BY: DR. RICHARD BOLES; PUBLISHED MAY 6, 2020

KEY POINTS:

  1. Recent scientific advances have determined that there are multiple biological pathways that can predispose an individual toward Autism Spectrum Disorder, with combinations of variants leading to pathway abnormalities unique to each individual. 
  2. Many of these pathways are modifiable by therapy, especially by targeted nutrition.  Mitochondrial Energy Metabolism is one such key pathway. 
  3. Highly individualized genetic factors among Autism Spectrum Disorder cases suggest that therapy should consist of many different nutrients.  The success of using a combination of essential nutrients will be discussed. 

Autism is no longer an idiopathic disease. This powerful statement has been made possible by an explosion in research into the underlying genetic, biochemical, and neuro-structural factors that can lead to autism. Autism is a behavioral outcome caused by a combination of genetic variants in hundreds to thousands of genes that are important in maintaining homeostasis regarding brain morphogenesis, physiology, and/or biochemistry. While the same can be said for intellectual disability, epilepsy, and many other neurodevelopmental conditions, the autistic phenotype is apparent when homeostasis fails in terms of brain connections important in highly integrative tasks such as language and social behavior.

Most autism-savvy families and clinicians are aware of the scientific research that supports the power of nutrition in autism. Nutritional interventions such as gluten-free, antioxidants, and microbiome-related are familial tools of progressive management. However, few understand how the emerging picture of what autism fundamentally is affects efforts and prospects for improved treatment. Does the new science suggest that autism is genetic, immobile, and untreatable, and that nutritional therapy is wishful thinking? Certainly not!  There are many ways in which the new science of autism actually informs favorably on treatment, in particular to the targeted use of nutrition. Many of the pathways in which homeostasis is disrupted leading to autism are treatable!

Mitochondrial energy metabolism is a key treatable pathway, and this lecture will discuss the evidence, clinical signs, diagnostic testing, and treatment; most of the latter is nutritional. Many other metabolic pathways are also implemented in autism pathogenesis, and can be readily treatable by nutritional means. Beyond metabolism, additional autism-related pathways that are amendable to nutritional interventions involve ion channels, neurotransmitters, receptors, and axonal transport. While many people with autism have poor and/or highly-restricted diets, nutritional therapy goes beyond providing dietary supplementation. Extremely-high dosing of targeted nutrients are used to push key metabolic pathways in the direction consistent with healing.

The extraordinary polygenic basis of autism results in extreme biological heterogeneity. No two patients share exactly the same factors, even if they are siblings. This situation leads to two realities in modern nutritional therapy for autism: First, is the utility of in-depth characterization of the underlying genetics and biology in each individual patient, followed by personalized therapy. This characterization will be addressed throughout the lecture in mini-case reports involving genetic testing following by targeted nutritional therapy aimed at the genetic factor(s) identified. Second, is the utility of combination products that include a large number of nutrients simultaneously targeted at many of the key pathways involved in autism pathogenesis.

In this 1 hour lecture titled “NUTRITION IN AUTISM AS INFORMED BY THE LATEST SCIENCE”, Dr. Boles shares several cases from his practice to show how autism-related pathways can be amendable to nutritional interventions, resulting in improved patient outcomes.  This lecture will also discuss one such product, SpectrumNeeds® by NeuroNeeds® (neuroneeds.com), which contains 33 active nutrients, including 20 that act on mitochondria.

For any questions, please email contact@neuroneeds.com.  

About Richard G. Boles, M.D.

Dr. Richard G. Boles completed medical school at UCLA, a pediatric residency at Harbor-UCLA, and a genetics fellowship at Yale.  For over two decades, Dr. Boles’ clinical and research focus has been on changes in genes involved in energy metabolism and additional pathways, and their effects on the development of common functional disorders. Examples include autism, pain syndromes, chronic fatigue, cyclic vomiting, intestinal dysmotility/failure, and depression. He has over 80 published papers. For 20 years, Dr. Boles was a faculty member at the Keck School of Medicine at USC and a practicing medical geneticist at Children’s Hospital Los Angeles. He was a Medical Director of the genetic testing companies, Lineagen and Courtagen. Dr. Boles became involved in genetic testing in order to facilitate the translation of the vast amounts of acquired genetic knowledge into applications that improve routine medical care. Dr. Boles has an active telemedicine practice.  Finally, Dr. Boles is the primary creator of SpectrumNeeds® in his position as a founder and the Chief Medical & Scientific Officer of NeuroNeeds®.

Disclosure: Dr. Boles is the Chief Medical & Scientific Officer for NeuroNeeds LLC, the start-up company that makes SpectrumNeeds®, QNeeds®, and CalmNeeds®.  You are under no obligation to purchase this or any products, whether recommended by Dr. Boles or another health care provider. As always, it is recommended that you contact your physician regarding these products and all other changes to disease management.

The Content within this article and NeuroNews Blog is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this Blog.