunction is associated with altered gene expression reflecting intestinal inflammation, impaired carbohydrate metabolism and transport, and dysbiosis. These findings may provide insights into pathogenesis and enable new strategies for therapeutic intervention.
Note that I’m not advocating that every child with autism has GI problems like this, but this is evidence that when children with autism have GI disorders of such severity that a biopsy is warranted, the condition is distinctly different than what is observed in children without that diagnosis. While not specific to GFCF, this is evidence of what some of us have been claiming all along; our child’s condition is not just an upset stomach, and indeed, is associated with their autism.
GFCF diets are not ‘harmless’ either and seem to be a ‘one size fits all’ approach by DAN!s. Another ‘throw it at the wall and see what sticks’ approach. GFCF diets do benefit those with actual allergies or intolerances but it is treated as a panacea, that is where the argument lay.
Can you validate your assertion that GFCF is ‘treated as a panacea’ by DAN doctors, or anyone? Regarding a harmless or non harmless, presumably you are referring to a study that found reduced bone density in children on CF diets compared to children not on that diet; a situation I would assert could (and should) be handled with relative ease via calcium supplementation.
Regarding allergies or intolerances, I’m curious how you would define that clinically? I think we had a short conversation @ RI on this at one point, but it was lost in the traffic, but the crux of my argument was that we have a great number of studies that show children with autism generate immunological responses at greater frequency to the proteins found in wheat or dairy when compared to children without that diagnosis.
http://www.ncbi.nlm.nih.gov/pubmed/15870662
http://www.ncbi.nlm.nih.gov/pubmed/17974154
http://www.ncbi.nlm.nih.gov/pubmed/16613867
http://www.ncbi.nlm.nih.gov/pubmed/12378124
http://www.ncbi.nlm.nih.gov/pubmed/15741748
To my knowledge, there has yet to be any study published that attempted this kind of test and failed to find an association in the autism population, though you may know of studies of which I am not aware. At this point, however, the definition of what constitutes a valid intolerance, measured either behaviorally, or clinically. My thoughts are that while these studies no doubt do not (edit!) prove wheat or dairy ’cause’ autism, they are evidence that some children with autism react differently to these proteins when compared with children without autism; and furthermore, I’m unconvinced that two negative studies involving thirty children is sufficient evidence to declare dietary restrictions dead.
In any case, I’d be curious on your thoughts on the studies I posted above?
http://www.clinicaltrials.gov/ct2/show/NCT01116388?term=gfcf&rank=1 — Now that looks like a pretty cool study! Curious, however, that the researchers at Massachusettes Hospital seem to be interested in studying subgroups of children, specifically those with sustained GI disturbances. I wonder what has caused them to think this is a worthwhile effort, and how you reconcile that with your opinion is that our ‘rigorous studies don’t support a sub-population benefit of GFCF diets’. Why study what is already established?
This study presents some very tricky issues, to my mind however. For good or bad, parents are trying GFCF diets. If you child meets the requirements for entry; i.e., autism and chronic GI problems, chances are very good that you’ve reached the Internet and found out about the GFCF diet already; likely having given it a shot. If it is working (or you feel it is working), and your child responded, are you going to enroll your child into a study where they may be given something that will worsen their condition? If you tried it previously and didn’t work, you are excluded. This reminds me of some problems cancer drugs are having getting participants. Difficult problem that I don’t know how to address.
http://www.clinicaltrials.gov/ct2/show/NCT00938054?term=gluten+casein+free&rank=4 — Another very cool study. I have personally recommended one friend of ours participate, whose child went from full blown autism diagnosis to undiagnosed. I know of one other child who went from an autism to PDD-NOS diagnosis. I do not know if they will take part. Tragically, my son is not eligible. [yet?]
– pD
ps – editing due to closing html tag fail. Sorry.
August 11, 2010 at 4:48 pm
pD, that may be the most intelligent discussion I have seen on this topic to date. I think it is very bizarre all this talk of how harmful the GFCF diet is. It could be, if a person were uneducated, but why does everyone assume that we are all too stupid to figure out how to do it properly? What is really ironic, is that no humans consumed non-human milk or grains until the introduction of agriculture, which was very recent in human history. For most of our history on this planet, every single human being was GFCF his or her whole life. They didn’t eat beans, either, which includes soy. When my son was first diagnosed, we tried the standard GFCF diet and saw little improvement. But after a lot of research, a year later we went on the Paleolithic diet, which involves a fairly simple principle: eat like most of our ancestors did for most of our history, and this may solve who knows what. I felt like this just made a great deal of common sense. Many experts believe that these agricultural foods were introduced so recently that many individuals in our species will not have completely adapted to some of these foods. Beans and grains are the foods we turned to when there was nothing else to eat, and they are easy to grow. They are cheap and abundant. But you can’t eat them without processing them in some way. They have an extraordinary amount of indigestible matter in them (i.e., fiber), which can in fact damage the intestines. But it makes perfect sense to me that there would be a lot of individuals who lack the enzymes to digest these difficult to digest foods, or who cannot tolerate them for who knows what reason, or even are more sensitive to other naturally occuring chemicals in these foods. But the idea that a human being cannot stay healthy without drinking cows milk or eating wheat is hardly an informed, scientific opinion.
August 11, 2010 at 10:27 pm
Hi Nyx –
Thanks for stopping by my blog. We are in agreement regarding the relatively recent addition of items such as wheat and dairy to the human diet; I looked into the Paleo diet for a while; generally I’m trying for almost nearly all whole foods, no gluten, and very limited animal protein of any type. The gluten free diet can be harmful in the same way that any dietary choice can be harmful. On a similar note, did you see the paper that came out last week regarding intestinal permiability? The authors report that children with autism on GFCF exhibited a reduced degree of permiability when compared to autistic children on a ‘normal’ diet.
I’ve yet to get my hands on a copy of this study, but if you look up work by some of the authors it becomes clear they know what they are doing in regards to gastro intestinal research.
– pD
August 12, 2010 at 12:20 pm
I know it’s not always easy to tell on the internet, so please let me start by saying that I am absolutely not here to argue with anyone! I’m just trying to learn and share … and so I wonder if you would mind sharing with me your thinking about avoiding animal protein. I guess I am doing pretty much precisely the opposite! Having eliminated all legumes (including soy) and grains (including corn), meat is really our only substantial source of protein, so I would like to understand more if you’ve discovered that this is a problem for your son, although of course I know all of our children are different. Actually, I should say that we were rather free until recently with the nuts, but I’ve figured out recently that the nuts are not agreeing with his system, and we’re laying off of them for a while. We’ve been on this particular diet only since the end of March, so of course I can’t really say that it is absolutely the best diet in the world, or even whether only certain parts of it are helpful. for example, for all I know he was allergic to corn, if you see what I mean. It was kind of an elimination/fewer foods diet, I guess you could say, but I haven’t done a lot of detailed analysis to try to pinpoint specific problem foods. So although we have seen clear improvements in our son’s GI situation, I can’t be sure why. So … I would appreciate knowing more about why animal protein in general might be problematic. Also, thank you for the link to the interesting study. I actually think that I can probably get this study. If you like, I will let you know if I get it, I am happy to share it with you if I can.
August 12, 2010 at 2:25 pm
Hi Nyx –
To be more clear, my son is eating animal protein (except cheese) much more often than I am. It isn’t an autism thing, so much as a cardiovascularproblem and cancer risk prevention thing for his parents. I’ve also found that my gastro health is vastly better if I only take mean two times a week or so, and then, as a part of a meal, as opposed to the center of interest. I can see how having no beans or corn would make this a very problematic choice. Then to drop out nuts too is very difficult. We went SCD for a while early on, which sounds similar to what you are doing, so I feel you pain.
You can get blood tests done for food sensitivities, but be very specific when asking your doctor about cost, they can vary greatly between servicing labs. I had one done a few years ago that revealed lots of small hits, but big triggers on wheat and cashews. I cut them out, and now if I try them I’m coughing and hacking for a few minutes afterwards. I also develop dark(er) circles under my eyes when I violate.
If you wind up getting a copy of the permiability paper, I’d love to take a look. I emailed the authors, but haven’t gotten a repsonse. passionless drone at yahoo dot com.
Thanks!
– pD
August 12, 2010 at 6:48 pm
Hi Science Mom –
Lets try discussing the diet stuff for a while. It’s a tricky area, but an important one for some children in my opinion. I’m also a bit torn about derailing the thread versus having actual traffic on my blog. Hah.
In any case,
The more rigorous studies don’t support a sub-population benefit of GFCF diets:
http://www.ncbi.nlm.nih.gov/pubmed/19033217
http://www.ncbi.nlm.nih.gov/pubmed/18600441
http://www.ncbi.nlm.nih.gov/pubmed/16555138
http://www.ncbi.nlm.nih.gov/pubmed/18425890
http://www.urmc.rochester.edu/news/story/index.cfm?id=2860
http://photoninthedarkness.com/?p=145
The links you provide do not seem to support your statement. In order:
http://www.ncbi.nlm.nih.gov/pubmed/19033217 — This is a review paper and not a study.
This reviews studies not included in my list above. If you found it lacking, you could have just referred to the primary literature. I found it to be a fair assessment and an easy read for others.
http://www.ncbi.nlm.nih.gov/pubmed/18600441 — This paper was on nutrient consumption, and not a study of GFCF per se.
That was meant to go under a different heading. I provided this to demonstrate the difficulties in maintaining nutrient-dense diets for many ASD children, even under the best of circumstances. As per Arnold et al. (2003) http://www.ncbi.nlm.nih.gov/pubmed/12959424 , children on GFCF diets had essential amino acid deficiencies, while control subjects on unrestricted diets did not. This isn’t an innocuous intervention.
http://www.ncbi.nlm.nih.gov/pubmed/16555138 — The very first attempt at a blinded GF trial. In this paper, the authors specifically state that some individual children did show benifits, but that at a group level these results were not significant. From Elder:
It is also interesting that even though grouped data were nonsignificant for each of the dependent variables, behavioral and language improvement could be seen in individual children
Also interesting were the unsolicited reports of one teacher and one respite worker who claimed to observe language and behavioral improvements in two of the children
A common problem in the study of children with autism is the wide variability among the children regarding behavioral and developmental traits and levels. Clearly this was a heterogeneous sample in reference to age, severity of autism, and cognitive abilities and thus it was difficult to draw meaningful conclusions about the group as a whole.
Finally:
Also, even though most parents were conscientious regarding the dietary restrictions, there were several reports of children ‘‘sneaking food’’ from siblings or classmates
If I had a pill for autism, and I ran a study with thirteen children in it, and the placebo group “snuck” actual medicine, would you consider that a rigorous study?
You are being selective regarding findings and interpretations:
Before unblinding, parents were asked to comment on whether they thought their child was on the GFCF diet the first or second 6 weeks. Five were correct, two had “no idea”, and six were incorrect.
…and no significant differences in
grouped data for urinary peptide levels of gluten (p=.44) and casein (p=.11).
So what, there were unsolicited reports, when did they occur? The whole point of conducting (particularly blinded) studies is to eliminated reporter biases. The authors were very reasonable in their interpretations and limitations of the study and yes, it is more rigorous than the couple that did find significant differences.
http://www.ncbi.nlm.nih.gov/pubmed/18425890 — Another review that states that while existing evidence supporting the diet is poor, what we need are good trials.
Large scale, good quality randomised controlled trials are needed.
[Note this was performed after Elder 2006, and the reviewers still felt the quality trials were lacking.]
And your point is? You like one review but not another? Of course there are limitations to all studies performed thus far. However, you are completely missing the fact that independent studies are beginning to multiply with similar conclusions. And equally interesting is that it is academics that are performing these studies and not a single decent study from ARI
http://www.urmc.rochester.edu/news/story/index.cfm?id=2860 — The authors of the study specifically state that there may be subgroups of children who would benifit from such a diet that their study would not be able to discern. From the link:
However, the study didn’t include children with significant gastrointestinal disease. It’s possible those children and other specific groups might see a benefit
And this being the ‘best’ study available, only 18 participants completed the study.
Again, a responsible, conservative interpretation of their results. No one I am acquainted with is against GFCF diets; it is the over-use of this diet as a panacea without any empirical evidence and without considerations as to potential need for such a restrictive diet. Not to mention close scrutiny of dietary deficiencies and imbalances that may accompany a restrictive diet.
Of your listings, we have two reviews, one paper on nutritional intake, two actual studies, and one blog posting that seems to assume that the only mechanism by which dietary restriction could be having an effect is opiods; a study on permiability, as opposed to diet. Of the actual studies that addressed GFCF specifically, we have a total of 31 children who completed trials of diets.
Your biases are showing. Arnold et al. had 36 children, Knivsberg et al., 20 children, Elder et al., 13 children and the Rochester study, 14 children. Nutritional deficiency studies are also necessary to justify dietary interventions, as ironically, autistic children whether via food selectivities, aversions or restrictive diets, can exhibit deficiencies that are detrimental for neurological development.
Prometheus did an outstanding job of discussing why the ‘opioid peptide excess hypothesis’ (widely used as a justification for GFCF diets by DAN!s) are not supported by the literature. This is very germane to the discussion. You may not like what he has said, but you also haven’t provided any rebuttal to his analyses; he also provides numerous links to other studies regarding GFCF diets and opioid peptides.
If this is your idea of ‘rigorous studies’, I’m starting to understand why we have such different ideas concerning the strength of our vaccine analysis. Considering the author acknowledged lack of attention towards children with gastro intestinal problems, the idea that our existing research suite appropriately begins to address the question of subgroups of children is one that you have failed to defend.
Strawman. I didn’t say that these were the ‘most’ rigorous studies, I said that the ‘more’ rigorous studies don’t support the use of GFCF diets. Given how articulate I know you to be, I would guess that it was intentional (and disingenuous). Again, restrictive diets can benefit some children and large-scale studies examining sub-populations of children are needed. Why isn’t ARI, GenRes or SafeMinds stepping up to bat?
Of potential salience in understanding if subgroups of children should be evaluated, this abstract from the last IMFAR, which tells us children with autism and GI disturbances are qualitatively different than children without autism and GI disturbances.
Intestinal Inflammation, Impaired Carbohydrate Metabolism and Transport, and Microbial Dysbiosis in Autism
Microarray and pathway analysis revealed significant changes in genes involved in carbohydrate metabolism and transport and inflammation in ileal biopsies from AUT-GI as compared to Control-GI subjects. Real-time PCR confirmed significant decreases in the AUT-GI group in the primary brush border disaccharidases, sucrase isomaltase (p=0.0013), maltase glucoamylase (p=0.0027), and lactase (p=0.0316) as well as in two enterocyte hexose transporters, sodium glucose co-transporter 1 (p=0.0082) and glucose transporter 2 (p=0.0101). In contrast, increases were confirmed for inflammation-related genes in AUT-GI subjects: complement component 1, q subcomponent, A chain (p=0.0022), resistin (p=0.0316), CD163 (p=0.0150), tumor necrosis factor-like weak inducer of apoptosis (p=0.015), and interleukin 17F (p=0.0220). No significant group differences were observed for the enterocyte-specific marker, villin. In conjunction with changes in intestinal gene expression, bacterial content differed between the AUT-GI and Control-GI groups: pyrosequencing and real-time PCR revealed lower levels of Bacteroidetes (ileum: 50% reduction, p=0.0027; cecum: 25% reduction, p=0.0220, and higher Firmicute/Bacteroidete ratios in AUT-GI children (ileum: p=0.0006; cecum: p=0.0220). High levels of Sutterella species were found in 47% of AUT-GI biopsies (7/15), whereas Sutterella was not detected in any Control-GI biopsies (0/7; ileum: p = 0.0220; cecum: p = 0.0368).
We describe a distinctive syndrome in autistic children wherein gastrointestinal dysfunction is associated with altered gene expression reflecting intestinal inflammation, impaired carbohydrate metabolism and transport, and dysbiosis. These findings may provide insights into pathogenesis and enable new strategies for therapeutic intervention.
Note that I’m not advocating that every child with autism has GI problems like this, but this is evidence that when children with autism have GI disorders of such severity that a biopsy is warranted, the condition is distinctly different than what is observed in children without that diagnosis. While not specific to GFCF, this is evidence of what some of us have been claiming all along; our child’s condition is not just an upset stomach, and indeed, is associated with their autism.
Of course the full study would be required but how do you know that this observation isn’t due to neurobaviours associated with food aversions and selectivity or restrictive diets?
”GFCF diets are not ‘harmless’ either and seem to be a ‘one size fits all’ approach by DAN!s. Another ‘throw it at the wall and see what sticks’ approach. GFCF diets do benefit those with actual allergies or intolerances but it is treated as a panacea, that is where the argument lay.”
Can you validate your assertion that GFCF is ‘treated as a panacea’ by DAN doctors, or anyone? Regarding a harmless or non harmless, presumably you are referring to a study that found reduced bone density in children on CF diets compared to children not on that diet; a situation I would assert could (and should) be handled with relative ease via calcium supplementation.
Please don’t act coy: http://autism.about.com/od/alternativetreatmens/a/GFCFaltview.htm
The diet is one of the very first recommendations we make, and consider it to be a cornerstone of the DAN! Approach. The reasons are many: first, many of the children lack the [dpp4] enzyme that allows them to break down the peptides from gluten and casein. As a result, a subset of autistic individuals have these improperly digested proteins which cross the intestinal membrane, travel in the blood, pass through the blood-brain barrier and interfere with neurotransmission. When this happens, Dr. Karl Reichelt, M.D., Ph.D., and other researchers have shown that these opioid-like substances can be responsible for poor attention, odd behavior, a deficit in socialization skills and poor speech.
Not just the study regarding bone density, but some of the other studies discussed here regarding nutritional deficiencies. Do you really think it is as simple as calcium supplementation? Useless if not in the correct amount and form and without proper vitamin D supplementation. What about other deficiencies? Are you confident that children are being adequately monitored to ensure proper nutrition?
The objection to the rampant use of GFCF is also that it is touted as a ‘cure’ for autism, rather than an intervention that may help with certain clinical symptoms. Do you really want to argue that Jenny cured Evan’s autism with GFCF and can ‘turn him autistic again with a damn cookie’? These proclamations are dangerous and cruel.
Regarding allergies or intolerances, I’m curious how you would define that clinically? I think we had a short conversation @ RI on this at one point, but it was lost in the traffic, but the crux of my argument was that we have a great number of studies that show children with autism generate immunological responses at greater frequency to the proteins found in wheat or dairy when compared to children without that diagnosis.
http://www.ncbi.nlm.nih.gov/pubmed/15870662
Remarkably underwhelming as support for increased wheat/casein allergies in autistic children.
http://www.ncbi.nlm.nih.gov/pubmed/17974154
Not available through my uni as an electronic publication so I can’t comment.
http://www.ncbi.nlm.nih.gov/pubmed/16613867
Also rather underwhelming as support for increased wheat/casein allergies in autistic children.
http://www.ncbi.nlm.nih.gov/pubmed/12378124
With the exception of higher IFN-Á/TNFα production against
dietary proteins in ASD PBMCs than in DPI or sibling PBMCs, this could indicate an immune response independent of IgE-mediated food hypersensitivities. This study doesn’t support increased dietary protein allergies in ASD children.
http://www.ncbi.nlm.nih.gov/pubmed/15741748
Found increased cytokine production in ASD children whether on elimination diet or unrestricted (slightly higher in unrestricted). Which does support something other than just IgE-mediated dietary intolerances/allergies.
To my knowledge, there has yet to be any study published that attempted this kind of test and failed to find an association in the autism population, though you may know of studies of which I am not aware. At this point, however, the definition of what constitutes a valid intolerance, measured either behaviorally, or clinically. My thoughts are that while these studies no doubt do not (edit!) prove wheat or dairy ’cause’ autism, they are evidence that some children with autism react differently to these proteins when compared with children without autism; and furthermore, I’m unconvinced that two negative studies involving thirty children is sufficient evidence to declare dietary restrictions dead.
In any case, I’d be curious on your thoughts on the studies I posted above?
No one is saying that some negative studies should declare dietary restrictions dead. It is the rampant use of them when not necessarily indicated and no empirical evidence. Now add other interventions into the mix, like chelation and that’s a recipe for disaster. Again, don’t you find it odd that those that are touting these interventions, are the ones blatantly avoiding conducting rigorous studies to demonstrate their efficacy?
http://www.clinicaltrials.gov/ct2/show/NCT01116388?term=gfcf&rank=1 — Now that looks like a pretty cool study! Curious, however, that the researchers at Massachusettes Hospital seem to be interested in studying subgroups of children, specifically those with sustained GI disturbances. I wonder what has caused them to think this is a worthwhile effort, and how you reconcile that with your opinion is that our ‘rigorous studies don’t support a sub-population benefit of GFCF diets’. Why study what is already established?
Again, strawman. Key word being ‘more’, not the ‘most’ rigorous on the spectrum of study quality.. The previous studies were good pilot studies that reasonably called for larger trials and with other sub-populations. I do hold you to a higher standard, so spare me the passive-aggressive nonsense, it doesn’t become you.
This study presents some very tricky issues, to my mind however. For good or bad, parents are trying GFCF diets. If you child meets the requirements for entry; i.e., autism and chronic GI problems, chances are very good that you’ve reached the Internet and found out about the GFCF diet already; likely having given it a shot. If it is working (or you feel it is working), and your child responded, are you going to enroll your child into a study where they may be given something that will worsen their condition? If you tried it previously and didn’t work, you are excluded. This reminds me of some problems cancer drugs are having getting participants. Difficult problem that I don’t know how to address.
I can understand that but given what has already been done and the sizeable cohort of ASD children, I don’t see why these concerns can’t be overcome.
http://www.clinicaltrials.gov/ct2/show/NCT00938054?term=gluten+casein+free&rank=4 — Another very cool study. I have personally recommended one friend of ours participate, whose child went from full blown autism diagnosis to undiagnosed. I know of one other child who went from an autism to PDD-NOS diagnosis. I do not know if they will take part. Tragically, my son is not eligible. [yet?]
Excellent and I brought it to (Twyla’s) attention mainly to start putting their money where their mouth is and enroll their ‘recovered’ children to demonstrate that their bio-med interventions may or may not have had any impact. Also, they can’t complain that no studies are being conducted, when in fact, they are.
I hope this post doesn’t turn into an HTML nightmare so please edit if it does.
@ScienceMom – Formatting modifications attempted. I do not know if this is a wordpress or a theme thing, but it becomes apparent my blog does not lend itself well to longer, threaded discussions. First one I’ve had. Sorry. – pD
August 16, 2010 at 5:52 pm
Hi ScienceMom –
I was out of Internet availability land for a while. I don’t have time for an in depth response right now, but I’m thinking that we may have somewhat similar views in some ways, something which I didn’t realize, which might contribute to some of our misunderstandings. I’ll try to write something in depth in a few days, but I do appreciate your tenacity and you raise some interesting points.
Thanks.
– pD
August 13, 2010 at 3:41 am
Science Mom, I don’t understand why you keep saying that the GFCF diet is treated as a “panacea”. A panacea is “a remedy for all diseases, evils, or difficulties — a cure-all”. Biomedical parents and practitioners say that this diet is very important, but they don’t stop with the diet. The diet is a starting point, but is not a cure-all for most.
Where is the harm in trying this diet? If it doesn’t help the person, no harm done. It does not take a huge investment of money and is not dangerous.
At this point there is no way to know in advance whether the GFCFSF diet will help a person. Yes, it is more likely to help if there are obvious GI symptoms, allergies, and/or celiac disease, but some people without any of these benefit tremendously from this diet. So, it is worth a try.
The vast majority of parents and practitioners who report success with this diet are not profiting from it. Their stories deserve attention, even if causal mechanisms are still not fully understood.
August 13, 2010 at 3:41 pm
Science Mom, I don’t understand why you keep saying that the GFCF diet is treated as a “panacea”. A panacea is “a remedy for all diseases, evils, or difficulties — a cure-all”. Biomedical parents and practitioners say that this diet is very important, but they don’t stop with the diet. The diet is a starting point, but is not a cure-all for most.
Please refer to my link above regarding GFCF as the ‘cornerstone’ of the DAN! protocol. It is used to ‘cure’ or ‘treat’ autism and that is simply not a valid application of restricted diets. It doesn’t matter that other interventions are used, GFCF is the ‘go to’ and it shouldn’t be.
Where is the harm in trying this diet? If it doesn’t help the person, no harm done. It does not take a huge investment of money and is not dangerous.
The harm? Let me count the ways. It is expensive and very time-consuming, if you’re doing it right. That means constant monitoring of a child’s diet in concert with a registered dietician to make sure nutritional needs are met. It isn’t just a matter of, “oh great, my child is eating, all’s good”.
Parents are often incapable of objectively assessing an intervention’s success or failure, the placebo effect, even by proxy is powerful. There is also pressure, both external and internal for something to work and the way GFCF is touted with all of its testimonials, parents put themselves through hell. Frankly, GFCF is based upon dubious findings and is lazy to promote when gluten and/or casein may not even be a source of a problem.
At this point there is no way to know in advance whether the GFCFSF diet will help a person. Yes, it is more likely to help if there are obvious GI symptoms, allergies, and/or celiac disease, but some people without any of these benefit tremendously from this diet. So, it is worth a try.
No, it isn’t more likely to help even when there are obvious GI symptoms or allergies. Careful, single elimination should be attempted first and again, monitoring diet for offending food(s) or adding other foods. GFCF isn’t some innocuous intervention, especially with ASD children that may already have food aversions and reduce the number of foods that would be acceptable to them. Restrictive diets reduce proper nutrition and it takes a lot of work to compensate for that. How do you know what cumulative or antagonising effects of other interventions have? Ever been tested? Did you see my post regarding even chelation and restrictive diets together? Why would you chance removing essential nutrients for neurodevelopment and physical development? And the fact is, is that most people who have their children on restrictive diets, do not work with registered dieticians and don’t fully understand what a balanced diet looks like.
Why would anyone without gluten or casein intolerances or allergies benefit from a GFCF diet?
The vast majority of parents and practitioners who report success with this diet are not profiting from it. Their stories deserve attention, even if causal mechanisms are still not fully understood.
DAN!s do profit by keeping parents coming back and parents feel validated when they can get other parents to do the same thing they are doing. If you want your ‘stories’ to garner attention, then put them to use by pressuring the ARI to perform double-blinded studies. Do you not see the hypocrisy of demanding studies from everyone else but not your own?
August 2, 2010 at 1:52 am
Hi Science Mom –
Thanks for coming by my blog. When I have created something you find of interest, I know I must be doing something halfway right.
To apply this to the real world, there has to be undiagnosed perinatal hypothyroidism correct?
That was a pretty strange link you sent me.
In any case, I think my short answer to this question is, not really. I tried to touch on the complexities in this type of interaction a little in my post, and my analysis goes deeper towards a the problems with our existing dataset, as opposed to what we do know. This will be good practice though, so here goes.
There are a couple of ways I believe that our chemical environment could be affected thyroid metabolism, and ultimately, autism rates in ways that would not be visible to the studies you describe. [I’d also like to state that thyroid metabolism need not be the only mechanism by which synthetics might be contributing to autism, however, we’ll stick to that for this discussion.]
First and foremost, if I understand correctly (you may understand better, and if so, please correct me), the hypothyroid in these studies is being checked almost immediately after birth. For example, Illinois attempts to evaluate for hypothyroidism within twenty four hours of birth.
http://www.idph.state.il.us/HealthWellness/fs/congenitalhypo.htm
Specimen collection prior to 24 hours of age, prematurity and illness can affect this screening. Infants with a presumptive positive screening test (seriously elevated TSH and/or low T4) require prompt follow-up and, when notified of these results, the clinician should immediately check on the clinical status of the baby and refer the infant to a pediatric endocrinologist
Furthermore, the driving force behind much of congenital hypothyroidism is an abnormally developed thyroid gland. In the case of an abnormal thyroid gland proper, we should expect to see differential thyroid levels at birth. My concerns are that our infants are being exposed to chemicals that achieve this physical effect through molecular mimicry, and exposure to those chemicals can easily occur subsequent to hospital based testing. If an infant comes into contact with agents that interfere with TSH or TSR after the screening process you describe, our diagnostic procedures would be unable to detect this effect. If, for example, ptythlates or other agents were introduced to the infant upon return the home, why should we expect a screening test given at the hospital to be able to detect this?
We have some preliminary evidence, in fact, that being an infant in homes with specific chemicals, and proxy measurements for increased breakdown of those chemicals is a risk factor for autism.
Associations between indoor environmental factors and parental-reported autistic spectrum disorders in children 6-8 years of age reported on an accidental finding of a relationship between specific flooring types (polyvinyl chloride) in the household, specifically the parents bedroom, and subsequent diagnosis of ASD.
This is a preliminary study, of course, and is liberally sprinkled with maybes, could bes, and requests for furhter investigation.
Secondary, I believe the existing tests look for reduced thyroid metabolites, but the fact that these findings are present at ‘normal’ levels does not necessarily indicate that metabolism is not being interferred with; as I understood it, this is the crux of endocrine disruption; the ability for sufficiently similarly structured molecules to interferre with normal physiological processes. By way of example, testing for estrogen levels won’t tell us very much about environmental exposure to estriadol.
Thirdly, the tests you describe make no allowances for either in utero disturbances, or maternal thyroid problems, already observed to be a risk factor for autism. For example, the Neuroendocrine pathways altered in autism. Special role of reelin went into some detail as towards the participation of reelin in nueronal migration. Given the make or break nature of this process, I do not think it is unreasonable to posit that even transitory disturbances of thyroid metabolism and subsequent reelin expression changes could contribute to ASD.
Lastly, and more nebulously, I’m entirely unconvinced that our only area of interest should be outlier regions i.e., classically defined hypothyroidism. The biggest problem to my mind is that our experience is that the ability to discern impact is largely a result of the granularity of our analysis; as we design more comprehensive tests, we find effects previously hidden from our view. For example, Blood lead level and kidney function in US adolescents: The Third National Health and Nutrition Examination Survey found that blood levels far less than the ‘official’ acceptable level were affecting kidney function in children. The blog posting I had, regarding an increase in special need services for children born between 37 and 39 weeks is another example. For that matter, any of our studies regarding BPA would fit this category. My concept of the precautionary principle, formed on my journey through autism, has me believing that it is a dangerous assumption to think that we can tinker around with thyroid metabolism just a little bit, but not to the level of classical hypothyroidism, and everything will work its way out.
When politically expeidient, the difficult to discern gradient between classical autism, aspergers, pdd, and a quirky uncle are used as proof that there is no increase in ASDs. Small changes are still changes. and the exposure to chemicals capable of masquerading into the thyroid dance are far from the only change our fetuses and infants are exposed to.
I have some thoughts regarding your thoughts on dietary interventions, but don’t have time to address them now. Maybe later in the week, depending on the breaks. In the meantime, I would be interested in your thoughts on hypothyroidism, reelin expression, and scary chemicals, if you have any.
– pD
August 2, 2010 at 1:57 am
Hello friends –
I also thought I’d share some other studies I ran into while trying to compose a response to Science Mom.
Subclinical hyperthyroidism and hyperkinetic behavior in children
and
Reduced thyroid-stimulating hormone response to thyrotropin-releasing hormone in autistic boys.
Both are pretty old, but do show some evidence of distrubed thyroid metabolism in older children with autism, though without any evidence one way or the other of the cause.
– pD
August 2, 2010 at 6:42 am
Isn’t the most common cause of hypothyroidism inflammation of the thyroid gland and/or an auto-immune reaction? This would be consistent with both being a susceptibility factor for autism (as people with autism tend to have more auto-immune issues among their family members than average) and with being a condition caused by the immune system dysregulation which seems to be a significant factor in autism.
August 11, 2010 at 4:52 pm
Yet another fascinating topic — actually, I have a thyroid goiter and my thyroid levels were a little off during my pregnancy. However, my doctors decided it was not enough to be significant or treated. Nor did they make any effort to figure out why or suggest that I should worry about it. I wish I knew more details, but I now can’t help but wonder if I in fact had/have subclinical hyperthyroidism. And by the way, I have urticaria, which at least some people believe is autoimmune in origin. Something else the conventional doctors just didn’t know what to do about. They just blamed it on stress.
August 11, 2010 at 10:29 pm
Hi Nyx –
Our very informal polling within our group of autism parents reveals a startling high presence of altered thyroid levels. Your findings and thoughts are not surprising to me.
– pD
August 2, 2010 at 4:42 pm
That was a pretty strange link you sent me.
It was and not the one I intended, http://genes-r-us.uthscsa.edu/nbsdisorders.pdf is the correct link just to demonstrate that thyroid function is part of the neonatal screen in all 50 states.
Furthermore, the driving force behind much of congenital hypothyroidism is an abnormally developed thyroid gland. In the case of an abnormal thyroid gland proper, we should expect to see differential thyroid levels at birth. My concerns are that our infants are being exposed to chemicals that achieve this physical effect through molecular mimicry, and exposure to those chemicals can easily occur subsequent to hospital based testing. If an infant comes into contact with agents that interfere with TSH or TSR after the screening process you describe, our diagnostic procedures would be unable to detect this effect. If, for example, ptythlates or other agents were introduced to the infant upon return the home, why should we expect a screening test given at the hospital to be able to detect this?
That is a valid point, particularly considering how much more sensitive infants and toddlers are due to size and mouthing behaviour.
Given the make or break nature of this process, I do not think it is unreasonable to posit that even transitory disturbances of thyroid metabolism and subsequent reelin expression changes could contribute to ASD.
I think it would depend upon what and when you define ‘transitory’. In other words, a substantial transitory disruption of thyroid function of a gestational mother could produce similar effects of chronic subclinical hypothyroidism in infants.
Lastly, and more nebulously, I’m entirely unconvinced that our only area of interest should be outlier regions i.e., classically defined hypothyroidism.
This is where you may be onto something given that infant subclinical hypothyroidism can contribute to cognitive function.
When politically expeidient, the difficult to discern gradient between classical autism, aspergers, pdd, and a quirky uncle are used as proof that there is no increase in ASDs. Small changes are still changes. and the exposure to chemicals capable of masquerading into the thyroid dance are far from the only change our fetuses and infants are exposed to.
I don’t disagree that we should be more cognisant and pro-active regarding the potential exposures that we all have.
August 4, 2010 at 1:20 pm
I have the impression that peanut oil may also be used for other purposes, such as emulsion. But I don’t have hard proof.
http://barbfeick.com/vaccinations/allergy/610-patents.htmAt any rate, this is off the main point of your article. There is a recent book on peanut allergies and vaccines, which will be interesting to read. In the meantime, I’m just wondering.
Context is everything and so is checking the voracity of your own claims. You linked to a collection of patent applications. It is easily seen that there are none of those oils in vaccines distributed in the U.S. and much of the EU: http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/appendices/b/excipient-table-2.pdf
August 11, 2010 at 4:53 pm
I think you meant veracity.
August 13, 2010 at 3:24 am
Yeah, I don’t think she meant that my claims are (or aren’t) voracious.
August 13, 2010 at 11:23 am
You may find this interesting (if you have not seen it before) –
http://www.newscientist.com/article/mg20727733.000-levels-of-controversial-soap-chemical-rise.html
August 16, 2010 at 5:49 pm
Hi MJ –
That would be terrifying if I already weren’t so jaded.
Thanks though.
– pD
[…] thе original: Autism Mashup – Hypothyroidism, Reelin Expression, аnԁ Scary … Share It: Hide […]
January 8, 2011 at 2:32 am
[…] to structural changes during development, and we also know that there is increasing evidence that endocrine disruptors can interferre with thyroid metabolism, or for that matter, a wide range of findings on endocrine disruptors and cognitive function. […]
May 6, 2013 at 12:32 pm
With havin so much written content do you ever run into
any issues of plagorism or copyright violation? My blog has a lot of exclusive content I’ve either authored myself or outsourced but it seems a lot of it is popping it up all over the web without my agreement. Do you know any solutions to help stop content from being stolen? I’d really appreciate it.
passionless Droning about autism 
July 29, 2010 at 3:36 pm
I’ve also read that fluoridated water impacts the thyroid?
re: “the focus on vaccines has contributed to the mindset that a static rate of autism (or nowadays, maybe a tiny increase), must be protected at all costs” Yes, it is bizarre how vaccine protectionism results in convoluted arguments. This seems to me to also impact the area of dietary intervention — else why so much arguing against simple harmless dietary intervention which is worth a try and often has great results? And studies that seem oddly skewed towards denial of what so many parents and people with autism witness (see Judy Converse’s 7/22 letter at http://pediatrics.aappublications.org/cgi/eletters/peds.2009-2391v1 ) It makes me wonder, why? Is positive response to dietary intervention evidence of vaccine causation? If not, why all the denial? Just narrow-mindedness, or something else being protected, or do certain high-up people know that the immune system responds abnormally to foods such as wheat and milk because vaccines contain substance such as casein hydrolosate (used as substrate to grow microbes for vaccines such as DPT) and wheat germ oil (which rumor has it is used in some vaccines, but I’m not sure of this). Not to mention peanut oil.
Sorry for going off on a tangent.
Thanks for all the very interesting info you provide.
July 31, 2010 at 4:22 pm
Hi Twyla –
I don’t know much about flouridated water and thyroid problems. (?)
The reasoning behind such a vigorous contempt over dietary interventions confuses me as well. I doubt the source of this is based in an attempt to obfuscate vaccine injury; that gives us (or someone) credit for a lot more knowledge than I think we have. My thoughts are that, where present, reactions to gluten or casein (or whatever), are not causal, but rather the inverse, something about having autism, (the chronic stress and resultant GI disturbances (?)) makes some children more likely to develop sensitivities to these proteins.
– pD
August 1, 2010 at 6:25 am
It seems to me that the reactions to foods may have to do with immune system dysregulation/inflammation/ sensitivity (which certainly could be related to vaccines), and also to enzyme deficiency (I have read that mercury can inhibit enzymes) and probiotic deficiency (partly caused by antibiotics). I see these sensitivities as part of much autism, but not necessarily the initial cause. Yet some kids are much less autistic without certain foods (especially gluten, casein, soy) than they are with those foodsh. So the foods may not be the original cause; maybe something else occurred to cause certain changes in the immune & digestive systems; but once these systems become sensitized, the foods can cause or exacerbate autistic behaviors, cognitive issues, etc.