http://insight.jci.org/articles/view/89376#.WFvrpdUE5Bk.twitter
I've just started reading this, it's a lot to chew through. Very exciting though.
I've just started reading this, it's a lot to chew through. Very exciting though.
Not having much experience with this subject I still think its really good...The one question mark - why did the cells in the ME/CFS patients serum use more oxygen not less than the cells in the healthy peoples serum? That sounds like they were more energetic but I don't know if cellular respiration is a marker for energy.
Not having much experience with this subject I still think its really good...The one question mark - why did the cells in the ME/CFS patients serum use more oxygen not less than the cells in the healthy peoples serum? That sounds like they were more energetic but I don't know if cellular respiration is a marker for energy.
I'm working on the blog now.
There is strong evidence for hypometabolism in the brain of patients with HD.
For example, glucose consumption is reduced, especially in the basal ganglia, even in presymptomatic mutation carriers.2,–4
Studies in animal models have revealed decreased adenosine triphosphate (ATP) concentrations in the brain of HD mouse models.5
There are also nonneurologic symptoms at the early stage of the disease, such as weight loss despite enhanced caloric intake, which suggest a hypercatabolism in HD.6
Reduced concentrations of branched-chain amino acids (BCAAs)—valine, leucine, and isoleucine—have been found in plasma samples of patients with HD as early as in presymptomatic carriers even when they were on a high-caloric diet.6
We hypothesized that decreased circulating levels of BCAAs reflect their mitochondrial oxidation in order to provide 2 key intermediates for the Krebs cycle: acetyl coenzyme A (acetyl-CoA) and succinyl-CoA.6 Consequently, therapies aiming at providing substrates to the Krebs cycle may be of special interest in HD.
We previously showed that dietary anaplerotic therapy—replenishing the pool of metabolic intermediates in the Krebs cycle—was able to improve peripheral energy metabolism in HD using 31P magnetic resonance spectroscopy (MRS) in muscle.7
How interesting - particularly the reduced metabolism in the basal ganglia.So any ideas why something like this triheptanoin hasn't been tried or looked at in ME/CFS? It seems fairly readily available, at least as a research chemical. It's a triglyceride.
This all relates to Huntington's disease...but sounds pretty familiar to what Fluge and Mella have found too, right?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4336068/
Reduced concentrations of branched-chain amino acids (BCAAs)—valine, leucine, and isoleucine—have been found in plasma samples of patients with HD as early as in presymptomatic carriers even when they were on a high-caloric diet.6
We hypothesized that decreased circulating levels of BCAAs reflect their mitochondrial oxidation in order to provide 2 key intermediates for the Krebs cycle: acetyl coenzyme A (acetyl-CoA) and succinyl-CoA.6Consequently, therapies aiming at providing substrates to the Krebs cycle may be of special interest in HD.