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Vitamin A (Autism)
Vitamin A
This study tests the effects of Vitamin A supplementation on a 5-year old autistic boy. The boy, who was being seen for a history of bilateral corneal ulceration, developed further ocular pathology that included a central ulcer in the right eye, a culture which yielded Streptococcus pneumoniae. After questioning his mother, it was found the boy had a very poor diet, consisting mainly of bacon, an occasional blueberry muffin, and Kool Aid. A serum vitamin A level measured less than 50 ug/L with the normal range being 360-1200 ug/L. He was given a vitamin A palmitate injection of 100,000 USP units intramuscularly and this was repeated 2 months later with a dose of 50,000 USP units intramuscularly. Three months later an ocular evaluation showed the surfaces of the eyes to be normal.
Steinemann, Thomas L., M.D. and Christiansen, Stephen P., M.D.: Vitamin A Deficiency and Xerophthalmia in an Autistic Child, Archives of Ophthalmology, March, 1998;116:392-393.
Food Allergy
Food Allergy
The etiopathogenesis of infantile autism is still unknown. It has been suggested that food peptides might be able to determine toxic effects at the level of the central nervous system by interacting with neurotransmitters. In fact a worsening of neurological symptoms has been reported in autistic patients after the consumption of milk and wheat.
This study attempted to verify the efficacy of a cow's milk free diet (or other foods which gave a positive result after a skin test) in 36 autistic patients. Also noted immunological signs of food allergy in autistic patients on a free choice diet.
There was a marked improvement in the behavioural symptoms of patients after a period of 8 weeks on an elimination diet and high levels of IgA antigen specific antibodies for casein, lactalbumin and beta-lactoglobulin and IgG and IgM for casein were found. The levels of these antibodies were significantly higher than those of a control group which consisted of 20 healthy children.
Results point to a relationship between food allergy and infantile autism as has already been suggested for other disturbances of the central nervous system.
Lucarelli S et al., Food allergy and infantile autism. Panminerva Med, 1995 Sep, 37:3, 137-41.
Hair Analysis
Hair Analysis
The concentrations of calcium, magnesium, zinc, copper, lead, and cadmium were determined in scalp hair samples from a group of 12 autistic children and a group of 12 nonautistic control children.
The only statistically significant difference between median concentrations of minerals in the hair from the two groups was a 62% decrease in the concentration of cadmium in the hair of autistic children. This decrease was probably not physiologically significant.
The nutrient intake of autistic children as a group was found to be adequate and typical of well-fed American children. It was concluded that the children in neither the autistic nor the nonautistic control group showed evidence of toxicity or deficiency of the minerals or nutrients studied, but because of food idiosyncracies nutrient intake should be monitored.
Shearer TR et al., Minerals in the hair and nutrient intake of autistic children. J Autism Dev Disord, 1982 Mar, 12:1, 25-34.
Immunogenetics
Immunogenetics
The major histocompatibility complex comprises a number of genes that control the function and regulation of the immune system. One of these genes, the C4B gene, encodes a product that is involved in eliminating pathogens such as viruses and bacteria from the body.
A deficient form of the C4B gene, termed the C4B null allele (no C4B protein produced) had an increased frequency in autism.
Confirmed the finding of an increased frequency of the C4B null allele in autism and found that the related disorders also had an increased frequency of this null allele. In addition, two alleles of the DR beta 1 gene also had significantly increased representation in the autistic subjects.
Warren RP et al., Immunogenetic studies in autism and related disorders. Mol Chem Neuropathol, 28(1-3):77-81 1996 May-Aug.
Metabolism (Autism)
Metabolism
Disorders in "purine" and pyrimidine "metabolism" may be difficult to recognize because their recent "description" means many are little known. They cover a broad spectrum of illnesses, can present from "birth" to the 80s, have multiple symptoms and lead to early death. Recognition of new disorders requires skill and serendipity. Often parents of affected children provide valuable clues.
These disorders should be suspected, particularly where the history involves siblings, in anemia, susceptibility to "infection", or neurological deficits including autism, delayed development, "epilepsy", self-mutilation, "muscle" weakness and - unusual in children and adolescents - "gout".
These disorders can be detected from the abnormal metabolites in body fluids and/or altered "enzyme" activity.
Simmonds-HA When and how does one search for inborn errors of purine and pyrimidine metabolism? Pharm-World-Sci. 1994 Apr 15; 16(2): 139-48.
Nutritional Ecology
Nutritional Ecology
Dietary intake was assessed in a sample population of 40 autistic and 34 control children with a 7-day diet record kept by the parent or primary caregiver. A questionnaire was completed by each participant to obtain descriptive data on nutrition and health issues, attitudes and beliefs about nutrition, and nutrition knowledge.
The autistic children had significantly greater intake of all nutrients with the exception of vitamins A and C, and fat; overall adequacy of diets was similar for both groups.
Parent/primary caregivers of autistic children reported a more positive belief in the relationship between diet and behavior, and a more positive attitude about the importance of nutrition. A higher incidence of food cravings, pica, and perceived eating problems were reported by the parent/caregivers of autistic children.
Raiten DJ & Massaro T Perspectives on the nutritional ecology of autistic children. J Autism Dev Disord, 1986 Jun, 16:2, 133-43.
Pterins
Pterins
Tetrahydrobiopterin is essential for brain cells to make monoamine neurotransmitters. It has been reported that the concentrations of tetrahydrobiopterin in plasma and urine are low in certain mental disorders and that oral supplements are beneficial.
A group of Japanese investigators have been conducting clinical trials of the effect of administration of tetrahydrobiopterin to autistic children and reported that it is beneficial with no significant side effects. Besides tetrahydrobiopterin, we also determined plasma and urinary levels of neopterin and monapterin in these individuals in order to evaluate the status of dihydroneopterin triphosphate, a key biosynthetic precursor of tetrahydrobiopterin.
Results indicated that the plasma and urinary levels of tetrahydrobiopterin are not statistically different between the two groups and, therefore, no simple explanation for the beneficial effects of administration of tetrahydrobiopterin on autistic children can be offered at the present time. In contrast, plasma and urinary levels of neopterin were depressed and plasma monapterin was also significantly depressed in autistic subjects compared with controls.
Levels of other pterins, including folate, were not statistically different between the two groups. The basis for this depression in neopterin and monapterin is unknown. It does not seem likely that this depression could be attributed to a difference in age or T-lymphocyte / macrophage activity. However, further studies are needed to investigate these possibilities.
Eto I et al., Plasma and urinary levels of biopterin, neopterin, and related pterins and plasma levels of folate in infantile autism. J Autism Dev Disord, 1992 Jun, 22:2, 295-308.
Rett Syndrome
Rett Syndrome
Nutrition is a major problem for the Rett patient. We have studied 21 girls with Rett syndrome (19 typical, two atypical). We report our experience in this population with the nutritional aspects of Rett syndrome, the typical dietary habits, and various nutritional deficiencies. Further experience with the use of high fat diets is reported.
Rice MA & Haas RH: The nutritional aspects of Rett syndrome. J Child Neurol, 1988, 3 Suppl:, S35-42.
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