Richard E. Frye

From Wikipedia, the free encyclopedia
Richard Eugene Frye
Alma materLong Island University C. W. Post Campus, Drexel University
Known forResearching possible environmental causes of autism, as well as the potential use of supplements to treat it.
Scientific career
FieldsChild psychiatry
InstitutionsUniversity of Arkansas for Medical Sciences, University of Texas Health Science Center at Houston
ThesisAn exploration of methods for evaluating the usefulness of new and existing aerodynamic equations in detecting nasal airway disease (1992)

Richard Eugene Frye is an American autism researcher and associate professor at Arizona Children's Hospital in Phoenix, and formerly of the University of Arkansas for Medical Sciences's department of pediatrics,[1] as well as the Director of the Autism Multispecialty Clinic at Arkansas Children’s Hospital.[2] Frye was formerly a faculty member at the University of Texas Health Science Center at Houston's division of child and adolescent neurology.[3]

Education[]

Frye received his bachelor's degree from Long Island University C. W. Post Campus in 1986 in psychobiology. Five years later, he obtained his M.S. from Drexel University in biomedical science/biostatistics. Frye went on to obtain his PhD and MD degrees both in 1998, and both from Georgetown University. From 1998 to 2000 Frye completed a residency in pediatrics at Jackson Memorial Hospital, before traveling to Children's Hospital Boston (CHB) to complete another residency, this time in pediatric neurology. After completing his residencies, he completed a research fellowship in behavioral neurology and learning disabilities, also at CHB, from 2003 to 2005. From 2004 to 2005 Frye completed another research fellowship, this time at Boston University in psychology.

Research[]

Frye's most cited paper is one published in 1990, which studied the effects of cigarette smoking on the sense of smell.[4] In fact, much of Frye's early research focused on olfaction.[5][6]

Frye's more recent research focuses on the potential environmental causes of autism, as well as physiological abnormalities that have been observed in autistic individuals. Specifically, he and his co-authors, who include Dan Rossignol, have concluded that it is possible that autistic individuals suffer from immune dysregulation and oxidative stress, as well as that mitochondrial dysfunction is more common in such individuals than in the general population.[7][8] In addition, Frye's research has concluded that autism may be caused by exposure to toxicants.[9] Frye has also published research on the use of dietary supplements as autism treatments, including melatonin[10] and tetrahydrobiopterin,[11] and recently coauthored a review regarding treatments for children with both autism and seizures, which concluded that "limited evidence is available on the effectiveness of treatments for seizures in children with autism." However, Frye also said that this paper "...demonstrates that certain treatments could be beneficial for treating both autism symptoms and seizures at the same time."[12][13] Another of Frye's studies concluded that many autistic children have abnormal levels of gut bacteria, and that these children exhibit abnormal energy metabolism as a result.[14][15] Some have speculated that the results of this research "could create blood tests for early screening of the condition [i.e. autism]."[16] In 2016, Frye contributed the foreword to a medical memoir of autistic siblings with abnormal gut bacteria and related biomarkers.[17]

Selected publications[]

  • Poling, J. S.; Frye, R. E.; Shoffner, J.; Zimmerman, A. W. (2006). "Developmental Regression and Mitochondrial Dysfunction in a Child with Autism". Journal of Child Neurology. 21 (2): 170–172. doi:10.1177/08830738060210021401. PMC 2536523. PMID 16566887.
  • Frye, R. E.; Rossignol, D. A. (2011). "Mitochondrial Dysfunction Can Connect the Diverse Medical Symptoms Associated with Autism Spectrum Disorders". Pediatric Research. 69 (5 Part 2): 41R. doi:10.1203/PDR.0b013e318212f16b. PMC 3179978. PMID 21289536.
  • Frye, R. E.; Sequeira, J. M.; Quadros, E. V.; James, S. J.; Rossignol, D. A. (2012). "Cerebral folate receptor autoantibodies in autism spectrum disorder". Molecular Psychiatry. 18 (3): 369–381. doi:10.1038/mp.2011.175. PMC 3578948. PMID 22230883.

References[]

  1. ^ "Richard E. Frye". University of Arkansas for Medical Sciences website. Retrieved 12 October 2013.
  2. ^ Richard Frye MD PhD
  3. ^ "Richard E. Frye". University of Texas Health Science Center at Houston website. Archived from the original on 13 May 2013. Retrieved 12 October 2013.
  4. ^ Frye, R. E. (1990). "Dose-Related Effects of Cigarette Smoking on Olfactory Function". JAMA: The Journal of the American Medical Association. 263 (9): 1233–1236. doi:10.1001/jama.1990.03440090067028.
  5. ^ Doty, R. L.; Deems, D. A.; Frye, R. E.; Pelberg, R.; Shapiro, A. (1988). "Olfactory Sensitivity, Nasal Resistance, and Autonomic Function in Patients with Multiple Chemical Sensitivities". Archives of Otolaryngology–Head & Neck Surgery. 114 (12): 1422–1427. doi:10.1001/archotol.1988.01860240072027. PMID 2461210.
  6. ^ Doty, R. L.; Frye, R. E.; Agrawal, U. (1989). "Internal consistency reliability of the fractionated and whole University of Pennsylvania Smell Identification Test". Perception & Psychophysics. 45 (5): 381–384. doi:10.3758/BF03210709.
  7. ^ Rossignol, D. A.; Frye, R. E. (2011). "Mitochondrial dysfunction in autism spectrum disorders: A systematic review and meta-analysis". Molecular Psychiatry. 17 (3): 290–314. doi:10.1038/mp.2010.136. PMC 3285768. PMID 21263444.
  8. ^ Brooks, Megan (31 January 2011). "Mitochondrial Dysfunction Linked to Autism". Medscape. Retrieved 6 November 2013.
  9. ^ Rossignol, D. A.; Frye, R. E. (2011). "A review of research trends in physiological abnormalities in autism spectrum disorders: Immune dysregulation, inflammation, oxidative stress, mitochondrial dysfunction and environmental toxicant exposures". Molecular Psychiatry. 17 (4): 389–401. doi:10.1038/mp.2011.165. PMC 3317062. PMID 22143005.
  10. ^ Rossignol, D. A.; Frye, R. E. (2011). "Melatonin in autism spectrum disorders: A systematic review and meta-analysis". Developmental Medicine & Child Neurology. 53 (9): 783–92. doi:10.1111/j.1469-8749.2011.03980.x. PMID 21518346.
  11. ^ Frye, R. E.; Huffman, L. C.; Elliott, G. R. (2010). "Tetrahydrobiopterin as a novel therapeutic intervention for autism". Neurotherapeutics. 7 (3): 241–249. doi:10.1016/j.nurt.2010.05.004. PMC 2908599. PMID 20643376.
  12. ^ "New Recommendations on Treatments for Seizures in Autism". PR Newswire. 25 September 2013. Retrieved 12 October 2013.
  13. ^ Frye, Richard E.; Rossignol, Dan A. (September 2013). "A review of traditional and novel treatments for seizures in autism spectrum disorder: findings from a systematic review and expert panel". Frontiers in Public Health. 1 (31). doi:10.3389/fpubh.2013.00031. PMC 3859980. PMID 24350200.
  14. ^ Frye, R. E.; Melnyk, S.; MacFabe, D. F. (2013). "Unique acyl-carnitine profiles are potential biomarkers for acquired mitochondrial disease in autism spectrum disorder". Translational Psychiatry. 3 (1): e220–. doi:10.1038/tp.2012.143. PMC 3566723. PMID 23340503.
  15. ^ Staff (29 January 2013). "Study Reveals Link between Gut Bacteria and Autism". Scitech Daily. Retrieved 13 October 2013.
  16. ^ "Potential Blood Test Found To Detect Autism". Medical News Today. 30 January 2013. Retrieved 13 October 2013.
  17. ^ Noonan, Jennifer (2016). No Map to This Country. Da Capo Lifelong. ISBN 978-0-7382-1904-2.

External links[]

Retrieved from ""