On top of that, the SSRI article you linked suggests a biochemical mechanism by which SSRIs might be acting (i.e. not by making something “fake” go away, by actually treating the cause of something real)

The article actually argues against that reading: IgG transferred from patients into mice reproduced the symptoms. Mice don't have a nervous disposition. That points to a physical mechanism.

"

Importantly, IgG fractions from the blood of these individuals cross-reacted with several types of mouse tissue in vitro, and transfer of this IgG to living mice reproduced symptoms such as pain, fatigue, coordination problems, temperature sensitivity and more. These effects were not seen with IGg transfer from unaffected patients. It hardly needs pointing out that you cannot transfer a nervous disposition or a persistent bad attitude by transfusing antibody fractions. Long Covid is a real a disease as lupus, MS, Hashimoto’s, or Type I diabetes, all of which are driven by production of antibodies to a person’s own tissues."

> In the first transfer experiment, most patient participants had been vaccinated prior to sampling, whereas the controls were not. Importantly, in our follow-up experiment, we used post-pandemic controls (exposed and vaccinated), and their IgG still did not induce the overt pain phenotype seen with long COVID IgG, suggesting vaccination alone is unlikely to explain the transfer effects.

Long COVID is much more prevalent among people who’ve experienced severe COVID symptoms, and unvaccinated people have the most severe symptoms. One doesn’t need a PhD to do the math here.

And of course people can have both.