Thread by @davidasinclair

/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
ncbi.nlm.nih.gov/pmc/articles/P…

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
ncbi.nlm.nih.gov/pmc/articles/P…

A: Randomized clinical trials failed to demonstrate an improved survival of ARDS patients treated with statins. /2.3
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?

Source: bloomberg.com/news/features/…

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?

Source:

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