...[in ME] gene variants may significantly, and in a negative manner, impact the functioning of key enzymes that process important metabolites involved in energy production, brain and immune functioning. When Phair added the impaired enzyme functioning to his metabolic modeling to determine if it could account for the strange metabolomic finding, he found that it could.
Testing the Hypothesis
That hurdle passed, it’s time to test the hypothesis experimentally — something, Davis noted, that Stanford has the tools to do.
The team will use “tracer” metabolites to determine if the cells with these mutations are, in fact, functioning less effectively. Phair said they should know if the metabolic trap is present in the white blood cells of ME/CFS patients by the end of summer.
The potentially very big news regarding Phair’s metabolic trap is that, as noted above, if it works out – Ron cautioned that’s a big “if” at this point – it could conceivably lead to a cheap, fast and effective treatment. It might also be able to help explain how some autoimmune diseases occur.
... treatment strategy would involve tweaking one of the major systems in the body