Rest periods and can CFS people get really well?

[Tunguska]

@Tunguska and others, do you read this study as saying we shouldn't be taking d ribose?

Agree with adreno, but moreover I read into the line:

Crucially, suppression of AGE formation using an AGEs inhibitor (aminoguanidine) effectively prevents hyperphosphorylation of Tau protein.

For ribose (seldom, was worth a shot but won't buy again) and fructose, I always take with AGE inhibitors like rutin (http://www.ncbi.nlm.nih.gov/pubmed/2354746 http://phm.utoronto.ca/~jeffh/Yanshan_paper.pdf) and carnosine.

 

[out2lunch]

Taken once in a while, if it helps you through a crash for example, is probably not a big deal. But I would avoid long term supplementation.

Based on what info, specifically? This study you're citing references T2DM patients, not ME/CFS.

While it's true that some of our patient population have both diseases, most of us do not. Therefore, to blindly apply the study findings to those who don't have diabetes is absurd, especially since the key reason for avoiding D-Ribose supplementation would be elevated levels of uric ribose found in diabetic patients.

Most of us who take D-Ribose do so because we lack the necessary enzymes to adequately convert glucose into ribose. Our pentose phosphorylation pathways are probably screwed up. Supplementing with D-Ribose gives us added energy because we need it for ATP manufacturing.

For those of us who used to get ATP directly through IV therapy with glutathione until the compounding pharmacists stopped selling it, D-Ribose has been the next best thing. Our muscles need it. So without individual testing to see if elevated uric ribose is a problem, stopping supplementation of D-Ribose makes no sense.

Personally, I'd like to see some tracking data for long-term heart failure patients who've taken D-Ribose for decades to see if they developed any dementia-related disease as a result. And I'd also like to see correlations between those HF patients on D-Ribose therapy who have T2DM vs those who do not. Seems to me that it's the diabetes which creates the risk and not just the D-Ribose supplementation itself.

 

[out2lunch]

For ribose (seldom, was worth a shot but won't buy again) and fructose, I always take with AGE inhibitors like rutin (http://www.ncbi.nlm.nih.gov/pubmed/2354746 http://phm.utoronto.ca/~jeffh/Yanshan_paper.pdf) and carnosine.

No can do.
Rutin, bromelain, quercitin... they all hate my gut. Nausea and pain galore.
I don't know how anyone can take these supplements.

 

[adreno]

Based on what info, specifically? This study you're citing references T2DM patients, not ME/CFS.

Actually, the study I quoted was a combined in vitro and animal model study, and did not involve diabetes. But you are correct those were not ME/CFS studies. Has there been any done with D-ribose?

Most of us who take D-Ribose do so because we lack the necessary enzymes to adequately convert glucose into ribose.

I will ask you the same question you asked me; based on what info? How do you know those enzymes are screwed up in ME/CFS? I have not seen any data on this.

I do not personally feel well with D-ribose, and I've seen negative reports from others as well. Some do feel better on it. I leave it to everyone to supplement as they see fit, but I personally choose to avoid D-ribose.

 

[out2lunch]

Actually, the study I quoted was a combined in vitro and animal model study, and did not involve diabetes. But you are correct those were not ME/CFS studies. Has there been any done with D-ribose?

Something in the back of my brain regarding a conference I attended years ago believes studies have been done. I think Teitelbaum was connected somehow. But I could be mistaken that he was directly involved. I know he was the first to promote D-Ribose supplementation at the IACFS/ME conference in January 2007. I spoke with the Corvalen researcher at that conference regarding their findings, and it all tied back to lack of ATP production. Ribose was the missing link. But perhaps this is more of an issue for FMS than ME/CFS. I have both.

I will ask you the same question you asked me; based on what info? How do you know those enzymes are screwed up in ME/CFS? I have not seen any data on this.

These enzymes are screwed up in some of us through G6PD deficiency testing. If you lack G6PD, your body isn't going to convert enough glucose to ribose for ATP. Again, this might be more of an issue for FMS since G6PD problems correlate high with spectrum disorders. And spectrum disorders correlate high with FMS.

I do not personally feel well with D-ribose, and I've seen negative reports from others as well. Some do feel better on it. I leave it to everyone to supplement as they see fit, but I personally choose to avoid D-ribose.

If you don't feel better on ribose then you don't need it. I know I need it because of how much better I felt when doing ATP therapy years ago. It gave my muscles more energy and stamina. I didn't crash as hard with PEM after doing chores around the house.

Granted, D-Ribose isn't as good as IV ATP. But it's better than nothing. And that's the key. If you feel better on it then you probably need it.


I've never really thought about this before, but this discussion is helping me to realize that several things I do for my health, like D-Ribose and FIR sauna, are more beneficial for my FMS than my ME/CFS. Or at least it seems that way to me.

Perhaps too many therapies we all discuss on these boards are best suited for one disease over another, but we often don't make the distinction and end up conflating them all. And perhaps this is one of those therapies. Some are helped by D-Ribose while others are not. And it might simply be a matter of comorbidity mucking up the works.

 

[ebethc]

My sister is hypothyroid and can not tolerate mfolate or methylB12 but does fine with folinic acid and hydroxyB12.

How does hypothyroidism impact methylation?

 

[Mij]

How does hypothyroidism impact methylation?

My sister has Hashiimoto and finds that mB12 and mfolate makes her feel too wired, whether this is a methylation issue I couldn't tell you.

 

[Gondwanaland]

My sister has Hashiimoto and finds that mB12 and mfolate makes her feel too wired, whether this is a methylation issue I couldn't tell you.

That is what happened to me too (I have Hashi's). MB12 and Mfolate apparently exhausted my thyroid. Probably at low doses they would have been beneficial (?)

 

[Mij]

That is what happened to me too (I have Hashi's). MB12 and Mfolate apparently exhausted my thyroid. Probably at low doses they would have been beneficial (?)

Possibly, I know she's changed her B Complex supplements frequently to find the right one, she said the one she takes now really helps her.

 

[Gondwanaland]

Possibly, I know she's changed her B Complex supplements frequently to find the right one, she said the one she takes now really helps her.

Now I am curious to know which one she liked best

 

[Mij]

@Gondwanaland I will email her. I remember her telling me that she found one that was lower dose and she could take 2 capsules throughout the day, rather than all at once.

 

[Mij]

@Gondwanaland she is now taking the Thorne Stress B Complex (not the regular Thorne B complex)

 

[Gondwanaland]

Thank you, @Mij I will check that out

 

[ahmo]

How does hypothyroidism impact methylation?

I produce negligible thyroid, have been medicated since adolescence. But also not active Hashimoto's. I proceeded w/ methylation protocol like anyone else, thyroid didn't seem to make a direct impact. Once my system was more functional, less adrenal stress, I was able to increase T3 medication to the correct dosage. For some time, T3 increased my heart rate too much, until adrenals were stronger.

 

[Jesse2233]

Given the latest research into PDH, and metabolomics generally, it seems that @Kimsie was ahead of her time with this post. Repairing the ETC will certainly help PDH (and other Krebs enzymes) function (as will reducing ROS in general). She also amazingly identified molybdenum deficiency as a crucial factor (this has since been supported by metabolomic research).

It's too bad she's no longer active on this board. I would love to get her thoughts on Drs Naviaux, Armstrong, Fluge/Mella, and Davis' metabolic research

In terms of autoimmunity / autoinflammation / infection, better mitochondrial function will allow for better NKC and T reg function, so her theory applies regardless of ongoing causal factor.

It also dovetails nicely with Dr Park's protocol (who claims a 90% recovery rate). He uses IVIG, nutrition, and rest (he says "you must rest like a monk meditates" very similar to Kimsie's total rest instructions). It seems that Dr Park is simultaneously calming immune dysfunction, supporting nutrition, and reducing ROS to create a synergistic combination for remission. I've tried to contact him but since he's in South Korea it has been difficult

 

[NotThisGuy]

yes, too bad @Kimsie is gone.... She really was ahead of her time....
I posted also something about her NADPH theory here: http://forums.phoenixrising.me/inde...thiamine-deficiency.24059/page-13#post-892852


I also found out that peroxynitrite inhibits the iron-sulphur-cluster.

If we she only have continued her work we might be cured by now.....