[Substitutive and dietetic approaches in childhood autistic disorder: interests and limits].

INTRODUCTION: Autism is a developmental disorder that requires specialized therapeutic approaches. Influenced by various theoretical hypotheses, therapeutic programs are typically structured on a psychodynamic, biological or educative basis. Presently, educational strategies are recommended in the treatment of autism, without excluding other approaches when they are necessary. Some authors recommend dietetic or complementary approaches to the treatment of autism, which often stimulates great interest in the parents but also provokes controversy for professionals. Nevertheless, professionals must be informed about this approach because parents are actively in demand of it.

LITERATURE FINDINGS: First of all, enzymatic disorders and metabolic errors are those most frequently evoked in the literature. The well-known phenylalanine hydroxylase deficit responsible for phenylketonuria has been described as being associated with autism. In this case, adapted diet prevents mental retardation and autistic symptoms. Some enzymatic errors are also corrected by supplementation with uridine or ribose for example, but these supplementations are the responsibility of specialized medical teams in the domain of neurology and cannot be applied by parents alone. Secondly, increased opoid activity due to an excess of peptides is also supposed to be at the origin of some autistic symptoms. Gluten-free or casein-free diets have thus been tested in controlled studies, with contradictory results. With such diets, some studies show symptom regression but others report negative side effects, essentially protein malnutrition. Methodological bias, small sample sizes, the use of various diagnostic criteria or heterogeneity of evaluation interfere with data analysis and interpretation, which prompted professionals to be cautious with such diets. The third hypothesis emphasized in the literature is the amino acid domain. Some autistic children lack some amino acids such as glutamic or aspartic acids for example and this deficiency would create autistic symptoms. However, for some authors, these deficits are attributed to nutritional deficits caused by the food selectivity of children. A fourth hypothesis concerning metabolic implication in autism is the suspicion that a food allergy phenomenon could interfere with development, and it has been observed that Ig levels are higher in autistic children than in control children. Autistic children with a positive reaction to food Ig would have a more favourable outcome with diet excluding some kinds of food; but most of those diets are drastic and ethically debatable. Fifth, glucidic catabolism could be deleterious with an excess of ketonic products that will initiate comitial seizures. Few studies with ketogenic diet have been conducted but, as it has been described with epileptic subjects, those diets would diminish autistic symptoms. Not enough studies have been conducted that would allow one to draw any firm conclusions. The sixth hypothesis is linked with vitamin deficiencies that are a notably important area of research in the treatment of autism. Vitamin B12 or B6 deficiencies have been studied in several articles, and many of them were controlled studies. French teams also emphasize an interest in supplementation with B12 or B6. The two last hypotheses concern auto-immune patterns and the toxic effects of heavy metals like mercury. There is a paucity of methodologically satisfying studies that support these two hypotheses and diet recommendations. Following these assumptions, some dietetic approaches have been recommended, even though the methodological aspects of supporting studies are poor. The most famous diet is the gluten-free and/or casein-free diet. Only two controlled studies attracted our attention. Even if for some autistic children such a diet was positive, for others, gluten-free or casein-free diets were poorly tolerated and, for some authors, not without considerable side effects, the more prejudicial of which was the Kwashiorkor risk. Ketogenic diets have been studied in one non controlled study, but even if positive results have been noted by the authors, the ketogenic diet is very restricting and the long term effects have not been evaluated. Vitamin supplementation is the one and only diet domain where there have been many repeated and placebo-controlled studies. Side effects are rare and mild even if high doses of vitamin B6 are advocated in these studies. In total, as evoked by Rimland, 11 controlled placebo-blind studies have been conducted and 50% of autistic children with this supplementation had improved autistic signs. However, these results still remain debated. Finally, more rarely, enzymatic abnormalities need specific diets which have some positive consequences, but such diets could not be applied by parents alone and are the responsibility of specialized teams. For discussion purposes we can emphasize that, in spite of the amount of studies concerning the effects of specialized diets, few are methodologically satisfying. We can not ignore that some side effects are possible with such approaches and parents need to be informed of them. Some are even potentially serious, such as diets with metal chelators. In spite of those results, vitamin supplementation seems to be the only one that some specialized teams in autism could apply, always with parent agreement. In conclusion, within this scientific field, studies on eating habits of autistic children should be conducted because of their food selectivity or avoidance.