B12 Vitamini Desteği Otizimli Çocukların Tedavisinde Etkili midir?

Yıl 2017, Cilt: 4 Sayı: 1, 15 - 27, 02.07.2017

Sümeyra Sevim , Aylin Ayaz

Öz

Otizm, tekrarlayan ve kısıtlı davranışlarla birlikte
sosyal iletişim kabiliyetinde bozukluklar ile karakterize kompleks
nörogelişimsel bir hastalıktır. Otizmin patojenik mekanizması henüz net olarak
açıklanamamaktadır. Ancak hücresel metilasyon kapasitesi ve antioksidan
kapasitesindeki değişiklikler metabolik bir bozukluk olduğunu göstermektedir. Bununla
birlikte yapılan çeşitli çalışmalarda özellikle bilişsel fonksiyonlar üzerinde
hayati rol oynayan folat ve B₁₂ vitaminin diyetle alımında ve plazma
seviyelerinde normal çocuklara göre değişiklik olduğuna dair kanıtlar
bulunmaktadır. Vitamin B₁₂, antioksidan sisteminde ve hücresel
metilasyonda rol alan önemli bir kofaktörtür. Bu nedenle otizmli çocukların
tedavisinde ve/veya çeşitli semptomların iyileştirilmesinde B₁₂ tedavisinin
etkin olabileceği düşünülmektedir. 

Anahtar Kelimeler

otizm, B12 vitamini, homosistein, metilasyon

Are B12 Vitamins Effective İn The Treatment Of Autistic Children?

Öz

Autism is a complex neurodevelopmental disorder
characterised by repetitive and restricted behaviors as well as social
communication behaviors. The pathogenetic
mechanism of autism has not yet been clarified. However, changes in cellular
methylation capacity and antioxidant capacity indicate a metabolic disorder.
After all there is evidence that diverse studies have shown that folate and vitamin B₁₂,
which play a crucial role in cognitive functions, are in dietary intake and
that plasma levels vary with normal children. Vitamin B₁₂ is an
important cofactor involved in antioxidant system and cellular methylation.
herefore, it is thought that B₁₂ therapy may be effective in the
treatment of autistic children and / or in the treatment of various symptoms.

Anahtar Kelimeler

autism, vitamin B12, homocysteine, methylation

Kaynakça

• Adams, J.B., Audhya, T., McDonough-Means, S., Rubin, R. A., Quig, D., Geis, E. ve diğerleri. (2011). Nutritional and metabolic status of children with autism vs. neurotypical children, and the association with autism severity. Nutrition & metabolism, 8(1), 1.
• Al-Farsi, Y.M., Waly, M.I., Deth, R.C., Al-Sharbati, M.M., Al-Shafaee, M., Al-Farsi, O. ve diğerleri. (2013). Low folate and vitamin B12 nourishment is common in Omani children with newly diagnosed autism. Nutrition, 29(3), 537-541.
• Ali, A., Waly, M.I., Al-Farsi, Y.M., Essa, M.M., Al-Sharbati, M.M., & Deth, R.C. (2011). Hyperhomocysteinemia among Omani autistic children: a case-control study. Acta Biochim Pol, 58(4), 547-551.
• Aponte, C.A., & Romanczyk, R.G. (2016). Assessment of feeding problems in children with autism spectrum disorder. Research in Autism Spectrum Disorders, 21, 61-72.
• Association, A.P., & Association, A.P. (1994). Diagnostic and statistical manual of mental disorders (DSM). Washington, DC: American psychiatric association, 143-147.
• Bent, S., & Hendren, R. (2015). Complementary and alternative treatments for autism part 1: evidence-supported treatments. AMA journal of ethics, 17(4), 369.
• Bent, S., & Hendren, R.L. (2010). Improving the prediction of response to therapy in autism. Neurotherapeutics, 7(3), 232-240.
• Bertoglio, K., Jill James, S., Deprey, L., Brule, N., & Hendren, R.L. (2010). Pilot study of the effect of methyl B12 treatment on behavioral and biomarker measures in children with autism. The Journal of Alternative and Complementary Medicine, 16(5), 555-560.
• Chauhan, A., Chauhan, V., Brown, W. T., & Cohen, I. (2004). Oxidative stress in autism: Increased lipid peroxidation and reduced serum levels of ceruloplasmin and transferrin-the antioxidant proteins. Life sciences, 75(21), 2539-2549.
• Coelho, D., Suormala, T., Stucki, M., Lerner-Ellis, J.P., Rosenblatt, D.S., Newbold, R.F. ve diğerleri. (2008). Gene identification for the cblD defect of vitamin B12 metabolism. New England Journal of Medicine, 358(14), 1454-1464.
• Cohen, D., Pichard, N., Tordjman, S., Baumann, C., Burglen, L., Excoffier, E. ve diğerleri. (2005). Specific genetic disorders and autism: clinical contribution towards their identification. Journal of autism and developmental disorders, 35(1), 103-116.
• Developmental, D.M.N.S.Y., & Investigators, P. (2014). Prevalence of autism spectrum disorder among children aged 8 years-autism and developmental disabilities monitoring network, 11 sites, United States, 2010. Morbidity and mortality weekly report. Surveillance summaries (Washington, DC: 2002), 63(2), 1.
• Fombonne, E. (2006). Past and Future Perspectives on Autism Epidemiology.
• Frustaci, A., Neri, M., Cesario, A., Adams, J.B., Domenici, E., Dalla Bernardina, B. ve diğerleri. (2012). Oxidative stress-related biomarkers in autism: systematic review and meta-analyses. Free Radical Biology and Medicine, 52(10), 2128-2141.
• Gilman, S. (2011). Neurobiology of disease: Academic Press.
• Hendren, R.L., James, S.J., Widjaja, F., Lawton, B., Rosenblatt, A., & Bent, S. (2016). Randomized, placebo-controlled trial of Methyl B12 for children with autism. Journal of child and adolescent psychopharmacology, 26(9), 774-783.
• Huguet, G., Ey, E., & Bourgeron, T. (2013). The genetic landscapes of autism spectrum disorders. Annual Review of Genomics and Human Genetics, 14:191–213.
• Howlin, P., Magiati, I., Charman, T., & MacLean, J., William E. (2009). Systematic review of early intensive behavioral interventions for children with autism. American journal on intellectual and developmental disabilities, 114(1), 23-41.
• James, S.J., Cutler, P., Melnyk, S., Jernigan, S., Janak, L., Gaylor, D.W. ve diğerleri. (2004). Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism. The American journal of clinical nutrition, 80(6), 1611-1617.
• Malhi, P., Venkatesh, L., Bharti, B., & Singhi, P. (2017). Feeding Problems and Nutrient Intake in Children with and without Autism: A Comparative Study. The Indian Journal of Pediatrics, 1-6.
• Malhotra, S., Subodh, B., Parakh, P., & Lahariya, S. (2013). Brief report: childhood disintegrative disorder as a likely manifestation of vitamin B12 deficiency. Journal of autism and developmental disorders, 43(9), 2207-2210.
• Moldin, S.O., & Rubenstein, J.L. (2006). Understanding autism: from basic neuroscience to treatment: CRC press.
• Pineles, S.L., Avery, R.A., & Liu, G.T. (2010). Vitamin B12 optic neuropathy in autism. Pediatrics, 126(4), 967-970.
• Postorino, V., Sanges, V., Giovagnoli, G., Fatta, L. M., De Peppo, L., Armando, M. ve diğerleri. (2015). Clinical differences in children with autism spectrum disorder with and without food selectivity. Appetite, 92, 126-132.
• Puig-Alcaraz, C., Fuentes-Albero, M., Calderón, J., Garrote, D., & Cauli, O. (2015). Increased homocysteine levels correlate with the communication deficit in children with autism spectrum disorder. Psychiatry research, 229(3), 1031-1037.
• Sandin, S., Lichtenstein, P., Kuja–Halkola, R., Larsson, H., Hultman, C.M., & Reichenberg, A. (2014). The familial risk of autism. JAMA, 311:1770–1777.
• Schmidt, R.J., Hansen, R.L., Hartiala, J., Allayee, H., Schmidt, L.C., Tancredi, D.J. ve diğerleri. (2011). Prenatal vitamins, one-carbon metabolism gene variants, and risk for autism. Epidemiology (Cambridge, Mass.), 22(4), 476.
• Yi, P., Melnyk, S., Pogribna, M., Pogribny, I.P., Hine, R.J., & James, S.J. (2000). Increase in plasma homocysteine associated with parallel increases in plasma S-adenosylhomocysteine and lymphocyte DNA hypomethylation. Journal of Biological Chemistry, 275(38), 29318-29323.