Every compound, correct dose, duration, and priority level — organized by goal (muscle, fat loss, longevity, cognition, libido, recovery, sleep). Link in the post, bookmark it. 📄 PDF added — scroll down and grab it. https://www.skool.com/biohacking-tony-huge/classroom/923d0785?md=5d8894556b0a4056875a8172d304165e

My hematocrit came back at 59, and that brought me back to something I think a lot of people on TRT overlook. Most people focus on testosterone, estrogen, and maybe PSA. But what about how thick your blood is? Testosterone can increase red blood cell production, so hematocrit can climb. The common solution is blood donation or therapeutic phlebotomy. The problem is that every draw also removes iron. So lowering hematocrit can help one issue while slowly draining ferritin if you are doing it too often. That’s why I think the real conversation is not just hematocrit. It is hematocrit plus ferritin. One tells you how concentrated your blood is. The other tells you what repeated blood removal may be costing you. I also get into hydration, why dehydration can make the numbers look worse, and why I think blood work matters more than guessing. Full video: https://www.youtube.com/watch?v=wTZAH92WmQY For those of you on TRT, are you checking ferritin too, or mostly just hematocrit?

Hey everyone! It’s a busy week for us filming new content, so this week’s live session is cancelled. Please disregard any previous announcement or email regarding this week’s live. Thanks for understanding! 💛

I pulled my genetics and blood work because I wanted to know exactly what I was dealing with. I have APOE4. I have multiple 9p21 cardiovascular risk markers. My genetics basically gave me a bad starting position when it comes to heart health. But genetics are not the final answer. In this video, I go through my actual blood work, LDL, HDL, Lp(a), hematocrit, liver markers, what I have experimented with over the years, what improved, and what still needs work. Some of the results surprised me, especially my Lp(a). This is also why I keep saying you need data. You cannot just guess what is happening inside your body based on how you feel. I am not saying anybody should copy what I do. I am showing you my own data, my own experiments, and how I think about managing risk. Watch the full breakdown: https://youtu.be/kIbZZiDcr4Q?si=kdTFcWDjhiHGMSvV If you found out tomorrow that your genetics put you at higher cardiovascular risk, what would you change first?

This is one of the more interesting longevity papers I have seen recently. A July 2026 Nature Communications study looked at an engineered enzyme called CMLase. The researchers designed it to target CML, one type of advanced glycation damage that can build up on long lived proteins over time. In isolated tissue, they reported major reductions in CML from collagen, aged human artery, skin, and eye lens samples. The important part is the limitation. This was not a human treatment trial. The work was done outside the body, and we still do not know whether the enzyme could be delivered effectively, whether the immune system would tolerate it, or whether removing CML would actually make tissues function younger. That is what makes this interesting to me. The research challenges the old assumption that this type of accumulated damage has to stay permanent, but there is still a big gap between an exciting laboratory result and something we can actually use in humans. I broke down the study, the measurement differences, the current evidence around glycation, and what we can realistically do today in the full video: https://youtu.be/XsUjonGMqzE?si=v0HQ-WtXUdUp7Et9 Community question: If scientists eventually prove that accumulated glycation damage can be safely removed in humans, where do you think the biggest impact would be: cardiovascular health, skin aging, eyesight, or longevity overall? Drop your take below. I want to hear how everyone here is looking at this research.