Is there a relationship between the microbiome and long covid?

If you follow us on Facebook and Instagram, you likely saw a couple of posts on the microbiome this week. The first showed a relationship between the microbiome and long COVID, as well as severe COVID19 illness. The second found some of the same members share a relationship with myalgic encephalomyelitis/chronic fatigue syndrome(ME/CFS).

This is interesting because both long COVID and ME/CFS seem to be very similar in presentation. Making the link even more intriguing is that getting COVID19 seems to cause long term changes in the microbiome that promote these changes. It’s not uncommon for viral infections to unleash ME/CFS.

It’s tough to say which way this relationship goes. Having COVID could cause the changes. Alternatively, having this dysbiotic microbiome could promote severe illness. Or, most likely, it could be a combination of the 2.

In today’s blog we discuss these changes and what we can do to prevent them.

The microbiome and long COVID

In this recently published paper, researchers looked at the microbiome of 100 people admitted to the hospital with COVID19. They found that the microbiome of these people was missing some key microbes.

In particular, Faecalbacterium prausnitzii and Bifidobacterium bifidum were significantly lower, with low F. prausnitzii associating most with severe illness. Furthermore, Eubacterium rectale and Bifidobacterium adolescentis were also lower, but this was not significant.

Of particular note, multiple studies consistently show decreased F. prausnitzii in COVID19 patients. You can check out discussions and studies on the topic here, here, and here.

F. prausnitzii is associated with reducing inflammation. This makes sense because the data points to dysregulated inflammation as the driver of severe COVID19.

Consequently, they peeped at COVID19 patients up to 30 days after recovery. The changes in the microbiome persisted, indicating that illness reinforced these changes.

As such, this paper indicates a link between the microbiome and long COVID. In particular, longer term changes to the microbiome may promote long COVID.

The microbiome and ME/CFS

In a separate paper, researchers looked at changes to the microbome in people with ME/CFS. They compared people with ME/CFS with control, as well as people with ME/CFS who also had IBS.

Again, they found certain microbes were lower between patients with ME/CFS and controls. This included Faecalibacterium prausnitzii, Faecalibacterium cf., Roseburia inulinivorans, Dorea longicatena, Dorea formicigenerans, Coprococcus catus, Odoribacter splanchnicus, Ruminococcus obeum, and Parabacteroides merdae. (Note: The ones in bold decreased in both studies)

Again, many of these microbes have anti-inflammatory effects. But interestingly, there was no difference in inflammation between ME/CFS patients and controls.

So, although these microbes provide an anti-inflammatory effect, inflammation may not drive all the symptoms. A decrease in these members of the microbiome may decrease vitality via other means. For example, by inducing fatigue, disturbing metabolism, or disturbing digestion and absorption of nutrients.

Facealbacterium prausnitzii: Keystone species in the human gut

People have a somewhat skewed view of the microbiome and how to leverage it for health. We often think of probitoic or prebiotic supplements as keys to maintaining gut health. Synbiotics and probiotic foods are two more methods.

But our gut is a complex ecosystem. As such, it’s a lot more complicated than simply tossing down some pills or powders. Ultimately, our lifestyle plays a much bigger role in our microbiome.

Like an ecosystem has apex predators, our gut has keystone species. When a keystone species is present, it promotes balance and harmony. The presence of a keystone species in the gut creates microbial networks that support gut health.

On the other hand, when a keystone species is missing, it destabilizes the whole network. F. Prausnitzii is a keystone species in our gut that supports gut health by producing butyrate and squashing inflammation.

Microbiome and long COVID: F. prausniitzi

Having F. prausnitzii in our gut promotes microbial diversity and stabilizes the gut. As a review mentions:

F. prausnitzii has been so far empirically validated as a keystone species for its ability to produce butyrate (Table 1). It’s loss has been associated with the development of IBD in several studies

When you lose this keystone species, you lose resilience in the gut, and create instability in the microbiome.

Promoting F. prausnitzii in the gut

Losing a keystone species such as F. prausnitzii has devastating effects on the gut. It lowers beneficial microbes, allows inflammation to run rampant, and promotes the growth of pathogenic microbes.

As such, it’s important to look at ways to keep F. prausniitzi hanging around in large numbers. This should not only provide a benefit to reducing the severity of COVID 19, it should also prevent COVID19 illness from destabilizing the gut.

So how do we do this? Here’s a list of factors that promote F. prausnitzii hyperlinked with studies:

Conclusion

Recent evidence links changes in the microbiome and long COVID. Essentially every study finds a decrease in F. prausnitzii, a keystone member of the microbiome that promotes health.

But this begs the question, does low abundance promote severe illness or does severe illness promote lower abundance?

Based on the data, it likely goes both ways. Ultimately, the link between the 2 may come down to behaviors that indirectly link them. For example, night shift decreases F. prausnitzii and triples the risk of COVID19. the risk increases to 7x in healthcare workers working nightshift.

In addition, people who are inactive had more than double the risk of hospitalization and death from COVID19 compared to people who meet physical activity guidelines.

Though we have no idea which way the relationship between the microbiome and long COVID goes, clearly behaviors that increase F. prausnitzii also decrease the risk of severe COVID19.

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