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Can anyone point me to articles, research, etc. on why CFIDS affects more women than it does men?
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Great question. I always wonder about this when theories about etiology are discussed. Why the male/female difference, unless this is an autoimmune disease? Any leads @Hip ?Can anyone point me to articles, research, etc. on why CFIDS affects more women than it does men?
Can anyone point me to articles, research, etc. on why CFIDS affects more women than it does men?
Maybe its just because women are just so much more fabulous than men
The other day I checked Naviaux' data for ATP and adenosine. ATP was normal but adenosine was low. Today I went back to have a look at AMP, which is the intermediate state between ATP and adenosine. My thinking was that maybe looking at it could tell us a bit more about exactly where any failure to breakdown eATP is occurring.
(We assume the source of AMP and Adenosine in serum is upstream ATP. If this assumption is a simplifying assumption and it seems fair but if not please let me know.)
AMP shows an interesting difference between patients and controls with a p value of 0.001. But the relative difference between female patients and controls is actually smaller in AMP than in Adenosine.
Here's the story, starting at the beginning with ATP, same as shown earlier.
ATP levels are the same, basically. The data is only available for Women. Patients are on the left of the chart in blue ,controls in red. At the bottom of the chart I give the levels and p values (two-tailed).
View attachment 24950
AMP, however, shows real differences, (including very big differences in men driven by very high variation.) (women on left in blue, controls in red, male patients in green, male controls purple.) This is a hint that we're not breaking down ATP to AMP
View attachment 24953
Adenosine, the purine that dampens the immune response, also shows big consistent differences. ME/CFS patients are low in it. (nb. The three male controls with the highest levels of adenosine are also the three with the highest levels of AMP in the previous chart.)
View attachment 24951
I also checked on this metabolite which is a basic purine building block. nothing to report.View attachment 24952
Why are levels of AMP so low? I wanted to see if I could use the data to check if ATP is being broken down to AMP.
I made this scatter plot of female patients showing a tantalising but weak negative correlation between them (-0.1). It *might* suggest that maybe people who build up high levels of eATP can't break them down into AMP ( it *really* looks like that if you're using your confirmation bias goggles but I remembered to take mine off just in time.)
View attachment 24945
Here's the equivalent scatter plot for the controls. As you see, not *so* different. (the slope on the line is 0.0006)
View attachment 24946
So maybe we have some very weak evidence for a failure in turning ATP into AMP. But we still need to explain the shortage of Adenosine. Let's look at the next step.
The next phase of the process is breaking down from AMP to adenosine. The relationshp between the levels looks fairly similar in patients and controls. The line of fit has roughly the same slope, suggesting maybe patients with ample AMP can make ample adenosine?
Female patients:
View attachment 24947
Female controls:
View attachment 24948
The shortage of adenosine can *probably* best be explained by a shortage of AMP, rather than a second problem in the process of breaking it down. (Although if you only look at variation of people with around 50,0000 to 60,000 level of AMP you see a big difference. Additional AMP above about 55000 seems to result in much higher levels of adenosine, suggesting a possible non-linear relationship).
Occams razor says one problem more likely than two. The big reason for the shortage of the immune-quelling particle adenosine is probably the shortage of AMP, not problems breaking AMP down.
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To conclude. I tried to answer the question of whether ATP was higher in patients than controls. It doesn't seem to be. I tried to answer whether other (more immuno-suppressive) purines AMP and adenosine were lower in patients than controls (they seem to be).
I tried to see if we can find where the process of dephosphorylation of ATP was broken. I found a slight but curious possible negative link from ATP and AMP. And not much to report on the relatonship between AMP and Adenosine.
It all fits (albeit weakly) with a failure in cd39, and could suggest AMP supplementation as a possible route for more exploration. More data needed!
Dr. Chia has also mentioned that men tend to recover under his protocols more often than women
more generally I recommend searching here for all your medical research needs! -> https://www.ncbi.nlm.nih.gov/pubmed
Great question. I always wonder about this when theories about etiology are discussed. Why the male/female difference, unless this is an autoimmune disease? Any leads @Hip ?
I would guess what you suggest may be correct, that ME/CFS is an autoimmune disease or has some autoimmune components, explaining the high female to male ratio.
What I don't understand is: If CFS is an autoimmune disease, then why don't we just take Methotrexate or something like that...
I take it you have not seen the Fluge and Mella's rituximab clinical trials, which show great promise for treating ME/CFS. Rituximab kills the B-cells that are causing autoimmune attack. There is a whole sub-forum on rituximab.
Fluge and Mella got involved in rituximab after they noted that an ME/CFS patient given methotrexate made a recovery. But they moved on to rituximab, as this is better.
Naviaux et al suggested based on their metabolic findings that men, more than women, may utilize endogenous protein catabolism to provide substrates for the TCA cycle. This could be related to hormones including anabolic-type steroids being higher in men and so might make women more prone to the symptoms of CFS mitochondrial metabolic defects than men.
Ah thank you. I just missed the fact that they used MTX before RTX! Okay that in fact sounds like inflammation is going on. But then I find it interesting why they can't find any inflammation in my blood...
Two things I would like to point:
-MTX (and so do many immunomodulatory drugs) is also efficient on inflammatory diseases like atopic dermatitis (not only on auto-immune diseases).
-Having no inflammatory markers in your blood doesn't mean you don't have inflammatory disease.
Actually a subgroup of ME/CFS patients have normal ESR and CRP (and fibrinogen), even when they have infection evidences. It may be because some protein synthesis are switched of by the disease.