Seems like it should be really straightforward to determine if this hypothesis is right by measuring bradykinin levels in Covid patients versus non-Covid patients.<p>One thing that I think strongly suggests that this hypothesis is wrong is that there is no strong relation between ACE-inhibitors and Covid mortality. Indeed, most of the studies that I've seen suggest that ACE-inhibitors have a somewhat protective effect whereas ARBs actually seem to have a minor detrimental effect [1]. So for the article to claim that covid behaves pharmacologically like ACE-inhibitors seems wrong at face value.<p>[1] <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2007621" rel="nofollow">https://www.nejm.org/doi/full/10.1056/NEJMoa2007621</a>
> Interestingly, Jacobson’s team also suggests vitamin D as a potentially useful Covid-19 drug. The vitamin is involved in the RAS system and could prove helpful by reducing levels of another compound, known as REN. Again, this could stop potentially deadly bradykinin storms from forming. The researchers note that vitamin D has already been shown to help those with Covid-19. The vitamin is readily available over the counter, and around 20% of the population is deficient. If indeed the vitamin proves effective at reducing the severity of bradykinin storms, it could be an easy, relatively safe way to reduce the severity of the virus.
They found out that some genes related to ACE in comparison to genes related to ACE2 are more 'expressed' in Covid patients than normally and they conclude that that must have resulted in too much bradykinine. Hmm - that strikes me as kind of roundabout - why they couldn't just measure bradykinine levels directly? Is that too hard?<p>"Here, we perform a new analysis on gene expression data from cells in bronchoalveolar lavage fluid (BALF) from COVID-19 patients that were used to sequence the virus. Comparison with BALF from controls identifies a critical imbalance in RAS represented by decreased expression of ACE in combination with increases in ACE2, renin, angiotensin, key RAS receptors, kinogen and many kallikrein enzymes that activate it, and both bradykinin receptors. This very atypical pattern of the RAS is predicted to elevate bradykinin levels in multiple tissues and systems that will likely cause increases in vascular dilation, vascular permeability and hypotension."
it's annoying that this is not a 'new' article/theory. It is an article talking about some research and analysis from TWO MONTHS ago. Almost want to request a (July 2020) marking in the title as we do with old link posts
The study itself:<p><a href="https://elifesciences.org/articles/59177" rel="nofollow">https://elifesciences.org/articles/59177</a><p>Excerpts from the abstract:<p><pre><code> Bradykinin is a potent part of the vasopressor system that induces
hypotension and vasodilation and is degraded by ACE and enhanced by
the angiotensin1-9 produced by ACE2.
</code></pre>
...<p><pre><code> This very atypical pattern of the RAS is predicted to elevate
bradykinin levels in multiple tissues and systems that will likely
cause increases in vascular dilation, vascular permeability and
hypotension.
</code></pre>
<a href="https://en.wikipedia.org/wiki/Bradykinin" rel="nofollow">https://en.wikipedia.org/wiki/Bradykinin</a>
This is a really interesting theory, and explains to some degree why those with darker complexions (lower vitamin-D levels) and obesity (increased rates of hypertension) have higher mortality rates. Would it explain why younger people are much less effected though?
Am I the only one bothered by the use of “theory” when this is a hypothesis and, in particular, the back and forth flipping between the two terms in the article?
Is this a fake news?<p>I could find only the article below on IBM's news section (they created this super computer). Speaking about the results of the 2 day analysis, Jeremy Smith, Governor’s Chair at the University of Tennessee, director of the UT/ORNL Center for Molecular Biophysics, and principal researcher in the study: “Our results don’t mean that we have found a cure or treatment for COVID-19. We are very hopeful, though, that our computational findings will both inform future studies and provide a framework that experimentalists will use to further investigate these compounds. Only then will we know whether any of them exhibit the characteristics needed to mitigate this virus.”<p><a href="https://newsroom.ibm.com/US-Dept-of-Energy-Brings-the-Worlds-Most-Powerful-Supercomputer-the-IBM-POWER9-based-Summit-Into-the-Fight-Against-COVID-19" rel="nofollow">https://newsroom.ibm.com/US-Dept-of-Energy-Brings-the-Worlds...</a>
I can't really see why you would need a supercomputer to do the analysis they did (it shows SC centers are getting desperate for users; I wouldn't even have been allowed to run this code on a supercomputer when I was an academic, because it didn't need interconnect for strong scaling.
The journal provides a good summary of the paper:<p><a href="https://elifesciences.org/articles/59177" rel="nofollow">https://elifesciences.org/articles/59177</a>
The anthropomorphization of computers (especially powerful ones) is pretty annoying. A _person used a supercomputer_ to analyze Covid-19, and I’m guessing the theory didn’t just ‘emerge’ from the computer.