Excessive Duplication ~ Narrow Focus ~ Wasted Funds ~ Future
Concerns, And Refocus
Autism science must diversify and refocus on understudied areas that impact autism, families. We know now that autism is epigenetic, creating chronic disease including; oxidative stress (neuron excitotoxicity), mitochondrial dysfunction, immune dysregulation/inflammation (immunoexcitotoxicity), decreased methylation, gastrointestinal disease, and salience network hyper connectivity (Rossignol, D., Frye, R., 2014; Anthes, E., 2013; Essa et al., 2013; Theoharides et al., 2013; Kang, E., 2013; Gorrindo et al., 2013; Goh et al., 2014; Rose et al., 2012). Another important element to consider when thinking of autism research regards the 54% regression into the disorder ( the University of California - Davis Health System, 2011).
There is a need to document the recovery process that I have seen on a larger scale. A collection of the initial metabalomic, microbiomic, genomic, and epigenetic information among participates with the individualized therapeutic protocols is needed and than document how their biology changes and health improvements. This is what is needed to prove on a large-scale evidence based practices, which insurance companies, general practitioners, and policy makers could not ignore.
Researcher should organize multidisaplinary teams in fields, such as epigenetics, systems biology, gut microbiology, nutrigenomics, metabolomics, neuroscience, gastroenterology, environmental science, and immunology. Scientific areas of focus should include;
- Autism and gastrointestinal disease, and interventions
- Environmental impacts and regressive autism
- Autoimmune interventions
- Food allergies and autism
- Brian inflammation, and interventions
- Immunomodulatory therapies
- BioMed... BioMed... BioMed...
- Yeast and fungal infection among those with autism
- Identify environmental risk factors and facilitate prevention
- Novel biomarkers in autism
- Mast cells, microglia and brain inflammation
- T-cell count in autism
- Research the ASD GI tissue sample bank
- Mitochondrial disorders in autism
- Demographics and active surveillance
- Case management protocols
- Prospective research establishing a role of gluten as a triggering factor in neuro-psychiatric disorders.
A prospective mother-child cohort, following subjects prenatally until adulthood could be used to relate data from neurotoxic exposure to information on behavior development throughout life, focusing on behaviour indicative of ASD. In addition, human risk assessment of developmental neurotoxicity should be improved, using collected exposure data in addition to information from toxicological testing. The significance of differences in dose, time and length of exposure as well as critical windows should be determined with respect to exposure to neurotoxic compounds, especially during early development, focusing on mechanisms to elucidate possible outcomes. In this way, the relation between exposure to neurotoxicants early in life and the onset of ASD in childhood can be further unravelled (Quaak et al., 2013).
Congressional Oversight Committee Hearing
Essa et al. (2013). Excitotoxicity in the pathogenesis of autism. Neurotox Res. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/23065398
GAO. (2013). Federal autism activities: Better data and more coordination needed to help avoid the potential for unnecessary duplication. Untied States government Accountability Office. Retrieved from http://www.gao.gov/assets/660/659147.pdf
Goh et al. (2014). Mitochondiral dysfunction as a neurobiological subtype of autism spectrum disorder. JAMA Psychiatry. Retrieved from https://archpsyc.jamanetwork.com/article.aspx?articleid=1859135
Gorrindo et al. (2013). Enrichment of Elevated Plasma F2t-Isoprostane Levels in Individuals with Autism Who are Stratified by Presence of Gastrointestinal Dysfunction. PLoS ONE. Retrieved from http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0068444
HHS. (n.d.). About IACC. U.S. Department of Health & Human Services. Retrieved from http://iacc.hhs.gov/about/index.shtml
Kang, E. (2013). Prenatal inflammation linked to autism risk. National Institutes of Health. Retrieved from http://www.nih.gov/news/health/jan2013/niehs-24.htm
Quaak, I., Brouns, M., & Van de Bor, M. (2013). The dynamics of autism spectrum disorders: How neurotoxic compounds and neurotransmitters interact. International Journal of Environmental Research and Public Health. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3774444/
Rose et al. (2012). Evidence of oxidative damage and inflammation associated with low glutathione redox status in the autism brain. Translational Psychiatry. Retrieved from http://www.nature.com/tp/journal/v2/n7/full/tp201261a.html
Rossignol, D., Frye, R. (2014). Evidence linking oxidative stress, mitochondrial dysfunction, and inflammation in the brain of individuals with autism. Frontiers in Physiology. Retrieved from http://journal.frontiersin.org/Journal/10.3389/fphys.2014.00150/abstract
Theoharides et al. (2013). Focal brain inflammation and autism. Journal of Neuroinflammation. Retrieved from http://www.jneuroinflammation.com/content/10/1/46
University of California - Davis Health System. (2011). Boys with regressive autism, but not early onset autism, have larger brains then age-matched healthy counterparts, study finds. Science Daily. Retrieved from http://www.sciencedaily.com/releases/2011/11/111128152410.htm