Ahoy everyone! Just thinking through something. I'm in month two of my first cycle of Terzepitide. Nice even body fat reduction, lower dosing as I am a hyper responder, minimum sides. Will be riding this out for a few more months. I wanted to get some opinions...maybe @Anthony Castore can chime in. I have one bottle of SLU in house. 30 capsules of 100mcg per capsule. How might I use this bottle of SLU to enhance the effects of this Terz cycle? I am wont to stay away from stacking because I don't want to over signal. What are the options here? Wait till I am done with Terz and just run that bottle of SLU? Wait till I am done with Terz and get more SLU and run a greater amount over a longer period of time? Throw the SLU in during my taper-off from Terz...so, a little bit of stacking? Or... Risk wasting the money I spent on the SLU and just throw it in to the middle of the Terz cycle and see what happens...for the sake of science? : ) Thoughts?

Hope everyone in the community is having a solid holiday season! Just wanted to let people know that I have just published a two part discussion with @Anthony Castore on the realities of mitochondrial health through the lens of the cascading problems of middle age. This is not a discussion about optimization of performance...it's a discussion about the observable avalanche of health problems that are now landing on men in their middle age and how we can use the cellular lens to turn things around. Also included: how to do it on a budget. Everyone uses a different platform, but here is the link to the first episode on Spotify: https://open.spotify.com/episode/6bzUPJ8Z4PGRhKVuvzndNa?si=hXym1a-4SNag5_A5-j8u0Q

One of the coolest things I’ve learned in this space came from Dr. Seeds. He is an extraordinary thinker and an exceptionally generous teacher, and this insight fundamentally changed how I understand inflammation. What makes it so powerful is not just the biochemistry, but the way it reframes old, familiar tools in an entirely new light. This concept connects aspirin, omega-3s, and resolution biology in a way that is both elegant and practical, and it’s a perfect example of Dr. Seeds’ ability to share deep, clinically meaningful knowledge with clarity and humility. At first glance, aspirin and fish oil look like simple, even old-fashioned tools. Aspirin has been around for more than a century, and fish consumption has been part of human diets far longer than supplements or pharmaceuticals. Yet when you zoom in to the molecular level, the interaction between aspirin and omega-3 fats reveals one of the clearest examples of how small biochemical changes can redirect entire inflammatory programs in the body. This is not about suppressing inflammation, but about teaching the body how to finish it. To understand why this matters, it helps to reframe inflammation itself. Inflammation is not a mistake or a flaw. It is a necessary biological response to injury, infection, or stress. The problem is not that inflammation turns on, but that in many modern contexts it does not properly turn off. The shutdown phase of inflammation is not passive. It is an active, enzyme-driven process governed by a class of signaling molecules called pro-resolving mediators, often abbreviated PRMs or SPMs. These molecules are the biochemical equivalent of a cleanup crew. They signal immune cells to stop recruiting reinforcements, clear debris, and restore tissue to normal function. The raw materials for these mediators come from fats stored in cell membranes. Specifically, long-chain fatty acids with 20 to 22 carbons. The most familiar of these are arachidonic acid, an omega-6 fat, and EPA and DHA, the omega-3 fats found in fish. These fats are not just calories. They are precursors to powerful signaling molecules. What determines whether they become inflammatory signals or resolving signals is the enzyme environment they encounter.