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Researchers Studying Century-Old Drug in Potential New Approach to Autism

Excerpts from article originally posted May 26, 2017 | Scott LaFee and Heather Buschman, PhD in Newsroom

Robert Naviaux, MD PhDIn a small, randomized Phase I/II clinical trial (SAT1), researchers at University of California San Diego School of Medicine say a 100-year-old drug called suramin, originally developed to treat African sleeping sickness, was safely administered to children with autism spectrum disorder (ASD), who subsequently displayed measurable, but transient, improvement in core symptoms of autism.

“The purpose of CDR is to help protect the cell and jump-start the healing process,” said Naviaux, by essentially causing the cell to harden its membranes, cease interaction with neighbors and withdraw within itself until the danger has passed.

“But sometimes CDR gets stuck,” Naviaux said. “This prevents completion of the natural healing cycle and can permanently alter the way the cell responds to the world. When this happens, cells behave as if they are still injured or in imminent danger, even though the original cause of the injury or threat has passed.”

At the molecular level, cellular homeostasis or equilibrium is altered, creating an abnormal cellular response that leads to chronic disease. “When this happens during early child development,” said Naviaux, “it causes autism and many other chronic childhood disorders.”

Suramin works by inhibiting the signaling function of adenosine triphosphate (ATP), a nucleotide or small molecule produced by cellular mitochondria and released from the cell as a danger signal. When CDR is activated, the effect of extracellular ATP is similar to a warning siren that never stops. Suramin inhibits the binding of ATP and similar molecules to key purinergic receptors, according to Naviaux. It silences the siren, “signaling the cellular war is over, the danger has passed and cells can return to ‘peacetime’ jobs like normal neurodevelopment, growth and healing.”

Robert Naviaux, MD, PhD

All five boys who received the suramin infusion displayed improvements in language and social behavior, restricted or repetitive behaviors and coping skills. Assessment of improvements was based upon observational examinations and interviews using standardized tests and questionnaires, such as the Autism Diagnostic Observation Schedule, 2nd edition (ADOS-2), the Expressive One Word Picture Vocabulary Testing (EOWPWT), the Aberrant Behavior Checklist (ABC), the Autism Treatment Evaluation Checklist (ATEC), the Repetitive Behavior Questionnaire (RBQ) and the Clinical Global Impression (CGI) questionnaire. To minimize misinterpretation of natural day-to-day variations in symptoms, parents were asked to mark a symptom as changed in the 6-week CGI only if the symptom lasted for at least one week.

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Low-dose suramin in autism spectrum disorder: a small, phase I/II, randomized clinical trial

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More from Dr. Naviaux on metabolics and Chronic Fatigue Syndrome

Science in Service of HumanityDr. Naviaux has responded to some comments on the groundbreaking paper, “Metabolic Features of Chronic Fatigue Syndrome”.

In this response he addresses the need for metabolic studies in other disease groups, whether metabolic studies determine the initial cause of sysmptoms, and how dauer states relate to what is seen in CFS.

We thank Vogt et al. for their comments (1). We respond to their three points in order. First, we are aware of the need to extend future metabolomics studies to include other disease groups. We stated this fact in the discussion of ref. 2 and are validating the results in independent cohorts. The detailed biochemical phenotype or signature that we found provides a first glimpse at a previously hidden biology. For example, disturbances in sphingolipid metabolism have important implications for immunobiology and neuroendocrine regulation relevant to myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS) (3). Sphingolipids are important mediators of the cell danger response (CDR) (4), and the CDR is an important regulator of the behavioral and functional changes produced by infection, and associated with sickness behavior (5). The biochemical phenotype of ME/CFS is distinct from other diseases that Vogt et al. (1) named. For example, in heart failure, metabolomics shows that long chain acyl-carnitines are increased (6), but these long chain acyl-carnitines were not changed in ME/CFS (2). In our view, chemistry and metabolism underlie all aspects of human biology. Our studies show that metabolomics can be used as a new lens to reveal unexpected biology that was invisible before…

Robert Naviaux, et all

Read full response.
Read the letter the response was based on.

PARTICIPATE in metabolomics research at SISOH.

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Press Democrat: Santa Rosa doctor’s study offers new insight into chronic fatigue syndrome

GUY KOVNER
THE PRESS DEMOCRAT | September 21, 2016

Eric Gordon MDA new study initiated by (Eric) Gordon and including Harrison as one of the subjects could provide that breakthrough.

The study, published last month, detected a “chemical signature” in the blood of chronic fatigue syndrome patients, establishing for the first time that chronic fatigue syndrome is an “objective metabolic disorder,” said co-author Dr. Robert Naviaux, the UC San Diego researcher who identified the blood chemical anomalies associated with the condition.

Gordon is a co-author of the study, and most of the patients in the study came from his practice.

Read PD Article

Read Full Study Paper

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New Study Published: Metabolic features of chronic fatigue syndrome

Robert NaviauxMetabolic features of chronic fatigue syndrome. Naviaux RK, Naviaux JC, Li K, Bright AT, Alaynick WA, Wang L, Baxter A, Nathan N, Anderson W, Gordon E. Proc Natl Acad Sci U S A. 2016 Aug 29.

Download a PDF copy – Metabolic features of chronic fatigue syndrome

The Metabolomics study done in collaboration with Robert Naviaux of the Naviaux Lab and Gordon Medical Associates is now available!

Here we report a metabolomics study of Chronic Fatigue Syndrome (CFS) in 45 CFS patients and 39 controls. Our data show that despite the heterogeneity of factors leading to CFS, the cellular metabolic response in patients was homogeneous, statistically robust, and chemically similar to the evolutionarily conserved persistence response to environmental stress known as dauer.

Read full paper…

Some people still argue that CFS is not a real illness but all in the mind. Does your discovery of a chemical signature help shatter this myth?

Yes. The chemical signature that we discovered is evidence that CFS is an objective metabolic disorder that affects mitochondrial energy metabolism, immune function, GI function, the microbiome, the autonomic nervous system, neuroendocrine, and other brain functions. These 7 systems are all connected in a network that is in constant communication. While it is true that you cannot change one of these 7 systems without producing compensatory changes in the others, it is the language of chemistry and metabolism that interconnects them all.

Metabolomics Q&A for CFS v6 

Support further research at the Gordon Medical Research Center