/1 I received many questions from my most recent newsletter. I will do my best to answer them in this thread:
Question from Lennart:
Is it possible that statins would impact lung recovery if infected with COVID-19?
A: There is evidence the anti‐inflammatory properties of statins in the lung could help with respiratory diseases. /2.1 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2104700/
A: Results from preclinical studies and observations in relevant patient populations support the protective potential of statins in ALI, paving the way now for definitive clinical trials. /2.2 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3555410/
A: Randomized clinical trials failed to demonstrate an improved survival of ARDS patients treated with statins. /2.3 https://www.ncbi.nlm.nih.gov/pubmed/27232279
/3 Question from Ana:
Some People say that certain medicines like Advil etc, worsen COVID-19. Aren't those anti-inflammatories?
A: There is currently no strong evidence to suggest that ibuprofen makes you more likely to catch coronavirus, or make the disease worse; however, certain expert organizations, including the FDA, are investigating the possibility further. /4.1
A: If you already take NSAIDs, such as ibuprofen or naproxen, for another condition, such as arthritis or pain-relief, ask your doctor for advice. /4.2
/5 Question from Rich:
This Colombia researcher is using a new method to speed up testing. Can this new method be applied to any of your work?
A: This is standard single-cell drug discovery and it could work, the problem is we need a solution in the next few weeks or sooner if we are to impact this first wave. /6.1
A: Chavez solved this problem by putting proteases from each virus into different cells, then creating what he calls nametags for each of the cells. /6.2
A: He adds possible drug compounds to the cells and uses genome sequencing to read the tags, which allows him to see whether any of the viral proteases are blocked by each drug. /6.3
/7 Question from Michael:
Dr. John P. A. Ioannidis of Stanford wrote an article saying that we are making decisions without reliable data. What is your opinion on this?
A: It is correct. We didn’t know the infection fatality rate because there were many asymptomatic people (or mild symptoms). The true fatality rate looks below 1%. It’s still very bad but not 4-6% as some data initially suggested. /8
/9 Question from Allison:
We've been hearing anecdotal stories about young people who are also impacted by the virus. Is that true? If so, why?
A: It’s not yet know but this could be the clue to susceptibility we are all waiting for. /10.1
A: Theories include previous exposure to a similar coronavirus, a genetic predisposition to an overactive immune and/or blood clotting system, genetic differences in the ACE2 gene that the virus needs for entry, or underlying health issues that are not yet diagnosed. /10.2
/11 Question from Todd:
Some companies are promoting thymosin for your immune system. What is it and does it really boost your immune system?
A: I’m seeing a lot of claims out there trying to increase sales. Unless there’s a placebo-controls clinical trial you can find in a scientific journal (e.g. PubMed), you can’t be sure any claims are true. /12.1
A: The small protein called thymosin comes originally from a thymus fraction and is thought to help with thymus function. Given that the thymus shrinks with age, it is hypothetically possible thymosin might help recover from COVID-19 ... /12.2
A: but I haven’t seen any clinical trials showing this so at best it’s speculation. If anyone has clinical data on thymosin in COVID-19 patients, it would be great to know. /12.3
A: Because if you have the flu and COVID-19 the prognosis is would be far worse. /14
/15 Question from James:
Dr. Todd Rider spoke about how DRACO's kill all viral infections in 2015. Why isn't this being talked about in 2020?
A: The technology is exciting. Finding RNA and killing cells that possess it using CRISPR/Cas9. There are two main issues I see. One is that SARS-CoV-2 is a singable-stranded RNA virus and this tech requires a double strand. /16.1
A: You will have transient double stranded RNA when it’s being copied or transcribed t this could be a limitation. The second is that delivery of genetic material to cells is not currently efficient and and less well studied in terms of safety. /16.2
/17 Question from Martin Alps:
Which kind of activity can you recommend for seniors while sitting at home?
A: Walk, stretch, video chat (we have Portals for our family). /18
/19 The Brighten Bar asked:
Can you please address whether it’s true that smokers and even COPD suffers are not more likely to get ill and in fact die to the ACE2 issue are not as at risk?
A: Chronic smoke exposure triggers expansion of mucus-secreting goblet cells and an increase in ACE2. Quitting smoking causes a decrease in lung ACE2 levels, which can explain why smokers are susceptible to severe SARS-CoV-2 infections. /20
/21 Anonymous question:
Is there any data indicating which immune-response cells attack the lung tissue?
A: Activated leucocytes and natural killer (NK) cells. When activated they secrete a variety of substances such as cytokines, proteases, and reactive oxygen species (free-radicals) that are the primary sources of tissue injury. /22
/23 Question from Robert:
Would you agree that to get back to some level of normalcy both active viral testing along with serology will be needed?
A: It would help, as it has in Hong Kong, the USA, and Singapore, but I don't think the USA is going to wait. Even with the tests, life wont be normal until a vaccine arrives. Herd immunity is unlikely, as only single digit percents have been infected. /24.1
A: Ultimately Id like to see every patient have a DNA sequence done, which would help track the virus, know if its “just” flu, and detect viral evolution. /24.2
Question from Alycia:
I was just reading about thrombotic complications in a study that came out a few days ago. Being someone that has a protein S deficiency and a previous pulmonary embolism, is the data suggesting that would put someone like me at high risk if infected? /25
A: Coagulopathy from the cytokine storm is being reported commonly, with a spike in D-dimer. There’s little known about cytokine storms and S deficiency. Im no MD, but I would think increased coagulation would be riskier for severe COVID-19 cases. /26
/27 Anonymous question:
Does vitamin D3 need to be taken with cofactors (vitamin K2, vitamin A, zinc etc...) to avoid malabsorption and imbalance?
A: K2 and Magnesium are often be supplemented with D3 (I take D3+K2). Some types of liver disease can reduce absorption or D3 metabolism. /28.1
A: Levels of the active form of D3 track with kidney and gut health. Conditions that affect the gut, like IBD and cystic fibrosis, can reduce vitamin absorption. /28.2
Q: What is the cytokine storm? What is it's relation to COVID-19? /29
A: Cytokines are small proteins secreted by immune cells that have an effect on other cells. Examples are interferons (IFNs), TNFalpha, interleukins (IL1,6), and transforming growth factors (TGFs). /30.1
During the course of COVID-19, some patients bring down viral numbers only to rapidly descend into a state of shock involving hyper-activation of the immune system and hyper-coagulation in small blood vessels. /30.2
This rapid and uncontrolled inflammatory signaling cascade, known as a “cytokine storm,” exacerbates the heavy breathing and low oxygenation, and triggers inflammation in major tissues such as the lungs, kidneys, heart, liver and brain. /30.3
The resulting vascular inflammation is emerging as a main cause of complement-associated microvascular injury and thrombosis in severe COVID-19 cases. /30.4
What do you think of ozone therapy to fight COVID-19? /31
A: There is no general agreement based on available evidence. There are a few clinical trials underway in Europe (none yet completed). The EPA says do not use ozone generators indoors. https://clinicaltrials.gov/ct2/show/NCT04366089
Q: What role does Quercetin play in relation to COVID-19? /33
A: It’s mostly theoretical at this stage. Quercetin, a polyphenol, inhibits both the SARS proteases, 3CLpro and PLpro, and the MERS 3CLpro protease, at least in the test tube. Im unaware of any placebo-controlled human trials in COVID-19 being reported. /34
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