Prevalence of "Long COVID" is hard to measure at this point, but based on symptom reporting, about 15% of people who test positive for COVID have some symptoms more than 2 months later.[1] More data is available for people who have had heart and brain MRI scans, which show inflammation. It may be possible to diagnose this with a special eye exam that detects inflammation in the eye's blood vessels. The tests are still very experimental, but there are objective measures of damage.
In support of this, I want to mention that there are known and measurable biomarkers that connect reported symptoms to undeniable physical symptoms.
Low cortisol is very common. That’s just one example. With low cortisol it’s hard to feel good or function 100%.
One paper of many that show this kind of relationship (a preprint): “Distinguishing features of Long COVID identified through immune profiling” — https://doi.org/10.1101/2022.08.09.22278592
It’s also important to note that there was a study that seemed to show that Long COVID was just anxiety or in people’s imagination. Because people who said they had Long COVID didn’t have SARS-CoV-2 antibodies. The thing is that not everybody seroconverts. Not everybody actually produces antibodies after infection; We simply can’t exclude Long COVID diagnoses based on looking at those particular antibodies. So that study can’t show what it has been said to show. (I can provide sources for this but am out of time. It’s on my honor.)
The best explanation I've seen thus far, assuming there aren't other complicating factors (which there often are) is that the immune system stays hyperactive in some people after infection. This causes excess production of IL-6 and IL-10, which in turn causes something called the kynurenine shunt. That in turn results in lowered central serotonin rates in the brain and heightened glutamate. This off balance results in lowered dopamine as the production of serotonin and dopamine are comingled. Dopamine usually breaks down to your typical epinephrine and norepinephrine levels. But since dopamine is at a lowered state, you get less epinephrine and norepinephrine. I'm guessing, but do not know the pathway, that lowered epinephrine and norepinephrine explain the lowered cortisol.
Either way, the treatment should be the same. Take a corticosteroid to lower the IL6 & 10 levels, ensure the patient is getting proper sleep and nutrients, and not doing anything to exacerbate lowered serotonin/dopamine levels, and cross your fingers.
I've started to hear of companies that are testing for elevated cytokines as a proof of long covid, and my family member's hospital has started educating their staff on cytokine release syndrome in the rare patient who has a reaction to a vaccine shot, both of which, for me, imply the industry might be moving in this direction for explanation. fingers crossed
[1] https://jamanetwork.com/journals/jamanetworkopen/fullarticle...