The three most common long COVID symptoms are shortness of breath, brain fog, and fatigue. The last post discussed senescent cells as a major mechanism that accelerates aging and chronic disease development. It turns out that senescent cells are also a prominent part of progression to long COVID disease which is a new chronic condition. COVID infection is highly variable ranging from mild disease to profound tissue damage, organ failure and death. Severe disease seems to be related to very high levels of inflammation which explains the protective effects of high dose steroid treatment. COVID changes cells from their normal function of replacing old cells into cells that don’t divide but instead put out high levels of inflammatory mediators. (Including interleukin 1-B). This also explains the much more dangerous disease in older people who have accumulated higher numbers of senescent cells over time. The new senescent cells add to the prior burden and already primed inflammatory state.
Metformin interferes with senescent cell formation and related inflammation. It reduces interleukin 1-B production and other mediators downstream. A recent study showed that metformin administered within 4 days of the onset of COVID symptoms reduces progression to long COVID by up to 63%. In the same study Ivermectin and fluvoxamine did not prevent long COVID. Other studies have shown benefit with the IL-1β blocker anakinra ($5200) and the anti-IL-6 receptor antibodies tocilizumab ($8000) and sarilumab ($5600). Metformin is $4 for a month’s supply, and it provides the same benefit. Diabetics are more than three times as likely to die of COVID. Diabetics on metformin reduce their risk of dying by almost two thirds. If you review the last post, you will see that we understand the mechanism of that benefit in great detail. Remember, metformin blocks the effect of ADMA very specifically to reduce the production of inflammatory mediators. An increased ADMA level is a powerful predictor of mortality in COVID infection.
So, long COVID fits into the unifying hypothesis of chronic disease and aging. We should all be thankful to the academic scientists who have done such a great job of laying the groundwork that allows us to understand aging and chronic disease at a level that offers better answers. That said, this research is itself a problem. It is usually very focused on a small piece of the puzzle. It seems almost all the effort is aimed at finding the next new very expensive thing. New scientific understandings of old medicines and ideas can provide much better health longer and at lower cost. Much more attention must be paid to translating this vast body of science for the benefit of patients and those who pay the bills.
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