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

ndn

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Earthpulse for sleep works, quantron resonance /QRS during the waking hours is higher intensity also necessary. Id do both
 

Texon

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I've never been a conforming kind of person. One of the most liberating things my psychotherapist ever provided to me (30+ years ago) was the mantra, "It's none of my business what other people think about me".

About focusing on one's mind and ruminations: When I was younger (before Peat) I was trapped in circular thinking and high anxiety. The therapist got a crawful of it one day and exclaimed, "oh, just stop with the catastrophizing!" I am here to tell you that my problem was body chemistry. Estrogen dominance, no progesterone, low thiamine, hypothyridism, high adrenaline, and heavy metals. For the past 6 years, (after finding Peat), I've improved my body chemistry with progesterone, some b-complex, and high dose thiamine, I am a different person.

The thing that slammed me a year ago that just about finished me off was a prescription for Bactrim antibiotic for a UTI. It blocked my thiamine function and just about killed me. I discovered thiamine because of an aside comment by Haidut on a Danny Roddy show; I tried some, it worked like magic, so I did a search for "Bactrim and thiamine" and found this article: Bactrim: An Anti-Folate, Anti-Thiamine, Potassium Altering Drug - Hormones Matter. Haidut and this article saved my life. Evidently, a lot of people get damaged by pharmaceutical drugs, mainly antibiotics, but Metformin too and there's others. I think that the way people become deficient in CO2 is their thiamine function gets blocked or they become deficient. The recommended daily requirement is pathetically low.

I've come to believe that thiamine is some amazing stuff.
Antibiotics deplete just about every important nutrient under the sun.

 

Texon

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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.
This is great information and rings completely true.
 

mostlylurking

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Antibiotics deplete just about every important nutrient under the sun.

Yeah, but some antibiotics are a whole lot worse than others. The problem is exacerbated by the inexcusable ignorance of the physicians prescribing them (I'm being generous). It's important to do your due diligence before you swallow any prescription.


and

 

mostlylurking

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This is great information and rings completely true.
B1 deficiency is such a dated idea; physicians assume it was eradicated when refined grains were "enriched" with it many years ago. They do not think to even consider it as a possibility.
 

Texon

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Yeah, but some antibiotics are a whole lot worse than others. The problem is exacerbated by the inexcusable ignorance of the physicians prescribing them (I'm being generous). It's important to do your due diligence before you swallow any prescription.


and

Absolutely agreed. I took only 1 dose of cypro one time...never again.
 

DonLore

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There seems to be evidence that Sars-cov2 can stay in the brain and CNS for a very long time, causing neuroinflammation. And this can powerfully mess up metabolism. So how could one kill the virus in the brain and CNS? Could iodine get to the brain via nasal spray? Or does anyone have any ideas?
 
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Zsazsa

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Addiction Drug Shows Promise Lifting Long COVID Brain Fog, Fatigue
CHICAGO (Reuters) - Lauren Nichols, a 34-year-old logistics expert for the U.S. Department of Transportation in Boston, has been suffering from impaired thinking and focus, fatigue, seizures, headache and pain since her COVID-19 infection in the spring of 2020.

Last June, her doctor suggested low doses of naltrexone, a generic drug typically used to treat alcohol and opioid addiction. After more than two years of living in "a thick, foggy cloud," she said, "I can actually think clearly ....
 

Validus

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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."
@haidut What are your thoughts specifically on Pentoxifylline from a high level? Safety, usefulness, mechanism of action etc?
 

Mauritio

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T3 as a covid treatment was rarely discussed but seems quite logical as most people dying are hypothyroid . To the point were the T3 level was an independent predictor of death.


"FT3 concentration was significantly lower in patients with severe COVID-19 than in non-severely ill patients. Reduced FT3 independently predicted all-cause mortality of patients with severe COVID-19."
 

Jam

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T3 as a covid treatment was rarely discussed but seems quite logical as most people dying are hypothyroid . To the point were the T3 level was an independent predictor of death.


"FT3 concentration was significantly lower in patients with severe COVID-19 than in non-severely ill patients. Reduced FT3 independently predicted all-cause mortality of patients with severe COVID-19."
 

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