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Diet & Autism/PDD/Asperger's
Often called the "Autism Spectrum Disorders"

Research Menu Page ||| Updated 11/18/13

Listed in date order, with the most recent first:

Dufault 2012 A macroepigenetic approach to identify factors responsible for the autism epidemic in the United States.
Curtis 2008 Nutritional and environmental approaches to preventing and treating autism and attention deficit hyperactivity disorder (ADHD): a review.
Patel 2007 A Comprehensive Approach to Treating Autism and Attention-Deficit Hyperactivity Disorder: A Prepilot Study.
Grandjean 2006     Developmental neurotoxicity of industrial chemicals.
Yel 2005     Thimerosal induces neuronal cell apoptosis by causing cytochrome c and apoptosis-inducing factor release from mitochondria.
Mutter 2005 Mercury and autism: Accelerating Evidence?
Mutter 2005 Amalgam risk assessment with coverage of references up to 2005 (Review)
Vojdani 2003 Infections, toxic chemicals and dietary peptides binding to lymphocyte receptors and tissue enzymes are major instigators of autoimmunity in autism.
Brown 2001 Theoretical estimation of blood mercury levels from Thimerosal injections using a one compartment biokinetic model. (An analysis to “bound” potential mercury tissue levels)
Cade 2000 Autism and Schizophrenia: Intestinal Disorders.
Fernstrom 2000     Can nutrient supplements modify brain function?
Alberti 1999 Sulphation deficit in "low-functioning" autistic children: a pilot study.
Cade 1999 A Peptide Found in Schizophrenia and Autism Causes Behavioral Changes in Rats.
Clark 1999 Autistic symptoms in children with attention deficit-hyperactivity disorder.
Harris 1998 Inhibition of phenolsulphotransferase by salicylic acid: a possible mechanism by which aspirin may reduce carcinogenesis.
McDougle 1996 Effects of tryptophan depletion in drug-free adults with autistic disorder.
Lucarelli 1995 Food allergy and infantile autism.
Leboyer 1993 Opiate hypothesis in infantile autism? Therapeutic trials with naltrexone.
Martineau 1985 Vitamin B6, magnesium, and combined B6-Mg: therapeutic effects in childhood autism.
Rimland 1978 The effect of high doses of vitamin B6 on autistic children: a double-blind crossover study.
Singh 1976 Wheat gluten as a pathogenic factor in schizophrenia.
Dohan 1973 Relapsed Schizophrenics: Earlier Discharge from the Hospital After Cereal-Free, Milk-Free Diet.


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  1. Sulphation deficit in "low-functioning" autistic children: a pilot study, Alberti A, Pirrone P, Elia M, Waring RH, Romano C, Biological Psychiatry 1999 Aug 1;46(3):420-4
    "The hypothesis that autistic behavior might be related to metabolic dysfunctions has led us to investigate in a group of "low functioning" autistic children and in an age-matched control group each made up of 20 subjects, the sulphation capacity available. ... RESULTS: The PS/PG ratio in the group of autistic subjects gave a significantly lower results than the control group ... CONCLUSIONS: The inability to effectively metabolize certain compounds particularly phenolic amines, toxic for the CNS, could exacerbate the wide spectrum of autistic behavior." [See also Harris study for info about salicylate & the PST enzyme]
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  2. Theoretical estimation of blood mercury levels from Thimerosal injections using a one compartment biokinetic model. (An analysis to “bound” potential mercury tissue levels), Brown, DR. Prepared for the IOM meeting on Thimerosal and Vaccines , Boston, July 16, 2001
    His Interpretations and Suggestions section contains what should be a strong indictment very carefully toned down:

    "(3) Because the risk to children is believed to be as much as 10 times greater than risk to adults, the fact that estimates are slightly below the toxic levels would not be considered evidence of safety;

    (4) . . . It is possible that single doses of Thimerosal would not be hazardous while repeated doses would bioaccumulate and be potentially toxic."

    Full text - Get Password

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  3. A Peptide Found in Schizophrenia and Autism Causes Behavioral Changes in Rats, Cade R & Sun Z. The National Autistic Society, Vol. 3(1) 85–95
    ". . . About 65 seconds after treatment with different doses of ß-CM7, [casomorphine] rats became restless and ran violently, with teeth chattering and with rapid respiration. Seven minutes later, the rats became inactive with less walking, distancing themselves from the other rat in the same cage, and sitting in, or putting their head against, the corner of the cage. The sound response was reduced and social interaction was absent. One hour later, the rats showed hyperdefensiveness. The above behavioral effects of ß-CM7 did not occur when rats were pretreated with naloxone (2 mg/kg, IP). The rats receiving saline did not show any behavioral changes throughout the 2 hour period of observation. ß-CM7 also demonstrated analgesic effects, which could be blocked by naloxone. The results suggest that ß-CM7 may play a role in behavioral disorders such as autism and schizophrenia"

    Full Text - Get Password

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  4. Autism and Schizophrenia: Intestinal Disorders, Cade R et al. Nutritional Neuroscience, March 2000
    ". . . A gluten-casein free diet was accompanied by improvement in 81% of autistic children within 3 months. Our data provide support for the proposal that schizophrenia and autism are due to absorption of exorphins formed in the intestine from digestion of gluten and casein."
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  5. Autistic symptoms in children with attention deficit-hyperactivity disorder, Clark T, Feehan C, Tinline C, Vostanis P, Eur Child Adolesc Psychiatry 1999 Mar;8(1):50-5
    "...This study estimates the rate of autistic symptoms in a sample of children with ADHD by using the parent-rated Autism Criteria Checklist. A high proportion of parents (between 65-80%) reported significant difficulties in social interaction (particularly in empathy and peer relationships), and communication (particularly in imaginative ability, nonverbal communication and maintaining conversation). The nature and relationship between ADHD and pervasive developmental disorders is considered, as well as implications for assessment, diagnosis and treatment."
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  6. Nutritional and environmental approaches to preventing and treating autism and attention deficit hyperactivity disorder (ADHD): a review., Curtis LT, Patel K. J Altern Complement Med. 2008 Jan-Feb;14(1):79-85.
    " OBJECTIVES: The purpose of this study was to concisely review the available literature of nutritional and environmental factors on autistic spectrum and attention deficit hyperactivity disorder (ADHD). DESIGN AND METHODS: Review of journal articles found on the PubMed database and from information from several conference proceedings. RESULTS: Many, but not all, studies link exposure to toxins such as mercury, lead, pesticides, and in utero smoking exposure to higher levels of autism and/or ADHD . . . CONCLUSIONS: Autistic spectrum disorders and ADHD are complicated conditions in which nutritional and environmental factors play major roles. Larger studies are needed to determine optimum multifactorial treatment plans involving nutrition, environmental control,medication, and behavioral/education/speech/physical therapies. "

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  7. Relapsed schizophrenics: earlier discharge from the hospital after cereal-free, milk-free diet. Dohan FC, Grasberger JC. American Journal of Psychiatry 1973 Jun;130(6):685-8.
    "Routinely treated schizophrenics, who on admission were randomly assigned to a diet free of cereal grains and milk while on the locked ward, were discharged from the hospital about twice as rapidly as control patients assigned to a high-cereal diet. What gluten secretly added to the cereal-free diet abolished this effect. These and previous findings suggest that cereal grains may be pathogenic for those hereditarily predisposed to schizophrenia just as they are for celiac disease, a disorder that may be genetically related. "

    Full Text - Get Password || text of Letter to British Medical Journal: Coeliac Disease and Schizophrenia (in Ireland)

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  8. A macroepigenetic approach to identify factors responsible for the autism epidemic in the United States. Dufault R, Lukiw WJ, Crider R, Schnoll R, Wallinga D, Deth R. Clinical Epigenetics 2012 Apr 10;4(1):6.
    " The number of children ages 6 to 21 in the United States receiving special education services under the autism disability category increased 91% between 2005 to 2010 while the number of children receiving special education services overall declined by 5%. The demand for special education services continues to rise in disability categories associated with pervasive developmental disorders. Neurodevelopment can be adversely impacted when gene expression is altered by dietary transcription factors, such as zinc insufficiency or deficiency, or by exposure to toxic substances found in our environment, such as mercury or organophosphate pesticides. . . . In the current review, we utilize a novel macroepigenetic approach to compare variations in diet and toxic substance exposure between these two geographical populations [Italy & U.S.] to determine the likely factors responsible for the autism epidemic in the United States."

    Full Text

    Quote: "Children with autism may be Zn (zinc) deficient and often have MT (metallothionein) dysfunction. Because of their diminished capacity to excrete toxic heavy metals, the severity of their condition is associated with their toxic metal burden. This macroepigenetic model proposes that autism prevalence is related to the consumption of HFCS and the overall exposure to Hg (mercury) in the U.S."

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  9. Can nutrient supplements modify brain function?    Fernstrom JD, American Journal of Clinical Nutrition 2000 Jun;71(6 Suppl):1669S-1673S
    "Over the past 40 y, several lines of investigation have shown that the chemistry and function of both the developing and the mature brain are influenced by diet. Examples are the effect of folate deficiency on neural tube development during early gestation, the influence of essential fatty acid deficiency during gestation and postnatal life on the development of visual function in infants, and the effects of tryptophan or tyrosine intake (alone or as a constituent of dietary protein) on the production of the brain neurotransmitters derived from them (serotonin and the catecholamines, respectively). ... "
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  10. Developmental neurotoxicity of industrial chemicals, Grandjean P, Landrigan PJ., Lancet 2006 Dec 16;368(9553):2167-78
    ". . . A few industrial chemicals (eg, lead, methylmercury, polychlorinated biphenyls [PCBs], arsenic, and toluene) are recognised causes of neurodevelopmental disorders and subclinical brain dysfunction. Exposure to these chemicals during early fetal development can cause brain injury at doses much lower than those affecting adult brain function. . . . Despite an absence of systematic testing, many additional chemicals have been shown to be neurotoxic in laboratory models. The toxic effects of such chemicals in the developing human brain are not known and they are not regulated to protect children. The two main impediments to prevention of neurodevelopmental deficits of chemical origin are the great gaps in testing chemicals for developmental neurotoxicity and the high level of proof required for regulation. New, precautionary approaches that recognise the unique vulnerability of the developing brain are needed for testing and control of chemicals."

    Full Text article - Get Password

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  11. Inhibition of phenolsulphotransferase by salicylic acid: a possible mechanism by which aspirin may reduce carcinogenesis, Harris RM, Hawker RJ, Langman MJ, Singh S, Waring RH, Gut 1998 Feb;42(2):272-5
    ". . .Salicylic acid consistently and selectively inhibited the P form of phenolsulphotransferase at subtherapeutic concentrations in both tissue samples. A 50% inhibition of sulphation by the P phenolsulphotransferase occurred at salicylic acid concentrations of about 40 and 130 microM in platelets and bowel mucosa respectively."> [While this is a possible benefit in inhibiting cancer, it may not be a benefit in ADHD and Autism. See ALBERTI STUDY HERE]
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  12. Opiate hypothesis in infantile autism? Therapeutic trials with naltrexone, Leboyer M, et al., Encephale 1993 Mar-Apr;19(2):95-102
    "The opioid hypothesis suggests that childhood autism may result from excessive brain opioid activity... This hypothesis has now received strong support and is currently based on three types of arguments: (1) similarity between autistic symptomatology and abnormal behaviors induced in young animals by injections of exogenous opioids, such as increasing social aloofness and decreasing social vocalization; (2) direct biochemical evidence of abnormalities of peripheral endogenous opioids being reported in autism and (3) therapeutic effects of the long lasting opioid receptor blocking agent naltrexone in autism. ... We performed an open trial with naltrexone in 2 autistic girls, displaying serious self-injurious behavior, reduced crying and a marked preference for salty and spicy foods, symptoms that could be related to a dysfunction of the opioid system. ... we observed an immediate reduction of hyperactivity, self-injurious behavior and aggressiveness, while attention improved. In addition, social behaviors, smiling, social seeking behaviors and play interactions increased..."

    Note: In our materials, we discuss treatment by removing the food items that produce the opioid proteins (the gluten-free, casein-free diet), and you can see more about this at www.gfcfdiet.com. The Leboyer et al study here shows the opioid presence, but recommends treatment by suppression of reaction to opioid by medication that blocks the receptors.

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  13. Food allergy and infantile autism. Lucarelli S, et al., Panminerva Med 1995 Sep;37(3):137-41
    "...We noticed a marked improvement in the behavioural symptoms of patients after a period of 8 weeks on an elimination diet ... Our results lead us to hypothesise a relationship between food allergy and infantile autism as has already been suggested for other disturbances of the central nervous system."
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  14. Vitamin B6, magnesium, and combined B6-Mg: therapeutic effects in childhood autism., Martineau J, Barthelemy C, Garreau B, Lelord G, Biol Psychiatry 1985 May;20(5):467-78
    "... The behavioral improvement observed with the combination vitamin B6-magnesium was associated with significant modifications of both biochemical and electrophysiological parameters: the urinary HVA excretion decreased, and EP amplitude and morphology seemed to be normalized. These changes were not observed when either vitamin B6 or magnesium was administered alone."
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  15. Effects of tryptophan depletion in drug-free adults with autistic disorder. McDougle CJ, et al., Arch Gen Psychiatry 1996 Nov;53(11):993-1000
    "...Tryptophan depletion led to a significant increase in behaviors such as whirling, flapping, pacing, banging and hitting self, rocking, and toe walking ... In addition, patients were significantly less calm and happy and more anxious...short-term reduction of serotonin precursor availability may exacerbate some symptoms characteristic of autism in some patients."

    Note: Tryptophan is contained in numerous foods such as milk and turkey. In a milk-free diet, it may be important to increase other foods containing tryptophan

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  16. Mercury and autism: Accelerating Evidence?, Mutter J, Naumann J, Schneider R, Walach H, Haley B. Neuro Endocrinol Lett. 2005 Oct;26(5):439-46.
    " Institute for Environmental Medicine and Hospital Epidemiology, University Hospital Freiburg, Germany. joachim.mutter@uniklinik-freiburg.de.

    . . . Recently, it was found that autistic children had a higher mercury exposure during pregnancy due to maternal dental amalgam and thimerosal-containing immunoglobulin shots. It was hypothesized that children with autism have a decreased detoxification capacity due to genetic polymorphism. In vitro, mercury and thimerosal in levels found several days after vaccination inhibit methionine synthetase (MS) by 50%. . . . Repetitive doses of thimerosal leads to neurobehavioral deteriorations in autoimmune susceptible mice, increased oxidative stress and decreased intracellular levels of glutathione in vitro. Subsequently, autistic children have significantly decreased level of reduced glutathione. Promising treatments of autism involve detoxification of mercury, and supplementation of deficient metabolites. "

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  17. Amalgam risk assessment with coverage of references up to 2005 Mutter J, Naumann J, Walach H, Daschner F., Gesundheitswesen. 2005 Mar;67(3):204-16.
    " Institut fur Umweltmedizin und Krankenhaushygiene, Universitatsklinik Freiburg. joachim.mutter@uniklinik-freiburg.de

    . . .Amalgam contributes substantially to human mercury load. Mercury accumulates in some organs, particularly in the brain, where it can bind to protein more tightly than other heavy metals (e. g. lead, cadmium). Therefore, the elimination half time is assumed to be up to 1 - 18 years in the brain and bones. Mercury is assumed to be one of the most toxic non-radioactive elements. . . . Review of recent literature suggests that mercury from dental amalgam may lead to nephrotoxicity, neurobehavioural changes, autoimmunity, oxidative stress, autism, skin and mucosa alterations or non-specific symptoms and complaints. The development of Alzheimer's disease or multiple sclerosis has also been linked to low-dose mercury exposure. There may be individual genetical or acquired susceptibilities for negative effects from dental amalgam. Mercury levels in the blood, urine or other biomarkers do not reflect the mercury load in critical organs. Some studies regarding dental amalgam reveal substantial methodical flaws. Removal of dental amalgam leads to permanent improvement of various chronic complaints in a relevant number of patients in various trials. Summing up, available data suggests that dental amalgam is an unsuitable material for medical, occupational and ecological reasons. "

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  18. A comprehensive approach to treating autism and attention-deficit hyperactivity disorder: a prepilot study. Patel K, Curtis LT. J Altern Complement Med. 2007 Dec;13(10):1091-7.
    " . . .This study examined 10 children aged 4-10 years old who had been diagnosed with both autistic spectrum disorder and ADHD by outside physicians or psychologists. These 10 children presented consecutively in an environmental medicine clinic in Buffalo, New York. The children were given comprehensive nutritional/environmental/chelation treatment for 3 to 6 months in addition to their usual behavioral, educational, speech, and physical therapies. . . . All 10 children showed significant improvement in many areas of social interaction, concentration, writing, language, and behavior. Urinary lead burden dropped significantly in all 10 children. . . . "

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  19. The effect of high doses of vitamin B6 on autistic children: a double-blind crossover study., Rimland B, Callaway E, Dreyfus P, Am J Psychiatry 1978 Apr;135(4):472-5
    The authors used data from an earlier nonblind study to identify 16 autistic-type child outpatients who had apparently improved when given vitamin B6 (pyridoxine). In a double-blind study each child's B6 supplement was replaced during two separate experimental trial periods with either a B6 supplement or a matched placebo. Behavior was rated as deteriorating significantly during the B6 withdrawal.
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  20. Wheat gluten as a pathogenic factor in schizophrenia. Singh MM, Kay SR, Science 1976 Jan 30;191(4225):401-2
    "...The observed effects seemed to be due to a primary schizophrenia-promoting effect of wheat gluten."

    This study is included because there appears to be overlap in both symptoms and treatment between schizophrenia and autism which was once called "childhood schizophrenia."

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  21. Infections, toxic chemicals and dietary peptides binding to lymphocyte receptors and tissue enzymes are major instigators of autoimmunity in autism Vojdani A, Pangborn JB, Vojdani E, Cooper EL., International Journal of Immunopathology and Pharmacology. 2003 Sep-Dec;16(3):189-99
    " Similar to many complex autoimmune diseases, genetic and environmental factors including diet, infection and xenobiotics play a critical role in the development of autism. In this study, we postulated that infectious agent antigens such as streptokinase, dietary peptides (gliadin and casein) and ethyl mercury (xenobiotic) bind to different lymphocyte receptors and tissue enzyme (DPP IV or CD26). ... A significant percentage of children with autism developed anti-SK, anti-gliadin and casein peptides and anti-ethyl mercury antibodies, concomitant with the appearance of anti-CD26 and anti-CD69 autoantibodies. ... bacterial antigens (SK), dietary peptides (gliadin, casein) and Thimerosal (ethyl mercury) in individuals with pre-disposing HLA molecules, bind to CD26 or CD69 and induce antibodies against these molecules. In conclusion, this study is apparently the first to demonstrate that dietary peptides, bacterial toxins and xenobiotics bind to lymphocyte receptors and/or tissue enzymes, resulting in autoimmune reaction in children with autism. "
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  22. Thimerosal induces neuronal cell apoptosis by causing cytochrome c and apoptosis-inducing factor release from mitochondria. Yel L, Brown LE, Su K, Gollapudi S, Gupta S., International Journal of Molecular Medicine. 2005 Dec;16(6):971-7
    " . . . In this study, we show that thimerosal, at nanomolar concentrations, induces neuronal cell death through the mitochondrial pathway. . . . Our data suggest that thimerosal causes apoptosis in neuroblastoma cells by changing the mitochondrial microenvironment."
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  23. Note on "negative" studies of gluten/casein-free diet for autism or schizophrenia:

    Several studies were done that showed no connection between gluten/casein control and autism. Close inspection of some of these studies is interesting:

    • In the Sponheim study of 1991, and the Vlissides study on schizophrenia of 1986, the diet used apparently did not exclude casein, but only gluten. Since both proteins have similar effects, it is not surprising that they saw no difference before and after the 6 month diet trial. "If you limp because you have 2 nails stuck in your shoe, and you take out one, you will still be limping."

    • The Storms study of 1982 used a gluten/casein diet but for only 10 days. It takes longer than that to see a response, according to Dr. Cade.

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