SARS-COV-2 Infection: The Possible Preventative Role Of Methylene Blue

Mito

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A COHORT OF CANCER PATIENTS WITH NO REPORTED CASES OF SARS-COV-2 INFECTION : THE POSSIBLE PREVENTIVE ROLE OF METHYLENE BLUE
Publié par Guérir du Cancer | Mar 28, 2020 | Bleu de Méthylène, Covid-19 | 7 |

Marc Henry1*, Mireille Summa2, Louis Patrick3, Laurent Schwartz4

1 Université de Strasbourg, Chimie Moléculaire du Solide, Institut Le Bel, Strasbourg.
2 Ceremade, Université Paris Dauphine
3 Association Espoir Métabolique
4 Assistance Publique des Hôpitaux de Paris, Paris, France.

Abstract

We report the case of a cohort of 2500 French patients treated among others with methylene blue for cancer care. During the COVID-19 epidemics none of them developed influenza-like illness. Albeit this lack of infection might be by chance alone, it is possible that methylene blue might have a preventive effect for COVID-19 infection. This is in line with the antiviral activity of Chloroquine, a Methylene blue derivative.

Both Chloroquine and Methylene blue have strong antiviral and anti- inflammatory properties probably linked to the change in intracellular pH and redox state.

Conclusion

With the current COVID-19 outbreak, the world is facing a challenge and every possibility of helping people should be considered. Our preliminary data suggest but do not prove that Methylene blue might be a good treatment for influenza- like illnesses. Both Methylene blue and its derivatives such as chloroquine may share similar mechanism of action. Time is ripe for a prospective randomized clinical trial for the treatment of this dreadful disease.

Old drugs which have been tested for other indications ( such as Methylene blue or Chloroquine) have a well-defined safety profile. They are often more effective than new drugs from the High Tech. The Covid 19 epidemics like cancer has a solution. Reporpusing of known molecules will help cure these deadly diseases.

A cohort of cancer patients with no reported cases of SARS-CoV-2 infection : the possible preventive role of Methylene Blue — Guérir du Cancer
 
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tankasnowgod

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Shhhhh! Don't tell the media that some of us here consume the Kordon product..........
 

burtlancast

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Yes, i read the article in french too.

They advise 75 mg three times a day.

Then i came back here and read the reactions of people to doses between 0.2 mg to 30 mg per day. It seems there's some remote danger of even very low doses of causing a serotonine syndrome, susceptible to send you to the ER, not exactly the safest place at the moment.

Has anyone on this forum ingested 225 mg per day of MB ?
 
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Has anyone on this forum ingested 225 mg per day of MB ?
I did 3x20mg per day. The only side effect was rapid weight gain. It made me fat very fast.
 

burtlancast

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Laurent Schwartz, the main leader of this research group, has some very interesting theories about cancer and other chronic diseases, very similar in many points to Peat.

He's the real french Ray Peat, as @haidut would say. :wink

Laurent Schwartz (oncologue) — Wikipédia
 
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burtlancast

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He also places the origin of chronic diseases on the energy malfunctioning in mitochondrias and all his compounds attempt to normalize this energy production.
 

LLight

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He advocates for resveratrol, ketogenic diet and metformin for cancer.
Yes but he is the only (french) scientist that I know who consider the metabolism regarding diseases.

They are rare.
 

Vinny

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A COHORT OF CANCER PATIENTS WITH NO REPORTED CASES OF SARS-COV-2 INFECTION : THE POSSIBLE PREVENTIVE ROLE OF METHYLENE BLUE
Publié par Guérir du Cancer | Mar 28, 2020 | Bleu de Méthylène, Covid-19 | 7 |

Marc Henry1*, Mireille Summa2, Louis Patrick3, Laurent Schwartz4

1 Université de Strasbourg, Chimie Moléculaire du Solide, Institut Le Bel, Strasbourg.
2 Ceremade, Université Paris Dauphine
3 Association Espoir Métabolique
4 Assistance Publique des Hôpitaux de Paris, Paris, France.

Abstract

We report the case of a cohort of 2500 French patients treated among others with methylene blue for cancer care. During the COVID-19 epidemics none of them developed influenza-like illness. Albeit this lack of infection might be by chance alone, it is possible that methylene blue might have a preventive effect for COVID-19 infection. This is in line with the antiviral activity of Chloroquine, a Methylene blue derivative.

Both Chloroquine and Methylene blue have strong antiviral and anti- inflammatory properties probably linked to the change in intracellular pH and redox state.

Conclusion

With the current COVID-19 outbreak, the world is facing a challenge and every possibility of helping people should be considered. Our preliminary data suggest but do not prove that Methylene blue might be a good treatment for influenza- like illnesses. Both Methylene blue and its derivatives such as chloroquine may share similar mechanism of action. Time is ripe for a prospective randomized clinical trial for the treatment of this dreadful disease.

Old drugs which have been tested for other indications ( such as Methylene blue or Chloroquine) have a well-defined safety profile. They are often more effective than new drugs from the High Tech. The Covid 19 epidemics like cancer has a solution. Reporpusing of known molecules will help cure these deadly diseases.

A cohort of cancer patients with no reported cases of SARS-CoV-2 infection : the possible preventive role of Methylene Blue — Guérir du Cancer
I bet there will be no clinical trial with MB. What are they going to do is to create another useless, and may be harmful vaccine for a single virus, that will pass and go by itself. Madness, madness is everywhere...
 

S.Seneff

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Haidut said it was the quinone structure that provides the benefit. Fermented product contains menaquinone. Natto is the one. Japan consumes it. So Japan has low covid-19 ?

Methylene blue seems to have a short half-life. Menaquinone-7 or plus seems to have longer hl.
 

Terma

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This is gonna be a bit rough. Not advice, etc. First off there's no way I could do 75mg safely and never went over 5mg usually < 1mg. The ALA dose (800mg x2) by comparison is less than I used to take. Note ALA famously increases glucose uptake from blood through AMPK, this can surprise.

The role of GR and TrxR is to keep GSH and redoxins in the reduced state in order to maintain cytosolic spaces under reduced conditions. The key point is that methylene blue could be a substrate for TrxR with production of the reduced neutral and colorless form (leuco-methylene blue or LMBH) absorbing in the UV-part of the electromagnetic spectrum (λ = 340 nm, ε = 3.3 mM-1·cm-1 and λ = 258 nm, ε = 17.4 mM-1·cm-1):
I think alternative explanation to lowering GSH (which essentially must be done in a localized way) is the impact on NADPH oxidase. NOX is destructive enzyme responsible for poor outcomes in viral infections, e.g. smoking. In some stressful experiments MB was able to halt NOX. That said there's a conversation missing here about cell-type specific effects like macrophages, but NOX also contributes to hypertension and affects ion movement and there's little question it participates in lung+cardiovascular injury.

They also tried MB in a combo with lipoic acid (which can buffer for GSH, but has pro-oxidant effects; my personal experience with LA was very good despite the preliminary warnings which were worth ignoring). I never tried MB with LA. There may be a specific preference for the form: Lipoic acid - Wikipedia
All the disulfide forms of LA (R/S-LA, RLA and SLA) can be reduced to DHLA although both tissue specific and stereoselective (preference for one enantiomer over the other) reductions have been reported in model systems. At least two cytosolic enzymes, glutathione reductase (GR) and thioredoxin reductase (Trx1), and two mitochondrial enzymes, lipoamide dehydrogenase and thioredoxin reductase (Trx2), reduce LA. SLA is stereoselectively reduced by cytosolic GR whereas Trx1, Trx2 and lipoamide dehydrogenase stereoselectively reduce RLA. (R)-(+)-lipoic acid is enzymatically or chemically reduced to (R)-(-)-dihydrolipoic acid whereas (S)-(-)-lipoic acid is reduced to (S)-(+)-dihydrolipoic acid.[38][39][40][41][42][43][44] Dihydrolipoic acid (DHLA) can also form intracellularly and extracellularly via non-enzymatic, thiol-disulfide exchange reactions.[45]
My guess (but you'd have to verify) is that R-ALA/RLA might be desirable by virtue of leaving the GR system alone (note that traditionally for R-ALA you're supposed to take less the dose of normal/SLA supplements but all the studies use the regular form), but can't make a big deal out of it without numbers.

However you can't lower NADPH systemically/indefinitely because it's cofactor for steroid conversions, kynurenine and life-critical systems (then again, it's theoretically possible that inhibiting kynurenine modified the immune system in a way specifically beneficial to SARS in the earlier or acute stages, but I haven't seen articles on that). Emphasis on: you want to throttle NOX during ARDS. Later you need NADPH to heal and compromising NADPH in regular/immune cells carries risk.

I know if I take MB for a few days I feel completely off and the doses aren't huge so I don't imagine serotonin as much but it could be from compromised steroids/pathways or higher H2O2 production in some conditions, which would normally be anti-viral if it's produced:
The antioxidant thiol-producing enzymes guarding the reducing milieu of cytosolic spaces are thus turned in contact with methylene blue into pro-oxidant H2O2-producing enzymes challenging the reducing milieu that they are meant to protect.
Then again there was a study suggesting MB at least somewhere has the ability to oxidize GSH without generating net extra H2O2, but I don't recall how that was resolved in vivo. May come down to catalase.

Of course this, but emphasis on tissue/subcellular action/distribution of the drugs:
In addition, there is less GSH available in the parasite as a substrate of GSH S-transferase for the detoxification of hemes and other lipophilic compounds.
[...]
The anti-bacterial effect of methylene blue then lies in the fact human GR reacts more slowly with methylene blue than parasites GR and that human TrxR is not present in erythrocytes. Accordingly, when parasitized red blood cells and normal erythrocytes are incubated together in MB-containing solution, the drug becomes concentrated selectively in the parasitized erythrocytes. A possible reason is that as LMBH bears no electrical charge, it easily permeates the membrane of digestive vesicles and is then auto-oxidized back to MB⊕, thus remaining trapped in the vesicles. It is finally worth noticing that synergistic effects have been found against P. falciparum in culture when using methylene blue in combination with artemisinin derivatives.20

Pointing out:
The half-life of MB in blood after intravenous administration is 5.25 h in humans.

LA is particular interest to me but form might matter, it seems powerfully therapeutic in various cases though it's not a guaranteed antioxidant (in my case that means I'd still consider NAC+glycine(or serine) for emergency symptoms, or in other words the point where NADPH/GSH in human cells is critically affected - remember GSH chaperones copper). Fast-acting and its half life is tiny so easy to titrate based on symptoms and stop. Logically through AMPK it drives glucose into cells so would help feed MB. This would be in any case a powerful therapy for something and I still have both. However you might worry about compromising eNOS too far in hypertension and circadian problems or increasing H2O2 which can already be pathogenic, and oxidative supplements can go wrong (personal+anecdotal experience and deduction), so I'll never do high doses right off the bat, and a minimum ascorbic acid must be in the system. It's the tissue localization that makes this convincing, hope it's correct.

I'm not sure how much oral AA I'd throw into this, but in my experience MB and LA are much stronger individually so I know what I'd pick in desperate situation with a gun. But that's not the final word because it was pointed out in the other thread that AA may be unique in protecting heme, and I'm not sure the relative contributions of these others... A minimum AA needs to be taken apart, but it might be valid to support AA recycling instead (LA seems to support AA but again can be pro-oxidative) in the right ways. The only potential risk AA carries is oxalic acid synthesis which would do damage especially during catastrophic Ca2+ overload, only acceptable for pathogens/cancer. Personally my experience with AA was never impressive while NAC and ALA pretty much kept me alive so in terms of oral potency no comparison. Most likely at the onset I'll start some AA daily and amino acids and swap if symptoms progress, to start with the safest and most approved. There are other things like selenium/zinc/magnesium/sodium/etc., B2/vitamins, rutin/hesperidin, aspirin (I reserve aspirin for very high fever, can't take it for long), especially cholesterol/steroids, and retinoic acid is critical lung factor, but even staying outside of prescription pharmaceuticals there's a point you can't predict the interactions, and among these MB/LA are wildcards. [inosine also good idea, incompatible with me]

There should be a convo about fibrosis and TGF-beta but I never compiled the effects of each of these on it (steroids/retinoids matter) and they're highly contextual, but generally the inclusion of NAD+/SIRT/AMPK/Thyroid-promoting effects restricts it:
TGF-b-and-AMPK-SIRT-crosstalk-The-negative-cross-regulation-between-TGF-b-signaling.png

Aside I think the risk of complications/fibrosis will be higher in hyperhomocysteinemia, as it may be symptomatic of broken serine/P5P-dependent transsulfuration compromising cellular defense and other reasons, so you can imagine the risk factors for people with existing cardiovascular disease even through non-causal associations, though this isn't exactly study material.
 
Last edited:

SOMO

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Small doses of Methylene Blue = brain and energy boost

Large doses of Methylene Blue = Drowsiness, stuffy nose and blue urine, but rapid clearing of infections and disinfection of oral and intestinal bacteria.
 

Terma

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e.g.: People with G6PD deficiency shouldn't take MB on their own, assumed to be due to compromised NADPH: Blue cures blue but be cautious (meanwhile supplementing ribose or malate during infection sounds risky if they fed the wrong bacteria)
However, known or suspected G6PD deficiency is a relative contraindication to the use of methylene blue. G6PD-deficient individuals generate insufficient NADPH to efficiently reduce methylene blue to leukomethylene blue, which is necessary for the activation of the NADPH-dependent methemoglobin reductase system. G6PD-deficient individuals are also prone to methylene blue-induced hemolysis. Methylene blue may also add to oxidative hemolysis. Moreover, in the presence of hemolysis, high-dose methylene blue can itself initiate methemoglobin formation.[7,8]
I guess the question is what minimum dose required for these effects, idk atm

It would be irresponsible to forget to point out that NOX is a primary justification for antagonizing angiotensin:
Angiotensin II, NADPH Oxidase, and Redox Signaling in the Vasculature
showing the overlap between therapies.
 
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Vinny

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This is gonna be a bit rough. Not advice, etc. First off there's no way I could do 75mg safely and never went over 5mg usually < 1mg. The ALA dose (800mg x2) by comparison is less than I used to take. Note ALA famously increases glucose uptake from blood through AMPK, this can surprise.


I think alternative explanation to lowering GSH (which essentially must be done in a localized way) is the impact on NADPH oxidase. NOX is destructive enzyme responsible for poor outcomes in viral infections, e.g. smoking. In some stressful experiments MB was able to halt NOX. That said there's a conversation missing here about cell-type specific effects like macrophages, but NOX also contributes to hypertension and affects ion movement and there's little question it participates in lung+cardiovascular injury.

They also tried MB in a combo with lipoic acid (which can buffer for GSH, but has pro-oxidant effects; my personal experience with LA was very good despite the preliminary warnings which were worth ignoring). I never tried MB with LA. There may be a specific preference for the form: Lipoic acid - Wikipedia

My guess (but you'd have to verify) is that R-ALA/RLA might be desirable by virtue of leaving the GR system alone (note that traditionally for R-ALA you're supposed to take less the dose of normal/SLA supplements but all the studies use the regular form), but can't make a big deal out of it without numbers.

However you can't lower NADPH systemically/indefinitely because it's cofactor for steroid conversions, kynurenine and life-critical systems (then again, it's theoretically possible that inhibiting kynurenine modified the immune system in a way specifically beneficial to SARS in the earlier or acute stages, but I haven't seen articles on that). Emphasis on: you want to throttle NOX during ARDS. Later you need NADPH to heal and compromising NADPH in regular/immune cells carries risk.

I know if I take MB for a few days I feel completely off and the doses aren't huge so I don't imagine serotonin as much but it could be from compromised steroids/pathways or higher H2O2 production in some conditions, which would normally be anti-viral if it's produced:

Then again there was a study suggesting MB at least somewhere has the ability to oxidize GSH without generating net extra H2O2, but I don't recall how that was resolved in vivo. May come down to catalase.

Of course this, but emphasis on tissue/subcellular action/distribution of the drugs:


Pointing out:


LA is particular interest to me but form might matter, it seems powerfully therapeutic in various cases though it's not a guaranteed antioxidant (in my case that means I'd still consider NAC+glycine(or serine) for emergency symptoms, or in other words the point where NADPH/GSH in human cells is critically affected - remember GSH chaperones copper). Fast-acting and its half life is tiny so easy to titrate based on symptoms and stop. Logically through AMPK it drives glucose into cells so would help feed MB. This would be in any case a powerful therapy for something and I still have both. However you might worry about compromising eNOS too far in hypertension and circadian problems or increasing H2O2 which can already be pathogenic, and oxidative supplements can go wrong (personal+anecdotal experience and deduction), so I'll never do high doses right off the bat, and a minimum ascorbic acid must be in the system. It's the tissue localization that makes this convincing, hope it's correct.

I'm not sure how much oral AA I'd throw into this, but in my experience MB and LA are much stronger individually so I know what I'd pick in desperate situation with a gun. But that's not the final word because it was pointed out in the other thread that AA may be unique in protecting heme, and I'm not sure the relative contributions of these others... A minimum AA needs to be taken apart, but it might be valid to support AA recycling instead (LA seems to support AA but again can be pro-oxidative) in the right ways. The only potential risk AA carries is oxalic acid synthesis which would do damage especially during catastrophic Ca2+ overload, only acceptable for pathogens/cancer. Personally my experience with AA was never impressive while NAC and ALA pretty much kept me alive so in terms of oral potency no comparison. Most likely at the onset I'll start some AA daily and amino acids and swap if symptoms progress, to start with the safest and most approved. There are other things like selenium/zinc/magnesium/sodium/etc., B2/vitamins, rutin/hesperidin, aspirin (I reserve aspirin for very high fever, can't take it for long), especially cholesterol/steroids, and retinoic acid is critical lung factor, but even staying outside of prescription pharmaceuticals there's a point you can't predict the interactions, and among these MB/LA are wildcards. [inosine also good idea, incompatible with me]

There should be a convo about fibrosis and TGF-beta but I never compiled the effects of each of these on it (steroids/retinoids matter) and they're highly contextual, but generally the inclusion of NAD+/SIRT/AMPK/Thyroid-promoting effects restricts it:
View attachment 17334

Aside I think the risk of complications/fibrosis will be higher in hyperhomocysteinemia, as it may be symptomatic of broken serine/P5P-dependent transsulfuration compromising cellular defense and other reasons, so you can imagine the risk factors for people with existing cardiovascular disease even through non-causal associations, though this isn't exactly study material.
I wish I had the brain to grasp this.....:banghead:
 

Terma

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It takes a lot of mistakes

Like this: to correct above I say ALA/LA increases AMPK and it does but it also increases Akt which is in the machinery actually responsible for the glucose sensitivity/uptake. Altogether meaning it behaves a bit like T3, and its precursor is caprylic acid which can be otherwise used for ketones meaning energy, and I'd say it's comparable in importance to ketones in the magnitude of its therapeutic effects, so even without MB I'm going to consider taking it again. But I don't think it fully substitutes for NAC, since that's de-novo GSH. So I'm going to be taking like 10 things.
 
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