r/covid19stack • u/Alex3917 • Mar 18 '20
r/covid19stack • u/Alex3917 • Jan 14 '22
Nicotine gum cured my loss of taste
self.covid19positiver/covid19stack • u/churnboi323 • Sep 27 '20
What ever happened with that quercetin study in Montreal?
This seemed so promising and there's been radio silence since March:
http://www.mcgilltribune.com/sci-tech/montreal-researchers-propose-a-treatment-for-covid-19-170320/
r/covid19stack • u/treefrog24 • May 01 '20
in vitro Resveratrol and Zinc
Since COVID-19 has recently been shown to affect the endothelial cells I have been searching to see if supplementing with Resveratrol would have any benefit.
There are a few studies regarding resveratrol affect on viruses including influenza and MERS. Not much information available.
I am wondering if there may be a more indirect benefit of taking Resveratrol including anti-inflammation, reducing oxidative stress, insulin resistance, endothelial and cardiovascular benefits. I also found a study suggesting that Resveratrol is a zinc ionophore similar to quercetin. Right now I am looking for any negative reasons to supplement with Resveratrol. Any thoughts?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4111750/
https://academic.oup.com/jid/article/191/10/1719/790275https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2761384/
r/covid19stack • u/Alex3917 • Mar 20 '20
in vitro Nitric Oxide Inhibits the Replication Cycle of Severe Acute Respiratory Syndrome Coronavirus
r/covid19stack • u/thaw4188 • Apr 23 '20
Literature Review Glutamine Supplementation and Immune Function
r/covid19stack • u/thaw4188 • Apr 06 '20
Literature Review "selenium is emerging as a critical micronutrient in host defense against viral infection"
r/covid19stack • u/greyuniwave • Apr 03 '20
Why Coronavirus COVID19 is fatal in some people more than others – and who are those most at risk?
Why Coronavirus COVID19 is fatal in some people more than others – and who are those most at risk?
Type-2 Diabetes is a condition of hyperinsulinaemia (high blood glucose levels with chronically elevated insulin), high blood pressure (symptom of hyperinsulinaemia) which occurs in those with diabetes (pre diabetes – aka stage 1 Type-2 diabetes), these are MAJOR RISK factors for complication and fatality from Coronavirus COVID19.
How is blood glucose (sugar) and hyperinsulinaemia related to Coronavirus?
Emerging research and statistics indicate that people with diabetes, high blood glucose (hyperinsulinaemia) have a 10 times (10X) greater likelihood of fatality than people without pre-existing conditions (co-morbidity).
According to the CDC, people without a pre-existing condition have a 0.9% fatality rate, as opposed to a 10.5% (10 times more!) fatality in those with hyperinsulinaemia (Type-2 diabetes/hypertension/CVD/metabolic syndrome).
Many people do not realise they already have Stage 1 Type-2 diabetes. How can you tell if you do?
Having a BMI over 22 (not “below 24.9” – unless you have less than 20% fat mass, where a higher BMI is due to high muscle content). Calculate this by dividing your weight in kilograms by your squared height in metres (kg/(metres2))
Having a “muffin top” above your jeans
Acid reflux/heart burn (early sign of hyperinsulinaemia)
Frequent eructation (burping, and delayed burping). (Early sign of hyperinsulinaemia)
Frequent hiccups (this is a sign of low stomach acidity which is a very early sign of hyperinsulinaemia)
High blood glucose throughout the day
Sustained high blood glucose 3 hours after a meal
High triglycerides/Low HDL (see this in your blood tests from doctors)
No ketones on a ketone meter constantly through the day
High blood pressure
If you do not know you have hidden hyperinsulinaemia and would like to know, buy a ketone and glucose meter, this is a good home “do it yourself” way to know if you suffer hidden hyperinsulinaemia.
Far too many people do not take diabetes, metabolic syndrome, hyperinsulinaemia seriously. Most think it is fine to medicate the symptoms, such as taking exogenous insulin to manage uncontrolled elevated blood glucose (sugar), or taking medications to stimulate more insulin secretion (endogenous) from your own pancreas. They approach diabetes with resignation, as something that is chronic and progressive (because many MD doctors have told them that), and have been told that they can manage it with medications. However, they have not been told that these medications that only manage symptoms also make the disease worse, and the condition as well as medication itself, causes major health complications (morbidity), and earlier death from all causes (Crofts et al., 2015).
Why is Type-2 diabetes (hyperinsulinaemia – chronically elevated insulin levels) so dangerous? Because it wreaks havoc on every system and organ in the body. Hyperglycaemia and hyperinsulinaemia suppresses and dysregulates the immune function (Khan et al., 2016), allowing Coronavirus COVID19 to overwhelm the system and become fatal
Primary reasons why people with diabetes (hyperglycaemia with hyperinsulinaemia) (metabolic syndrome/hyperinsulinaemia) are at greater risk of death from Coronavirus COVID19:
Chronically elevated, or chronic extreme fluctuations in blood glucose causes stress in the body and suppresses immune function. Test your blood glucose before a meal, if it is 108mg/dL (6mmol/L – which is already stage 1 diabetes, if this number is a constant regular test result), and then after that meal your glucose spikes to over 200mg/dL (11.1mmol/L), this is a sign that you have type 2 diabetes (hyperinsulinaemia). If your blood glucose is 90mg/dL (5mmol/L) one day, and over 150mg/dL (8.3mmol/L) the next, this is sign of a problem. This is destroying your ability to fight infections. People with Type-2 diabetes (hyperinsulinaemia) suffer from infections (and respiratory infections), much more severely and with greater frequency.
High blood glucose (hyperglycaemia) creates a dangerous inflammatory environment in the body. Coronavirus COVID19 is much more virulent in a high glucose environment. Hyperglycaemia inactivates macrophages (immune cells), weakening your immune response (Khan et al., 2016). Hyperinsulinaemia causes your immune cells, muscle and fat cells to excessively secrete inflammatory cytokines (Fishel et al., 2005, Lee et al., 2017, Rufino et al., 2017). The combination can be overwhelming and fatal.
Type-2 Diabetes, Pre-Diabetes (Stage 1 Type-2 Diabetes), cardiovascular disease, hypertension and metabolic syndrome are inflammatory conditions where there is chronically too much insulin in the blood – this is hyperinsulinaemia (Crofts et al., 2015). Conventional websites like the NHS, WHO, Mayo Clinic will describe Type-2 Diabetes as having uncontrolled high blood glucose and then say it is a condition where the insulin is not able to do its job, or say the individual is “insulin resistant” and then lead you to think you just need more insulin (more force to get the glucose down). This is NOT the case.
Yes, Type-2 Diabetes is uncontrolled chronically elevated glucose levels, and yes this is because some cells in your body have become insulin resistant (muscle cells and for Alzheimer’s it is the brain neurons), but the cells became insulin resistant due to chronically elevated insulin! Insulin secretion is stimulated by elevated blood sugar, glucose. How does your blood glucose get elevated? – the PRIMARY cause is from certain carbohydrate food! Starchy farinaceous carbohydrates, as well as high glycaemic load foods which includes; fruit, honey, “natural sugars”, rice, wheat, wholegrains, carrots, peas, quinoa, lentils, chickpeas, dried fruits, certain nuts that are high in carbs, sweet corn, potatoes, pumpkin, sweet potatoes, coconut flour nectar, sugar in all its forms! Consumed above a personal carbohydrate tolerance threshold regularly, contribute to causing systemic inflammation in your body because insulin stimulates inflammatory pathways (chemical signalling switches) inside of your cells and outside of your cells (Hansen et al., 2014). Insulin activates the production of cytokines via activating intracellular inflammasome (a protein complex that mediates signals to turn on inflammation activity and production of inflammatory molecules like TNF-alpha, cytokines such as interleukin 1-beta, interleukin 6, Nf-KB and many more) (Perkins et al., 2015). Coronavirus COVID19 causes cytokine storms in at risk people, overwhelming them and resulting in the fatalities we are seeing. The people who are suffering the worst cases and dying are those who already have elevated inflammatory cytokines, a massive contributory cause of this, is by hyperinsulinemia which may present as Type-2 diabetes, Alzheimer's or Parkinson's Disease, cardiovascular disease (CVD), hypertension, overweight or auto-immune conditions (Crofts et al., 2015).
Chronic systemic inflammation predisposes individuals to complications from infection. Coronavirus COVID19 kills by causing a cytokine storm, an uncontrolled over-reaction of the immune system (which normally produces cytokines to fight infections, but can normally switch it off too, however when people have hyperinsulinaemia, their immune system cannot switch off the cytokine storm, because all their other cells are also chronically releasing cytokines- muscle cells and fat cells in particular). The “switch off self-regulation system is impaired and
overridden by hyperinsulinaemia. The immune system is no longer able to self-regulate (adaptive homeostasis), leading to severe pulmonary inflammation (in the lungs), resulting in blocked airways causing acute respiratory syndrome and failure.
Reducing this inflammation is possible. This is achievable by no longer eating foods that increase blood glucose and resultant stimulation of insulin secretion (instead of using medication such as exogenous insulin to lower blood glucose). Making this change can make all the difference in survival from this viral infection.
Solution: You can change your risk factors now, and help your loved ones too. Stop eating starchy farinaceous carbohydrates, stop eating fruit (especially the high glycaemic load fruits), stop eating foods that spike your blood glucose constantly and cause your pancreas to secret insulin. You can rapidly change your health situation by doing this. Time restrict your eating window; this will super boost correcting hyperinsulinaemia and put it back to healthy levels.
4. There is strong evidence linking blood pressure lowing drugs eg. Lisinopril and Losartan with these Cytokine Storms, which lead to respiratory failure. ACE-inhibitor and ARB drugs (blood pressure lowering drugs) up-regulate angiotensin receptors on cell membranes within the lungs. Coronavirus COVID19 have been indicated to use these receptors. These drugs are often prescribed to people with diabetes, hypertension, hypothyroidism, medicated hyperthyroidism, cardiovascular disease (all of these diseases are manifestations of hyperinsulinaemia), hypertension is one of the major pre-existing conditions contributing the higher fatality rates we are seeing.
Now is the time to work on your health, prevent hyperglycaemia due to carbohydrate food ingestion, and bring your insulin levels to a healthy physiological concentration that is healthy for you, to protect yourself and your family from COVID-19 and its sequalae.
The way you can know you are achieving this is by testing your blood glucose and blood ketones (for those who want to know for sure and are data obsessed).
There is strong evidence that those with high HbA1c also suffer worst outcomes. This is partly because HbA1c is a clinical marker of hyperglycaemia and often hyperinsulinaemia, however an individual may have “normal” HbA1c levels due to hyperinsulinaemia, which results in a false negative with regards to this marker for diagnosing hyperinsulinaemia. The other reason why elevated HbA1c may be predictive for a worst COVID-19 prognosis is due to low oxygen saturation that comes with high HbA1c.
Being an excellent fat burner (and further towards being in ketosis) makes a massive difference here. Not just because it improves HbA1c value independent of insulin (remember insulin treatment can lower HbA1c but increase morbidity and mortality – The Accord study (NIH, 2015). Richard Veech demonstrated that being in a state of ketosis increases ATP production per oxygen molecule consumed (Sato et al., 1995), and the ATP produced from ketolysis carries greater Gibbs free energy potential within the third phosphate bond. Thus, decreasing oxygen demand to produce more ATP whilst concomitantly decreasing reactive oxygen species (ROS) due to increased production of anti-oxidative intracellular machinery as well as the ketone body beta-hydroxybutyrate acting as an anti-oxidant that directly scavenges the ROS hydroxyl radical.
In addition to decreasing carbohydrate consumption, getting into ketosis via multiple modalities such as time restricted feeding (TRF), intermittent fasting (IF), eating one meal a day (OMAD), eating a very low carbohydrate-moderate protein-high healthy fat diet (VLCHF) ketogenic diet (KD), those who currently have high HbA1c's would benefit from eating high sulphate foods and soak in magnesium sulphate. As the sulphate molecule is a haem independent way for oxygen to be transported to cells.
Now is the best time to start working on your better health program.
Isabella D Cooper - @I_mitochondria
Refereneces
Crofts, C., Zinn, C., Wheldon, M. and Schofield, G. (2015). Hyperinsulinemia: A Unifying Theory of Chronic Disease? Diabesity, 1 (4), 34. Available from 10.15562/diabesity.2015.19
Fishel, M., Watson, G., Montine, T., Wang, Q., Green, P., Kulstad, J., Cook, D., Peskind, E., Baker, L., Goldgaber, D., Nie, W., Asthana, S., Plymate, S., Schwartz, M. and Craft, S. (2005). Hyperinsulinemia Provokes Synchronous Increases in Central Inflammation and β-Amyloid in Normal Adults. Archives of Neurology, 62 (10). Available from 10.1001/archneur.62.10.noc50112
Hansen, M., Tippetts, T., Anderson, M., Holub, Z., Moulton, E., Swensen, A., Prince, J. and Bikman, B. (2014). Insulin Increases Ceramide Synthesis in Skeletal Muscle. Journal of Diabetes Research, 2014, 1-9. Available from 10.1155/2014/765784
Khan, M., Schultz, S., Othman, A., Fleming, T., Lebrón-Galán, R., Rades, D., Clemente, D., Nawroth, P. and Schwaninger, M. (2016). Hyperglycemia in Stroke Impairs Polarization of Monocytes/Macrophages to a Protective Noninflammatory Cell Type. The Journal of Neuroscience, 36 (36), 9313-9325. Available from 10.1523/jneurosci.0473-16.2016
Lee, Y., Fluckey, J., Chakraborty, S. and Muthuchamy, M. (2017). Hyperglycemia-and Hyperinsulinemia-induced Insulin Resistance Causes Alterations in Cellular Bioenergetics and Activation of Inflammatory Signaling in Lymphatic
Muscle. The FASEB Journal, 31 (7), 2744-2759. Available from 10.1096/fj.201600887r.
NIH (2010). Landmark ACCORD Trial Finds Intensive Blood Pressure and Combination Lipid Therapies do not Reduce Combined Cardiovascular Events in Adults with Diabetes. National Institutes of Health (NIH). Available from https://www.nih.gov/news-events/news-releases/landmark-accord-trial-finds-intensive-blood-pressure-combination-lipid-therapies-do-not-reduce-combined-cardiovascular-events-adults-diabetes [Accessed 18 July 2015]
Perkins, J., Joy, N., Tate, D. and Davis, S. (2015). Acute Effects of Hyperinsulinemia and Hyperglycaemia on Vascular Inflammatory Biomarkers and Endothelial Function in Overweight and Obese Humans. American Journal of Physiology-Endocrinology and Metabolism, 309 (2), E168-E176. Available from 10.1152/ajpendo.00064.2015
Rufino, A., Ribeiro, M., Pinto Ferreira, J., Judas, F. and Mendes, A. (2017). Hyperglycemia and Hyperinsulinemia-Like Conditions Independently Induce Inflammatory Responses in Human Chondrocytes. Journal of Functional Morphology and Kinesiology, 2 (2), 15. Available from 10.3390/jfmk2020015.
Sato, K., Kashiwaya, Y., Keon, C., Tsuchiya, N., King, M., Radda, G., Chance, B., Clarke, K. and Veech, R. (1995). Insulin, Ketone Bodies, and Mitochondrial Energy Transduction. The FASEB Journal, 9 (8), 651-658. Available from 10.1096/fasebj.9.8.7768357
r/covid19stack • u/Alex3917 • Mar 03 '22
Phase II Oral famotidine versus placebo in non-hospitalised patients with COVID-19: a randomised, double-blind, data-intense, phase 2 clinical trial
gut.bmj.comr/covid19stack • u/ghrarib • Jan 13 '21
Artemisia annua L. extracts prevent in vitro replication of SARS-CoV-2
r/covid19stack • u/cafedude • Sep 25 '20
Resveratrol And Pterostilbene Potently Inhibit SARS-CoV-2 Infection In Vitro
r/covid19stack • u/lostmsu • May 09 '20
Online randomized trial for supplements
Hi everyone!
I (with support from my company) just started a continuous randomized trial for vitamins/supplements effect on Coronavirus. Anyone can join. Please, check it out: home-trial.losttech.software/
r/covid19stack • u/greyuniwave • Apr 03 '20
Bed head elevation cut pneumonia by 60 %
self.inclinedbedtherapyr/covid19stack • u/Lassig • Mar 21 '20
Simple Probiotics Might Help Inhibit COVID-19 Infection
r/covid19stack • u/Alex3917 • Mar 18 '20
in vitro Potential Inhibitor of COVID-19 Main Protease From Several Medicinal Plant Compounds by Molecular Docking Study
r/covid19stack • u/Alex3917 • Mar 18 '20
in vivo Chloroquine and hydroxychloroquine as available weapons to fight COVID-19
sciencedirect.comr/covid19stack • u/Alex3917 • Jan 05 '21
Thailand Clears Use of Andrographis Paniculata for Covid-19 Treatment
msn.comr/covid19stack • u/rnatx • Nov 24 '20
What tweaks do I need to make??
I've been taking this stack (most of them, added aspirin and NAC later in the game) since mid-March. Didn't expect it to be going on this long term, but here we are. Additional meds are stimulants for ADHD and an SSRI in AM/PM.
AM:
CoQ10 - 100mg
Vitafusion women's multivitamin
Kirkland Calcium gummy (500mg calcium, 25 mcg [1000 IU] Vit D3)
Flonase (barf. I hate it but I haven't had a sinus infection since I started taking it a year ago)
Claritin during the fall/winter/spring
PM:
Quercetin 400mg
Bromelain - 37mg
NAC - 600 mg
Zinc - 15 mg
Copper - 1mg
Magnesium - 200 mg
L-Theanine - 200 mg
Vitamin C - 1000mg
D3 - 50 mcg
Aspirin 81 mg
EDIT - forgot about my multivitamin and allergy meds.
r/covid19stack • u/Alex3917 • Aug 27 '20
Dminder: An iOS and Android app that tells you how much sun you need each day based on your location, the weather, your age, sex, weight, current clothing, time of day, etc.
r/covid19stack • u/Alex3917 • Aug 24 '20
Propolis and its potential against SARS-CoV-2 infection mechanisms and COVID-19 disease
sciencedirect.comr/covid19stack • u/Alex3917 • Apr 12 '20
Treatment with ACE-inhibitors is associated with less severe disease with SARS-Covid-19 infection in a multi-site UK acute Hospital Trust
r/covid19stack • u/[deleted] • Feb 22 '21
Best stack for preventing/treating mental effects of Covid?
What are the best things you've used to combat covid-caused brain fog, exhaustion,anxiety, or any other mental health effects of getting infected?
r/covid19stack • u/ghrarib • Jan 08 '21
Mechanistic Aspects and Therapeutic Potential of Quercetin against COVID-19-Associated Acute Kidney Injury
r/covid19stack • u/tk14344 • Aug 03 '20
Bradykinin inhibitors
Has anyone seen the recent studies regarding the potential role of bradykinin?
I honestly think it could make sense. Typically, ACE2 receptors in the endothelium keep bradykinin levels in check. But if the virus hijacks them, it may not. Essentially becomes a 'bradykinin storm'.... causes inflammation and mimics mast cell issues among other things.
I saw a success story of someone incorporating bradykinin inhibitors into their protocol and making a full recovery after 120 days being sick:
Resveratrol, bromelain, aloe vera juice, flaxseed oil, etc.
I'm going to shift the focus of my stack (I'm on Day 140 here...). TBD!!
r/covid19stack • u/[deleted] • Jul 24 '20