Comment · Thu, March 19, 2020
What do the makers of Nootropics take themselves?
Original post in this thread
varvela · 23 points
To the team at Nootropics Depot, I’m curious to know what are some in-house favorites among the products you sell?
What stacks do you guys take that drive development of such great products?
What they were answering
redditinface · 1 points
u/MisterYouAreSoDumb, shouldn't we skip the EGCG at this point given that it acts as an ACE inhibitor and there's speculation that COVID-19 is exacerbated by ACE inhibitors?
u/MisterYouAreSoDumb
I'll copy it here, too.
We know ACE2 up-regulation is a pathway to allowing SARS-CoV-2 to enter and infect the body. However, we do not have conclusive evidence that ACE inhibitors increase the risk. We also don't have any evidence that EGCG leads to an up-regulation in ACE2 expression. In fact, EGCG looks to non-competitively inhibit ACE through an allosteric mechanism, which may not affect ACE2 expression at all. It actually seems to not happen if you take it with vitamin C, which I am.
We investigated the molecular mechanisms involved in the angiotensin-converting enzyme (ACE) inhibition by (−)-epigallocatechin-3-gallate(EGCg), a major tea catechin. EGCg inhibited both the ACE activity in the lysate of human colorectal cancer cells and human recombinant ACE(rh-ACE) in a dose-dependent manner. Co-incubation with zinc sulfate showed no influence on the rh-ACE inhibition by EGCg, whereas it completely counteracted the inhibitory effect of ethylenediaminetetraacetic acid, a chelating-type ACE inhibitor. Although hydrogen peroxide was produced by the autoxidation of EGCg, hydrogen peroxide itself had little effect on the ACE activity. Conversely, the co-incubation of EGCg with borate or ascorbic acid significantly diminished the EGCg inhibition. A redox cycling staining experiment revealed that rh-ACE was covalently modified by EGCg. A Lineweaver–Burk plot analysis indicated that EGCg inhibited the ACE activity ina non-competitive manner. These results suggested that EGCg might allosterically inhibit the ACE activity through oxidative conversion into an electrophilicquinone.
Furthermore, physicians are telling their patients to continue taking their ACE inhibitors, as the science is not settled yet.
I would personally currently avoid things that we know up-regulate ACE2 specifically. However, I would not freak out and eliminate anything that has any ACE inhibitory effects. If physicians are saying to not discontinue even stronger competitive ACE inhibitors, I don't think we need to freak out over the minor effects of EGCG; especially when combined with vitamin C.