William Shaw, Ph.D. is an American chemist and the founder of the Great Plains Laboratory, Inc.

William Shaw Ph.D., biochemist, and toxicologist, specialized in integrative treatments for autism and maintenance of brain health, founder of Great Plains Laboratory, Inc., expert witness, biochemical and nutritional consultant, accomplished teacher and speaker.

Center for Disease Control

After obtaining his Ph.D. in biochemistry and human physiology at The Medical University of South Carolina, Shaw worked at the Center for Disease Control (CDC) for six years. His first position was as a supervisory research chemist in the National Health and Nutrition Examination Survey (NHANES) which conducts a nutritional adequacy and toxic exposure assessment of the population of the entire United States. This information was used by the FDA to make nutritional recommendations for supplements to commercial foods like breakfast cereals. He coauthored a chapter on methods for vitamin testing in human body fluids in a widely used clinical chemistry textbook (1). During this time at CDC, Shaw also developed an interest in the field of testing for organic acids, a test used to detect genetic diseases called inborn errors of metabolism and evaluated different approaches to testing and first developed the idea of testing for Clostridia bacteria metabolites using human body fluids following extended conversations with researchers in the Analytical Bacteriology Section of CDC and a review of their scientific papers. These researchers tested for the presence of phenolic compounds in cultures of Clostridia bacteria (2,3) to identify the species but did not test for the presence of similar metabolites of the same compounds in body fluids of humans infected with Clostridia. Shaw later used this information to detect the presence of Clostridia metabolites modified by human metabolism in human urine. 

 His last four years at CDC were in the Endocrinology and Immunoassay Departments, where he developed the first theoretical and mathematical basis for radioimmunoassay data reduction calculations (4,5), demonstrating the algebraic equivalency of nine different data reduction methods. Prior to Shaw’s work, the theoretical chemical reasons for the linearity of such data reduction methods with certain mathematical transforms were unknown.  

He also solved a major medical mystery involving thyroid hormone (T4) testing that affected virtually all laboratories in the United States and many other countries, especially during summer weather. The majority of T4 tests performed throughout the world yielded falsely elevated values in warm weather, sometimes leading to incorrect therapy. Shaw found that certain blood fats such as phospholipids and triglycerides broke down during transport of samples for thyroid testing when the weather was warm. The breakdown products, called lysolecithins and nonesterified (free) fatty acids, were powerful detergents that denatured the protein reagents used in the thyroid test, leading to falsely high values (6,7). Based on this original discovery, Shaw proposed that a similar mechanism, the breakdown of fats to form detergents, operating in the human body was a likely major cause of diseases such as diabetes, pancreatitis, Reye’s syndrome, and schizophrenia (8,9).

Mercer University and SmithKline Beecham Clinical Laboratories

Shaw then moved into the field of toxicology and became board certified in this field with an additional board certification in the field of clinical chemistry, one of a handful of people in the world with double board certifications in these fields.  He was a professor at Mercer University School of Pharmacy and became Forensic Toxicology Director at SmithKline Beecham Clinical Laboratories, one of the world’s largest clinical laboratories at the time.  During this time, Shaw developed his expertise in drug metabolism and testing, liquid chromatography, and gas chromatography- mass spectrometry and served numerous times as an expert witness in cases of alcohol and drug abuse and later in homicide cases. 

Shaw then moved into a position as Director of Clinical Chemistry, Toxicology, Endocrinology, and organic acid testing at Children’s Mercy Hospital, one of the teaching hospitals of the University of Missouri at Kansas City School of Medicine where he was appointed an associate professor. During this time, he revived his previous interest in organic acids and mass spectrometry to set up a test for inborn errors of metabolism for patients at the hospital and many outside clients. This testing led to a discovery that certain metabolites of microorganisms in the intestinal tract appeared to be a factor in some cases of autism and in other psychiatric diseases (10-16). He obtained a grant from Pfizer to evaluate the usefulness of antifungal treatment as a therapy in autism. The therapy appeared promising and antifungal therapy is now widely used by integrative physicians throughout the world as a treatment for autism and other chronic illnesses such as chronic fatigue syndrome, fibromyalgia, and vulvodynia. Shaw was one of the members of the first group to meet to discuss new integrative treatments for autism called “Defeat Autism Now”.  Based on the efforts and stimulation of this group, Shaw published two books on the treatment of autism that are popular worldwide with more than a million copies sold and that have been translated into multiple languages including French, Spanish, Portuguese, Italian, German, Hungarian, Korean, Japanese, Chinese, Arabic, and Indonesian: Biological Treatments for Autism and PDD (14) and Autism: Beyond the Basics (15) which deal with many of the underlying causes of autism and the related disease pervasive developmental disorder (PDD). Shaw is now working on a third book on the causes and treatments for autism. 

Clostridia & Neuropsychiatric Diseases 

During his research at Children’s Mercy, Shaw also found that certain Clostridia bacteria produced metabolic byproducts in the intestinal tract in very high amounts in patients with autism, schizophrenia, and many other neuropsychiatric diseases (11-14). One of these compounds was ultimately identified (13) as 3-(3-hydroxyphenyl)-3-hydroxypropionic acid (HPHPA). Subsequently, his discovery of high HPHPA in urine samples of children with autism was confirmed by research groups in Turkey (18), China (19), Italy (20,21), and Latvia (22). The Chinese study (19) indicated that elevated HPHPA was >96% specific for the diagnosis of autism. Shaw proposes (13,16) that this compound is one of the major causes of both autism and a variety of neuropsychiatric diseases such as schizophrenia, Parkinson’s disease, depression, anorexia nervosa, and many others.  

Shaw proposes that HPHPA and other phenols from Clostridia species inactivates a key enzyme called dopamine-beta-hydroxylase (DBH) in the brain and peripheral nervous system but that genetic deficiencies of this enzyme cause diseases like autism and many other neurological diseases (17). The DBH enzyme converts the neurotransmitter dopamine to norepinephrine, leading to excessive dopamine. At high concentrations dopamine causes severe oxidative stress and converts to toxic byproducts that cause severe brain damage, leading to neuropsychiatric diseases. Shaw’s research on HPHPA is presented in detail in the book Integrative Therapies for Depression (16).  Shaw is also responsible for the formation of the scientific group and conference “Integrative Medicine for Mental Health” (IMMH) which was founded to delineate and treat the underlying causes of neuropsychiatric illnesses.

Great Plains Laboratory, Inc.

After starting the Great Plains Laboratory, Shaw published two books on the underlying causes of autism (14,15) including: genetic factors, mitochondrial dysfunction, nutritional deficiencies such as folate and cholesterol deficiencies, food allergies, abnormal intestinal flora, toxic chemical exposures, immune deficiencies, mold exposure and others.  Shaw proposed (23) that acetaminophen toxicity is one of the major factors leading to increased rates of autism, asthma, and attention deficit. His theory is consistent with a significant number of other studies (24-32). In 2022, a lawsuit alleging that acetaminophen was a cause of autism and attention deficit was filed (33). In the same year, 18 such cases were consolidated into a class action multi-district litigation, which subsequently added an additional 48 cases. The increase in the rates of autism, asthma, and attention deficit started with the substitution of acetaminophen (paracetamol) for baby aspirin because of a concern about Reye’s syndrome. In response to a Johnson and Johnson criticism (a major Tylenol producer) that proof of his theory would require a double-blind study, Shaw states that such a double-blind study would be unlikely to ever be done because parents would not want to subject their healthy children to the drug.   

Shaw published the first case study (34) linking autism with exposure to the weedkiller glyphosate and is preparing a much larger study to determine if this chemical may be a major cause of autism. Glyphosate kills normal intestinal bacteria and has been shown to increase Clostridia in animals and agricultural fields. Two of the three children with autism in Shaw’s study on triplets exposed to glyphosate from their corn tortillas had very high glyphosate and high clostridia metabolites in their urine samples (34)

Shaw started the commercial laboratory, The Great Plains Laboratory, Inc in 1996 and served as its laboratory director for 25 years. The laboratory has continuously operated in CLIA (federal group regulating laboratories) compliance since that date. He obtained a US patent (35) for his discovery of the abnormal metabolites found in urine samples of children with autism. The Great Plains Laboratory, grew to offer a variety of tests for the medical community such as food and inhalant allergies, opiate peptides in urine, organic acids, glyphosate, mycotoxins, and toxic chemicals. Shaw expanded its services to provide education, consultation, and testing to physicians in most of the countries of the world. The laboratory was sold in 2021 after which Shaw remained an employee.

Shaw was the recipient of the 2013 award for outstanding research in child brain research by the International Academy of Child Brain Research for his research in the field of autism. In 2021 Shaw was awarded the Jonathan Forman Award by the American Association of Environmental Medicine for his outstanding contributions to the field of Environmental Medicine. In 2022, Shaw received the Herbert J. Rinkel Award from the American Association of Environmental Medicine for his contributions in teaching in the field of environmental medicine. Shaw has been the keynote speaker at the National Autism Society of America National Meeting, the National Meeting of the American Association for Environmental Medicine, and the National Meeting of the American Academy for the Advancement of Medicine, the Pan American Allergy Association, The American Academy of Anti-Aging Medicine, and many others. He has spoken to numerous medical groups and has provided medical training in virtually every state in the United States and in most of the developed countries of the world in approximately 500 scientific presentations. He was personally contacted and congratulated for his research work on autism by the office of then Vice-President Al Gore and was greeted by the personal physician of Mao Tse-tung during a speaking tour at Chinese medical schools and other institutions.

In 2020, Shaw and Sidney Baker MD published a case study (36) of a complete recovery from autism after treatment with the antifungal agent itraconazole of a child with autism who had high levels of compounds associated with mold growth. These compounds markedly decreased after antifungal treatment and the child recovered completely. The child has continued to be symptom-free several years after his recovery. 

Wikipedia Distortion of the Facts in Article About Shaw

Wikipedia is sometimes useful but is also subject to misinformation in that anyone can print anonymous incorrect, biased, or invalid information that is difficult to correct. In the Wikipedia essay about William Shaw PhD, the article misinformation was changed 3 times by his staff and then changed back to the false information by anonymous Wikipedia “editors”, after which the incorrect information was “locked”, presumably to prevent further corrections by Shaw’s team.

Below is some of the Wikipedia slanted information:

Wikipedia: “William Shaw became focused on autism in 1993 and has claimed that acetaminophen may be a major cause of autism. Nevertheless, as of 2017, there still was no good evidence to claim that acetaminophen caused autism.”

Shaw : As noted in his published article (23), there was plenty of proof that acetaminophen was a contributing cause of autism, and many references were cited. The accuracy of the article was confirmed by a large John Hopkins study (46) that showed “Cord biomarkers of fetal exposure to acetaminophen were associated with significantly increased risk of childhood ADHD and ASD in a dose-response fashion. Our findings support previous studies regarding the association between prenatal and perinatal acetaminophen exposure and childhood neurodevelopmental risk and warrant additional investigations.” The evidence was so compelling that lawsuits against the makers of acetaminophen have been launched (47).

Wikipedia: “Shaw has also alleged without credible scientific evidence that yeast infections cause autism. He was accused of "exploit[ing] the parents' understandable and desperate search for a cause of their children's autism."

Shaw: The reference cited by Wikipedia is an article about a sippy cup lawsuit brought by a parent and their lawyer who alleged that the sippy cup was contaminated with Candida. He had nothing to do with the lawsuit except for saying that the urine organic acid test of the child indicated the presence of Candida metabolite. He never stated that the sippy cup caused the Candida problem or the child’s autism. How is stating the result of a lab test “exploit[ing] the parents' understandable and desperate search for a cause of their children's autism."? The article is slanted in such a way that he appears to be the instigator or a partner to the “sippy cup” lawsuit. He has devoted a good portion of his life to assisting people with autism and their families in identifying and understanding potential causes and treatments that reduce the symptoms of autism. In each and every case, he ensured that his information is supported by science.

Furthermore, a number of articles connecting Candida and autism have been published, three by Shaw (10-12) and others from around the world (37-40).

Wikipedia: “Shaw has endorsed dangerous and discredited chelation treatments for autism.”

Shaw: Shaw has never recommended chelation treatment for autism unless metal testing revealed abnormal elevations of toxic metals. Beneficial results of chelation treatment for autism and hyperactivity (common in autism) have been published for autism in peer-reviewed medical journals (41-45).

Recommendations Regarding Wikipedia and Quack Watch

Do not contribute to Wikipedia fund raising until Wikipedia requires that the authors of different articles be completely identified. This is very important when dealing with controversial issues. If material is deliberately defamatory, the authors of such material should not remain anonymous but should be made accountable, especially if they are an agent of a major corporation or the government of any country. The Wikipedia user needs to know the biases or conflicts of interest that the Wikipedia editor may have.

If there is a difference of opinion, all opinions should be included in the article, rather than “locking out” different opinions.

Quack Watch and Wikipedia should list all of their financial contributors, so the reader is aware of any conflicts of interest involved in their assessments.

References

  1. Nino, H.W., and Shaw, W. 1976. “Nutritional Biochemistry”. In Fundamentals of Chemistry, Second Edition.  W.B.  Saunders Co., Philadelphia, Pennsylvania.

  2. Moss, C., Hatheway, C.,Lambert, M., McCroskey, L 1980. Production of Phenylacetic and Hydroxyphenylacetic Acids by Clostridium botulinum Type G. Journal of Clinical Microbiology  11(6):743-745. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC273498/pdf/jcm00179-0223.pdf

  3. Elsden SR, Hilton MG, Waller JM. The end products of the metabolism of aromatic amino acids by Clostridia. Arch Microbiol. 1976 Apr 1;107(3):283-8. doi: 10.1007/BF00425340. https://pubmed.ncbi.nlm.nih.gov/1275638/

  4. Shaw, W., Smith, J., and Spierto, F.W.  1977. Linearization of data for saturation-type competitive protein binding assay and radioimmunoassay. Clin. Chim. Acta 76:15. https://www.ncbi.nlm.nih.gov/pubmed/852137

  5. Shaw, W.  1982.  Theoretical and mathematical conditions of use of linearization methods for saturation-type radioassay data. Clin.  Chem. 28(5): 1196. http://clinchem.aaccjnls.org/content/clinchem/28/5/1196.full.pdf

  6. Shaw, W., Powell, M.K., Hubert, I. L., and Spierto, F. W. 1976. A comparison of   the interference of fatty acids in the competitive protein binding radioassay and radioimmunoassay for serum T4. Clin. Chim. Acta 73:25. https://www.ncbi.nlm.nih.gov/pubmed/?term=1000836

  7. Shaw W, Hubert IL, Spierto FW. Interference of fatty acids in the competitive protein-binding assay for serum thyroxine. Clin Chem. 1976 May;22(5):673-8. https://www.ncbi.nlm.nih.gov/pubmed/1261016

  8. Shaw, W. 1985. Possible role of lysolecithins and nonesterified fatty acids in the pathogenesis of Reye’s syndrome, sudden infant death syndrome, acute pancreatitis, and diabetic ketoacidosis. Clin. Chem. 31:1109. http://clinchem.aaccjnls.org/content/clinchem/31/7/1109.full.pdf

  9. Shaw, W. 1988.  Possible synergistic effects of nonesterified fatty acids and lysolecithins, a toxic methionine metabolite, and ammonia in the production of hepatic encephalopathy and schizophrenia.   Orthomolecular Medicine 3: 87. https://isom.ca/wp-content/uploads/2020/01/JOM_1988_03_3_02_Possible_Synergistic_Effects_of_Nonesterified_Fatty-.pdf http://orthomolecular.org/library/jom/1988/pdf/1988-v03n03-p087.pdf

  10. Shaw, W., Kassen, E., and Chaves, E. 1995. Increased urinary excretion of analogs of Krebs cycle metabolites and arabinose in two brothers with autistic features. Clin. Chem. 41(8): 1094-1104. http://clinchem.aaccjnls.org/content/clinchem/41/8/1094.full.pdf

  11. Shaw, W., Kassen, E., and Chaves, E. Assessment of antifungal drug therapy in autism by measurement of suspected microbial metabolites in urine with gas chromatography-mass spectrometry. Clinical Practice of Alternative Medicine: 15-26, 2000. https://www.researchgate.net/publication/238069252_Assessment_of_Antifungal_Drug_Therapy_in_Autism_by_Measurement_of_Suspected_Microbial_Metabolites_in_Urine_with_Gas_Chromatography-Mass_Spectrometry

  12. W Shaw, J Baptist, D Geenens. Immunodeficiency, Gastrointestinal Candidiasis, Wheat and Dairy Sensitivity, Abnormal Urine Arabinose, and Autism: A Case Study. North America J. Med Sci 3:1-8,2010 https://www.scribd.com/document/258750196/candida-immunodeficiency

  13. Shaw W. Increased urinary excretion of a 3-(3-hydroxyphenyl)-3-hydroxypropionic acid (HPHPA), an abnormal phenylalanine metabolite of Clostridia spp. in the gastrointestinal tract, in urine samples from patients with autism and schizophrenia. Nutr Neurosci. 2010 Jun; 13(3):135-43. https://www.ncbi.nlm.nih.gov/pubmed/20423563

  14. Shaw, W., Rimland, B., Seemon, B., Scott, P., and Seroussi, K. 2002. Biological Treatments for Autism and PDD. https://www.amazon.com/Biological-Treatments-Autism-William-Shaw/dp/0966123859

  15. Shaw, W. 2009. Autism, Beyond the Basics. Sunflower Press. 11813 W 77th St, Lenexa, KS 66214 https://www.amazon.com/Autism-Beyond-Basics-William-Shaw/dp/0966123867

  16. Shaw, W.  Clostridia bacteria in the gastrointestinal tract as a major cause of depression and other neuropsychiatric disorders. Role of Clostridia metabolites 3-(3-hydroxyphenyl)-3-hydroxypropionic acid (HPHPA) and 4-cresol in the alteration of dopamine and norepinephrine metabolism. In: Integrative Psychiatry for Depression: Redefining Models for Assessment, Treatment, and Prevention of Mood Disorders. James Greenblatt and Kelly Brogan, Editors. Taylor and Francis, N.Y., N.Y., 2015 https://www.amazon.com/Integrative-Therapies-Depression-Redefining-Assessment/dp/1498702295 

  17. Shaw, W. Dopamine excess and/or norepinephrine and epinephrine deficiency in autistic patients due to prenatal and/or postnatal deficiency of dopamine beta-hydroxylase. J. Orthomolecular Medicine 36 (1):1-25, 2021. https://isom.ca/article/dopamine-excess-and-or-norepinephrine-and-epinephrine-deficiency-in-autistic-patients-due-to-prenatal-and-or-postnatal-deficiency-of-dopamine-beta-hydroxylase/

  18. Recep Kesli, Cem Gokcen, Ufuk Bulug, and Yuksel Terzi Investigation of the relation between anaerobic bacteria genus Clostridium and late onset autism etiology in children. Journal of Immunoassay and Immunochemistry, 35:101–109, 2014. https://pubmed.ncbi.nlm.nih.gov/24063620/

  19. Xiyue Xiong, Dan Liu, Yichao Wang, Ting Zeng, and Ying Peng.Urinary 3-(3-Hydroxyphenyl)-3-hydroxypropionic Acid, 3-Hydroxyphenylacetic Acid, and 3-Hydroxyhippuric Acid Are Elevated in Children with Autism Spectrum Disorders. BioMed Research International Volume 2016, Article ID 9485412, 8 pages. http://dx.doi.org/10.1155/2016/9485412

  20. Noto A, Fanos V, Barberini L, Grapov D, Fattuoni C, Zaffanello M, Casanova A, Fenu G, De Giacomo A, De Angelis M, Moretti C, Papoff P, Ditonno R, Francavilla R. The urinary metabolomics profile of an Italian autistic children population and their unaffected siblings. J Matern Fetal Neonatal Med. 2014 Oct;27 Suppl 2:46-52. doi: 10.3109/14767058.2014.954784. https://pubmed.ncbi.nlm.nih.gov/25284177/ 

  21. Mussap M, Siracusano M, Noto A, Fattuoni C, Riccioni A, Rajula HSR, Fanos V, Curatolo P, Barberini L, Mazzone L. The Urine Metabolome of Young Autistic Children Correlates with Their Clinical Profile Severity. Metabolites. 2020 Nov 23;10(11):476. doi: 10.3390/metabo10110476 https://pubmed.ncbi.nlm.nih.gov/33238400/ 

  22. Daneberga Z, Nakazawa-Miklasevica M, Berga-Svitina E, Murmane D, Isarova D, Cupane L, Masinska M, Nartisa I, Lazdane A, Miklasevics E. Urinary organic acids spectra in children with altered gut microbiota composition and autistic spectrum disorder. Nord J Psychiatry. 2021 Dec 22:1-7. doi: 10.1080/08039488.2021.2014954. https://pubmed.ncbi.nlm.nih.gov/34935590/

  23. Shaw W. Evidence that Increased Acetaminophen use in Genetically Vulnerable Children Appears to be a Major Cause of the Epidemics of Autism, Attention Deficit with Hyperactivity, and Asthma. Journal of Restorative Medicine 2:1-16, 2013. http://jeffreydachmd.com/wp-content/uploads/2015/05/Tylrnol_Acetaminophen_Glutathione__Autism_William-Shaw_2013.pdf

  24. Claudia B. Avella-Garcia,Jordi Julvez, Joan Fortuny,Cristina Rebordosa, Raquel Garcıa-Esteban, Isolina Riano Gaan,Adonina Tardon, Clara L. Rodrıguez-Bernal, Carmen Iniguez, Ainara Andiarena, Loreto Santa-Marina and Jordi Sunyer. Acetaminophen use in pregnancy and neurodevelopment: attention function and autism spectrum symptoms. International Journal of Epidemiology, 2016, 1–9 doi: 10.1093/ije/dyw115 https://www.researchgate.net/publication/304577447

  25. Ghanizadeh A. Acetaminophen may mediate oxidative stress and neurotoxicity in autism. Med Hypotheses 2012 ;78:351. http://www.medical-hypotheses.com/article/S0306-9877(11)00581-0/abstract

  26. Liew Z, Ritz B, Rebordosa C, Lee P-C, Olsen J. Acetaminophen use during pregnancy, behavioral problems, and hyperkinetic disorders. JAMA Pediatr. 2014;168:313–20. http://jamanetwork.com/journals/jamapediatrics/fullarticle/1833486

  27. Brandlistuen RE, Ystrom E, Nulman I, Koren G, Nordeng H. Prenatal paracetamol exposure and child neurodevelopment: a sibling-controlled cohort study. Int J Epidemiol 2013;42: 1702–13.  http://jamanetwork.com/journals/jamapediatrics/fullarticle/1833486

  28. Bauer AZ, Kriebel D. Prenatal and perinatal analgesic exposure and autism: an ecological link  Environ Health 2013;12:41. http://ehjournal.biomedcentral.com/articles/10.1186/1476-069X-12-41

  29. Thompson JMD, Waldie KE, Wall CR, Murphy R, Mitchell EA. Associations between acetaminophen use during pregnancy and ADHD symptoms measured at ages 7 and 11 years. PLoS One 2014 ;9:e108210. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0108210

  30. Good P. Did acetaminophen provoke the autism epidemic? Altern Med Rev 2009;14: 364–72. www.altmedrev.com/publications/14/4/364.pdf

  31. Schultz ST, Klonoff-Cohen HS, Wingard DL,Akshoomoff NA, Macera CA, Ji M. Acetaminophen (paracetamol) use, measles-mumps rubella vaccination, and autistic disorder: The results of a parent survey.Autism. 2008;12 (3):293–307. http://onlinelibrary.wiley.com/doi/10.1111/j.1742-7843.2011.00767.x/references

  32. Schultz ST. Can autism be triggered by acetaminophen activation of the endocannabinoid system? Acta Neurobiol Exp. 2010;70(2):227–31. https://www.researchgate.net/publication/45185683_Can_autism_be_triggered_by_ acetaminophen_activation_of_the_endocannabinoid_system

  33. https://acetaminophen.autism-lawsuits.org/?utm_medium=paid_search&utm_source=google&utm_campaign=autism-lawsuits-ll-ops-221005&utm_content=acetaminophen&utm_term=acetaminophen%20autism%20lawsuit&gclid=CjwKCAiAjs2bBhACEiwALTBWZeTu5U3bVSmWmQA2aSwHj8ukU2RRk2JE2feC1PFgSs-1ZGSL6we5FhoCd3sQAvD_BwE

  34. Shaw, W.  Elevated urinary glyphosate and Clostridia metabolites with altered dopamine metabolism in triplets with autistic spectrum disorder or suspected seizure disorder: a case study. Integrative Medicine; a Clinical Journal. Feb-March 2017 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5312745/

  35. Diagnosis of autism and treatment therefor. https://uspto.report/patent/grant/5686311

  36. Baker, S. and Shaw, W. Case study: Rapid complete recovery from an autism spectrum disorder after treatment of Aspergillus with the antifungal drugs itraconazole and Sporanox. Integrative Medicine 19(4) 20- 27, 2020. https://pubmed.ncbi.nlm.nih.gov/33132781/

  37. Hughes HK, Ashwood P. Anti-Candida albicans IgG Antibodies in Children With Autism Spectrum Disorders. Front Psychiatry. 2018 Nov 26;9: 627. doi: 10.3389/fpsyt.2018.00627. https://pubmed.ncbi.nlm.nih.gov/30534090/ 

  38. Ekiel A, Aptekorz M, Kazek B, Wiechuła B, Wilk I, Martirosian G. Mikroflora jelitowa dzieci autystycznych [Intestinal microflora of autistic children]. Med Dosw Mikrobiol. 2010;62(3):237-43. Polish. https://pubmed.ncbi.nlm.nih.gov/21114016/ 

  39. Kantarcioglu AS, Kiraz N, Aydin A. Microbiota-Gut-Brain Axis: Yeast Species Isolated from Stool Samples of Children with Suspected or Diagnosed Autism Spectrum Disorders and In Vitro Susceptibility Against Nystatin and Fluconazole. Mycopathologia. 2016 Feb;181(1-2):1-7. doi: 10.1007/s11046-015-9949-3. Epub 2015 https://pubmed.ncbi.nlm.nih.gov/26442855/

  40. Strati F, Cavalieri D, Albanese D, De Felice C, Donati C, Hayek J, Jousson O, Leoncini S, Renzi D, Calabrò A, De Filippo C. New evidences on the altered gut microbiota in autism spectrum disorders. Microbiome. 2017 Feb 22;5(1):24. doi: 10.1186/s40168-017-0242-1. https://pubmed.ncbi.nlm.nih.gov/28222761/ 

  41. David OJ, Hoffman SP, Clark J, Grad G, Sverd J. The relationship of hyperactivity to moderately elevated lead levels. Arch Environ Health. 1983 Nov-Dec;38(6):341-6. doi: 10.1080/00039896.1983.10545818. https://pubmed.ncbi.nlm.nih.gov/6667034/ 

  42. Blaurock-Busch E, Amin OR, Dessoki HH, Rabah T. Toxic Metals and Essential Elements in Hair and Severity of Symptoms among Children with Autism. Maedica (Bucur). 2012 Jan;7(1):38-48. https://pubmed.ncbi.nlm.nih.gov/23118818/ 

  43. Adams JB, Audhya T, McDonough-Means S, Rubin RA, Quig D, Geis E, Gehn E, Loresto M, Mitchell J, Atwood S, Barnhouse S, Lee W. Toxicological status of children with autism vs. neurotypical children and the association with autism severity. Biol Trace Elem Res. 2013 Feb;151(2):171-80. doi: 10.1007/s12011-012-9551-1. Epub 2012 Nov 29. https://pubmed.ncbi.nlm.nih.gov/23192845/ 

  44. Yassa HA. Autism: a form of lead and mercury toxicity. Environ Toxicol Pharmacol. 2014 Nov;38(3):1016-24. doi: 10.1016/j.etap.2014.10.005. Epub 2014 Nov 6. https://pubmed.ncbi.nlm.nih.gov/25461563/ 

  45. Adams JB, Baral M, Geis E, Mitchell J, Ingram J, Hensley A, Zappia I, Newmark S, Gehn E, Rubin RA, Mitchell K, Bradstreet J, El-Dahr JM. The severity of autism is associated with toxic metal body burden and red blood cell glutathione levels. J Toxicol. 2009; 2009:532640. doi: 10.1155/2009/532640. Epub 2009 Aug 26. https://pubmed.ncbi.nlm.nih.gov/20107587/ 

  46. Ji Y, Azuine RE, Zhang Y, Hou W, Hong X, Wang G, Riley A, Pearson C, Zuckerman B, Wang X. Association of Cord Plasma Biomarkers of In Utero Acetaminophen Exposure With Risk of Attention-Deficit/Hyperactivity Disorder and Autism Spectrum Disorder in Childhood. JAMA Psychiatry. 2020 Feb 1;77(2):180-189. doi: 10.1001/jamapsychiatry.2019.3259. PMID: 31664451; PMCID: PMC6822099. https://pubmed.ncbi.nlm.nih.gov/31664451/ 

  47. https://lawsuits.org/tylenol-autism/?utm_medium=paid_search&utm_source=google&utm_campaign=lawsuits-mt-ops-221201&utm_content=mt-lawsuits&utm_term=class%20action%20lawsuit%20tylenol%20autism&gclid=Cj0KCQiA1sucBhDgARIsAFoytUtQdE24z-cbKhj7H8_4MFFD5iZ8bFGt9bvY3PJ-xJFqomziAFKzB8AaAjtKEALw_wcB