Deeply appreciate your emphasis on sleep, here. Since COVID, I have had more nights of not more than 2 or 3 hours of sleep than ¨great nights¨ when I can sleep between only 5 and 6 hours. I do have a history of insomnia, but like others here, I know, without a doubt, that my sleep deprivation now, however much related to a pre-COVID vulnerability, is a whole new animal for me that coincides quite exactly with the beginning of my COVID recovery. If doctors simply would treat reported symptoms that are new or very different from our health histories, and that coincide with a COVID infection, wouldn´t this open new areas of inquiry in a direction that could conceivably lead to finding a UNIFIED root cause (or limited set of root causes) of long COVID? In other words, whoever maintains the databases of reported long COVID symptoms could be channeling each newly reported symptom (even if not 1000% confirmed to be COVID-related) to the thinkers who are earnestly searching for a single or small cluster of common pre-COVID backgrounds that seem to predispose particular people to long COVID, with the expectation that these thinkers will try to identify links across many or most of the reported symptoms, on a road to hypothesizing a key set of predisposing factors that may be reversible. We already know that post-viral inflammatory dysregulation DESCRIBES many reported long COVID symptoms/disorders, but that is simply an observation of the immune status of many long COVID patients, rather than something that points to a deeper root vulnerability that gave rise to this post-viral dysregulation. Sure, long haulers can sometimes feel better on courses of systemic steroids and other immunity-suppressing medications, but suppression of one of the common characteristics of many of our symptoms is far from being something that reaches deeper and helps our bodies to reverse this inflammatory abnormality. For these reasons, I am most intrigued by the emerging interest in chronic B1 (sometimes only subacute) deficiency as a factor possibly predisposing us to long COVID, because this, in my view, does reach deeper and potentially points to a possible solution (and a surprisingly simple one) that might spare us from lives of living permanently on steroids, biologics, and other superficial fixes. This is not to say we should reject pharmacological palliatives. We need these desperately in order to keep as active as possible, but what I want to see lots more of is greater study of what predisposed us followed by proposed solutions arising out of any predisposing factors that may be correctible via currently available therapies. With respect to B1 deficiency, when seen as a possible predisposing cause, this is a bit tricky, since those who measure B1 levels are finding, today, that about 85% of patients tested for thiamine deficiency are, in fact, deficient. Moreover, there is a burgeoning movement of people currently not deficient in B1 undertaking high-dose B1 supplementation for nootropic and immunity-enhancing benefits. (This movement relies heavily on the fact that it is nearly impossible to suffer toxicity even from high B1 supplementation.) Regardless, I see the B1 protocols that some long haulers use these days to be an expression of a yearning for a unified cause theory that I hope will become a valid goal of the ongoing medical research into long COVID.