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Autism: Dietary Treatment Options

by Sandra and Max Desorgher(more info)

listed in medical conditions, originally published in issue 57 - October 2000

An Autism Epidemic

The diagnosis and recognition of autism spectrum disorder has risen, according to some, to epidemic proportions.[1] Once considered a rare psychological condition, recent advances and communication have propelled autism to the front headlines in medical journals[2] as well as the news media.[3] Funding for research has been slow and provided almost exclusively to genetic studies. Population studies[4] lag behind, with forthcoming information being too little too late for many who have and will suffer the 'lifelong' disability of autism. The cost to family and community for providing lifetime care for individuals with moderate to severe autism, estimated at $2,000,000 per individual, is forcing governments to take a close look at the possible causes for the increase in diagnosis, educational impact and long-term commitment and cost of continued ignorance.[5]

Image of children

At the time when autism was first described by Dr Leo Kanner and thus given an identity, there was little debate as to the field of medicine which would be called upon to develop expertise and treatments for this rare psychological condition. Under the psychological paradigm, advances have not been forthcoming.

Physicians, researchers and specialists, often driven by personal agendas, have sometimes made 'findings' which are called 'pieces of the puzzle' by the autism community. These pieces do not always seem to fit together or even belong to the same puzzle.

In our theory, a single cause, these pieces do fit together. In our theory autism is not a psychological condition – it is a neuro-gastro-immunological disorder resulting from an immuno-genetic error during foetal development. At the time when the immune system is developing, the first immune cells must select a non-self substance which has crossed the placental barrier and react to this non-self substance in order for the immune system to proliferate. In the developing foetus there is no apparent function for a substance called lutein, a pigment which is used by the human at birth to protect the eyes from ultraviolet light. The immune system is developing just after neural tube closure which has been the time of reference given by some research that corresponds to brain imaging differences that are identified in autists.[6] However, the slightly earlier 'neural tube closure' time frame would likely correlate to a population with co-occurring spina bifida – no such correlation exists. An immune system which identifies lutein as the non-self substance would result in a correlation to Retinopathy of Prematurity. This correlation does exist.[7,8] An immune system reaction of this type would result in a correlation to a disturbance in pterin metabolism. This correlation does exist,[9] and it would result in a correlation to mitochondrial disturbance and again this correlation does exist.[10]

Vitamin A Deficiency in a 'Low Fat' Society

The World Health Organization (WHO) and Federal Agricultural Organization (FAO), in 1967, determined that humans could obtain their vitamin A from vitamin A precursor foods i.e. beta-carotene.[11] Studies have since shown that whole populations cannot convert precursor beta-carotene to usable vitamin A (retinol).[12,13] During this same time period commercial baby formulas were replacing home-made formulas and do not provide essential nutrients such as arachidonic acid. Improved agricultural practices allowed foods that had been consumed seasonally (such as coloured fruits and vegetables) to become available as year round foods. Prenatal vitamins included the precursor vitamin A (beta-carotene). The amount of pigment produced by a plant depends on many factors but research has shown that lutein production increases when the plant is exposed to direct sunlight, increased sunlight or is under stress. We are consuming more pigments from fruits and vegetables than ever before. At the same time research confirms that vitamin A deficiency continues to result in adverse reactions to vaccination, blindness and death at alarming rates, even in the most developed countries.[14-19]

Successful Results of a Lutein-free Diet

The theory, lutein intolerance, is simple and as yet has not been subject to rigorous research. Since 1995 we have worked to provide recommendations to families and physicians treating individuals with autism. Our results include that 80% of our clients report significant and measurable results when a nutrient balanced, lutein free, soy protein free and casein/gluten restricted diet is implemented with an adequate and balanced intake of essential nutrients. 10% report complete alleviation of symptoms or declassification from autism.[20] The complexity of the dietary intervention results from the unique needs of each individual, their current diet and the age at which sufficient dietary intervention is applied.

The complexity of the dietary intervention needed results from the self-limited or restricted diets of the autists[21] as well as the cascade of biochemical abnormalities that are a result of the immune system's response to the non-self pigment pathogen, environmental factors as well as the unique make-up of each individual's genetic information. This can be further complicated when a co-occurring disease, disorder or condition is present.

The Unique Nutritional Needs of the Autist

Pigments from plant foods are removed from the human body via binding to tryptophan and vitamin B6. Tryptophan is an amino acid containing 'indole', a pigment. Serotonin is derived from tryptophan, and altered tryptophan metabolism is an established biochemical marker for autism.[22] Positive results have been reported and validated in studies published by the Autism Research Institute (ARI), San Diego, California with vitamin B6 supplementation in 20% of the study group.[23] Information from these studies does not share whether the individuals who had measurable results previously had diets deficient in vitamin B6, whether the individuals were provided additional supplements, or whether the individuals maintained self-limited or restricted diets. Further research also published by the ARI describes positive results with the use of N,N, dimethylglycine commonly called DMG.[24] A recent study of four autistic individuals given DMG did not corroborate the positive findings associated with DMG supplementation.[25] Again, no information on the children's diets was provided with the study results. Dr Mary Megson reports her findings with vitamin A supplementation, in the form of fish liver oil.[26] The findings by Dr Megson and media coverage send parents of autists scurrying to locate sources of vitamin A for their autistic children. Parents want and need to provide supplements and foods that their autistic children will accept and this is not always an easy task. As a result of the difficulty of getting supplements and indeed many foods into the autist's diet, the parent may settle for vitamin A precursor beta-carotene which tastes good, whereas some parents report that their child will literally take the bottle of cod liver oil and drink the contents voraciously before they can be stopped.

Opioid Excess Theory and the GFCF Diet

In addition to trypotophan/serotonin abnormalities, B6 and DMG reports, natural vitamin A supplementation and outcome there is research by Paul Shattock, Autism Research Unit (Sunderland), Dr Kalle Reichelt (Norway) and Dr Robert Cade, University of Florida which identify abnormal opioid levels in the autistic population.[27,28,29] The opioid excess theory has resulted in vigorous use of gluten- and casein-restricted diets being implemented for autists around the world. The results vary and are complicated by factors that include that some autists are natural lutein avoiders while others crave lutein foods. Foods used to replace gluten- and casein-containing foods may include soy protein which contains genistein, forcing the conversion of tryptophan to kynurenine,[30] another biochemical marker which is often elevated in the autist and in my research has been shown in some cases to be normal prior to the implementation of the gluten/casein-restricted diet and elevated after implementation of the gluten/casein-restricted diet and correlating to soy protein foods being added to the diet.[31] "Pellagra with colitis due to a defect in tryptophan metabolism: A nine-year-old girl presented with a red scaly rash confined to sun-exposed areas which started at two years of age and had the appearance of pellagra. Investigation of urinary tryptophan metabolites following an oral tryptophan load, showed increased excretion of kynurenine and kynurenic acid but reduced excretion of 3-hydroxy-kynurenine, xanthurenic acid and N1-methyl nicotinamide. These results indicated a defect in the hydroxylation of kynurenine, an important reaction in the synthesis of the nicotinamide nucleotide coenzymes, NAD and NADP, from tryptophan. The patient went on to develop severe colitis and psychological changes. All her symptoms responded to treatment with nicotinamide."[32]

Natural Painkillers from our Immune System

Another biochemical marker, is the reported discovery of dermorphin and deltorphin in the autist's urine.[33] These opioids, which are said to be 2000 times more potent than pharmaceutical morphine, provide more evidence that the human immune system is responsible for the unique make-up of the autist. It has been established that the immune system macrophages release haemorphins[34] and opioid substances through cathepsin manufacture.[35,36] My personal experience as an asymptomatic individual with biochemical abnormalities similar, if not identical, to many autists has resulted in my life's work – dietary intervention and autism. The release of the D-amino acid mu-opioids is very possibly a direct result of the immune systems error during foetal development targeting lutein as non-self, leading to a cascade of biochemical (immunogenetic) responses. The elevated levels of immune phagocytozing cells, which would result as dietary intake of lutein foods were added to the child's diet, could result in the reported vaccine reactions. My adopted daughter was diagnosed severe delayed disordered at 20 months but at 22 months she coded after her DPT/MMR vaccinations – she was fed lutein-containing fruit just a few hours after her vaccinations. As the immune cells break down and remove the lutein pigment, this could also result in the release back into the body of the formic acid. The development of the vaccine, originally a live, attenuated virus inside a lipid-filled chloroplast, may have been the initiating factor which has altered the way that our immune system reacts to the structure which houses the plant pigments. The diet of the dart frog includes poisonous insects. The immune system may interact with gut bacteria to produce this natural painkiller for the dart frog and this same reaction could be taking place as the immune system of the autist seeks to protect the host resulting in the production of natural painkillers from our immune system.

The Need for a Comprehensive Approach

Dr Rosemary Waring and J M Ngong have produced substantial peer-reviewed documentation of the abnormal sulphation metabolism in the autistic population.[37,38] This research clearly substantiates the need for molybdenum, the trace element required to produce sulphating enzymes. A primary source of molybdenum in the human diet is wheat (gluten), and when a gluten-restricted diet is implemented often there is no one to provide recommendations for replacement nutrients that may be inadvertently left out of the restricted diet. Removing casein (dairy protein) eliminates one of the two natural sources of essential vitamin A (retinol), and yet there was no one to recommend that a dairy-restricted diet results in the need to supplement vitamin A, until Dr Megson's research made headline news. So, a simple immune system error has resulted in the need for providing a comprehensive approach to dietary intervention. The individual's genetic make-up and pigment metabolism reveal information usually considered to be inconsequential and include co-occurring 'benign' conditions such as carotenaemia and vitiligo and the occurrence of strange bumps and/or blisters on the skin of autists.[20] On the other hand, devastating disorders of pigment metabolism also co-occur with an autism diagnosis, the most well documented being tuberous sclerosis[39] and PKU.[40]

Autism, Serotonin and Pellagra

One of the first markers identified to be different in the autists was abnormal serotonin metabolism.[41] To understand how an abnormal serotonin metabolism can result in some of the symptoms and characteristics seen amongst the autistic population, we can examine the similar presentation of a disorder that was once much more frequently diagnosed, and is most commonly known as a condition of B-vitamin deficiency – Pellagra:

"Serotonin metabolism is pellagra: Altered mental status is common in pellagrins."[42] "…Pellagra in the 1940s (the triad: dermatitis, diarrhoea, dementia) and its clinical aspects today: sun-exposed teguments revealing erythema and rapidly becoming pigmented and parchment like, dried, parched lips, angular stomatitis, lead-like sclera fine cornea vascularization; gastro-intestinal disturbances: constipation, unjustified diarrhoea, strange migratory abdominal feelings accompanied by ubiquitous dysesthesias. Other characteristics of this form of disease are: unexpressive look, continuously concerned, thoughtful, anxious or frowning, labile mind, headaches, insomnia. Villager's neurosis sometimes may be considered, in an appropriate clinical context, as a facet of nutritional deficiency."[43]

The comparison to Pellagra can be broadened when we consider autism as a disorder of pigment metabolism:

"Skin diseases associated with photosensitivity are numerous and may be divided into three main groups: photo-aggravated dermatoses, genophotodermatoses and metabolic photodermatoses. Genophotodermatoses are genodermatoses that are made photosensitive by a recognized or as yet unidentified deficiency of the natural photoprotection system. In this group are albinism, vitiligo, xeroderma pigmentosum and poikiloderma. Metabolic photodermatoses are diseases in which photosensitization reactions, often revealing, are due to the accumulation in the skin of an endogenous chromophore as a result of a congenital (porphyria) or acquired (pellagra) enzymatic disorder."[44]

Autism and Pellagra can also be viewed as a deficiency in essential fatty acids: "The major psychoses and neuroses as omega-3 essential fatty acid deficiency syndrome: substrate pellagra: Pellagra was once a major cause of three behaviourally different mental disorders – schizophreniform, manic-depressive-like, and phobic neurotic – plus drying dermatoses, autonomic neuropathies, tinnitus, and fatigue. Present-day mental diseases are found to exhibit, statistically, the same pellagraform physical disorders but to ameliorate not so much with vitamins as with supplements of a newly discovered trace omega-3 essential fatty acid (w3-EFA), which provides the substrate upon which niacin and other B vitamin holoenzymes act uniquely to form the prostaglandin 3 series tissue hormones regulating neurocircuits en bloc. Since present-day refining and food selection patterns, as well as pure corn diets, deplete both the B vitamins and W3-EFA, the existence of therapeutically cross-reacting homologous catalyst and substrate deficiency forms of pellagra are postulated, the first contributing to the B vitamin deficiency epidemics of 50-100 years ago, the second to the more recent endemic 'Diseases of Western Civilization' which express in certain genetic subgroups as the major mental illnesses of today."[45]

Autism – A Disorder of Pigment Metabolism

Pineal gland regulation via ocular pigments has been illuminated in recent research.[46a,b] The altered serotonin metabolism is another biochemical marker easily understood when the lutein theory is explored. Lutein is macular yellow, a photoprotective pigment.[47]

The visual anomalies, such as nystagmus[48], Scotopic Sensitivity Syndrome[49] and blindness7, that are associated with autism can be fully understood when the immune system interference with this pigment is recognized.

"Although one of the first biological treatments of a major psychiatric disorder was the dietary treatment of pellagra, the use of diet and dietary components in the study of psychopathology has not aroused much interest."[50] In Unconjugated Pterins in Neurobiology[51] Dr Robert Levine explores the neurochemistry of PKU and benefits of folic acid supplementation. Toxic overload is a feature of autism, and therapies such as chelation are sometimes reported by environmental medicine doctors, immunologists and parents to result in positive outcome for the autist. The anecdotal evidence is now available in overwhelming proportions. The need for funding to determine a comprehensive dietary intervention protocol for autists is long overdue.

References

1. Iver Peterson. School districts groan under weight of autism 'epidemic': high rewards and high costs as states draw autistic pupils. NY Times. 2000.
2. Wakefield AJ et al. Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children. Lancet. 351: 637-64. 1998.
3. Brennan Fleur. Can diet offer hope to autistic children? Sunday Times (family health section). 16 May 2000.
4. Center for Disease Control, Atlanta Ga. CDC Confirms Brick Township 'Epidemic' as 1 in 149.
5. FEAT. "According to the Department of Developmental Services, in the case of just one neurodevelopmental disorder, autism, the cost per lifetime of care is $2 million for every person with autism in the developmental services system." 18 May 2000.
6. Courchesne E et al. The brain in infantile autism: posterior fossa structures are abnormal. Neurology. 1994.
7. Brown R et al. Are there 'autistic-like' features in congenitally blind children? J. Child. Psychol. Psychiatry. 38(6): 693-703. 1997.
8. Ek U et al. Relation between blindness due to retinopathy of prematurity and autistic spectrum disorders: a population-based study. Dev. Med. Child. Neurol. 40(5): 297-301. 1998.
9. Messahel S et al. Urinary levels of neopterin and biopterin in autism. Neurosci. Lett. 241(1): 17-20. 1998.
10. Lombard J. Autism: a mitochondrial disorder? Med. Hypotheses. 50(6): 497-500. 1998.
11. Shils ME and Young VR. Modern Nutrition in Health and Disease. 7th Edition. 1988.
12. de Pee S et al. Lack of improvement in vitamin A status with increased consumption of dark-green leafy vegetables. Lancet. 346(8967): 75-81. 1995.
13. Fallon S. Health and nutrition in isolated traditional societies. Online article.
14. Traoré L et al. Strategies to control vitamin A deficiency. Sante. 8(2): 158-62. 1998.
15. van Stuijvenberg ME et al. Response to an iron fortification programme in relation to vitamin A status in 6-12-year-old school children. Int. J. Food Sci. Nutr. 48(1): 41-9. 1997.
16. Hussey GD and Klein M. Routine high-dose vitamin A therapy for children hospitalized with measles. J. Trop. Pediatr. 39(6): 342-5. 1993.
17. Sommer A. Vitamin A, infectious disease, and childhood mortality: a solution? J. Infect. Dis. 167(5): 1003-7. 1993.
18. Arrieta AC et al. Vitamin A levels in children with measles in Long Beach, California. J. Pediatr. 121(1): 75-8. 1992.
19. Coutsoudis A et al. Vitamin A deficiency among children in a periurban South African settlement. Am. J. Clin. Nutr. 57(6): 904-7. 1993.
20. Sara's Diet Website. http://personal.atl.bellsouth.net /~sojmed/sara's-diet.html
21. Desorgher ME and SJ. Self-selective diets in autism spectrum disorders. Online paper. 2000.
22. Launay JM et al. Serotonin metabolism and other biochemical parameters in infantile autism. A controlled study of 22 autistic children. Neuropsychobiology. 20(1): 1-11. 1988.
23. Bonisch E. Experiences with pyrithioxin in brain-damaged children with autistic syndrome. Prax. Kinderpsychol. Kinderpsychiatr. 17(8): 308-10. 1968.
24. http://www.autism.com/ari/dmg1.html and http://www.autism.com/ari/dmg2.html
25. Bolman WM and Richmond JA. A double-blind, placebo-controlled, crossover pilot trial of low dose dimethylglycine in patients with autistic disorder. J. Autism Dev. Disord. 29(3): 191-4. 1999.
26. Media release. Autistic children are 'waking up' – Richmond paediatrician may have found link to vitamin A Deficiency and autism. August 1999.
27. Reichelt KL et al. Biologically active peptide-containing fractions in schizophrenia and childhood autism. Adv. Biochem. Psychopharmacol. 1981.
28. Shattock P et al. Role of neuropeptides in autism and their relationship with classical neurotransmitters. Brain Dysfunction. 3: 328-345. 1990.
29. UF Health Science Center. University of Florida Researchers Cite Possible Link Between Autism, Schizophrenia And Diet. Office of Public Information. 16/3/1999.
30. Freese, A. et al. Kynurenine metabolites of tryptophan: implications for neurologic diseases. Neurology. 40(4): 691-5. 1990.
31. Desorgher ME and SJ. Sara's Diet – Exploding the Myths. 1999.
32. Clayton PT. Pellagra with colitis due to a defect in tryptophan metabolism. Eur. J. Pediatr. 150(7): 498-502. 1991.
33. Dermorphins and Deltorphins; Sara's Diet Website; 2000.
34. Dagouassat N et al. Generation of VV-hemorphin-7 from globin by peritoneal macrophages. FEBS Lett. 382(1-2): 37-42. 1996.
35. Allen JR et al. Two short-chain dehydrogenases confer stereoselectivity for enantiomers of epoxypropane in the multiprotein epoxide carboxylating systems of Xanthobacter strain Py2 and Nocardia corallina B276. Biochemistry. 38(1): 247-56. 1999.
36. Zhao Q et al. Neokyotorphin formation and quantitative evolution following human hemoglobin hydrolysis with cathepsin D. Peptides. 19(4): 759-66. 1998.
37. Waring RH and Ngong JM. Sulphate Metabolism in Allergy-Induced Autism: Relevance to the Disease Aetiology. 1993.
38. Alberti A et al. Sulphation deficit in 'low-functioning' autistic children: a pilot. Biol. Psychiatry. 46(3): 420-4. 1999.
39. Smalley. Autism and tuberous sclerosis. J. Autism Dev. Disord. 28(5): 407-14. 1998.
40. Miladi N. Phenylketonuria: an underlying etiology of autistic syndrome. A case report. J. Child Neurol. 7(1): 22-3. 1992.
41. Hanley HG. Hyperserotonemia and amine metabolites in autistic and retarded children. Arch. Gen. Psychiatry. 34(5): 521-31. 1977.
42. Raghuram TC et al. Serotonin metabolism is pellagra. Arch. Neurol. 32(10): 708-10. 1975.
43. Dumitrescu C et al. Particular features of clinical pellagra. Rom. J. Intern. Med. 32(2): 165-70. 1994.
44. Amblard P. et al. Skin diseases with photosensitivity. Rev. Prat. 42(11): 1365-8. 1992.
45. Rudin DO. The major psychoses and neuroses as omega-3 essential fatty acid deficiency syndrome: substrate pellagra. Biol. Psychiatry. 16(9): 837-50. 1981.
46a. Hsu DS et al. Putative human blue-light photoreceptors hCRY1 and hCRY2 are flavoproteins. Biochemistry. 5:35(44): 13871-7. 1996.
46b. Griffin EA Jr et al. Light-independent role of CRY1 and CRY2 in the mammalian circadian clock. Science. 22:286(5440): 768-71. 1999.
47. Ernström U et al. A yellow component associated with human transthyretin has properties like a pterin derivative, 7,8-dihydropterin-6-carboxaldehyde. FEBS Lett. 360(2): 177-82. 1995.
48. Denis D et al. Ophthalmologic signs in children with autism. J. Fr. Ophtalmol. 1997.
49. Edelson Stephen M. Scotopic Sensitivity Syndrome and the Irlen Lens System. Center for the Study of Autism, Salem, Oregon.
50. Young SN. The use of diet and dietary components in the study of factors controlling affect in humans: a review. J. Psychiatry Neurosci. 18(5): 235-44. 1993.
51. Lovenberg Levine. Unconjugated Pterins in Neurobiology – Basic and Clinical Aspects. 1987.

Additional and General References

1. Fischer KM. Expanded (CAG)n, (CGG)n and (GAA)n trinucleotide repeat microsatellites, and mutant purine synthesis and pigmentation genes cause schizophrenia and autism. Med. Hypotheses. 51(3): 223-33. 1998.
2. Nussbaum JJ et al. Historic perspectives. Macular yellow pigment. The first 200 years. Retina. 1(4): 296-310. 1981.
3. Desorgher Sandra and Max. Autism, pigments and the immune system: immune system regulation of pain and stress – evidence for the utilization of chiral substances. Natural painkillers in the autist. Published online at the Sara's Diet Website (see below) (revised version). 1999.
4. Sara's Diet – A comprehensive dietary approach to autism. http://www.desorgher.fsnet.co.uk

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About Sandra and Max Desorgher

Sandra J. Desorgher is a nutritional researcher and developer of Sara's Diet. She is co-author of Sara's Story: Adoption of an Autistic Child. Together with her husband Max and daughter Sara she teaches dietary intervention therapy as a treatment method to reduce and alleviate the symptoms of autism. Max Desorgher is a certified healer, Le Plan International School of Healing, Bandol, France. Max works closely with his wife Sandra to develop a comprehensive approach to healing mind, body and spirit. Max and Sandra's paper, Autism, pigments and the immune system (published online), is a basic introduction to the science behind the diet. Max is also the developer of the Sara's Diet website. Sara came to live with Sandra in 1989 and was adopted in 1994. She was evaluated by the TEACCH autism centre in autumn 1993 and was diagnosed as moderately autistic with 18 primary characteristics. In 1994 she was placed on her 'special diet'. By autumn 1995 she had achieved 'honour roll' status at school and continues to make progress on all levels. She was declassified from autism by the Marcus Institute, Atlanta, Georgia in August 1999. For further information, please visit their website at http://www.desorgher.fsnet.co.uk

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