Hoy folks, wow, there are a lot of posts to read already! Well, without having read the previous messages, I just wanted to share my analysis on the paper that I have made in Spanish:
http://www.sfc-em-investigacion.com/viewtopic.php?p=31521#p31521
Maybe my view is shared by some of you. What I wrote in Spanish after reading the paper is essentially, that these results are mostly a confirmation of the altered metabolic/biochemical pathways already published and therefore known on ME/CFS, such as the mitochondrial failure, oxidative damage, catabolism, altered redox status, problems in the methylation cycle and adjacent pathways such as nucleotides metabolism, etc. There are some things I think are new, such as the lipid metabolism, although it is something we already knew--indirectly from the lipid oxidation, unbalanced omega 3-6 ratio, lipid peroxidation, etc.
Those of us who studied in depth the Yasko’s protocol for autism ,years ago , and its application the ME/CFS proposed by Richard A. Van Konynenburg, do know many of the found abnormalities--and it's great that they are confirmed and published!.
As for the hypometabolic state, well, I remember having read this several times years ago,from for example Dr. Myhill in her book. It is great that this study actually points out this fact, giving to it a grade of evidence it didn’t have before.
I would also like to remember that the concept of putting together some metabolites in order to draw a diagnostic tool is not new, and has been carried out various times in the past, with even better sensibilities than this paper finds: Dr. Myhill made it with 5 parameters; I think it was Dr Klimas who published the potencial diagnostic value of a few cytokines put together, and in the same vein, recently, Dr. De Meirleir and his team published how more than 400 SNPs (12 of these in the “transcriptional region” of the DNA) with a very low P value, could also distinguish between patients and controls.
For me, and in my very humble opinion, the most relevant part of this study are the following assertions:
(…)ultimately may represent a fundamental response to oppose the spread of persistent viral and intracellular bacterial infections. (…)This pattern is also opposite of what is found during acute inflammation and infection (…) Plasma FAD was decreased in both males and females with CFS (...)FAD is mobilized from tissues, increased in the plasma, and renal secretion is increased under conditions of stress or infection (…) Hydroxyproline was increased(...)Another metabolic fate of hydroxyproline is glyoxylate, which can be transaminated in mitochondria to produce glycine and metabolized in peroxisomes to oxalate and peroxide for cell defense and innate and antiviral immunity (…) Arg levels were also increased in chronic fatigue(...)Increased Arg is associated with a decreased risk of infection after operative stress and is used to synthesize the antimicrobial molecule agmatine under conditions of active infection (…) HICA was decreased in both males and females with CFS.(..)HICA has antibacterial and antifungal activity.(…)
In short, no matter if papers look at the immune system, or at the biochemical/metabolic signature of ME/CFS—like this one does--, they find the same:
multiple aetiological events lead to a similar state of chronic inflammation, immune activation and immune-suppression (yes, at the same time), probably caused by intracellular viral or bacterial infections… Well, this sounds quite familiar, doesn't it!
I just wanted to share my 2 cents!
Best,
Sergio
