Robert Naviaux

Source: gordonmedical.com

Robert K. Naviaux, MD, PhD, is a Professor in Residence at the University of California, San Diego, California, US. His work "has focused on the role of mitochondrial DNA replication, copy number regulation, DNA damage, and nucleotide signaling in development, aging, healing and regeneration in mitochondrial mechanisms of disease and development." He was invited to join the Open Medicine Foundation's research team in 2016, following a announcement that the ME/CFS Severely Ill, Big Data Study had a significant result in the area of mitochondria.

Dr. Naviaux directs the Robert Naviaux Laboratory at University of California, San Diego (UCSD) whose work is "divided into two groups: 1) Mitochondrial Mechanisms of Disease and Development, and 2) Evolutionary Systems Biology and Marine Metagenomics." He is founder and co-director of the Mitochondrial and Metabolic Disease Center at UCSD, the co-founder and a former president of the Mitochondrial Medicine Society, as well as, a founding associate editor of the journal, Mitochondrion.

Dr. Naviaux "discovered the cause and created the diagnostic test for Alpers syndrome, a mitochondrial disease... [and] is the director of the first FDA-approved clinical trial to study suramin [an antiparasitic drug] as a treatment for autism."

Currently, Dr. Naviaux is using his mitochondria expertise, especially in metabolomics, to look for a biomarker and potential treatment for ME/CFS.

In May 2016, a study was launched, led by Dr. Naviaux and Dr. Ronald Davis, in collaboration with Dr. Eric Gordon, Dr. Paul Cheney, and the Stanford Genome Technology Center in order "to validate earlier findings of a possible diagnostic signature for ME/CFS by measuring metabolites and to evaluate the contribution of genetics to the variation in observed metabolic signatures in this disease." The initial phase, with a total of 90 participants, has been completed and suggests "the mitochondria is in hypometabolism due to a chronic cell danger response state in ME/CFS patients."

Education

• 1977-1978 - Undergraduate (Biochemistry), Georg August Universität, Göttingen, Germany
• 1979 - B.S. (Biological Sciences), University of California, Davis, California
• 1981 - M.S. (Zoology), Indiana University, Bloomington, Indiana
• 1986, 1989 - M.D., Ph.D. (Genetics, Virology), Indiana University School of Medicine, Indianapolis, Indiana
• 1986-1990 - Internship and Residency, Internal Medicine, American Board of Internal Medicine (ABIM), Clinical Investigator Pathway, University of California, Davis
• 1990-1994 - Postdoctorate (Retrovirology, Gene Therapy), The Salk Institute, La Jolla, California
• 1994-1997 - Fellowship (Biochemical Genetics, mtDNA Replication), University of California, San Diego Medical Center, San Diego, California

Notable studies

• 2004, Developing a systematic approach to the diagnosis and classification of mitochondrial disease
• 2008, Mitochondrial control of epigenetics
• 2014, Metabolic features of the cell danger response (Full Text)
• Sep 13, 2016, Metabolic features of chronic fatigue syndrome(Full Text)

• Nov 15, 2016, Reply to Vogt et al.: Metabolomics and chronic fatigue syndrome
• Feb 7, 2017, Reply to Roerink et al.: Metabolomics of chronic fatigue syndrome

• 2017, A robust, single-injection method for targeted, broad-spectrum plasma metabolomics(Full Text)
• 2020, Human Herpesvirus-6 Reactivation, Mitochondrial Fragmentation, and the Coordination of Antiviral and Metabolic Phenotypes in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (Full text)

Awards and Honors

• 2002, Honored in a non-fiction book entitled, Anna’s Friends — Lessons Learned from a Short and Beautiful Life
• 2007, Thomson ESI - Science Citation Index “Fast Moving Front Article”
• 2007, United Mitochondrial Disease Foundation Mitochondrial Medicine - Best Abstract Award
• 2008, Hailey’s Wish Foundation - Hailey’s Hero Award, For Outstanding Research and Clinical Care of children with mitochondrial disease

Talks and interviews

• 2011, Mitochondria and Autism (Spring 2011) - Robert K. Naviaux, M.D., Ph.D.
• Aug 12, 2017, Community Symposium on the Molecular Basis of ME/CFS - 2017
• Sep 28, 2017, Robert Naviaux, MD, PhD | ME/CFS Cell Danger Response, Metabolic Features, Low-energy in Nature

(with Spanish subtitles)

Articles

• 2016, "Mitochondria Man Gets His Money and the UK Goes Mega: Chronic Fatigue Syndrome Research Moving Forward"

• 2018, "UCSD Researcher Suggests Chronic Illness Could Be Breakdown in Normal Healing"

Online presence

• Health Rising Forum for Robert Naviaux
• PubMed
• University of California, San Diego Faculty Website
• Youtube - Talks on Autism

Learn more

• Robert Naviaux Laboratory at UC San Diego
• The Significance of Reversing Autism-Like Features in Two Distinct Mouse Models With a Single Drug, Suramin

See also

• Metabolomics
• Mitochondrion
• Dauer
• Metabolic features of chronic fatigue syndrome

mitochondria Important parts of the biological cell, with each mitochondrion encased within a mitochondrial membrane. Mitochondria are best known for their role in energy production, earning them the nickname "the powerhouse of the cell". Mitochondria also participate in the detection of threats and the response to these threats. One of the responses to threats orchestrated by mitochondria is apoptosis, a cell suicide program used by cells when the threat can not be eliminated.

mitochondria Important parts of the biological cell, with each mitochondrion encased within a mitochondrial membrane. Mitochondria are best known for their role in energy production, earning them the nickname "the powerhouse of the cell". Mitochondria also participate in the detection of threats and the response to these threats. One of the responses to threats orchestrated by mitochondria is apoptosis, a cell suicide program used by cells when the threat can not be eliminated.

mitochondria Important parts of the biological cell, with each mitochondrion encased within a mitochondrial membrane. Mitochondria are best known for their role in energy production, earning them the nickname "the powerhouse of the cell". Mitochondria also participate in the detection of threats and the response to these threats. One of the responses to threats orchestrated by mitochondria is apoptosis, a cell suicide program used by cells when the threat can not be eliminated.

genome an organism's complete set of DNA, including all of its genes

See myalgic encephalomyelitis.

See chronic fatigue syndrome.

metabolite A chemical compound produced by, or involved in, metabolism. The term is often used to refer to the degradation products of drugs in the body.

metabolomics The analysis of the chemical metabolism within cells, tissues or organisms. The term is often used to refer to the full set of metabolites found in a cell in a given environment.

myalgic encephalomyelitis (M.E.) - A disease often marked by neurological symptoms, but fatigue is sometimes a symptom as well. Some diagnostic criteria distinguish it from chronic fatigue syndrome, while other diagnostic criteria consider it to be a synonym for chronic fatigue syndrome. A defining characteristic of ME is post-exertional malaise (PEM), or post-exertional neuroimmune exhaustion (PENE), which is a notable exacerbation of symptoms brought on by small exertions. PEM can last for days or weeks. Symptoms can include cognitive impairments, muscle pain (myalgia), trouble remaining upright (orthostatic intolerance), sleep abnormalities, and gastro-intestinal impairments, among others. An estimated 25% of those suffering from ME are housebound or bedbound. The World Health Organization (WHO) classifies ME as a neurological disease.