William Shaw (autism researcher)

William Shaw is an American chemist, autism researcher and the founder of the Great Plains Laboratory, based in Lenexa, Kansas.

William Shaw Ph.D.
Alma materUniversity of Georgia, Medical University of South Carolina
Spouse(s)Yes
ChildrenFour sons, one stepson, one stepdaughter
Scientific career
FieldsAutism, clinical chemistry, toxicology, integrative healthcare
ThesisSome effects of maternal folate deficiency on the development of newborn mice (1971)

Education

Shaw has a bachelor's degree in biochemistry from the University of Georgia (1967) and a PhD from the Medical University of South Carolina (1971), also in biochemistry.

Career

After obtaining his PhD, Shaw spent six years working at the Centers for Disease Control and Prevention, where he was a supervisory research chemist and the chief of the radioimmunoassay laboratory. He then worked at Mercer University in Atlanta for a year as an assistant professor of pharmacy, before beginning a twelve-year stint at Smith Kline Beecham Clinical Laboratories, also in Atlanta. From 1991 until 1996, he worked at Children's Mercy Hospital in Kansas City, Missouri.[1] His laboratory, the Great Plains Laboratory, which he founded in 1996, specializes in metabolic and nutritional testing, particularly as it pertains to autism.[2] The Great Plains Laboratory is fully certified under the federally mandated Clinical Laboratory Improvement Amendments (CLIA) Clinical Laboratory Improvement Amendments (listed CLIA #17D0919496).[3]

Autism

He began studying autism in 1993, and has contended that acetaminophen may be a major cause of autism,[4][5] a hypothesis which he advanced in a paper published in 2013 in the Journal of Restorative Medicine.[6] Shaw has also contended that yeast infections may also cause autism, and has also endorsed chelation therapy as an autism treatment.[7] Another topic Shaw has researched has been the excretion of certain metabolites of clostridia bacteria, such as 3-(3-hydroxyphenyl)-3-hydroxypropionic acid. This research has concluded that autistic children excrete higher levels of this compound, and that antibiotics may therefore be useful as an autism treatment.[8][9][10] He is the author of "Biological Treatments for Autism and PDD," and gave a speech to the organization Parents Helping Parents in Santa Clara, California in 2008.[11]

gollark: Apiomemetically speaking, I favour "plastic cup" technology for practicality.
gollark: Idea: asynchronous heavforth.
gollark: lyric badhis purging of <#614050573167362079> made me sadlyric badhis poor management during his long reign drove me mad
gollark: Yes, anarchy is bad, bees will be deployed, etcetera.
gollark: No. Deploying counterbees.

References

  1. William Shaw's CV
  2. Kirk, Sally (2008). Hope for the Autism Spectrum. Jessica Kingsley Publishers. pp. 100.
  3. Clinical Laboratory Improvement Amendments (CLIA) Directory Listings Search
  4. Johnson, Heather (7 November 2013). "Researcher sees link between drug, autism". North Platte Telegraph. Retrieved 28 November 2013.
  5. Kirk, Hanno (16 April 2012). "Hanno Kirk: New link to autism epidemic". The Charleston Gazette. Retrieved 28 November 2013.
  6. 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
  7. Tsouderos, Trine (7 December 2009). "Chelation based on faulty premise". Los Angeles Times. Retrieved 28 November 2013.
  8. Shaw, W. (2010). "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". Nutritional Neuroscience. 13 (3): 135–143. doi:10.1179/147683010X12611460763968. PMID 20423563.
  9. James, Susan Donaldson (12 September 2013). "Anxiety In Your Head Could Come From Your Gut". ABC News. Retrieved 28 November 2013.
  10. Probiotic Diet as an Intervention
  11. Dr. William Shaw at the PHP website
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