Diet and autism: fresh evidence
Gluten free and Casein free (GF/CF) diets have been suggested for autism for many years. A survey of parent members of the National Autistic Society in 2005 found that even though only 7.5% cited gastro-intestinal (GI) difficulties as an issue for their child around half had used special diets of one sort or another. Between 10 and 20 percent reported improvements following the diet and around 10 percent wanted more research into diets and other biomedical interventions. Although most of the GI issues were reported in children with autistic disorder parents of children with Aspergers Syndrome supported the use of special diets in comparable numbers. In line with Paul Shattock’s oft quoted remark that nobody ever died of a gluten deficiency parents have often regard the GF/CF diet as essentially benign. It may be expensive and time consuming to implement but it cannot do any harm and may help with behaviour. So where is the harm in trying it?
The most obvious source of harm is the nutritional effect of limiting the type of foods offered to a growing child. Foods that contain gluten and casein also contain essential nutrients that may not be present in the GF/CF alternatives. Two years ago the National Institutes of Health reported on problems with bone density in autistic boys
The researchers believe that boys with autism and ASD are at risk for poor bone development for a number of reasons. These factors are lack of exercise, a reluctance to eat a varied diet, lack of vitamin D, digestive problems, and diets that exclude casein, a protein found in milk and milk products. Dairy products provide a significant source of calcium and vitamin D. Casein-free diets are a controversial treatment thought by some to lessen the symptoms of autism.
A recent study due to be presented at IMFAR this year went to great lengths to ensure that children on the GF/CF diet did not miss out on essential nutrients.
The researchers took on the difficult yet crucial task of ensuring participants received needed nutrients, as children on gluten-free, casein-free diets may eat inadequate amounts of vitamin D, calcium, iron and high quality protein.
They also tried to control for the effects of different treatments and therapies that might confound the results of a dietary trial by ensuring that all the subjects received the same early intensive behavioural intervention during the trial. Twenty two children aged between thirty and sixtysix months were enrolled in the trial but only fourteen completed it. One withdrew after proving positive for celiac disease. Another had an iron deficiency and the rest were unable to adhere to all the study requirements.
The trial lasted for eighteen weeks. A month into the trial each child received a cleverly disguised snack containing either gluten, casein, a combination of both or neither and went on to receive three of each type of snack in random order at one week intervals. The snacks were disguised so that neither the researchers, the children, their parents nor their teachers could identify them. The result was that there was no difference to sleep patterns, bowel movements, language or behaviour in any of the children.
The authors acknowledge the obvious weaknesses in this study. it had a small sample size and did not include children with GI disorders. However it was very well designed and provides a model for future studies. Another study, Absence of urinary opioid peptides in children with autism (Cass et al 2008) found no evidence of increased urinary peptides i autistic children compared to non-autistic controls. This is in line with Hunter et al (2003).
All this suggests that unless your child has an obvious GI disorder you should not even consider a GF/CF diet. Even if there are GI problems it is highly unlikely that urinary peptides are to blame. And if the peptides are not there why use the diet? The commercial labs that claim to routinely detect these peptides in samples from autistic children stand in marked contrast to the university and hospital labs that have failed to detect these peptides even when using very sensitive testing procedures. The study by Cass et al found evidence that suggested the presence of peptides in 25 out of 68 samples from children with an ASD. However that was not the whole story.
By HPLC analysis alone, 25 urine samples from the autism/Asperger group were selected as showing peaks in approximately the correct locations to be opioid peptides. For all 25, MALDI-TOF MS analysis of the relevant fraction found no instances of ions of m/z corresponding to opioid peptides. These results indicate that the peaks observed on the HPLC trace were not opioid peptides.
Then we have the evidence from America. Ibrahim et al 2009 found no evidence of increased GI disease in autistic subjects. A recent review published by the American Association of Pediatrics found no evidence base for an increase in GI disorders or for the effectiveness of dietary interventions in autism.
This does not mean that there is no connection between autism and GI disorders. Ibrahim et al conclude that
As constipation and feeding issues/food selectivity often have a behavioral etiology, data suggest that a neurobehavioral rather than a primary organic gastrointestinal etiology may account for the higher incidence of these gastrointestinal symptoms in children with autism.
And the AAP review stressed that some so-called autistic behaviours may be indicative of gastro-intestinal distress and these children should not have these behavioural symptoms disregarded because they are autistic. As I wrote in my very first blog post
The first thing we have to be clear about is that the child’s symptoms are real. Some parents have had their worries dismissed because it is assumed that autistic children will have poor sleep patterns, scream a lot and be difficult to feed anyway. [...]
The second point is that some of these symptoms may be connected to a child’s autism. But we do not know how. If you are non-verbal and you have constant earache, you will head-bang. That does not mean that your earache caused your autism. Nor does it mean that alleviating your distress will cure your autism. It means you are autistic and you have an earache.
Anyone with an autism diagnosis should be given a full medical work up in case there are any other conditions that need treatment. Too often the diagnostic process stops when autism is identified. There are autistic children who have other conditions that may respond to safe, targeted biomedical interventions.
I would only add that “biomedical” in this context refers to evidence based medicine delivered by qualified professionals in a proper medical facility and not to the store front clinics of the alternative therapy business.
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Comment by María Luján | May 22nd, 2010
There are many problems with this study… and the trial was only 4 weeks, after the challenge was introduced therefore it was very short.
Comment by María Luján | May 22nd, 2010
The number of children studied in this study was by far higher in terms of GI issues, even when the goal was to study GI issues in ASD.
[2320.7] GI Symptoms in Autism Spectrum Disorders (ASD): An Autism Treatment Network Study
Kent Williams, George J. Fuchs, Glenn Furuta, Margaret Marcon, Daniel L. Coury, Autism Treatment Network GI Committee. Vanderbilt University, Nashville, TN; University of Arkansas for Medical Sciences, Little Rock, AK; University of Colorado at Denver, Denver, CO; Hospital for Sick Children, Toronto, Canada; Nationwide Children’s Hospital, Columbus, OH.
BACKGROUND: The prevalence of GI symptoms in children and adolescents with ASD is uncertain, with studies reporting conflicting results.
OBJECTIVE: To determine the frequency of GI symptoms as reported by parents in a large ASD registry, and to identify factors associated with GI symptoms in children with ASD.
DESIGN/METHODS: Autism Treatment Network Registry enrolled 1420 children, age 2-18 years, with an ADOS-confirmed ASD diagnosis (autism, Asperger disorder, or PDD-NOS) at 15 sites in the US and Canada. Parents completed a GI symptom inventory tailored to the needs of nonverbal children, as well as Child Behavior Checklist (CBCL), Child Sleep Health Questionnaire (CSHQ) and Pediatric Quality of Life (PedsQL) at time of enrollment.
RESULTS: GI symptom data were available for 1185 children. Overall 45% of children were reported to have GI symptoms at time of enrollment. Of GI complaints that occurred within the 3 months prior to enrollment, abdominal pain was most common (59%) followed by constipation (51%), diarrhea (43%), other (40%), nausea (31%) and bloating (26%). Reports of GI symptoms increased with age, ranging from 39% in those under 5 years to 51% in those 7 years and older (p<0.0001). Children ages 1 to 5 years with GI symptoms had higher CBCL t-scores for total problems and for the emotionally reactive, anxious/depressed, somatic complaints, sleep problems, internalizing problems, affective problems, and anxiety problems subscales, all p<0.05. Children ages 6 to 18 years with GI symptoms had higher CBCL t-scores for total problems and for all subscales (p<0.01). Sleep problems occurred more frequently in children with than those without GI symptoms (70% versus 30%, p<0.0001). Children with GI symptoms had lower PedsQL scores (overall score and all five subscales, p<0.01) compared to children without GI problems. Presence of GI problems did not differ by gender, ASD subtype, race, or IQ.
CONCLUSIONS: Parents of children with ASD report a high prevalence of GI symptoms in their children. This prevalence increases with age. GI complaints are significantly associated with behavioral abnormalities in all age groups. GI symptoms are also significantly associated with sleep disturbances and decreased health-related quality of life. Further definition is needed on the role and potential impact of treatment of GI disorders on behavior, sleep disturbance, and quality of life in children with ASD.
Date: Sunday, May 2, 2010
Poster Symposium Session: Autism (10:15 AM – 12:15 PM)
Presentation Time: 10:15 AM
Room: East Ballroom C – Vancouver Convention Centre
Board Number: 7
Course Number: 2320
Comment by María Luján | May 22nd, 2010
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.
Hunter and Ibrahim have been very much analyzed and criticised because of flaws in analysis, design and conclussions
Comment by David N. Andrews M. Ed., C. P. S. E. | May 24th, 2010
“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.”
In the absence of a placebo condition, the study is pretty much useless, but I do agree with the ‘further studies’ bit: the aim of science in investigating interventions is to find out:
1- what works;
2- how it works;
3- for whom it works;and,
4- why it works (for them and not others).
Incidentally, my ex-wife (formerly plant physiologist/geneticist/biochemist and now applied developmental social psychologist) was looking at the gut issues studies, and she came up with some interesting observations. Not going to say what they are, because it’s for her to weigh in on this with a letter to an editor somewhere.