Understanding Cell Death in Human Health

🥇‼️😎A fungus from an abandoned uranium mine just made cancer cells self-destruct Scientists have discovered a bizarre strain of fungus growing deep within a uranium-contaminated site in Ukraine. But instead of just surviving the radiation, this organism may offer one of the most promising anti-cancer treatments in decades. The fungus, tentatively named Cladosporium radtoxicum, produces a compound that triggers apoptosis — programmed cell death — in aggressive cancer lines without harming healthy tissue. The site where this fungus was found has long been considered a dead zone for life. But the extreme radiation appears to have caused an evolutionary twist. Researchers found that the fungus thrives by converting radiation into chemical energy, like photosynthesis — a process called radiosynthesis. In doing so, it secretes a dark melanin-rich compound to shield itself. This compound, it turns out, can also penetrate and destabilize tumor cell membranes. Early lab tests at Germany’s Max Planck Institute show that when human glioblastoma cells were exposed to the fungal extract, over 75% of the cancer cells collapsed within 48 hours. Normal human cells remained unaffected. This selectivity is extremely rare — and it's what makes the compound so exciting for oncologists. The team has now isolated and synthesized the active molecule, naming it "radmycin." Unlike chemotherapy, radmycin doesn’t flood the body with toxic agents. Instead, it hijacks the cancer cell’s energy cycle, switching on a cascade of internal breakdowns. It's like making the tumor turn against itself. Animal trials have already begun, with preliminary results showing tumor reduction in mice by over 60% in two weeks. If these findings continue, human trials could begin as early as next year. The hope is a new class of therapies that doesn’t rely on radiation or aggressive toxins — but on biology evolved in the most radioactive corners of the Earth. This is one of the few times in medical history where radiation didn’t just cause cancer — it accidentally bred the cure

What happens when there is rust in the brain's wires and cells? We continue to struggle with understanding iron and neuroferroptosis and whether there will be an 'iron age' of the brain and disease? The just published paper in Nature Reviews Neuroscience by Lei, Walker and Layton makes the case that our aging brains accumulate iron like rust on a wire. The buildup, if left unchecked, can trigger cell death referred to as neuroferroptosis. This isn’t just theory, it's a process that could underlie Parkinson's, Alzheimer's, ALS, stroke, and brain cancer. Key Points: - The way the brain is built it is at high risk for the effects of iron. It's lipid-rich, iron-loaded, and oxygen-hungry. - These represent a 'perfect storm' of conditions for ferroptosis, an iron-dependent, lipid-peroxidizing cell death pathway. - Neurons possess a massive membrane surface and limited self-renewal capacity. Their defenses rely on selenium, GPX4, glutathione, and antioxidants like vitamin E. They are thus very susceptible. - The connective tissue of the brain, the microglia, can spread the process. When microglia undergo ferroptosis, they activate astrocytes and propagate damage to neurons. - Once started, the process triggers and propagates neuroinflammation and degeneration. - Elevated iron, reduced antioxidants, and genetic risk factors all link neuroferroptosis to Alzheimer's, Parkinson's, ALS, stroke, MS, and neurodegeneration w/ iron accumulation disorders. - Chelating or removing the iron may actually backfire. Iron is essential for brain metabolism and dopamine production. Trials using iron chelators worsened outcomes in Alzheimer's and Parkinson's. My take: I have 3 big takeaways: 1- Iron is a double-edged sword. We need it for brain health, however too much can rust the brain’s wiring, leading to a worrisome cascade of damage. 2- Cell death isn’t just a final act, it actually may start earlier than you think. Neuroferroptosis likely begins long before symptoms of Parkinson’s or Alzheimer’s appear. 3- Antioxidants and selenium may matter, however remember, they are not magic bullets. Nutrients like vitamin E and selenium help protect the brain, but we’ll need smarter, targeted therapies to truly make a dent in neuroferroptosis. This gives us one more reason to take one multivitamin a day until we sort out the specifics. https://lnkd.in/ebA4YmpY Nature Magazine Norman Fixel Institute for Neurological Diseases Parkinson's Foundation Alzheimer's Association® The ALS Association

What happened to us? Over the last 50 years, we’ve seen a dramatic rise in chronic, complex disease. • Diabetes • Fatty liver • Autism spectrum disorders • Autoimmunity • Infertility • Alzheimer’s, Parkinson’s, ALS Metabolic dysfunction is no longer rare. It’s the norm. We’ve blamed the usual suspects: Too much sugar. Too much fat. Bad genes. But these explanations don’t fully account for the scale—or the timing. There’s another variable. One that’s been largely ignored. Iron Fortification: A Global Experiment In 1963, the Codex Alimentarius Commission—formed by the WHO and FAO—mandated iron fortification of processed foods worldwide. The form used? Inorganic, non-heme iron salts—cheap, synthetic, and unbound. A form the human body: • Cannot regulate • Cannot safely store • Cannot eliminate Since then, we’ve been chronically exposed through: • Fortified grains, cereals, and flours • Prenatal vitamins • Standard iron supplements This policy was intended to prevent iron-deficiency anemia. But it introduced a new kind of problem: chronic, low-grade iron overload at the tissue level. The Silent Collapse of Cellular Metabolism Excess iron doesn’t float harmlessly in the blood. It deposits in tissues. It fuels reactive oxygen species. It disrupts redox balance. And it triggers ferroptosis—iron-driven cell death. The cascade looks like this: • Mitochondrial collapse • Glutathione depletion • DNA damage and epigenetic instability • Immune dysfunction and chronic inflammation Iron overload poisons the fundamental processes of energy production and repair. But perhaps the most critical system it disrupts is erythropoiesis—the production of red blood cells. Healthy erythropoiesis is the metabolic engine that powers oxygen delivery. But iron overload breaks the system. • Iron becomes trapped in tissues instead of recycled • Erythropoietin signaling becomes erratic • Bone marrow output falters • Oxygen transport collapses • Cells become hypoxic—even in the presence of excess iron The body misreads this as iron deficiency and tries to compensate—absorbing even more iron, fueling even more oxidative stress. This is a closed loop of dysfunction: Iron overload → impaired erythropoiesis → oxygen starvation → increased iron demand → more overload → more damage It’s a self-sustaining metabolic trap. And it’s happening silently, beneath lab markers that often appear “normal.” The Great Misdiagnosis Patients are told they’re iron deficient. But what we’re really seeing is iron dysregulation—iron in the wrong place, at the wrong time, doing the wrong thing. This explains why so many people are anemic and inflamed. Fatigued and oxidized. Diagnosed with one disease but slowly unraveling across multiple systems. This isn’t just about iron. It’s about the collapse of the metabolic system that governs energy, immunity, repair, and cognition. This is the root cause no one is talking about. Until now.