Overlap between ME/CFS and Covid-19 information - e.g. oxidative stress (MedCram), vitamin supplements, etc

[ZeroGravitas]

I've been watching a whole bunch of PeakProsperity and MedCram (excellent and respectable teaching doctor) to digest the medical info coming out about Covid-19 studies, etc (as I've been caught up blogging about it for ~6 weeks, etc).

In previous weeks they've each described quite similar supplement regiments, for supporting their own (healthy) immunity, that wouldn't be at all out of place in our community (although relatively small, heh):

• Dr Chris Martenson (Peak Prosperity) - Zinc, Quercetin, D3, then if sick Elderberry, NAC (for covid 19) and vit-c to bowel tolerance (as Dr Myhill advises too).



• Roger Seheult, MD (Med Cram) - Vit-c (whole food), D3 (2500IU/day), quercetin (500mg x2), zinc (50mg), contrast shower (max hot/cold for immune stimulation), + obsessively intense anti-contamination hygiene routines (he describes at length and I wouldn't worry about) as he works with critically ill Covid patients.

Anyway, MedCram videos have dealt with seemingly all aspects of Covid-19 in a very approachable but technical manner. And perhaps most other aspects of medicine, previously, including treating septic shock with vitamin C...

... And today gave a fantastic overview of mitochondria's ATP production as a line up to talking about oxidative stress for his theory of what's the primary mechanism behind Covid-19; Sars-Cov-2 attacking the endothelium of the circulatory system with associated massive oxidative stress not controlled because ACE2 is also knocked out by the virus:

I found it helpful just for generally helping me get to grips with what "reduced" means (can never internalise it) as well as where the SOD (and other anti-oxidant) enzymes (glutathione and catalase) fit in :

 

[ZeroGravitas]

MedCram has continued explaining [0:48 - YouTube] their (very sound looking) hypothesis that serious Covid-19 illness/death is primarily caused by greatly increased oxidative stress on blood vessel epithelia, leading it to dysfunction, releasing excess von Willebrand's Factor, which causes (excess clotting and) thrombosis.

How this theory can account for the marginal protection for those with type-O blood, much greater risk for black individuals and even the up-tick in Kawasaki-like illness in children!

► But the mechanism and dysfunctions he talks about might have a some elevance to ME/CFS that I don't remember being mentioned. Specifically:

• Angiotensin (1-7) has an anti-oxidant effect on super-oxide.

• Angiotensin II creates more superoxide. (I've not seen him explain the mechanism for either of those effects, can anyone explain, off hand?)

• ACE2 enzyme, that converts ATII to AT(1-7), is destroyed from cell surfaces by virus entry, causing a strong imbalance, favouring superoxide production.

• Ace I Inhibitors and Angiotensin Receptor Blockers (both for treating high blood pressure) effectively work to enhance ACE2 and reduce superoxide production (particularly with blood vestles).

Covid patients also tend to suffer from problematically low blood pressure, because of ACE2 destruction - the angiotensin system normally signals (certain) blood vessels to constrict.

Hypotension common in ME/CFS too. I wondered if there could be a direct link (I expect not - I'm just being medically naive). Like, could ACE2 expression be upregulated in our blood vessels, for its secondary purpose of helping to deal with raised oxidative stress?


@Learner1 - you're very much into anti-oxidant systems. Do you make anything of the above couple of posts...?

 

[Learner1]

@ZeroGravitas I'm wondering what effect an ACE deletion would have - do you know?

The info I've seen to date implicates the increase in oxidative and nitrosative stress with worsening of COVID-19.

There have been papers on use of antioxidants for COVID-19:

https://www.cebm.net/covid-19/n-ace...dence-for-effectiveness-in-treating-covid-19/

https://reader.elsevier.com/reader/...611B74AB01587BAA54DA6321A1E55E3DDAA71F8013667

https://onlinelibrary.wiley.com/doi/10.1002/jmv.25707

And, Lyme doctor Richard Horowitz has had success with giving IV glutathione to a couple of his Lyme patients who contracted COVID-19.

https://www.sciencedirect.com/science/article/pii/S2213007120301350



Additionally, low vitamin D seems to correlate with more severe COVID-19 and higher death rates.

https://www.medrxiv.org/content/10.1101/2020.04.08.20058578v3

 

[ZeroGravitas]

I'm wondering what effect an ACE deletion would have - do you know?

You mean ACE (1) enzyme? Not a personal genome question, eh? I don't know, but I imagine there might have been a mouse study on it....? (Ther usually is - I think someoene I looked at talked of one for ACE2 knockout... Maybe....)

There have been papers on use of antioxidants for COVID-19

Oh, absolutely. A lot. MedCram's waiting for some of the high dose IV C studies to be published. Will be great to see him peer review them, really special to be able to see that kind of thing properly done in approachable videos.

His video, I linked above, goes over some of the evidence that justifies his supplement regiment.



Incidentally - there was much talk (from PeakProsperity and him) about the lack of zinc (or controlling for zinc levels) in the hydroxychloroquine trials, that reportedly failed. Zinc's supposedly required for it's mechanism of action.

But of course zinc's also essential for a couple of the SOD enzymes, and commonly deficient. So adding it as part of a drug cocktail might work more on that basis, in augmenting SOD and controlling ROS.

Anyway, @Learner1 - you've told me that imbalanced anti-oxidant supplementation could be detrimental... So wondering if you think something like Myhill's "Just drink as much ascorbic acid as physically possible!" (my paraphrasing) approach could backfire? In severe cases of Covid-19.

The covid-ME/CFS similarity is also that both have been likened to sepsis, too (covid unlike typical pnumonia or ARDS which is way more lung centric).

I think I'll have take the time (some time, not soon) to look up the metabolic/mechanism link between angiotensin and oxidation...

 

[ZeroGravitas]

Odd co-occurrence: Cort just posted on Simmaron Research about this paper (posted on PR, here) that's hypothesising a blood vessel related overarching explanation of ME/CFS. In it (my emphasis):

The real mystery, though, involves what’s going on with the renin-angiotensin-aldosterone system (RAAS) in ME/CFS. Low blood volumes should automatically activate that system to increase the blood volumes, but paradoxically, instead of being increased, RAAS activity appears to be reduced in this disease. Because, as noted above, low blood volume sends the sympathetic nervous system into overdrive, the inability of the RAAS to do its job could play a major role in ME/CFS. For some reason the RAAS has hardly ever been looked into in this disease.


[Wikipedia]

So, another unexpected link with the angiotensin imbalance theory of severe Covid-19 illness (mentioned above).

No mention of anti-oxidant effects.

 

[ZeroGravitas]

I didn't have the energy, a couple months back, to repost this tweet here (via Brian Vastag):

https://twitter.com/i/web/status/1427349779705581587

The refered paper, published in PNAS, directly compares Long Covid and ME/CFS, primarily in terms of oxidative stress/redox imbalance:

Concluding Remarks

People with acute COVID-19 and people with ME/CFS share redox imbalance, systemic inflammation and neuroinflammation, impaired production of ATP and other abnormalities in common (Fig. 2), abnormalities that have bidirectional connections (169).

The syndrome of long COVID-19 that can develop in some COVID-19 survivors (people called “long haulers”) is very similar to ME/CFS, so it may well be that the group of abnormalities seen in acute COVID-19 and in ME/CFS also will be seen in long COVID-19. Presumably, redox abnormalities in COVID-19 are secondary to the infection with SARS-CoV-2. The same may be true among those ME/CFS patients whose illness began with an “infectious-like” illness.

Edit: Oh, and here was an article about it by author Anthony Komaroff, MD (via Solve MECFS Initiative Facebook).