GFCF Double Blind Study

9 Aug

Washington, Aug 8 : In one of the first double-blind, clinical studies, scientists at The University of Texas Health Science Center at Houston will be seeking to determine if gluten and dairy products have a role to play in autistic behaviour, as has long been claimed by parents.


This should be interesting.

Personally, I don’t have much of an issue with the GFCF diet, aside from the lack of evidence supporting it. Regulating someone’s diet is nowhere near as dangerous as chelation or Lupron injections or industrial cleaner being marketed as chelators. But maybe a nutritionist will correct me on that.

I am a little bit worried about a statement attributed to one of the study authors:

A lot of children with autism have gastrointestinal problems such as constipation and diarrhea.

Do they? Is there any actual evidence beyond the anecdotal that backs that statement up? I can’t recall seeing any myself. Not that I’m omniscient on the subject you understand.

We tried our autistic child on the diet shortly after xyr diagnosis and it did absolutely nothing. But then I think we misunderstood it. Xe didn’t have any diet or gastro issues to begin with. We were still in that rather naive ‘must cure at all costs’ phase and there was only a small handful of websites dedicated to autism or autism treatments. Indeed, one of the things that amazes me is how autism has become something of an industry over the five years or so.

Anyway, I’ll be interested to see how this one pans out. How ’bout you?

14 Responses to “GFCF Double Blind Study”

  1. _Arthur August 9, 2008 at 23:21 #

    What would be truly fascinating, would be a discovery that bad gluten (or other foods) digestion is “co-morbid” with autism; that the pathways of some proteins involved in digestion are common with brain developpement.

    On a completely different tack, I have sometimes been flabbergasted by biomed parents who have their kid on 100+ pills of food supplements (selenium, secretin, vitamins, etc…), and then attribute his or her finicky digestion on either autism or gluten. From my standpoint, any of those pills could be the cause of constipation or diarrhea, and they wouldn’t have a clue.

  2. CS August 9, 2008 at 23:27 #

    The MET gene study was very interesting but I don’t see much talk about it. There are a few adult autistics on Youtube doing a GFCF diet and reporting their progress on it.

  3. Alli August 10, 2008 at 01:31 #

    we have had no gut problems at all and as our little one has such a limited diet, bread making up 90% of it I don’t think a gluten free bread would have gone down well. He doesn’t or does eat things based on mouth feel as sensory overload is one of our biggest challenges.

    I think that not enough is told to parents about co-morbid conditions and how they can be present ALONG with autism not actually part of autism.

  4. _Arthur August 10, 2008 at 02:25 #

    From the article: “Researchers will study intestinal permeability (leaky gut) through urine collection and behavior through psychometric testing.”

    Yeah, leaky gut. You cannot ever dispell or disprove such “theories”.

  5. María Luján August 10, 2008 at 06:08 #

    Hi Kev
    To avoid the self- repetition, this is an analysis from Elder et al, some time ago we- Jonathan Semetko and I- discussed that I think apply here.

    KEv , I disagree strongly on the diet part. Of course I am not a nutricionist but I consider myself an informed mom, someone that has discussed a lot of aspects with doctors in practice and researchers-nutricionists, peditricians, gastroenterologists, etc-especially on the topic of the GFCFSF diet and how to do it to avoid nutritional defficiencies or problems.IT all depends on why the diet is done, with what tests, what controls and what supplementation- based properly on clinical studies of the child and under what kind of medical supervision. My son- without apparent GI issues more than sporadic gastroenteritis- tested positive for IgA severe defficiency- an atypical presentation- and celiac disease and casein allergy and abnormal gut flora and I can go on and on …and he was 97 % in height and weight for his age and otherwise “absolutely normal” for the peditrician- “wait wait wait” at 2.6 years- except that he was not talking and other problems-with food to begin with considered only behavioral and “normal”. Therefore he had a lot of undetected medical conditions, “asymptomatic”, that to be detected they should have been properly tested BEFORE with the knowledge about what to search and why.
    What I do not understand is why with the knowledge in the impact of gluten allergy/intolerance in the malabsorption of vitamins, minerals- including Ca/Mg/Zn and for example folic acid and related compounds, these trials are not designed with selected clinical data before and during the diet. Even more I can not understand why other tests to avoid the impact of confounders in the potential benefit or not of the diet are not included in these studies (GI issues , abnormal flora, GERD, malabsorption?, Ca/Mg/Zn, kidney and liver function? other essential and non-essential elements before/during the diet). If a child is having some kind of malabsorption, a GFCFSF diet without Ca supplementation or folic acid supplementation or even the proper detection of iron defficiency or abnormal status may be problematic- such as our doctor talked with us considering the diet.
    Without these clinical studies, the group of children under the diet may be so strongly heterogenous, IMHO, in nature than the results may be not of more value than if the diet ALONE has some benefit- something that it is known that even from the anecdotic only happens very few times.

    It is not simple.

  6. Kev August 10, 2008 at 07:16 #


    So you’re saying even something as simple _sounding_ as an altered diet needs to be implemented very carefully?

    And congrats on this comment going straight through 😉

  7. lurker August 10, 2008 at 07:30 #

    Snotty arguments againt GFCF and acknowledgement of digestive problems shouldn’t be respected when mainstream researchers won’t even look into it. All of that talk about digestive problems among parents wouldn’t have become so prevalent if the observations came from only a few parents who were misinterpreting unconnected digestive problems.

    It’s ridiculous that those who complain about anecdotal evidence, accept anecdotal refutations of what they’re trying to ignore. There should be a lot of attention into this because of the possible intense pain that could be caused by such digestive problems. But the “evidence” proponents just moan about and demand proper evidence which seems to me to be just them saying that they will not acknowledge it unless it is approved by the research establishment.

  8. María Luján August 10, 2008 at 07:54 #

    Hi Kev
    Yes, I do think that dietary changes should be implemented very carefully.It happened to us. My son had several problems besides the celiac condition. Only with the proper treatment of them he demonstrated progress and improvement in many aspects. But also, the diet- with proper support- was the beginning that allowed us to find other problems.

    I disagree with the idea of the GFCF diet as useless or the idea of the GFCF as a requirement without the proper procedure to know why, how and with what proper analysis of confounders or concomitant problems. My main issue has been on the topic what simple the analysis of many doctors has been in terms for example of the clinical results-in my experience.

    Yes, finally one comment that don´t get trapped! 🙂

  9. Kev August 10, 2008 at 08:45 #

    _”Snotty arguments againt GFCF and acknowledgement of digestive problems shouldn’t be respected when mainstream researchers won’t even look into it.”_

    But they _are_ looking into it. That’s what this post is about.

    _”All of that talk about digestive problems among parents wouldn’t have become so prevalent if the observations came from only a few parents who were misinterpreting unconnected digestive problems.”_

    I disagree. You’re assuming that the parents who _do_ talk about it are in the majority. Do you have evidence to back up that opinion?

    _”It’s ridiculous that those who complain about anecdotal evidence, accept anecdotal refutations of what they’re trying to ignore.”_

    Such as?

    _”There should be a lot of attention into this because of the possible intense pain that could be caused by such digestive problems. But the “evidence” proponents just moan about and demand proper evidence which seems to me to be just them saying that they will not acknowledge it unless it is approved by the research establishment.”_

    We have to be able to say if:

    a) It just so happens that a few (relative to the entire population of) autistic people have gastric issues that need treating

    b) A significant percentage of autistic people have gastric issues as a comorbidity of their autism

    c) A significant percentage of autistic people have gastric issues that are directly related to the fact they are autistic.

    Without that, proceeding medically must be difficult.

    That is _not_ to say that in any of these scenarios the gastric discomfort should be ignored, just that we need to define its role in relation to autism.

  10. farmwifetwo August 10, 2008 at 12:07 #

    Going to wade in on this one some of the best Univ’s around so you can trust the article.

    Eldest had nightmares, terrors, diahhrea and rashes that made you cry… daily. The Dev Ped said “Some children with autism are like that”. I read Karen Serrousi’s book and said.. lets try dairy. Within 48hrs it was ALL gone. A week later my Dh put a tiny bit of butter on a freezer pancake and my 2.75yr old son went INSANE after about an hour. He screamed, head slammed, it was horrible. We put him in the playpen, I held his little bro (6mths old) and simply cried. By noon he’d calmed enough to eat, had a nap and had another terror. Then went calm.. too calm. Went out the front with his Dad to bbq, looked at me through the kitchen door and SLAMMED his head off the front porch (concrete) hard enough to leave a bruise and a bump. Took 24hrs for it to clear his system and he’s never had dairy again and he’s nearly 9.

    The butter got tossed.

    We didn’t do it for a cure, we did it to get rid of the other symptoms. Gluten did ziltch, we weaned it (you don’t stop gluten cold) and tried it for a year.

    Dairy removal did nothing for the little one, we started it the same day eldest had the above reaction. Eldest now has NVLD (started at mild PDD), youngest has severe, non-verbal PDD.

    It is NOT a cure. But knowing now, watching the other… he was stoned on it. He’d fall and his hands never came out to break the fall… little boys’ do and he’s on the other end of the spectrum.

    But our family has a history of IBS, my bro can’t have dairy…. I think it totally depends on the child and whether or not they already have symptoms – like never ending diahhrea.

    It is the ONLY bio-med treatment we have tried and we will not try others.


  11. Sullivan August 10, 2008 at 16:48 #

    But they are looking into it. That’s what this post is about.

    It isn’t like this is the first study either.

    For example, U Rochester has been conducting a study for years.

  12. María Luján August 10, 2008 at 18:58 #

    But they are looking into it. That’s what this post is about.
    How?Considering what confounders and other CMPs that may mask the potential benefits or not of a GFCF diet.?
    This kind of studies are the same line of Elder therefore they are incomplete and potentially misleading in their results.

    I am not who you are responding to but there are a lot of subgroups with GI issues detected. I am included some comments on different published manuscripts. Especially those marked with *
    One of the most recent published manuscripts form the Dr Horvath group (2002) reported for 36 children with ASD symptoms like chronic diarrhea, abdominal discomfort and distension. The histological examination revealed grade I or II reflux esophagitis in 69.4 % (25/36), chronic gastritis in near 40 %(15/36) and chronic duodenitis in near 66.6 % (24/36). Twenty two of the 25 children with reflux (88%) had night awakenings, signs of abdominal disconfort and pushing on the abdomen. None of the patients had H. Pylori.
    Low intestinal carbohydrate digestive enzyme activity was reported in 21 children of 36 (58.3 %), even when no abnormality was found in pancreatic function. 27 of 36 children had an increased pancreatico billiar fluid output after intravenous secretin administration. 21 of 36 children had diarrhea (near 60 %). Low lactase was found in 14 patients. One kind of cells, the Paneth cells, showed similar results to studies done to Chron´s patients.

    *Sucrase degrades sucrose, Lactase to lactose, Isomaltase to dextrins and maltase to maltose-All of the enzymes (finished in ase) are disaccharidases or oligosaccharidases that is they degradate bigger sugars to more little ones.
    *Lactase deficiency is by far the most common. Produces “lactose intolerance”
    These are medical conditions related to deficiencies of enzymes – in amount and/or activity or how it functions- related to carbohydrates.

    Kushak R and Buie T reported lactase deficiency in 58-65 %, isomaltase/palatinase deficiency in 30 to 40 % in ASD. Children with intestinal inflamation are 77 % deficient in lactase and 64 % in isomaltase.

    From the Journal of Pediatric Gastroenterology and Nutrition
    Gastrointestinal Symptoms And Intestinal Disaccharidase Activities In Children With Autism
    Kushak, Rafail I; Winter, Harland S; Farber, Nathan S; Buie, Timothy M
    Journal of Pediatric Gastroenterology & Nutrition. 41(4):508, October 2005

    Disaccharidase activities in 308 autistic (AI) and 206 non-autistic individuals (NAI) with different GIP (gastrointestinal problems).

    *Disaccharidase is the enzyme that degradates disaccharides to monosaccharides. Otherwise, sugars as disaccharides are not adsorbed, but they can produce negative effects on intestinal mucosa.

    The frequency of GIP among AI and NAI was: diarrhea, 38 vs 18 %; abdominal pain, 36 vs 59 %; food sensitivity, 14 vs 11%; constipation, 4 vs. 0.5%; GER (reflux), 3 vs. 11%; FTT (failure to thrive), 2 vs. 6%; diarrhea with abdominal pain, 6 vs 5%; diarrhea with food sensitivity, 6 vs 3%; and abdominal pain with food sensitivity, 4 vs 3%. AI with diarrhea (n = 206) demonstrated significantly lower maltase (P < 0.05) activity than NAI with diarrhea. Frequency of lactase deficiency in AI with FTT (n = 5) was significantly higher (80% vs 25%; P < 0.05) than in NAI with FTT and frequency of palatinase deficiency in AI with diarrhea was significantly higher than in NAI (28% vs 11%; P < 0.05) with the same GIP. AI and NAI with other GIP had similar frequency of disaccharidase deficiencies.

    Gastroesophageal Reflux In Children With Autism: How Do Children Present And Can One Test These Children? Buie, Timothy M
    Journal of Pediatric Gastroenterology & Nutrition. 41(4):505, October 2005
    Same author studied the possibility of GER (Gastroesophageal reflux) with GI complaints and aggression or self-injurious behavior GER was identified in 5 of 5 patients tested by wireless pH testing. Esophagitis was seen in 3 of 6 patients biopsied.
    *pH testing data are reported in a scale called de Meester score. Normal is less than 14.72. Autistic Children showed from 19.7 to 75.1.
    *Author concludes that aggressive or self injury behavior may be a manifestation of pain from GERD

    Distinct Changes In Colonic Epithelial Glycosylation In Children With Autism Compared To Classical IBD And Developmentally Normal Controls, June 2004
    Rosseneu, S. L. M.1; Murch, S.1; Heuschkel, R.1; Philips, A.1
    Journal of Pediatric Gastroenterology & Nutrition. 39 Supplement 1:S333, June 2004.
    Data show quite distinct patterns of O-glycosylation within the glycocalix in children with autism, not simply due to inflammation.This may contribute to alterations in the colonic mucosal flora. As clinical improvement has been reported in autistic children when enteric dysbiosis is treated, these changes warrant further study if confirmed in larger series.

    *The glycocalix is the polysaccharide-containing material (that is a covering of polymers of monosugars) lying outside the cells of the gut.
    *Glycosylation is a process by which the glycocalix is modified by other sugars ( involving other enzymes for example). Abnormalities associated with disease states are major contributors to diversity in glycan expression
    *It seems that not only inflammation, but altered glycosilation pathways of glycocalix can be found in gut in ASD.

    Intestinal Permeability Test In Children With Autism
    Boukthir, S.2; Rocchiccioli, F.1; Dlala, S. Ben2; Mrad, S. Mazigh2; Zenaidi, M.2; Belhadj, A.3; Helayem, M.3; Abdennebi, M.4; Barsaoui, S.2
    Journal of Pediatric Gastroenterology & Nutrition. 39 Supplement 1:S242-S243, June 2004
    The intestinal permeability test (IPT) is regarded as a valuable and non-invasive test for monitoring small intestinal mucosal damage in children. An abnormal IP was seen in 26.6% of our autistic children.

    Although constipation occurs in 2% to 5% of healthy children, its clinical diagnosis is often difficult in children with behavioral disorders. Despite this, moderate or severe constipation was more frequent in the autistic group than in the control subjects (36% vs 10%). 54.4% of autistic children had moderate/severe loading or acquired megarectum compared with 24.1% of control subjects. Milk was the strongest predictor of constipation in the autistic group, whereas stool frequency, gluten consumption, soiling, and abdominal pain were not predictive of constipation (Dr Heuschkel / Dr Afzal publication).

    Autism and gastrointestinal symptoms

    Autistic disorder and gastrointestinal disease

    Gastrointestinal abnormalities in children with autistic disorder

    Constipation With Acquired Megarectum in Children With Autism

    Kind of food allergies related to milk/gluten/others

    *Therefore there are 7 medical conditions that can be related to milk/gluten/food allergies, not only Celiac disease, mediated by IgE or not. Food allergy is not the same as food intolerance

    From J Child Neurol. 2008 Jan;23(1):6-13. .
    Autism spectrum disorders: concurrent clinical disorders.Xue Ming , Brimacombe M, Chaaban J, Zimmerman-Bier B, Wagner GC.
    .. This study characterized the clinical co-occurrences and potential subgroups in 160 children with autism spectrum disorders who presented to The Autism Center between 1999 and 2003. Medical and psychiatric co-occurrences included sleep disorders, epilepsy, food intolerance, gastrointestinal dysfunction, mood disorder, and aggressive and self-injurious behaviors. Sleep disorders were associated with gastrointestinal dysfunction (P < .05) and mood disorders (P < .01). Food intolerance was associated with gastrointestinal dysfunction (P = .001). Subjects with mood disorder tended to develop aggressive or self-injurious behaviors (P < .05). Developmental regression was not associated with increased co-occurrence of medical or psychiatric disorders. Medical co-occurrence did not present as a risk factor for psychiatric co-occurrence, and vice versa. These results showed a high prevalence of multiple medical and psychiatric co-occurrences. There may be common pathophysiologic mechanisms resulting in clinical subgroups of autism spectrum disorders. Recognition of the co-occurrence of concurrent disorders may provide insight into the therapeutic strategy.

    Biol Psychiatry. 2007 Feb 15;61(4):492-7.
    Relationship of dietary intake to gastrointestinal symptoms in children with autistic spectrum disorders.
    Levy SE, Souders MC, Ittenbach RF, Giarelli E, Mulberg AE, Pinto-Martin JA.

    Gastrointestinal (GI) symptoms and abnormalities in stool consistency are frequently reported by parents of children with autism spectrum disorders (ASD). The purpose of this study was to 1) describe dietary intake of a cohort of children with ASD compared with normative data and 2) determine whether GI symptoms and stool consistency are related to dietary intake. METHODS: Data from diet diaries of children (3-8 years) with ASD (n = 62) were analyzed by a registered pediatric dietician to compare to RDA standards for total calories, protein, carbohydrate, and fat. Dietary intake was correlated with descriptors of stool consistency using cumulative logistic regression methods. RESULTS: Intake of calories, carbohydrates, and fat were in the average range; protein intake was increased (211% of RDA). Reported frequency of GI abnormalities, including abnormal stool consistency (e.g., bulky or loose), was increased (54%). No statistically significant relationships between stool consistency and dietary intake were observed. CONCLUSIONS: In this sample, there was a high rate of reported gastrointestinal symptoms, despite lack of medical causes.
    And a very recent one
    Novel therapeutic targets for autism.
    OK, how your questions are going to be answered? With the kind of approach “Let´s go to see the benefits of GFCF diet using such behavioral parameters or symptoms under the DSMIV or other to test impact?” It does not seem accurate or even useful- considering the partial reported literature that is availalbe on the topic of GI issues in ASD.Again, to answer your questions (that I think are relevant and we are all concerned about) these studies should be better designed to include the published information on clinical correlates on GI abnormalities in ASD subgroups- and they are not doing so.
    Sorry by the length of the post.

  13. Kev August 10, 2008 at 19:05 #

    Ma, I’m curious, do you see this study as potentially as dangerous as some of _us_ see the currently postponed chelation study?

    _”How?Considering what confounders and other CMPs that may mask the potential benefits or not of a GFCF diet.?”_

    I guess that’s the million dollar question. In your experience do you think its even possible?

  14. María Luján August 10, 2008 at 20:24 #

    Hi Kev
    Thank you for the freedom of the trapped comment 🙂 and for your question.
    On chelation
    I have been always concerned about
    a- how easily has been dismissed the potential problems in transport, management, metabolism and excretion of toxic/essential elements in ASF by many and
    b- how easily the diagnosis in susceptible children, with potentially other CMPs in terms of aminoacids and proteins management and or liver /kidney other metabolic problems, has been promoted in terms of simple analysis- such as hair only or the provocation test per se.
    I have been concerned by BOTH because neither of these situations help to detect a real problem of – for example- bioaccumulation or altered metabolism of xenobiotics in general- beyond the controversial I am talking of antibiotics antiepileptics and others. My son for example has awful reactions to common antibiotics and only with a lot of care we -withn his doctors- found a group that it has not so many impact on him,
    Yes, I think that bioaccumulation is a problem. A problem that has not been properly studied or analyzed in ASD- but neither in other medical conditions. But there is a deep lack of knowledge about how the toxic elements are managed to avoid negative effects in the average population-Even when transport and management is being more and more analyzed but from other fields than ASD- such as molecular biology. There is no test to know about bioaccumulation and the provocation test has a lot of criticisms. Then I wonder why instead of going to the clinical trial- the final step for me- more interest and research is not focused in metabolism and management of toxic elements in different forms- including the management of xenobiotics in general (transporters, role of glutathione and other conjugates and so on) in ASD.
    I do think that there is a lot of anecdotic evidence that in this topic remains not properly studied. The difference between us is that you consider that the problem does not exist looking at the scientific consensus; I think that nobody can say that the problem does not exist because there is no test- consensuated and beyond criticism- to assure that bioaccumulation or sequestration in tissues is present or not in ASD and there is a profound lack of knowledge on mechanisms. Therefore I am not conviced about the chelation study but by different reasons. I would want that the study has strong background in terms of tests to confirm the bioaccumulation and /or the need of the chelation approach.
    For example, autistic children – at least an important subgroup – demonstrate to have problems with aminoacids metabolism. Proteins are build from aminoacids. Transporters are proteins; what is the impact on transporters and other proteins /enzymes of a GFCF diet-especially if there are CMPs such as lack of nutrients ? What is the impact of gluten and casein if altered protein management is present? Where are the clinical studies that explore this in ASD subgroups? Where are the clinical studies on GFCF diet in blood/urine and fecal stool of essential and toxic elements before and during the diet – in autistic children properly clinically studied and supported in terms of the treatment of CMPS- except for example aminoacids? AND on time on diet- not puntual studies?
    Please note that this is far beyond mercury, it includes medication needed for problems autistic population has. If there is no knowledge about how autistic subgroups manage and metabolize xenobiotics, the potential of very negative reactions to xenobiotics many autistics need as medication- such as antiepileptics- is very important. Therefore IMO the problem is much wide and profound that only the toxic elements per se.
    In your experience do you think its even possible?
    Yes, I would say that it is even probable.Of course my experience is individual with my son.Looking at the published literature I do think that it is a situation that happened before. You know it all depends on how the questions are done. All manuscript should answer a well defined question . And the questions are once and again done the same way
    a-Is the GFCF diet a way to improve ASD symptomatology?
    b-Is the ….. a cause of ASD?
    c.Is…..a cure for ASD?
    and in this way because the questions are not formulated with the increasingly important clinical knowledge about ASD subrgroups the answers you will find will be of very limited use or practicallly useless. The questions should be formulated including this knowledge and information. Of course, this makes the formulation of the question much more difficult. But it would be the only pathway to real progress. Otherwise, the repetition of the same Why is it going to produce a different result if almost always the same aspects with the same information is presented once and again? And why if the different result exists is then going to be evident?

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