I continue to follow any new research on the relationship of the gut to COVID outcomes. Late last week, I saw a review article on Medical Dialogs about the potential of using probiotics therapeutically to treat COVID.[i] There was not much new in it – I have already covered most of what it said, in posts like this one and this one. However, there were a couple of tidbits I thought I’d mention.
The author concludes that, “..there is clinical evidence progressing along the direction that modulation of gut microbiota, resolving the gut dysbiosis, can positively influence COVID-19 outcomes. This is further substantiated by the positive effects of probiotics reported against other coronavirus strains…Lactobacillus and Bifidobacterium can be safely considered.”
(By the way, back in 2017, I actually wrote about probiotics and the ordinary flu. Have a read! )
The 2nd article, that got a fair amount of virtual paper last week was about how an enzyme that appears to be targeted by COVID also influences inflammation in the gut, raising the “…possibility that anti-inflammatory drug therapies for IBD [inflammatory bowel diseases] may aid recovery from coronavirus.”[ii] This was a large (1000 individuals), multi-center study which looked at an enzyme called angiotensin converting enzyme 2 (ACE2) which is well studied in terms of regulating blood pressure. (There are several medications which target ACE and angiotensin for treating high blood pressure.) In this case though, it turns out that COVID virus actually binds to ACE2 and uses it to invade and infect cells.
Dysregulation of ACE2 is associated with IBD: levels are low in those with Crohn’s disease and high in those with ulcerative colitis. “The differing ACE2 levels were associated with poorer outcomes and more severe disease in the IBD patients.” Once again, we see that too much or too little are equally bad. It turns out that the effects of ACE2 is dependent on where it is in the GI tract. One of the researchers involved called it a “double edged sword.” (There is evidence that the microbiome has a big role to play in the workings of ACE…which makes perfect sense.)
When treated with a powerful anti-inflammatory, infliximab, ACE2 normalized in those with IBD, which suggests that it might prove useful in those with COVID. After all, those with higher levels of ACE2 enzyme may be at higher risk for contracting COVID. This line of research is so promising that several government agencies have awarded almost $700K in grants to continue their work.
This is not new news, really, by the way. There are several papers published over these last 10 months or so showing that ACE inhibitors and ACE receptor blockers reduce the risk of COVID, and that evidence is mounting. According to a very recent article in the Journal of the American Heart Association, data from more than 700 patients (50 years and older) found that using an ACE inhibitor prior to hospitalization was associated with reduced mortality from the disease. The same was found with angiotensin receptor blockers, although the trend was weaker. [iii]
The upshot of it all: the condition of the biome seems to play a big role in the risks of COVID. Treating dysbiosis and inflammation is a very good idea at the moment: and even when/if a vaccine does become available, the immunity you develop to the disease may also very well be reliant on the state of your biome.