6/8 — THE PROTOCOL Strength train 2-4x weekly. Compound movements that load the hips and spine — the sites that actually break. Squats, deadlifts, hip thrusts, overhead press, rows. Train hard enough that the final reps are genuinely challenging. Jump. 10-20 daily — hops, skips, jumping jacks, rope. One of the most proven osteogenic stimuli that exists. Skip only if your joints or physician say otherwise. Protein at every meal. Bone is roughly half protein by volume. Most older adults are underfed on protein at exactly the moment they need more. Calcium 1,000-1,200mg daily, food first. Dairy, leafy greens, sardines with bones, fortified foods. Spread it out — absorption is better in smaller doses. Vitamin D. Test it. Calcium is nearly useless without it. Take D3 with a fatty meal. Magnesium and K2. Magnesium activates vitamin D. K2 helps direct calcium into bone rather than arteries — which, as a cardiologist, I care about a great deal.

I'm a cardiologist. A review published this morning just took a sledgehammer to the protein-maxxing era. And the most important detail isn't in the headline — it's buried in the human data. Lamming's lab at Wisconsin reviewed over 350 studies on protein restriction and aging, published today in Cell Press Blue. As @EricTopol put it, they define — for the first time — the hallmarks of protein restriction: Improved metabolic health. Induction of nutrient-sensing pathways. Decreased senescence. Improved mitochondrial function. An altered epigenome. And the promotion of healthy aging. Six hallmarks. From eating less protein, while still meeting your needs. 𝗧𝗵𝗲 𝗻𝘂𝗺𝗯𝗲𝗿𝘀 𝗳𝗿𝗼𝗺 𝘁𝗵𝗲 𝗺𝗼𝗱𝗲𝗹𝘀 Flies: up to 122% longer life. Rodents: 10-50%+ gains. Methionine restriction alone: 7-42% lifespan extension. Cutting isoleucine and valine: 23-65% in various setups — with less frailty and less cancer. 𝗧𝗵𝗲 𝗺𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺 𝘀𝗵𝗼𝘂𝗹𝗱 𝘀𝗼𝘂𝗻𝗱 𝗳𝗮𝗺𝗶𝗹𝗶𝗮𝗿 Excess protein — especially leucine, isoleucine, valine, and methionine — keeps mTOR switched on. mTOR is the growth accelerator. Keep it humming and autophagy shuts down, cells stop cleaning house, and senescent "zombie" cells accumulate. Restrict protein and it reverses. mTOR quiets. GCN2 activates autophagy. And FGF21 surges — driving fat burning, insulin sensitivity, and lower inflammation. This is the exact pathway rapamycin targets. The exact pathway fasting targets. We've been chasing it with drugs while telling everyone to eat more of the thing that blocks it. 𝗧𝗵𝗲 𝗵𝘂𝗺𝗮𝗻 𝗱𝗮𝘁𝗮 — 𝗮𝗻𝗱 𝘁𝗵𝗲 𝗳𝗶𝗻𝗱𝗶𝗻𝗴 𝘁𝗵𝗮𝘁 𝗰𝗵𝗮𝗻𝗴𝗲𝘀 𝗲𝘃𝗲𝗿𝘆𝘁𝗵𝗶𝗻𝗴 Levine's landmark Cell Metabolism study followed adults for 18 years. Those aged 50-65 with high protein intake had a 75% increase in overall mortality and a four-fold increase in cancer death. But here's the line nobody quotes: those associations were abolished or attenuated when the protein was plant-derived. Same amount of protein. Different source. Different outcome. And the age flip matters enormously: over 65, high protein was associated with reduced mortality. Your protein needs change with age — in the opposite direction from what the influencers say. 𝗧𝗵𝗲 𝗵𝗼𝗻𝗲𝘀𝘁 𝗰𝗮𝘃𝗲𝗮𝘁𝘀 Topol's own caution is right: this review rests largely on model organisms. So does most of the healthspan literature, including rapamycin — but "true in mice" isn't "true in humans," and I won't pretend otherwise. And Lamming himself gave the nuance that saves this from being clickbait: athletes consume enormous protein without developing metabolic disease. He suspects exercise protects them — the protein goes into building muscle instead of idling in growth pathways. So the finding isn't "protein is bad." It's that protein without exercise may be the problem. A sedentary person drinking protein shakes, eating protein cereal and protein water is chronically flooring a growth pathway with nothing demanding growth. 𝗪𝗵𝗲𝗿𝗲 𝗜 𝗹𝗮𝗻𝗱, 𝗮𝘀 𝗮 𝗰𝗮𝗿𝗱𝗶𝗼𝗹𝗼𝗴𝗶𝘀𝘁 If you're sedentary and eating 1.5-2g/kg because an influencer told you to — the data doesn't support it, and it may be working against you. If you lift hard 3-4x a week, that protein has somewhere to go. Different equation. And if you're over 70 or frail — do not cut your protein. Sarcopenia will kill you faster than mTOR will. Older adults and pregnant women need more, and the authors say so explicitly. I still believe the Mediterranean diet is the best diet on earth, and this review is the mechanistic explanation of why. It delivers moderate protein — mostly plants, legumes, nuts, fish. Lower methionine density. Olive oil, fiber, polyphenols. It hits every lever this paper describes without a single scoop of powder. Lamming's own lab tested it: a low-protein diet modeling the traditional Mediterranean and Okinawan patterns, head-to-head against Western and ketogenic diets. Western and keto increased fat mass and frailty. The Mediterranean-style diet reduced both and improved cardiometabolic markers. Traditional Okinawa ran about 9% of calories from protein. The blue zones didn't drink protein shakes. They ate beans, and they moved every single day.

A remarkable case report has drawn attention after an elderly woman with advanced Alzheimer’s disease appeared to show unexpected improvements following supervised treatment with psilocybin mushrooms. The woman, a Japanese American in her 80s, had experienced progressive cognitive decline for around ten years. During the previous five years, she was largely limited to speaking single words, relied on others for everyday activities, had difficulty walking and dressing herself, and experienced persistent urinary incontinence. Under professional supervision, she received a 5-gram dose of psilocybin-containing mushrooms. Within approximately 19 hours, her caregivers noticed significant changes. They reported that she began speaking in full sentences, reminiscing about past experiences, and interacting more with those around her. Over the following days and weeks, she became more engaged, recognized family members, walked with greater independence, dressed herself, and even regained bladder control. A month later, she underwent a second supervised session using a 3-gram dose. Caregivers again observed improvements in her speech, mobility, and overall responsiveness. Although these observations are striking, they should not be interpreted as evidence that psilocybin can cure or reverse Alzheimer’s disease. This describes only a single patient rather than a controlled clinical study. Her Alzheimer’s diagnosis was made from her medical history and clinical assessment, without confirmation using brain imaging or biomarker testing such as spinal fluid analysis. The report also lacked standardized cognitive assessments before and after treatment, a comparison group, and any evidence that the underlying brain changes associated with Alzheimer’s had been repaired. Even so, the case has generated scientific interest. Psilocybin primarily acts on serotonin receptors in the brain and has demonstrated effects in laboratory and animal research on neuroplasticity, communication between brain networks, inflammation, and the formation of new connections between nerve cells. Some scientists speculate that these changes might briefly improve the efficiency of remaining healthy brain circuits, allowing abilities that had become difficult to express to emerge more clearly. However, this idea remains a hypothesis and has not yet been confirmed in people with Alzheimer’s disease. It’s also important to remember that psilocybin is not without risks, particularly for older adults or those with significant medical conditions. In this case, the woman reportedly experienced excessive sweating, a possible fever, and an unusually prolonged sleep-like period after treatment.