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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)
SSRIs do not “work on” those other conditions, but depression is highly comorbid with serious chronic illnesses. SSRIs improving some symptoms is to be expected when depression symptoms overlap with the condition.
I've seen healthy, active and successful people be affected, where the cause of "long covid" seems unlikely to be psychological. But there is no denying that, shall we say "a certain type" of person seems to be overrepresented in these cases, and for them it is very attractive to attach the label "long covid" to something that previously existed.
I guess that until we have discovered the biological mechanism underlying this phenomenon, it will be hard to cleanly separate these two cases, but from what I've seen I find it likely that this bipartition really exists.
It is possible for someone with depression to misdiagnose themself with Long COVID or CFS if they don’t understand the conditions. A lot of people will avoid mental health diagnoses in favor of other explanations because they don’t want to accept that they have a mental health condition.
Where you’re confused is that these conditions are not exclusively defined by “brain fog” and lack of energy.
CFS has specific criteria such as specific post-exertional malaise that set it apart from depression in a very concrete way. Any informed practitioner or screener for study acceptance is going to identify the difference.
Onset also matters. If someone claims they developed Long COVID and the trigger was a bad breakup with no known case of COVID it’s easy to dismiss. A key feature of Long COVID is that it starts with a case of COVID.
As for your posts: The fact that you included Morgellon’s (a fictitious disease akin to delusional parasitosis) with other real conditions suggests that you are picking up some weird information from somewhere. Please don’t speak so confidently about these topics you don’t understand. Curiosity is good, but dismissing other people’s conditions as mental illness is really awful.
To use a computing analogy, which doesn't map perfectly onto the body, if consciousness awareness is userland, you can have things go wrong which are localised in ring 0 - brain drugs will be to some degree effective on those, that doesn't mean it's fake or made up.
In reality there are fuzzy boundaries and feedback loops everywhere. SSRIs treating this isn't any more mysterious than NSAID painkillers being somewhat effective for acute depression.
It's probably a whole set of feedback processes that get screwed up, hence the panoply of symptoms, inserting a hard stop into one part of the loop can be enough to kick the system back into a better functioning state.
The classic psychological explanation is the patient only thinks they are sick. But the reality is their body is behaving like they are sick. Worse the classic explanation why you feel sick is 'toxins' from an infection and that is wrong. It's your reaction to feedback from your immune system.
For example, we have a concept of "energy" for which calories is a rough proxy, but there's no particular reason why fighting an infection should draw on the same reserves that running either endurance or peak muscle does, especially as most people operate in a state of calorie surplus, and their respiratory system is more than capable of supplying a bit of extra O2 unless they're severely ill. And yet clearly the immune/autonomic system forces people into a "rest" state in case of infection.
Or another one, there's no particular biological reason for older people to have less "energy". Like yes there's loss in muscle mass and some small drop-offs in the efficiency of various systems, but it doesn't seem like directly compensating for those makes all that much difference.
We do have devices that can measure mitochondrial energy production. There are two I think, forgot their names.
Like we know at a crude physical level, we can give someone a bit of a boost with glucose and sympathomimetic stimulants, but sometimes it works a lot better than others. And it's ineffective for fatigue syndromes, but they can't be the other mechanical things commonly associated with fatigue either. (lactic acid, micro-tears and so on).
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.
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Serotonin is among other things a nausea and thermoregulation neurotransmitter, and has to do with cognition. Most serotonin in the body is synthesized in the gut – a highly enervated endothelial membrane – transported by platelets, and metabolized in the lung.
SARS-CoV-2 is known to damage endothelium, known to cause really weird platelet and blood clotting issues like platelet necroptosis and infection and alteration of bone marrow platelet progenitor cells, known to cause lung injury. In a whole bunch of ways.
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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."
There are studies that show significant immunomodulatory effects of SSRIs.