Friday, January 9, 2015

Prof Ronald Davis: I don't think people understand how horrible this disease is

Miriam E. Tucker, January 08, 2015:

Chronic Fatigue Syndrome: Wrong Name, Real Illness

The condition is tragically real for Ronald W. Davis, PhD, professor of biochemistry and genetics at Stanford University and director of the Stanford Genome Technology Center, whose work with genetic linkage mapping enabled the Human Genome Project. His 31-year-old son developed ME/CFS 3 years ago and is now completely bedridden and unable to speak.
"I don't think people understand how horrible this disease is. They don't look that sick. Even my son, who is incredibly debilitated, doesn't look sick," Dr Davis told Medscape Medical News.
In his new position as ME/CFS scientific advisory board director of the Open Medicine Institute, Dr Davis has recruited Nobel laureates James D. Watson, PhD, and Mario R. Capecchi, PhD, and other esteemed scientists as advisors to create what he envisions as a collaborative ME/CFS research effort akin to the Human Genome Project.
"I think it will yield if we get sufficient funding, quite frankly. It may be a tough nut to crack...I'm looking at this long-term. I don't like the long-term because my son is ill, but I'm realizing this won't be temporary," Dr Davis told Medscape Medical News.
Numerous physical abnormalities have been identified in ME/CFS patients, with stronger biological signals seen in studies measuring response to exercise[3] that differentiate patients from controls and far exceed the effects of mere deconditioning, experts say.
Such evidence includes significantly reduced oxygen consumption and workload for ME/CFS patients after treadmill tests,[4] and altered gene expression compared with controls following moderate exercise.[5]

Other biological evidence includes a recent finding of bilateral white matter atrophy in ME/CFS patients compared with controls,[6] several studies documenting significant decreases in natural killer cell cytotoxic activity, and increased levels of multiple proinflammatory cytokines.[7]

A highly significant elevation in non-Hodgkin lymphoma—which, like ME/CFS, has been linked to Epstein-Barr virus[8]—was found among ME/CFS patients aged 66-99 years in a National Cancer Institute study of data from the Surveillance, Epidemiology, and the End Results (SEER) and Medicare registries of approximately 1.2 million cancer cases and 100,000 controls, with an odds ratio of 1.29 andP value of .0000017.[9]
In a novel study of 165 consecutive patients with ME/CFS who underwent upper gastrointestinal endoscopies and antrum biopsies, 135/165 (82%) stained positive for enterovirus viral capsid protein 1 compared with just 7/34 (20%) of controls (≤ .001).[10]
And in another novel finding that speaks to the phenomenon's heterogeneity, approximately 2% of ME/CFS cases were found to have chromosomally integrated human herpesvirus-6 (HHV-6) as compared to just 0.2%-0.85% of the general population,[11] suggesting a specific etiology for a small proportion of cases.[12]
Responses to treatment in randomized, blinded, placebo-controlled trials also point to biological causation, including improvements with valganciclovir in a study of ME/CFS patients with elevated antibody titers to HHV-6 and Epstein-Barr virus,[13] and a preliminary trial (now being repeated in a larger patient group) in which ME/CFS patients responded to rituximab, a monoclonal antibody that destroys immune system B cells and is approved in the United States for the treatment of non-Hodgkin lymphoma and other B-cell–mediated conditions.[14]



Geoff said...

Excellent post with lots of interesting information, thanks Dr Speedy.

Dr Speedy said...

Thx that's what I thought Geoff


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