Niacin and Covid

submitted by EddieC from self.Coronavirus

Work In Progress

Placeholder for understanding the effects of Niacin against Covid

The COVID-19 Burden or Tryptophan Syndrome: Autoimmunity, Immunoparalysis and Tolerance in a Tumorigenic Environment:

"The chronic disease of #COVID19 is due to changes in the metabolism of tryptophan and the lack of niacin (NAD/NADH+)."

Pre-print: Sufficient niacin supply: the missing puzzle piece to COVID-19, and beyond? by Dmitry Kats

"Lack of tryptophan causes sustained anaemia due to insufficient stimulation of the bone marrow"

"We noted common severe disease predictors among those patients whose profiles were pronated to a worse evolution. They show an intracellular aerobic respiratory chain cycle that is completely shaken by lack of essential vitamin B3, which originated from the tryptophan cycle.

This explains some studies findings for a positive outcome found in the replacement of complex B vitamins in critically ill patients, not found for other vitamins. Covid-19 patients are under high-intensity metabolic stress, with depleted NAD/NADH+ to connect aerobic metabolism to anaerobic respiration. Also, in this highly intense stress period, blood cortisol is found in high concentrations.

COVID-19 is a complex combination of viral action and metabolic deficits triggered by infection and aerobic metabolism to anaerobic respiration. Also, in this highly intense stress period, blood cortisol is found in high concentrations.

COVID-19 is a complex combination of viral action and metabolic deficits triggered by infection and ternalisation of ACE-2, modifying the RASS axis to inflammatory vasospasm and thrombotic pathway, and reaches its maximum when immunoparalysis and tolerance allow the development of neoplasms, which the immune system should contain."

"We have been following these patients after hospital discharge due to Covid-19. Their main complaint, in the vast majority of cases, is muscular pain and fatigue. Myalgia and eosinophilia syndrome with chronic fatigue is related to the tryptophan metabolite cascade alterations. The magnitude of the syndrome may be hypoxemia dependent. The longer time under hypoxemia, the less niacin and the more tryptophan will deviate to Kynurenine in an inflamed environment."

Essentially, if you don’t have sufficient niacin supply, you get hypoxemia and thus progressed further along #COVID19 pathology

To put it concretely:

A lack of niacin is the underlying cause of #COVID19.

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[–]EddieC[S] 2 insightful - 2 fun2 insightful - 1 fun3 insightful - 2 fun -  (0 children)

Niacin and its metabolites as master regulators of macrophage activation

"This study reveals for the first time that niacin and its metabolites possess antioxidant, reprogramming and antiinflammatory properties on human primary monocytes and monocyte-derived macrophages

Our findings imply a new understanding of the mechanisms by which niacin and its metabolites favor a continuous and gradual plasticity process in the human monocyte/macrophage system."

[–]EddieC[S] 2 insightful - 1 fun2 insightful - 0 fun3 insightful - 1 fun -  (0 children)

Niacin-mediated rejuvenation of macrophage/microglia enhances remyelination of the aging central nervous system:

"These results identify niacin as a novel stimulator of macrophage/microglia phagocytosis in culture that acts through Hcar2 to upregulate CD36 culminating in myelin engulfment.

We conclude that niacin is not affecting circulating monocytes or the recruitment of macrophages/microglia into lesions in middle-aged animals, but that it promotes the intralesional phagocytic clearance of inhibitory myelin debris.

These results demonstrate that systemic treatment with niacin improves remyelination in the aging CNS, specifically in larger caliber axons that otherwise would not be remyelinated in aging after lysolecithin-induced demyelination.

Recently, it was shown that the ability for macrophages/microglia to export phagocytosed cholesterol is important for preventing the formation of cholesterol crystals and lysosomal rupture within macrophages/microglia in demyelinated lesions, and that this is reduced in aging.

As niacin has an extensive clinical history when used in dyslipidemia and is well tolerated, we examined whether systemic niacin treatment would be effective in improving the deficient remyelination observed in middle-aged mice.

Indeed, daily treatment with niacin enhanced myelin debris clearance, promoted OPC recruitment, as well as enhanced remyelination in lesions.

Altogether, these results identify a novel clinically approved medication that is able to significantly stimulate the innate immune system to enhance remyelination in the aging central nervous system.

These cells have also been shown to be detrimental through the secretion of free radicals and reactive oxygen species in addition to the release of potentially harmful pro-inflammatory cytokines [40].

As we found that niacin was able to significantly upregulate the secretion of several pro-inflammatory cytokines in vitro, including TNF-α which has been shown to be toxic in its soluble form through TNFR1 on oligodendrocytes [4], we were concerned that niacin treatment in middle-aged mice may exacerbate neurotoxicity. We do not think that this is the case, however, as we found no difference in axonal density with niacin treatment.

Furthermore, niacin treatment of mice induced with experimental autoimmune encephalomyelitis, an inflammatory model of MS, improved disease score and minimized the degree of inflammatory infiltrates in the CNS [52].

As pro-inflammatory macrophages/microglia have been previously shown to be important for remyelination [1, 26, 30], we may be harnessing the beneficial aspects of these cells without causing significant cell death or neurotoxicity.

It is also reassuring that we did not find elevation of pro-inflammatory monocytes in the circulation of niacin-treated mice, suggesting its safety in patients with inflammatory demyelinating diseases including MS.

Altogether, these results further emphasize the potential clinical utility of using niacin for remyelination.

We have identified niacin as a novel clinically approved medication that enhances macrophage/microglia phagocytosis of inhibitory debris, resulting in increased OPC recruitment and ultimately remyelination in the aging CNS."

[–]infocom6502 1 insightful - 2 fun1 insightful - 1 fun2 insightful - 2 fun -  (0 children)

It's going to take a while to read and digest.... but looking at your highlights it seems like an amazing find.

I take niacin in conjunction with creatine. This combo seems to have synergistic effects that are noticeable.

For anyone with a weakened condition glutathione or stimulating its production in liver (eg milk thistle+ glycine+ NAC+glutamine) this can greatly help recovery.

[–]EddieC[S] 1 insightful - 1 fun1 insightful - 0 fun2 insightful - 1 fun -  (0 children)

Niacin promotes cardiac healing after myocardial infarction through activation of the myeloid prostaglandin D2 receptor subtype 1:

"niacin increased PGD2 release in macrophages and shifted macrophages to M2 polarization both in vitro and in vivo by activation of DP1 and accelerated inflammation resolution in zymosan-induced peritonitis in mice.

Moreover, niacin treatment facilitated wound healing and improved cardiac function after MI through DP1-mediated M2 bias and timely resolution of inflammation in infarcted hearts. In addition, we found that niacin intake also stimulated M2 polarization of peripheral monocytes in humans. Collectively, niacin promoted cardiac functional recovery after ischemic myocardial infarction through DP1-mediated M2 polarization and timely resolution of inflammation in hearts."

[–]EddieC[S] 1 insightful - 1 fun1 insightful - 0 fun2 insightful - 1 fun -  (0 children)

Nicotinic acid modulates intracellular calcium concentration and disassembles the cytoskeleton:

"In conclusion, the present study indicated that NA disassembles F-actin and microtubule systems, thereby blocking cytoskeleton-dependent intracellular transport."

[–]EddieC[S] 1 insightful - 1 fun1 insightful - 0 fun2 insightful - 1 fun -  (0 children)

[Niacin increases cellular free & decreases ester cholesterol] https://www.jlr.org/article/S0022-2275(20)39224-5/fulltext

HDL-C-mediated cholesterol efflux & selective cholesterol transport become dysfunctional in chronic metabolic diseases such as obesity or atherosclerosis, consistent with the increased mortality observed in elderly patients & patients w/obesity or diabetes

Niacin increases serum total and HMW adiponectin concentrations and decreases lipolysis within minutes following GPR109A receptor activation. Because adiponectin concentrations are generally low and adipose tissue lipolytic activity high in obese individuals with the metabolic syndrome, niacin may be an ideal pharmacological approach to reduce CVD in this population.

Protection against/risk of #SARS_CoV_2 infection (& similarly for progression of #COVID19 severity as shown in another report) is (independently) associated with only HDL-C (/ApoA-I) and not LDL-C, ApoB, triglycerides, or anything else.

a 10 mg/dl increase in serum HDL-cholesterol or apolipoprotein A1 levels was associated with ∼10% reduced risk of SARS-CoV-2 infection, after adjustment for age, sex, obesity, hypertension, type 2 diabetes, and coronary artery disease. https://www.jlr.org/article/S0022-2275(21)00043-2/fulltext

a 0.2 mmol/L increase in HDL-C was associated with a corresponding 9% reduction in risk for COVID hospitalization. A very similar pattern of association was apparent when COVID-19 mortality was the outcome of interest.