Acid glycosaminoglycan (aGAG) excretion is increased in children with autism spectrum disorder, and it can be controlled by diet
- 622 Downloads
Autism research continues to receive considerable attention as the options for successful management are limited. The understanding of the autism spectrum disorder (ASD) etiology has now progressed to encompass genetic, epigenetic, neurological, hormonal, and environmental factors that affect outcomes for patients with ASD. Glycosaminoglycans (GAGs) are a family of linear, sulfated polysaccharides that are associated with central nervous system (CNS) development, maintenance, and disorders. Proteoglycans (PG) regulate diverse functions in the central nervous system. Heparan sulfate (HS) and chondroitin sulfate (CS) are two major GAGs present in the PGs of the CNS. As neuroscience advances, biochemical treatments to correct brain chemistry become better defined. Nutrient therapy can be very potent and has minimal to no side effects, since no molecules foreign to the body are needed. Given GAGs are involved in several neurological functions, and that its level can be somewhat modulated by the diet, the present study aimed to evaluate the role of GAGs levels in ASD symptoms. Both tGAG and its different fractions were evaluated in the urine of ASD and healthy control childrens. As levels differed between groups, a second trial was conduted evaluating if diet could reduce tGAG levels and if this in turn decrease ASD symptoms. The present study found that tGAG concentration was significantly higher in the urine of children with ASD compared to healthy control children and this was also evident in all GAG fractions. Within groups (controls and ASD), no gender differences in GAG excretion were found. The use of a 90 days elimination diet (casein-free, special carbohydrates, multivitamin/mineral supplement), had major effects in reducing urinary tGAG excretion in children with ASD.
KeywordsAutism Glycosaminoglycans Proteoglycans Neurodevelopment disorders Epigenetics Nutrition
The authors thank the children with ASD and their parents for their consensus, collaboration, and hard work as participants in this research study. Further, the physicians Denes Kovendi and Eva Satorhegyi are thanked for help with diagnosis.
Compliance with ethical standards
Conflict of interest
The authors declare no potential conflicts of interest with respect to the authorship, and/or publication of this article.
All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.
- 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 (2011) Nutritional and metabolic status of children with autism vs. neurotypical children, and the association with autism severity. Nutr Metab (Lond) 8:34. doi: 10.1186/1743-7075-8-34 CrossRefPubMedCentralGoogle Scholar
- APA - American Psychiatric Association (1994) Diagnostic and statistical manual of mental disorders: DSM-IV, 4th edn. American Psychiatric Association, WashingtonGoogle Scholar
- Bjørklund G (2013) The role of zinc and copper in autism spectrum disorders. Acta Neurobiol Exp (Wars) 73:225–236Google Scholar
- Blumberg SJ, Bramlett MD, Kogan MD, Schieve LA, Jones JR (2013) Changes in prevalence of parent-reported autism spectrum disorder in school-aged U.S. children: 2007 to 2011–2012. National health statistics reports; no 65. National Center for Health Statistics, HyattsvilleGoogle Scholar
- CDC - Centers for Disease Control and Prevention (2012) Prevalence of autism spectrum disorders–autism and developmental disabilities monitoring network, 14 sites, United States, 2008. MMWR Surveill Summ 61(3):1–19Google Scholar
- James SJ, Melnyk S, Jernigan S, Cleves MA, Halsted CH, Wong DH, Cutler P, Bock K, Boris M, Bradstreet JJ, Baker SM, Gaylor DW (2006) Metabolic endophenotype and related genotypes are associated with oxidative stress in children with autism. Am J Med Genet B Neuropsychiatr Genet 141B:947–956CrossRefPubMedPubMedCentralGoogle Scholar
- Macedoni-Lukšič M, Gosar D, Bjørklund G, Oražem J, Kodrič J, Lešnik-Musek P, Zupančič M, France-Štiglic A, Sešek-Briški A, Neubauer D, Osredkar J (2015) Levels of metals in the blood and specific porphyrins in the urine in children with autism spectrum disorders. Biol Trace Elem Res 163:2–10. doi: 10.1007/s12011-014-0121-6 CrossRefPubMedGoogle Scholar
- Rusiecki JA, Baccarelli A, Bollati V, Tarantini L, Moore LE, Bonefeld-Jorgensen EC (2008) Global DNA hypomethylation is associated with high serum-persistent organic pollutants in Greenlandic Inuit. Environ Health Perspect 116:1547–1552. doi: 10.1289/ehp.11338 CrossRefPubMedPubMedCentralGoogle Scholar