𝕊𝕔𝕙𝕄𝕀𝔻𝔾𝔼 🐝🧢😷 #PutN95sInHealthcare

These are probably the exact same folks who refused to wear masks during the pandemic

i still think the worst spreaders of covid & covid disinformation are healthcare workers. unlike many laypeople, most of them can't use illiteracy as an excuse for treating it like a bad cold. it's literally your job to have an accurate basic understanding

i still think the worst spreaders of covid & covid disinformation are healthcare workers. unlike many laypeople, most of them can't use illiteracy as an excuse for treating it like a bad cold. it's literally your job to have an accurate basic understanding

These are probably the exact same folks who refused to wear masks during the pandemic

His 20-year-old son has ulcerative colitis, and he said nearly everyone in the treatment center was under 30. Food, environment, antibiotics, stress, microplastics, gut microbiome, whatever it is, pretending this is normal seems insane. Hopefully AI can figure this out sooner rather than later

⚠️‼️‼️ Maybe Bryan Johnson’s case is being interpreted too late in the chain. If you want to live longer, maybe you should not only measure aging. You should also ask what is chronically activating your immune system. His case may not be just about the stomach, ferritin or thyroid. Low ferritin may not be the real starting point. Autoimmune gastritis may not even be the first autoimmune event. What if the real story started years earlier, with loss of immune tolerance? This case is much more interesting than “my stomach is eating itself.” What I see here is a possible immune story that started years before the autoimmune gastritis was diagnosed. First, autoimmune thyroid disease. Then, years of low ferritin that nobody could explain properly. Now, autoimmune gastritis. Medicine often treats these as separate boxes: -thyroid problem -iron problem -stomach problem But immunologically, they may be connected. If someone develops autoimmune thyroid disease early in life, I would always ask what broke tolerance in the first place. Genetics matter, of course. But the immune system usually does not attack a healthy organ out of nowhere. In many autoimmune diseases, the pattern may be: susceptibility -persistent antigenic stimulation -chronic inflammation → loss of tolerance → autoimmunity. That persistent stimulus could be EBV, another herpesvirus, SARS-CoV-2, Borrelia, Toxoplasma, H. pylori or another pathogen able to persist, evade immune control or create chronic inflammatory pressure. One persistent trigger does not have to create only one autoimmune disease. Over years, it may create an immune environment where more targets appear. This is why autoimmune diseases often cluster. Thyroid autoimmunity and autoimmune gastritis are already known to travel together. This is sometimes called thyrogastric syndrome. So the combination is not random. Now look at the stomach. Autoimmune gastritis targets parietal cells. Parietal cells produce stomach acid and intrinsic factor. If they are damaged, stomach acid falls. And if stomach acid falls, iron absorption can fail. That explains why ferritin can stay low for years even when hemoglobin and hematocrit still look normal. The body keeps blood values normal by draining iron stores first. So low ferritin can be the early warning sign before anemia appears. But the deeper question is not only: “Why was ferritin low?” The deeper question is: “Why did the immune system start attacking the stomach?” Chronic mucosal inflammation is one possible answer. The gut is one of the largest immune surfaces in the body. If there is persistent infection or persistent antigenic stimulation, immune cells can keep being recruited into the tissue. Over time, chronic inflammation can create ectopic lymphoid structures — immune aggregates inside tissues where antigen presentation continues and immune responses are amplified. In that environment, self-antigens are repeatedly exposed. If the person is genetically susceptible, autoreactive T and B cells that should remain silent may become activated. That is how chronic inflammation can turn into organ-specific autoimmunity. This is especially important because many tissues do not normally express high levels of MHC-II. But under inflammatory signals such as interferon, epithelial or glandular cells can begin presenting antigen in a way they normally should not. That can be dangerous for tolerance. In the thyroid, that may contribute to thyroid autoimmunity. In the gastric mucosa, it may contribute to autoimmune gastritis. In the pancreas, under a different context, it may contribute to diabetes. The organ affected may depend on where the immune conflict is happening. So his three problems could be part of one connected process: (1/2)🧵👇🏻

⚠️‼️‼️ Maybe Bryan Johnson’s case is being interpreted too late in the chain. If you want to live longer, maybe you should not only measure aging. You should also ask what is chronically activating your immune system. His case may not be just about the stomach, ferritin or thyroid. Low ferritin may not be the real starting point. Autoimmune gastritis may not even be the first autoimmune event. What if the real story started years earlier, with loss of immune tolerance? This case is much more interesting than “my stomach is eating itself.” What I see here is a possible immune story that started years before the autoimmune gastritis was diagnosed. First, autoimmune thyroid disease. Then, years of low ferritin that nobody could explain properly. Now, autoimmune gastritis. Medicine often treats these as separate boxes: -thyroid problem -iron problem -stomach problem But immunologically, they may be connected. If someone develops autoimmune thyroid disease early in life, I would always ask what broke tolerance in the first place. Genetics matter, of course. But the immune system usually does not attack a healthy organ out of nowhere. In many autoimmune diseases, the pattern may be: susceptibility -persistent antigenic stimulation -chronic inflammation → loss of tolerance → autoimmunity. That persistent stimulus could be EBV, another herpesvirus, SARS-CoV-2, Borrelia, Toxoplasma, H. pylori or another pathogen able to persist, evade immune control or create chronic inflammatory pressure. One persistent trigger does not have to create only one autoimmune disease. Over years, it may create an immune environment where more targets appear. This is why autoimmune diseases often cluster. Thyroid autoimmunity and autoimmune gastritis are already known to travel together. This is sometimes called thyrogastric syndrome. So the combination is not random. Now look at the stomach. Autoimmune gastritis targets parietal cells. Parietal cells produce stomach acid and intrinsic factor. If they are damaged, stomach acid falls. And if stomach acid falls, iron absorption can fail. That explains why ferritin can stay low for years even when hemoglobin and hematocrit still look normal. The body keeps blood values normal by draining iron stores first. So low ferritin can be the early warning sign before anemia appears. But the deeper question is not only: “Why was ferritin low?” The deeper question is: “Why did the immune system start attacking the stomach?” Chronic mucosal inflammation is one possible answer. The gut is one of the largest immune surfaces in the body. If there is persistent infection or persistent antigenic stimulation, immune cells can keep being recruited into the tissue. Over time, chronic inflammation can create ectopic lymphoid structures — immune aggregates inside tissues where antigen presentation continues and immune responses are amplified. In that environment, self-antigens are repeatedly exposed. If the person is genetically susceptible, autoreactive T and B cells that should remain silent may become activated. That is how chronic inflammation can turn into organ-specific autoimmunity. This is especially important because many tissues do not normally express high levels of MHC-II. But under inflammatory signals such as interferon, epithelial or glandular cells can begin presenting antigen in a way they normally should not. That can be dangerous for tolerance. In the thyroid, that may contribute to thyroid autoimmunity. In the gastric mucosa, it may contribute to autoimmune gastritis. In the pancreas, under a different context, it may contribute to diabetes. The organ affected may depend on where the immune conflict is happening. So his three problems could be part of one connected process: (1/2)🧵👇🏻

i still think the worst spreaders of covid & covid disinformation are healthcare workers. unlike many laypeople, most of them can't use illiteracy as an excuse for treating it like a bad cold. it's literally your job to have an accurate basic understanding

COVID and development delays. This study reports: COVID+ during pregnancy associated with 2x rates of their babies DX'd w/developmental delays than controls (6.3% vs 3.0% respectively) What could COVID infection(s) be doing to kids' development, even after they're born?

spoke to a woman whose 35 year old daughter just died of an "aggressive" cancer. She said, "cancer seems to be taking more and more young people."