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This is a huge and very detailed write-up on Corona from the perspective of a genomic analysis firm that I am not previously familiar with. It goes through many approaches listed in this thread. It is nuanced and goes into many of the pros and cons of different approaches.
At the end you get to the gist of what the author think is important (a consultation with them)
If you are dealing with challenges in physical health or cognitive ability and need additional insights into how to develop aggressive and effective strategies for immune resilience / protection, I encourage you to reach out today and book a consultation with Transcend Genomics. Your needs, as an individual, cannot be determined by broad, generalized studies that draw conclusions based on limited evidence. Everyone needs their own, specific approach, tailored to their history, current health challenges, genetics, and all other vital markers that define how you function biochemically.
Skip to the very end for a list of what the article author considers to be the main approaches.
Therapeutic Candidates Resveratrol
This natural phenol is produced by several plants in response to pathogen-induced injury. While it is more well known for its beneficial effects on cardiovascular disease, cancer, metabolism, and (controversially) lifespan, it actually has some very interesting properties that may make it a powerful ally in the fight against COVID-19.
Zinc
Decreases neutrophil and macrophage chemotaxis693694
Improves glutathione-conjugation of toxins in liver695
Modulates haptoglobin production696
Inhibits NLRP3 inflammsome and ameliorates lung injury697698699
Promotes mitochondrial biogenesis700701702
Directly lowers the expression of TMPRSS2703
Zinc is absolutely vital for proper immunity and deficiency is common in tuberculosis, pneumonia, acute lower respiratory tract infection, and the common cold.704
Quercetin
Inhibits replication potential in coronaviruses705
Useful in the early stages of the disease by directly improving interferon-mediated antiviral immunity706
If taken during cytokine storm, it will suppress IL10, amplify chemotaxis, and increase inflammatory potential, so care must be taken with timing.707
This flavonoid is most abundantly found in citrus fruit, buckwheat, and onions. It is mostly known for its ability to inhibit allergic-type inflammation, though antioxidant and protein kinase enzyme inhibition activities have also been noted. Before implementing this compound, it should be noted that it is decidedly estrogenic, with binding potential for both alpha and beta estrogen receptors. Nonetheless, other potential attributes have been documented that could prove useful in COVID-19.
Simvastatin
Reduces angiotensinogen expression, thereby preventing elevations in angiotensin II708
Suppresses excessive inflammation709
Protects against vascular injury / remodeling710
Beyond lipid-lowering effects, this statin also has a wide range of potentially protective effects throughout the course of coronavirus infection.
Low-Dose Dipyridamole (LDD)
Ameliorates angiotensin-II induced endothelial dysfunction711
Decreases excessive granulocyte chemotaxis712
May decrease viral loads and mitigate inflammation713
Has shown the ability to inhibit the NLRP3 inflammasome714
Dipyridamole is a nucleoside transport inhibitor and a PDE3 inhibitor medication that inhibits blood clot formation and prevents stroke when given chronically, long-term. Short-term use, however, promotes blood vessel dilation and lowers blood pressure.
Lately, low-dose dipyridamole (LDD) has been proposed for the treatment of insomnia, dry eye, dry mouth, erectile dysfunction, and fibromyalgia. Most notably, however, is its ability to prevent and treat viral diseases in both adults and children. Though very little is known regarding its off-label mechanisms, much may be presumed about its molecular activity, given it is an analogue of adenosine.715
Metformin
Modulates lung epithelial inflammation via adenosine receptor A2a716
Augments IL10 response717
Protects mitochondrial membranes against iron-induced lipoperoxidation718
Decreases metalloproteinase expression and release by monocytes719
Originally marketed as an anti-diabetic drug, Metformin is now gaining traction for its anti-aging potential. While it would be beyond the scope of this article to explain why Metformin may actually be a dangerous option, long-term, for either blood glucose control or attainment of longevity, it nonetheless possesses some very useful properties in the context of COVID-19.
N-Acetyl-Cysteine (NAC)
Reduces chemokine expression720
Inhibits intravascular inflammation721
May improve antiviral protection by up-regulating type I interferon signaling722
Increases mitochondrial biogenesis723
Inhibits NLRP3 inflammasome724
Acetylcysteine is an N-acetyl derivative of the amino acid L-cysteine. L-cysteine, along with glycine and glutamine, is an essential precursor for the formation of master-antioxidant glutathione. I have already described the potential in COVID-19 for massive depletion of all antioxidants systemically. Glutathione plays a particularly important role in red-blood-cell antioxidant capacity, without which there is a greater risk for hemolysis.
Compounds to Avoid during COVID-19 Acetaminophen
Inhibits ACE (angiotensin converting enzyme)725
Reduces AngII receptor binding726
Reduces macrophage hyperactivity and promotes dormancy727
Reduces vascular inflammation by inhibiting AGEs / glycation728
Improves parameters of COPD729
Reduces excess mucous in the lungs, though this may be problematic for those with genetics for lower mucin production.730
Marketed as Tylenol, this non-steroidal anti-inflammatory drug’s safety for SARS-CoV-2 infection has not been thoroughly proven. Nonetheless, the medical community at large has mostly focused on ibuprofen’s risks and recommended, with impunity, the use of acetaminophen for pain and inflammation reduction. Let’s look at various ways this drug could be problematic for COVID-19.
Dexamethasone
Decreases intracellular glutathione in pulmonary macrophages and type II pneumocytes, resulting in profoundly diminished antioxidant capability in the lungs731
Depletes glutathione in the liver, potentially leading to hepatic necrosis, especially in the presence of pre-existing, systemic oxidative stress732
May increase systolic and diastolic blood pressure in patients with pre-existing cardiovascular disease733
The use of corticosteroid medications has been mostly discouraged for COVID-19 patients, due to their potential to suppress immune response. Obviously, timing is everything — suppressing immune response at the early stages of infection can inhibit antiviral potential whereas at later stages when immune processes are out of control (e.g. during cytokine storms), a certain amount of suppression might be desirable. That being said, there are other mechanisms of action that make corticosteroids such as dexamethasone problematic for this disease.
Copper
Increases gene expression of angiotensin II type 1 receptors734
Induces ACE expression in monocytes, paradoxically increasing their inflammatory potential735
Can alter T-cell expression, amplify chemokine response, and trigger autoimmunity, especially in the elderly736
Substantially decreases glutathione in alveolar epithelial cells, enhancing potential for oxidative damage737
We have already discussed the dangers of excessive serum iron and how that might be exacerbated by high-dose ascorbic acid intake. Copper, however, also plays a significant role in disease outcome. Not only does it compete for transluminal transport with iron and zinc, but it can, at increasing levels, also suppress zinc’s immune-benefits.
Copper is required for inflammasome activation, and chelation blocks NLRP3 induction738
Excess copper transport in pulmonary arteries contributes to the development of hypoxia-induced pulmonary hypertension.739
Ascorbic acid “auto-oxidizes” in the presence of copper, in a dose-dependent manner740
This is not to mean that copper should be avoided altogether. On the contrary, a proper zinc to copper ratio (generally from 15-30:1 zinc:copper) fosters not only robust immunity but also balanced expression of superoxide neutralizing SOD2, protecting mitochondria from oxidative stress. As copper levels rise in the direction of (or higher than) zinc, hydrogen peroxide from superoxide dismutation can further react with free copper to form hydroxyl radicals — a reaction that would be promoted by ascorbic acid. Therefore, the admonition is to keep zinc and copper in the right ratio and avoid large doses of ascorbic acid which have already been described above to be decidedly unpredictable and potentially dangerous.
DHEAThis naturally occurring adrenal steroid hormone is a metabolic intermediate in the production of both testosterone and estrogen. Its popularity has risen over the years, especially among longevity proponents because its levels are known to decline with age. While its potential benefits (in those that are deficient) are numerous, there may be several reasons why it may need to be avoided during SARS-CoV-2 infection.
May induce T-cell proliferation and increase natural killer cell count, but these effects are only seen at higher doses after at least 12 weeks time.741
Inhibits antiviral interferon-gamma and induces expression of IL10 and TGF-beta, both of which are immuno-suppressive. This effect occurs about 1 month into supplementation.742
Protects against vascular inflammation, pulmonary hypertension, and lung remodeling / fibrosis.743
Improves nitric oxide levels and increases vaso-relaxation744
Directly opposes corticosteroid effects, potentially promoting TNF-alpha induced inflammation745
Overall, the immune-modulating effects of DHEA appear to have a delayed onset, but may be in effect for people that have already been supplementing with it prior to infection. Nonetheless, it could inhibit antiviral immunity and promote inflammation (through corticosteroid opposition) at the wrong times, so using it in a clinical context would be challenging, to say the least.
NicotineIt might surprise you to see nicotine in the list, but apparently, it has been recommended (in chewing gum form) by certain fringe health groups, so a brief discussion of its dangers is in order here.
Synthroid / Excess T4
The most obvious problem is nicotine’s ability to transiently but nonetheless powerfully stimulate vasoconstriction, and thereby elevate blood pressure.746
Nicotine enhances ACE2 expression directly in the lung (via inhaled products) but more systemically if taken sublingually or via patch.747
Induces pro-inflammatory potential in alveolar macophages748
Enhances adhesion potential in endothelial cells, promoting macrophage-mediated inflammatory damage749
Provokes cathepsin-dependent activation of NLRP3 inflammasome750
Activates dendritic cells and augments their capacity to stimulate T-cell proliferation and cytokine secretion751
Last but certainly not least, we have the thyroid hormone T4, administered in either synthetic form (Synthroid) or as part of naturally desiccated thyroid products (NDT). The problem with these therapies is that in individuals that have slow or impaired conversion of T4 to the active form, T3, there is the potential for T4 pooling and higher conversion to reverse T3. This results in an overall down-regulation of metabolic rate — something that is already happening during infection. To make matters worse, excess T4 can also have other undesirable effects.
Thyroxine (T4) up-regulates angiotensinogen, thereby promoting higher AngII and increasing blood pressure.752
Directly induces the expression of pro-inflammatory cytokines such as IL1B and TNF-alpha753
Provokes superoxide production in alveolar neutrophils and macrophages754
Nonetheless, proper levels of thyroxine, in balance with T3, are vitally important for immune balance. Studies have shown thyroxine’s ability to potentiate interferon-gamma mediated antiviral activity, so if you suffer from hypothyroidism and are taking medication that contains T4 / thyroxine, the advice is simply to ensure you are not in excess. This can be confirmed by measuring free-T4/free-T3 ratio along with reverse T3.
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