Both "long" COVID-19 and CFS are likely caused by hypometabolism

[nejdev]

A good study that examines the remarkable parallels between the so-called "long" COVID-19 (i.e. chronic display of symptoms associated with COVID-19) and the (in)famous chronic fatigue syndrome (CFS). Namely, increases inflammation, excessive glycolysis, suppressed mitochondrial function and decreased synthesis of ATP. Despite all of these known signs of both pathologies, no study so-far (including the new one below) has suggested treatments with thyroid or other pro-metabolic therapies. For some reason, the therapies suggested by mainstream doctors revolve around antioxidants, and hydration therapies, which, while likely helpful, do not address the underlying cause. Considering both COVID-19 and its common therapies such as glucocorticoids suppress thyroid function, IMO addressing the thyroid angle as well as the inflammatory response should be the primary goal in regards to treating both "short" and "long" COVID-19, as well as CFS. Something as simple as progesterone administration could be a game-changer for these conditions due to both the pro-metabolic effects of progesterone, as well as its direct anti-viral effects combined with anti-inflammatory and (contrary to glucocorticoids) pro-immunity effects. Btw, based on the evidence available so far it is rather clear that CFS is little more than chronic hypometabolic state triggered by a cytokine storm or the stress reaction associated with either the original viral infection or its "treatments".

Redox imbalance links COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome
"...Although most patients recover from acute COVID-19, some experience postacute sequelae of severe acute respiratory syndrome coronavirus 2 infection (PASC). One subgroup of PASC is a syndrome called “long COVID-19,” reminiscent of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). ME/CFS is a debilitating condition, often triggered by viral and bacterial infections, leading to years-long debilitating symptoms including profound fatigue, postexertional malaise, unrefreshing sleep, cognitive deficits, and orthostatic intolerance. Some are skeptical that either ME/CFS or long COVID-19 involves underlying biological abnormalities. However, in this review, we summarize the evidence that people with acute COVID-19 and with ME/CFS have biological abnormalities including redox imbalance, systemic inflammation and neuroinflammation, an impaired ability to generate adenosine triphosphate, and a general hypometabolic state. These phenomena have not yet been well studied in people with long COVID-19, and each of them has been reported in other diseases as well, particularly neurological diseases. We also examine the bidirectional relationship between redox imbalance, inflammation, energy metabolic deficits, and a hypometabolic state. We speculate as to what may be causing these abnormalities. Thus, understanding the molecular underpinnings of both PASC and ME/CFS may lead to the development of novel therapeutics."

"...Several therapies targeting redox imbalance already have been utilized or proposed for the treatment of disease. NO inhibits the replication of SARS-CoV-2 in vitro (154) and improves oxygenation in people with COVID-19 when administered by inhalation (155). Small studies of ubiquinol (156) and of a combination of NADH and CoQ10 (157) have reported clinical benefit. Many other potential treatments targeting redox imbalance also deserve consideration: for example, glutathione (and glutathione donors), N-acetyl cysteine, cysteamine, sulforaphane, ubiquinol, nicotinamide, melatonin, selenium, vitamin C, vitamin D, vitamin E, melatonin plus pentoxyfylline, disulfiram, ebselen, and corticosteroids. In two cases of acute COVID-19, glutathione administered therapeutically counteracted dyspnea associated with COVID-19 pneumonia and reduced pulmonary inflammation (158)."

"...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. Clearly, COVID-19–induced permanent damage to the lungs (chronic hypoxia), heart (congestive failure), and kidneys (fluid and acid-base abnormalities) could cause some of the persisting symptoms seen in long COVID-19. In both long COVID-19 and ME/CFS other symptoms (e.g., fatigue, brain fog) may be generated by neuroinflammation, reduced cerebral perfusion due to autonomic dysfunction, and autoantibodies directed at neural targets, as summarized elsewhere (170). As many as 2.5 million people suffer from ME/CFS in the United States (6). The COVID-19 pandemic may generate a similar number of cases of long COVID-19 in the coming 1 to 2 y (5). It therefore is imperative that increased research be focused on both long COVID-19 and ME/CFS. Fortunately, the United States and several other countries have committed substantial funding to study chronic illnesses following COVID-19, one of which is long COVID-19. Two registries and associated biobanks of people with long COVID-19 and/or ME/CFS are available to aid research.* We suggest that the study of the connections between redox imbalance, inflammation, and energy metabolism in long COVID-19 and in ME/CFS may lead to improvements in both new diagnostics and therapies."

Are hypometabolism and hypothyroidism related? I just got my blood results back from the doctor and my P-Cystatin C(mg/L) levels were just above the lowest threshold at .65, whereas the reference range is .65 - 1.10. According to the testing lab:

Low levels of cystatin-C are very rarely seen. In some cases, untreated long-term hypothyroidism (hypothyroidism) may result in decreased cystatin-C.

 

[Jam]

Are hypometabolism and hypothyroidism related? I just got my blood results back from the doctor and my P-Cystatin C(mg/L) levels were just above the lowest threshold at .65, whereas the reference range is .65 - 1.10. According to the testing lab:

Low levels of cystatin-C are very rarely seen. In some cases, untreated long-term hypothyroidism (hypothyroidism) may result in decreased cystatin-C.

Cystatin C levels are decreased in atherosclerotic (so-called 'hardening' of the arteries) and aneurysmal (saccular bulging) lesions of the aorta.[67][68][69][70] Genetic and prognostic studies also suggest a role for cystatin C.[71][72] Breakdown of parts of the vessel wall in these conditions is thought to result from an imbalance between proteinases (cysteine proteases and matrix metalloproteinases, increased) and their inhibitors (such as cystatin C, decreased)... Non-Hispanic blacks and Mexican Americans had lower normal cystatin C levels.[85].

 

[nejdev]

Cystatin C levels are decreased in atherosclerotic (so-called 'hardening' of the arteries) and aneurysmal (saccular bulging) lesions of the aorta.[67][68][69][70] Genetic and prognostic studies also suggest a role for cystatin C.[71][72] Breakdown of parts of the vessel wall in these conditions is thought to result from an imbalance between proteinases (cysteine proteases and matrix metalloproteinases, increased) and their inhibitors (such as cystatin C, decreased)... Non-Hispanic blacks and Mexican Americans had lower normal cystatin C levels.[85].

Thanks for mentioning. I checked out the Wikipedia for the references on this, the Stanford paper that this was based on said the median range was around .51 for the "decreased" levels you referenced, so not really worried about hardening arteries or legions. I'm at .65 in a reference range of .60-1.10 (I think I mistyped the reference range up there).

I am interested about this foot note in the testing info: Low levels of cystatin-C are very rarely seen. In some cases, untreated long-term hypothyroidism (hypothyroidism) may result in decreased cystatin-C.

So while still within the acceptable ranges, I wonder if this could point to something with the thyroid (maybe, possibly, eventually?). I should mention though that literally all the tests they gave me came back completely normal (40+ blood panel). Super confusing considering my long haul situation.

 

[nejdev]

In addition to what @ecstatichamster mentioned above, I would also add that tests for "free" steroids, thyroid or otherwise, are even more meaningless. The only thing they show is how much TBG you produce, which is the protein that carries the thyroid hormones in the blood. High free T3 means low TBG, which is not a good sign as it implies hypothyroidism and potentially liver issues as well as that protein is produced by liver. It is the total T3/T4 tests, which are better indication of how well the thyroid gland is working.

Thyroxine-binding globulin - Wikipedia

en.wikipedia.org

So, if thyroid tests are done they should always include at a minimum TSH, and both free and total T4/T3, and ideally reverse T3 (rT3) as well. tests for liver function done at the same time as thyroid help even more with intereting thyroid results, but even those are not enough without considering temps/pulse as well.

Heya there, new to Peating, found my way here looking for help with my COVID long haul. It's been 7 months, was positive in March 2021 and got over the acute phase, have been dealing with a plethora of symptoms since, listed here: COVID Long Hauler for 7 months, need help

I recently had a full blood panel done (43+ tests) and literally everything came back normal. I have been to the doctor multiple times, everything comes back fine, but I'm still feeling like I got hit by a car, weird neuro problems, fatigue etc.

My tests for thyroid/liver function:

Thyroid
S-T4, free (ModE) (pmol / L) - 15 (ref 12-22)
S-TSH (ModE) (mE/L) - 2.9 (ref 0.3 - 4.2)

Liver
P-ASAT (microcat / L) - 0.36 (ref <0.76)
P-ASAT (microcat / L) - 0.47 (ref <1.1)
P-GT (microcat / L) - 0.30 (ref <1.4)

As you can see I'm within reference ranges. My entire panel looks normal. Not understanding how this reflects hypometabolism or hypothyroidism. Forgive my ignorance, I'm just getting into all these granular aspects of my health - before long COVID I was super healthy, never had to think about any of this.

 

[DonLore]

Heya there, new to Peating, found my way here looking for help with my COVID long haul. It's been 7 months, was positive in March 2021 and got over the acute phase, have been dealing with a plethora of symptoms since, listed here: COVID Long Hauler for 7 months, need help

I recently had a full blood panel done (43+ tests) and literally everything came back normal. I have been to the doctor multiple times, everything comes back fine, but I'm still feeling like I got hit by a car, weird neuro problems, fatigue etc.

My tests for thyroid/liver function:

Thyroid
S-T4, free (ModE) (pmol / L) - 15 (ref 12-22)
S-TSH (ModE) (mE/L) - 2.9 (ref 0.3 - 4.2)

Liver
P-ASAT (microcat / L) - 0.36 (ref <0.76)
P-ASAT (microcat / L) - 0.47 (ref <1.1)
P-GT (microcat / L) - 0.30 (ref <1.4)

As you can see I'm within reference ranges. My entire panel looks normal. Not understanding how this reflects hypometabolism or hypothyroidism. Forgive my ignorance, I'm just getting into all these granular aspects of my health - before long COVID I was super healthy, never had to think about any of this.

Your TSH is really high. Lab range for TSH is bull****, anything over 1 is already not good

 

[mostlylurking]

Heya there, new to Peating, found my way here looking for help with my COVID long haul. It's been 7 months, was positive in March 2021 and got over the acute phase, have been dealing with a plethora of symptoms since, listed here: COVID Long Hauler for 7 months, need help

I recently had a full blood panel done (43+ tests) and literally everything came back normal. I have been to the doctor multiple times, everything comes back fine, but I'm still feeling like I got hit by a car, weird neuro problems, fatigue etc.

My tests for thyroid/liver function:

Thyroid
S-T4, free (ModE) (pmol / L) - 15 (ref 12-22)
S-TSH (ModE) (mE/L) - 2.9 (ref 0.3 - 4.2)

Liver
P-ASAT (microcat / L) - 0.36 (ref <0.76)
P-ASAT (microcat / L) - 0.47 (ref <1.1)
P-GT (microcat / L) - 0.30 (ref <1.4)

As you can see I'm within reference ranges. My entire panel looks normal. Not understanding how this reflects hypometabolism or hypothyroidism. Forgive my ignorance, I'm just getting into all these granular aspects of my health - before long COVID I was super healthy, never had to think about any of this.

TSH very high, free T3 is missing. Without the free T3, test doesn't tell you much. Other things in addition to hypothyroidism can block oxidative metabolism. Thiamine deficiency/functional blockage will do it too. There have been correlations drawn between thiamine deficiency/blockage and long haul covid. Here are some articles for your consideration: You searched for covid and thiamine - Hormones Matter

 

[nejdev]

Your TSH is really high. Lab range for TSH is bull****, anything over 1 is already not good

What is this based on? Not doubting, just would like to know what your reference range is based on so I can better understand. Thanks.

 

[nejdev]

TSH very high, free T3 is missing. Without the free T3, test doesn't tell you much. Other things in addition to hypothyroidism can block oxidative metabolism. Thiamine deficiency/functional blockage will do it too. There have been correlations drawn between thiamine deficiency/blockage and long haul covid. Here are some articles for your consideration: You searched for covid and thiamine - Hormones Matter

Great, I'm going to read these. Thanks so much for the feedback. Here are my B complex levels:

S-Cobalamin (ModE) (pmol / L) - 370 (ref 150-650)
S-Folate (nmol / L) - 26 (ref >7)
P-Homocysteine (micromol / L) - 9.3 (ref <15)

I have upped my Thiamine intake, currently added liver pate and sunflower seeds to the diet...although the seeds aren't very Peaty, I think I'm going to start eating cooked beef liver for the extra thiamine. Also have some B complex coming in the mail today.

 

[DonLore]

What is this based on? Not doubting, just would like to know what your reference range is based on so I can better understand. Thanks.

"Normal" TSH Above 2 As A Cause Of Unexplained Infertility

As most of the people on this forum know, Peat has spoken many times about the optimal values of TSH and has said that its value should be as close to 0 as possible. I posted a study some time ago showing that "normal" TSH levels above 2 are associated with a number of health issues that baffle...

raypeatforum.com

I found this and there is a link going into further detail in the opening post

 

[mostlylurking]

Great, I'm going to read these. Thanks so much for the feedback. Here are my B complex levels:

S-Cobalamin (ModE) (pmol / L) - 370 (ref 150-650)
S-Folate (nmol / L) - 26 (ref >7)
P-Homocysteine (micromol / L) - 9.3 (ref <15)

I have upped my Thiamine intake, currently added liver pate and sunflower seeds to the diet...although the seeds aren't very Peaty, I think I'm going to start eating cooked beef liver for the extra thiamine. Also have some B complex coming in the mail today.

Sunflowers seeds are not a good idea; very high in PUFA. Doctors don't usually check for thiamine deficiency/function. Understanding what exactly to ask for is helpful. This guy in the video below explains the testing a short way in (10-15 min?). If you are trying to correct a functional blockage from covid, high doses of thiamine (hcl or TTFD) may be required. The official recommended RDA is woefully inadequate.

View: https://www.youtube.com/watch?v=mG3m3tbEGU0

 

[nejdev]

Sunflowers seeds are not a good idea; very high in PUFA. Doctors don't usually check for thiamine deficiency/function. Understanding what exactly to ask for is helpful. This guy in the video below explains the testing a short way in (10-15 min?). If you are trying to correct a functional blockage from covid, high doses of thiamine (hcl or TTFD) may be required. The official recommended RDA is woefully inadequate.

View: https://www.youtube.com/watch?v=mG3m3tbEGU0

Thanks so much for the feedback, very much appreciated. Been in a world of hurt these past 7 months.
Starting your video now. What is the difference between HCL and TTFD? And how do I know which one is required? I think the complex I ordered from life extension contains 150mg of HCL.

Also do you know if there are any cofactors with thiamine? Do I need to pair it with something?

Lastly do you see a connection between Thiamine and Niacin? I have been hearing more and more info recommending B3 as well.

 

[DonLore]

Thanks so much for the feedback, very much appreciated. Been in a world of hurt these past 7 months.
Starting your video now. What is the difference between HCL and TTFD? And how do I know which one is required? I think the complex I ordered from life extension contains 150mg of HCL.

Also do you know if there are any cofactors with thiamine? Do I need to pair it with something?

Lastly do you see a connection between Thiamine and Niacin? I have been hearing more and more info recommending B3 as well.

TTFD goes into cells (also inside brain) much faster and more efficiently, so it is more potent stuff. Magnesium, potassium and other b-vitamins are said to be required with thiamine

 

[mostlylurking]

Thanks so much for the feedback, very much appreciated. Been in a world of hurt these past 7 months.
Starting your video now. What is the difference between HCL and TTFD? And how do I know which one is required? I think the complex I ordered from life extension contains 150mg of HCL.

I got slammed last year by taking Bactrim antibiotic. It blocked my thiamine function and just about finished me off. I'm pretty sure I was already having a thiamine blockage issue caused by heavy metals. I had been taking about 75-100mg/day of thiamine for 6 years but it wasn't enough post Bactrim and I got really sick. I tried about 250-300mg pure thiamine hcl powder and experienced massive improvement within 45 minutes. That experience showed me my problem was with thiamine. I had to increase the dosage over time to maintain the same benefit. I wound up following Dr. Costantini's protocol here: HDT Therapy I have been taking 2 grams of thiamine hcl/day since the first of February and I'm doing well on it. Higher doses of the hcl type are needed because of absorption issues in the gut. My brain symptoms resolved just fine on the hcl.

I tried to take the TTFD thiamine but it gave me a headache (for 36 hours) so I stuck with the hcl. It is the old fashioned type that has a very long track record and is considered a safe supplement. You have to take it with water, not juice.

Excellent info on Dr. Costantini's site. Also excellent info on EONutrition's youtube channel here: https://www.youtube.com/channel/UCFqXidfUsI0vm73xsBMIQdQ

The safe way to supplement with potassium is to simply drink 8 oz of orange juice. I drink more of it though. Magnesium is helpful; I use magnesium glycinate. I also take a b-complex pill every day.

 

[mostlylurking]

Starting your video now. What is the difference between HCL and TTFD? And how do I know which one is required? I think the complex I ordered from life extension contains 150mg of HCL.

Hcl is the old fashioned (and safe) thiamine that's been around so long nobody is interested in doing new studies on it. TTFD is new(ish) and synthetic and has lots of interesting studies available on it. I think you can pretty much extrapolate the findings for TTFD over to the hcl in order to understand thiamine in general.

The spiel on TTFD is that it gets into the cells easier or without some helper transporter thingy (technical term) that some people are low on (genetics) and so have a harder time responding to the thiamine hcl. Seems to be a little turf war going on to me. TTFD fans (Dr. Lonsdale, Dr. Chandler Marrs, Elliot Overton) swear it gets into the brain whereas other types don't. Dr. Costantini swore by thiamine hcl and has said it is the only thiamine that gets into the "neurons". I wandered around the studies and did find a single study that said Benfotiamine (yet another thiamine type) doesn't cross the blood brain barrier and TTFD does.

I think that bad reactions are much more common with TTFD than thiamine hcl. Elliot Overton has a video about it and one of his suggestions/solutions if you react badly to TTFD is to take thiamine hcl for a while first. I got better on the hcl so I never tried TTFD a second time.

I've learned from reading that thiamine deficiency causes the blood brain barrier to become compromised. So if you can get this resolved via thiamine supplementation, your brain symptoms will improve.

Also do you know if there are any cofactors with thiamine? Do I need to pair it with something?

Some magnesium, some potassium (from orange juice), a good b-complex.

Lastly do you see a connection between Thiamine and Niacin? I have been hearing more and more info recommending B3 as well.

I take about 200mg of niacinamide/ day, about 50mg riboflavin (B2), and a little extra biotin (maybe 20-25mg) in addition to my b-complex. I take a gram or two of aspirin too; I've been diagnosed with rheumatoid arthritis (in remission) and I find the aspirin helpful. Just be sure to get niacinamide, not niacin. I use the pure powders from BulkSupplements.com.

here's a collection of Ray Peat quotes about niacinamide: Ray Peat, PhD Quotes on Therapeutic Effects of Niacinamide – Functional Performance Systems (FPS)

I also take progesterone and I take pregnenolone too. I doubled the pregnenolone for a while and I did see more improvement when I did that so I think pregnenolone is helpful. Progesterone is anti-inflammatory and I've taken about 40mg/day for over 6 years. I'm female, age 71. Progesterone is helpful for males too, especially for emergencies, like strokes for example. It lowers brain inflammation.

 

[mostlylurking]

Thanks so much for the feedback, very much appreciated. Been in a world of hurt these past 7 months.
Starting your video now. What is the difference between HCL and TTFD? And how do I know which one is required? I think the complex I ordered from life extension contains 150mg of HCL.

Also do you know if there are any cofactors with thiamine? Do I need to pair it with something?

Lastly do you see a connection between Thiamine and Niacin? I have been hearing more and more info recommending B3 as well.

You may want to research further; here's a link to a great RP search engine: PeatSearch: a Ray Peat-specific search engine - Toxinless Use the cell on the left to search Peat's articles; ignore the google ads at the top of the search results.

 

[nejdev]

You may want to research further; here's a link to a great RP search engine: PeatSearch: a Ray Peat-specific search engine - Toxinless Use the cell on the left to search Peat's articles; ignore the google ads at the top of the search results.

What a wealth of knowledge! Thank you SO much....this is a great place to start. So I've started my dosing with Thiamine HCL, nothing too noticeable yet (in fact I think I almost felt worse) but I think that was because I stopped taking antihistamines. I'm taking Loratadine and Famotidin for H1/H2 blockage, they really make a difference in the general fatigue/brain fog throughout the day. So I started back up on those again.

So I'm taking a B Complex that includes thiamine 150mg, the recommendations are to take two of those, twice daily, so I'm slowly ramping up my dosage to see what effect I get. On top of that I do my regular Vitamin D3, Magnesium, and Liposomal C which has potassium with it. Added Niacin (50mg/day) and Melatonin (3mg/day) but considering ramping up. Been eating liver pate, scored some veal liver recently that I need to cook as well. I have a whole host of symptoms over at my other thread, some days are worse, some days are better. I'm hoping your recommendations help.

I'll look into progesterone/pregnenolone, already taking a ton of ***t so might need to back off some other stuff to give my body a break. Last question, I have seen other users here favor niacinimide over nicotinc acid? Is there a particular reason?

Thanks again for this info, and I'm glad you've found it to work. I hope I can improve my condition myself, it has been an awful time and doctors have been pretty much useless through all this.

 

[mostlylurking]

On top of that I do my regular Vitamin D3, Magnesium, and Liposomal C which has potassium with it.

Beware of liposomal anything. It's PUFA (polyunsaturated fatty acid). I think I made myself pretty sick with liposomal C about 7 years ago. Beware of dosing with potassium; it's tricky. Better/safer to just drink some orange juice.

I think it's important to research thiamine as it can be a little tricky in some people. I found EONutrition videos very educational and helpful: https://www.youtube.com/channel/UCFqXidfUsI0vm73xsBMIQdQ also the articles about thiamine on hormonesmatter.com: You searched for thiamine - Hormones Matter I found Dr. Costantini's information on his site very helpful too: HDT Therapy

Although I personally did not experience much in the way of negative effects from it, some people can have heart palpitations (?) from high dose thiamine; I think that is tied to how the body has compensated for the deficiency and how much the deficiency has affected the heart. Things can take a little while to unwind. Take it slow, pay attention to your body, increase your dosage over some time (several weeks).

Added Niacin (50mg/day) and Melatonin (3mg/day) but considering ramping up.

Beware of niacin. Niacinamide is safe. Melatonin isn't a Peat recommendation either. Are you having trouble sleeping? Is that why you are taking Melatonin? Taking all your thiamine by 3:00pm improves sleep. Drinking a glass of milk before bed helps too. Progesterone an hour or so before bed helps too. I've also found that taking some aspirin and some (maybe 90-100mg) niacinamide before bed is helpful. Always take thiamine with water, never fruit juice as the sugar cancels it out.

I'll look into progesterone/pregnenolone, already taking a ton of ***t so might need to back off some other stuff to give my body a break.

Ray Peat has said he has helped a lot of people by talking them into stopping their supplements. He does not recommend supplementing with C as it is now all contaminated with lead in the manufacturing process and you can get too much in the way of anti-oxidants. Oxidation is positive and important. Drinking organic NO PULP orange juice is much safer than taking a C supplement. The added "pulp" is actually processing refuse they dissolve with mystery enzymes and put in the product to get rid of their refuse so the EPA doesn't fine them.

Last question, I have seen other users here favor niacinimide over nicotinc acid? Is there a particular reason?

Nicotinic acid = niacin; it is stressful to the body. Niacinamide is much safer and Peat clarifies that point on a regular basis. Something about niacin (aka nicotinic acid) forcing the mast cells to release histamine which is stressful to the body (the "niacin flush"). Niacinamide doesn't do that to you. If you are taking antihistamines, taking niacin may be why you feel you need them.

 

[mostlylurking]

On top of that I do my regular Vitamin D3, Magnesium, and Liposomal C which has potassium with it.

Ray Peat has said many times that he has helped a lot of people get well just by getting them to stop taking their supplements. Please listen carefully to this video, queued up to the start of the topic:
View: https://youtu.be/PuSfV43Quuo?t=419


I found this clip using this search engine: Bioenergetic Search You may find it helpful to find information that is available in Ray Peat interviews.

 

[mostlylurking]

"...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.

So is it beri-beri?

The Pandemic Within a Pandemic - LewRockwell
snippet: Furthermore, long-term Covid-19 symptoms (racing heart, crushing fatigue, shortness of breath, headache, muscle pain, sleeplessness, etc.) go unexplained. These symptoms are better explained by a vitamin B1 deficiency.

-and-

Fear and anxiety; the need of a relaxant

The lockdowns and frightening news reports that a mutated virus was about to eradicate human populations led to high levels of fear and anxiety. Subsequently, the consumption of alcohol and sugary foods, combined with sleeplessness which increased coffee and tea drinking, led to an unprecedented and widespread dietary deficiency. These foods and beverages block the absorption and transport of a key vitamin (B1, thiamine, pronounced thi-a-meen) that controls the human autonomic nervous system, which in turn controls the immune system.

The alcohol/B1 deficiency epidemic does not conveniently fit the profit-making objectives of vaccine makers nor the desires of politicians to control populations, and therefore it is conveniently overlooked.

The confounder

How do we know this?

A vitamin B1 deficiency, known as beriberi, continues to confound American medicine. How do we know this?

We know this because of data showing increased consumption of alcohol, coffee and tea during the pandemic.

The human body of an adult only has about 30 milligrams of vitamin B1 (thiamine). It is easily depleted.

The unexplained incidence of long-term Covid symptoms such as racing heart, chronic headache, crushing fatigue and even shortness of breath can only be explained by a deficiency of vitamin B1. No coronavirus, flu bug, or any other infection produces the symptoms observed with Covid-19.

The hidden epidemic preceded the Covid-epidemic

America was already experiencing a vitamin B1 epidemic when the Covid-19 pandemic was announced. With lockdowns the consumption of vitamin-B1-depleting alcohol at home rose 500%. Even prior to the pandemic in March of 2020, alcoholism accounted for 24% of adult emergency room/ambulance-delivered admissions. Alcoholism costs a staggering $100 billion in medical care, before Covid-19.

also this one: Do You Have Beri-Beri? - LewRockwell :

Modern beri beri is subtle. It is not the same vitamin deficiency disease that was traced to removal of bran from polished rice decades ago and quelled with vitamin fortified foods. As Dr. Lonsdale says, modern beri beri as a disease characterized by high calorie intake and where the diet is rich in carbohydrates. It occurs in over-fed human populations. As early as 1914 it was known that the risk for beriberi increases with greater carbohydrate and sugar consumption.

Dr. Lonsdale says there are often surprisingly clear clues to the disease found in the diet. Sugary foods, particularly those with sucrose and fructose, are the primary offenders. A classic example would be a person who consumes three or four cans of soda pop a day. A shortage of vitamin B1 then results in inefficient use of oxygen in the body and tissues that require high amounts of oxygen, such as the heart and brain, suffer the most.

The beri beri drum beats on

The list of maladies linked to vitamin B1 deficiency is extensive. It goes beyond heart failure, fibromyalgia and atrial fibrillation mentioned above.

In fact, in virtually every nerve disorder, including multiple sclerosis and glaucoma (optic nerve) a shortage of vitamin B1 should be ruled out with a strong repeated dose of a highly absorbable form of thiamin.

Today doctors may misdiagnose thiamin deficiency symptoms as Alzheimer's disease, congestive heart failure, amnesia, anorexia, cancer, ringing in the ears (tinnitus), peripheral neuropathy, irritable bowel (ulcerative colitis), loss of vision (amblyopia, cataract), epilepsy, schizophrenia, Guillain-Barré syndrome, glaucoma, arthritis, hearing loss, and psychosis.

Vitamin B1 requirements

But still, it is difficult for physicians to fathom that a shortage of a simple vitamin is what causes such widespread disease. After all, the daily requirement for vitamin B1 is just 1.5 milligrams per day, which should easily be met in a world of fortified foods and multivitamins. Furthermore, the body stores about 30-50 milligrams. But body stores can be depleted fairly rapidly, within 4-6 weeks. It is not fully appreciated that the human body's reserve pool of thiamin, can be fully depleted within days.

Beri beri modernus: it's in the tea cup, coffee mug and beer stein

The problem of thiamin deficiency may be traced to another daily practice, the consumption of coffee, tea or beer. Many millions of people consume coffee or tea at the same time they take their morning multivitamin. What's the problem with tea or coffee? They contain tannins (bitter parts) that alter vitamin B1 and render it useless. Sulfite preservatives, as found in wine, are another antagonist to B1. Alcohol also interferes with B1 absorption. In fact, about 30-80% of alcohol users have low circulating levels of B1. The lesson here is not to take vitamin B1 pills with coffee, tea or alcohol.

another article: Not the First Time a Vitamin Deficiency Was Confused For a Viral Epidemic

This article makes good points but it won't let me copy to paste here. So go take a look at it via the link.

 

[Sam321]

A good study that examines the remarkable parallels between the so-called "long" COVID-19 (i.e. chronic display of symptoms associated with COVID-19) and the (in)famous chronic fatigue syndrome (CFS). Namely, increases inflammation, excessive glycolysis, suppressed mitochondrial function and decreased synthesis of ATP. Despite all of these known signs of both pathologies, no study so-far (including the new one below) has suggested treatments with thyroid or other pro-metabolic therapies. For some reason, the therapies suggested by mainstream doctors revolve around antioxidants, and hydration therapies, which, while likely helpful, do not address the underlying cause. Considering both COVID-19 and its common therapies such as glucocorticoids suppress thyroid function, IMO addressing the thyroid angle as well as the inflammatory response should be the primary goal in regards to treating both "short" and "long" COVID-19, as well as CFS. Something as simple as progesterone administration could be a game-changer for these conditions due to both the pro-metabolic effects of progesterone, as well as its direct anti-viral effects combined with anti-inflammatory and (contrary to glucocorticoids) pro-immunity effects. Btw, based on the evidence available so far it is rather clear that CFS is little more than chronic hypometabolic state triggered by a cytokine storm or the stress reaction associated with either the original viral infection or its "treatments".

Redox imbalance links COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome
"...Although most patients recover from acute COVID-19, some experience postacute sequelae of severe acute respiratory syndrome coronavirus 2 infection (PASC). One subgroup of PASC is a syndrome called “long COVID-19,” reminiscent of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). ME/CFS is a debilitating condition, often triggered by viral and bacterial infections, leading to years-long debilitating symptoms including profound fatigue, postexertional malaise, unrefreshing sleep, cognitive deficits, and orthostatic intolerance. Some are skeptical that either ME/CFS or long COVID-19 involves underlying biological abnormalities. However, in this review, we summarize the evidence that people with acute COVID-19 and with ME/CFS have biological abnormalities including redox imbalance, systemic inflammation and neuroinflammation, an impaired ability to generate adenosine triphosphate, and a general hypometabolic state. These phenomena have not yet been well studied in people with long COVID-19, and each of them has been reported in other diseases as well, particularly neurological diseases. We also examine the bidirectional relationship between redox imbalance, inflammation, energy metabolic deficits, and a hypometabolic state. We speculate as to what may be causing these abnormalities. Thus, understanding the molecular underpinnings of both PASC and ME/CFS may lead to the development of novel therapeutics."

"...Several therapies targeting redox imbalance already have been utilized or proposed for the treatment of disease. NO inhibits the replication of SARS-CoV-2 in vitro (154) and improves oxygenation in people with COVID-19 when administered by inhalation (155). Small studies of ubiquinol (156) and of a combination of NADH and CoQ10 (157) have reported clinical benefit. Many other potential treatments targeting redox imbalance also deserve consideration: for example, glutathione (and glutathione donors), N-acetyl cysteine, cysteamine, sulforaphane, ubiquinol, nicotinamide, melatonin, selenium, vitamin C, vitamin D, vitamin E, melatonin plus pentoxyfylline, disulfiram, ebselen, and corticosteroids. In two cases of acute COVID-19, glutathione administered therapeutically counteracted dyspnea associated with COVID-19 pneumonia and reduced pulmonary inflammation (158)."

"...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. Clearly, COVID-19–induced permanent damage to the lungs (chronic hypoxia), heart (congestive failure), and kidneys (fluid and acid-base abnormalities) could cause some of the persisting symptoms seen in long COVID-19. In both long COVID-19 and ME/CFS other symptoms (e.g., fatigue, brain fog) may be generated by neuroinflammation, reduced cerebral perfusion due to autonomic dysfunction, and autoantibodies directed at neural targets, as summarized elsewhere (170). As many as 2.5 million people suffer from ME/CFS in the United States (6). The COVID-19 pandemic may generate a similar number of cases of long COVID-19 in the coming 1 to 2 y (5). It therefore is imperative that increased research be focused on both long COVID-19 and ME/CFS. Fortunately, the United States and several other countries have committed substantial funding to study chronic illnesses following COVID-19, one of which is long COVID-19. Two registries and associated biobanks of people with long COVID-19 and/or ME/CFS are available to aid research.* We suggest that the study of the connections between redox imbalance, inflammation, and energy metabolism in long COVID-19 and in ME/CFS may lead to improvements in both new diagnostics and therapies."

Alot of people are curing long covid with limbic reset courses as well as CFS.

Limbic overdrive due to massive fear campaigns is on par with CFS. Crazy