Health rising article, by Cort Johnson 18 March 2016: End ME/CFS Severe Patient Study Turns to the Mitochondria
The mantra at the Severely Ill/Big Data study at the Open Medicine Foundation is to follow the evidence where it leads. We don’t know exactly what Davis has found or if will be ultimately validated. We do know that something eyebrow raising involving the mitochondria has shown up in the early stages of the Open Medicine Foundation’s End ME/CFS Severely Ill study. Something eyebrow raising enough for a mitochondrial expert to join the fold.
Davis has found abnormalities before but this is the first one, he told me, that has really leapt off the charts. It was orders of magnitude different from normal.
Whatever the finding is it has apparently lead to a mitochondrial expert, Robert Naviaux, MD, PhD being added to the Open Medicine Foundation’s Scientific Advisory Board.
We’ve had mitochondrial findings before but not from researchers of his ilk. Naviaux is not a doctor and sometime researcher. He’s a full-time mitochondrial researcher. His first paper on the subject occurred about 15 years ago. Since then he’s co-authored more than 80 studies on the mitochondria, genetics, metabolism and metabolomics. The metabolomics study that highlighted the possible mitochondrial issue in ME/CFS has been submitted to the Journal of the American Medical Association (JAMA). Publication, if it comes, is hoped for in early spring/summer.
He runs the Robert Naviaux Laboratory at UC San Diego, and is the founder and co-director of the Mitochondrial and Metabolic Disease Center at UCSD.. He’s also the co-founder and a former president of the Mitochondrial Medicine Society, and a founding associate editor of the journal Mitochondrion. This man is steeped in the mitochondria – but he also has an interesting immune side.
Naviaux trained at the NIH in tumor immunology and natural killer cell biology, and at the Salk Institute in virology and gene therapy. With all that experience he seems perfectly placed to understand the role infection/inflammation may play on mitochondrial issues, should they continue to show up, in ME/CFS. In conversation Ron Davis has suggested that mitochondrial problems with the immune cells could conceivably be driving the immune dysfunction in ME/CFS.
A busy researcher in a hot field, his joining of the OMF Scientific Advisory board speaks volumes about the possible significance of Davis’s recent finding. Naviaux wouldn’t sign on if something very intriguing hadn’t sparked his interest. One patient reported Naviaux replied to her email.
“I have only been working in the CFS world for a year, but we have already made several discoveries that have a chance to offer real hope for people who have suffered for so long. We have a paper in review at JAMA. If it is published, we will have a real start on seeing CFS in a new light, and having real tools for new ways to treat patients as individuals, and not just as a patient with CFS.”
Davis has stated that Dr. Nath of the NIH’s Clinical Center study has been informed of what they’ve found.
The Chronic Fatigue Initiative’s Mitochondrial Emphasis
J Transl Med. 2016 Jan 20;14(1):19. doi: 10.1186/s12967-016-0771-6.Mitochondrial DNA variants correlate with symptoms in myalgic encephalomyelitis/chronic fatigue syndrome. Billing-Ross P1, Germain A2, Ye K3, Keinan A4, Gu Z5, Hanson MR6.
The Chronic Fatigue Initiative’s move to the mitochondria recently resulted in a paper published by Maureen Hanson of Cornell University. The study involved sequencing the entire mitochondrial genome of almost 400 ME/CFS patients from five sites across the U.S. It determined whether single or groups of variations in mitochondrial genes or something called heteroplasmy were more common in ME/CFS.
The study found no evidence of inherited genetic disease or heteroplasmy in ME/CFS but one finding suggested that people whose genome gives them an increased tolerance of oxidative stress may be at reduced risk of coming down with ME/CFS. (The mitochondria produce large numbers of free radicals). ME/CFS patients with a group of variations in some mitochondrial genes also tended to display more joint pain, bloating, chemical or light sensitivity, disrupted sleep and experience more dead/heavy feelings after exercise.
This study did not suggest that variations in the mitochondrial genome caused ME/CFS but it did suggest that once you have ME/CFS some mitochondrial variations might make it worse. That could suggest that something affecting mitochondrial functioning could be present in ME/CFS.
One study that found evidence of mitochondrial genetic issues in ME/CFS and other “functional disorders” concluded that the “pathophysiology likely involves broad effects on the autonomic nervous system.”
There’s the genetics of mitochondrial disease and then there’s mitochondrial functioning. If an autoimmune or some other process is affecting the mitochondria then genetic problems need not be present for a disease to have a mitochondrial basis. The next step for Maureen Hanson and the CFI is to determine if mitochondrial problems caused by an autoimmune or another process are impairing the functioning of immune cells in ME/CFS.
Conclusion
The mitochondria are finally getting some serious attention in ME/CFS. Mitochondrial problems have been found before in the disease and interest is growing in the subject. Newton recently showed for the first time that mitochondrial disorders can cause fatigue as severe as that found in ME/CFS. She found comparable levels of fatigue in about a third of people with mitochondrial disorders. She suggested that future treatments developed to assist mitochondrial patients may be able to help people with ME/CFS. With results like that and researchers like Naviaux and Hanson in the mix, mitochondrial issues should be getting more attention in ME/CFS.
