Home > Awareness, Science, Uncategorized > Tune-In: “Good Morning America” Story on Gluten-Free, Casein-Free Diet

Tune-In: “Good Morning America” Story on Gluten-Free, Casein-Free Diet

Tune-in on Thursday, May 20 during the 8:00 a.m. hour of ABC’s “Good Morning America” for an interview with Susan Hyman, M.D., University of Rochester School of Medicine. Dr. Hyman will discuss her research on the efficacy of the much discussed gluten-free,casein-free diet, a study she is releasing at the International Meeting for Autism Research taking place this week in Philadelphia. Check your local listings for more information. Learn more about IMFAR here.

  1. May 19, 2010 at 9:42 pm

    I don’t have cable and am in Canada, so I am out of luck but I’ll try to find a way to see it…
    But I do have to say, we put my son on this diet when he was 3 and saw quite a huge change in him in just a few days. It was like night in day in how he behaved, looked at us, ‘stimmed’… just a radical difference.
    I realize the diet doesn’t work for all Autistics though, which is really too bad.

    My entirely family has no switched to brown rice pasta and other gluten free foods because as far as we can tell, gluten isn’t good for anyone, Autistic or not! So why bother?

  2. María Luján
    May 19, 2010 at 10:20 pm

    I can´t understand why this kind of studies are so poorly designed at this point. Even more, the time of the study is too short, being longer the needed time to show benefits looking at the research of Shattock et al
    Nutr Neurosci. 2010 Apr;13(2):87-100.

    The ScanBrit randomised, controlled, single-blind study of a gluten- and casein-free dietary intervention for children with autism spectrum disorders.
    Whiteley P, Haracopos D, Knivsberg AM, Reichelt KL, Parlar S, Jacobsen J, Seim A, Pedersen L, Schondel M, Shattock P.

    Dept of Pharmacy, Health & Well-being, Faculty of Applied Sciences, University of Sunderland, UK.
    Abstract
    There is increasing interest in the use of gluten- and casein-free diets for children with autism spectrum disorders (ASDs). We report results from a two-stage, 24-month, randomised, controlled trial incorporating an adaptive ‘catch-up’ design and interim analysis. Stage 1 of the trial saw 72 Danish children (aged 4 years to 10 years 11 months) assigned to diet (A) or non-diet (B) groups by stratified randomisation. Autism Diagnostic Observation Schedule (ADOS) and the Gilliam Autism Rating Scale (GARS) were used to assess core autism behaviours, Vineland Adaptive Behaviour Scales (VABS) to ascertain developmental level, and Attention-Deficit Hyperactivity Disorder – IV scale (ADHD-IV) to determine inattention and hyperactivity. Participants were tested at baseline, 8, and 12 months. Based on per protocol repeated measures analysis, data for 26 diet children and 29 controls were available at 12 months. At this point, there was a significant improvement to mean diet group scores (time*treatment interaction) on sub-domains of ADOS, GARS and ADHD-IV measures. Surpassing of predefined statistical thresholds as evidence of improvement in group A at 12 months sanctioned the re-assignment of group B participants to active dietary treatment. Stage 2 data for 18 group A and 17 group B participants were available at 24 months. Multiple scenario analysis based on inter- and intra-group comparisons showed some evidence of sustained clinical group improvements although possibly indicative of a plateau effect for intervention. Our results suggest that dietary intervention may positively affect developmental outcome for some children diagnosed with ASD. In the absence of a placebo condition to the current investigation, we are, however, unable to disqualify potential effects derived from intervention outside of dietary changes. Further studies are required to ascertain potential best- and non-responders to intervention.

    Ann Clin Psychiatry. 2009 Oct-Dec;21(4):205-11.

    The possibility and probability of a gut-to-brain connection in autism.
    Reichelt KL, Knivsberg AM.

    Department of Pediatric Research, Rikshospitalet Medical Centre, University of Oslo, Oslo, Norway.

    Abstract
    BACKGROUND: We have shown that urine peptide increase is found in autism, and that some of these peptides have a dietary origin. To be explanatory for the disease process, a dietary effect on the brain must be shown to be possible and probable. METHODS: Diagnosis was based on DSM-III and DSM-IV criteria. We ran first morning urine samples equivalent to 250 nm creatinine on high-performance liquid chromatography (HPLC) reversed phase C18 columns using trifluoroacetic acid acetonitrile gradients. The elution patterns were registered using 215 nm absorption for largely peptide bonds, 280 nm for aromatic groups, and 325 nm for indolyl components. We referred to a series of published ability tests, including Raven’s Progressive Matrices and the Illinois Test of Psycholinguistic Ability, which were administered before and after dietary intervention. The literature was also reviewed to find evidence of a gut-to-brain connection. RESULTS: In autistic syndromes, we can show marked increases in UV 215-absorbing material eluting after hippuric acid that are mostly peptides. We also show highly significant decreases after introducing a gluten- and casein-free diet with a duration of more than 1 year. We refer to previously published studies showing improvement in children on this diet who were followed for 4 years and a pairwise matched, randomly assigned study with highly significant changes. The literature shows abundant data pointing to the importance of a gut-to-brain connection. CONCLUSIONS: An effect of diet on excreted compounds and behavior has been found. A gut-to-brain axis is both possible and probable.
    there are reports about gluten intolerance with presentation without even abnormal biopsies- only behavioral manifestat

    Minerva Pediatr. 2010 Apr;62(2):119-123.

    [Increasing prevalence of celiac children with negative serum antigliadin antibodies.]

    Caristo E, Tognato E, Di Dio G, Rapa A, Fonio P.

    Clinica Pediatrica, Università del Piemonte Orientale, Novara, Italia –

    Abstract
    AIM: In the last few years we noted an increasing number of children with celiac disease with negative serum anti-gliadin antibodies (AGA) a useful serologic test to monitor compliance to gluten-free diet. The aim of this study was to verify diagnostic accuracy of AGA and compare clinical characteristics of AGA-negative with AGA-positive celiac children. METHODS: The authors analyzed serum of AGA-negative celiac children with 3 Elisa kits, and compared clinical and anthropometric data of AGA-negative with AGA-positive celiac children. Celiac disease was diagnosed with small bowel biopsy, and total IgA were determined. Children with IgA-deficiency were excluded. RESULTS: When retested with two other commercial kits, serum values of AGA-negative children were confirmed in all but one. In the last 14 years a diagnosis of celiac disease was performed in 166 children, in 56 of them (33.7%) antigliadin antibodies were negative. Preva-lence of AGA-negative celiac children increased significantly in the last years (from 23% before 2002 to 39.8% after 2002, P=0.04). AGA-negative children were significantly older (7.8 years vs. 3.7 years, P=0.0007) they complained more frequently of abdominal pain (55%, vs. 25,4% P=0.04) and less frequently of anaemia (8% vs. 24.5% P=0.012) and were less likely to have a classical celiac triad (5.3 vs. 22%, P=0.004) than AGA-positive children. CONCLUSION: Serum AGA seem no longer useful for monitoring compliance to gluten-free diet. In children where AGA are negative at diagnosis, when the child eats a normal amount of gluten, they are going to remain negative even after poor compliance.

    No data related to Aminoacids testing before the diet or even more Toxic elements were included. In protein avoidance and looking for behaviors the role of neurotransmitters metabolism was completely dismissed.Many anecdotic evidence show that on diet and on time on diet leves of Hg/Al/Pb/Cd/As in urine/blod/fecal stool increase and aminoacids profiles chamnge. No data on aminoacids testing in 24 hours urine and blood were included to detect potential protein mismanagement and to detect subgroups of aminoacids metabolism problems. No data on fungal or bacterial problems in gut were included- no Fungal antibodies in blood, no culture testing, no other parasites analyzed. No data on abnormal metabolites or fungus were included. No data on liver enzymes -.whole hepatogram-or renal status were included. No data on vitamin status were included /(A, B, C, D3, E), no data on essential elements status were included and how they changed on time (Ca/Mg//Zn/Se/Li/Cu/Cr).
    J Proteome Res. 2010 May 13. [Epub ahead of print]

    Urinary Metabolic Phenotyping Differentiates Children with Autism from Their Unaffected Siblings and Age-Matched Controls.
    Yap IK, Angley M, Veselkov KA, Holmes E, Lindon JC, Nicholson JK.

    Biomolecular Medicine, Division of Surgery and Cancer, Faculty of Medicine, Imperial College London, Sir Alexander Fleming Building, South Kensington Campus, London SW7 2AZ, United Kingdom, and Sansom Institute, Division of Health Sciences, University of South Australia.

    Abstract
    Autism is an early onset developmental disorder with a severe life-long impact on behavior and social functioning that has associated metabolic abnormalities. The urinary metabolic phenotypes of individuals (age range=3-9 years old) diagnosed with autism using the DSM-IV-TR criteria (n = 39; male = 35; female = 4), together with their nonautistic siblings (n = 28; male = 14; female = 14) and age-matched healthy volunteers (n = 34, male = 17; female = 17) have been characterized for the first time using (1)H NMR spectroscopy and pattern recognition methods. Novel findings associated with alterations in nicotinic acid metabolism within autistic individuals showing increased urinary excretion of N-methyl-2-pyridone-5-carboxamide, N-methyl nicotinic acid, and N-methyl nicotinamide indicate a perturbation in the tryptophan-nicotinic acid metabolic pathway. Multivariate statistical analysis indicated urinary patterns of the free amino acids, glutamate and taurine were significantly different between groups with the autistic children showing higher levels of urinary taurine and a lower level of urinary glutamate, indicating perturbation in sulfur and amino acid metabolism in these children. Additionally, metabolic phenotype (metabotype) differences were observed between autistic and control children, which were associated with perturbations in the relative patterns of urinary mammalian-microbial cometabolites including dimethylamine, hippurate, and phenyacetylglutamine. These biochemical changes are consistent with some of the known abnormalities of gut microbiota found in autistic individuals and the associated gastrointestinal dysfunction and may be of value in monitoring the success of therapeutic interventions.
    Now, with this lack of clinical knowledge, with the short term of the study how the conclussions can be of the kind that are being reported?

  3. August 12, 2011 at 7:15 am

    I’ve just been diagnosed with Celiac Disease does anyone know of any gluten free foods that taste good?

  1. March 15, 2011 at 10:51 am

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