Hello everyone! There’s been much talk about SGLT2 inhibitors and its benefits in terms of longevity and overall optimization. I’m really interested in trying it. Has anyone tried it and what are your experiences? My concern in my situation is that I don’t eat a lot of carbs and my fasting insulin is already low, below 3. Wouldn’t that give me the risk of having eu glycemic keto acidosis? Any insights? About Trehalose, I read Anthony recommending taking it fasted for autophagy. Great. However, taking it fasted wouldn’t it break the fast since it’s an actual sugar? And for the autophagy activating benefits what dose should be taken at once?

I went back and forth on whether to write this for a long time. Part of me never wanted this community to become another place that just sells access. There are already enough of those. When I started this group it was really just an extension of the conversations I was having anyway. Interesting papers. Questions I couldn’t stop thinking about. Mechanisms that seemed important but weren’t getting much attention. Things I was learning from my own training, my own health, and the people I have the privilege of working with. Somewhere along the way it grew into something much bigger than I expected. That part is exciting. But it also created a problem. A lot of the conversations I actually want to have don’t fit into a social media post. They don’t fit into a reel. And they definitely don’t fit into a comment section. Some topics need an hour. Some need ten. Because understanding something and hearing about something are not the same thing. Most people today know more than they ever have. And yet somehow they are more confused than ever. They have collected protocols, saved posts, screenshots, stacks, peptides, supplements. But if you changed one variable tomorrow, they wouldn’t know what to do next. That is not a criticism. I have been there myself. The deeper I get into this field, the more convinced I become that understanding is the real asset. Not information. Information is cheap now. Understanding is rare. So that is what this place is built around. Not protocols. Not secret compounds. Not some exclusive club. A classroom. We take a topic that matters and pull it apart, piece by piece, until it actually makes sense. We talk about the things everyone is excited about, and the things nobody is paying attention to yet. We bring in smart people who challenge the way I think. We do live Q&As. And I spend real time showing not just what I am doing, but how I am thinking through decisions as they happen. Because that is the skill that transfers. That is the thing that stays useful when the next study comes out and changes the conversation.

There’s a really interesting shift happening in veterinary medicine right now and most pet owners probably haven’t noticed it yet. For years, canine osteoarthritis care was largely framed around symptom suppression. Dog slows down. Dog limps. Dog struggles getting onto the couch or into the car. Maybe there’s stiffness after rest. The solution pathway usually looked pretty predictable. Anti-inflammatory medications. Weight loss recommendations. Joint supplements. Maybe laser therapy or rehab if someone was lucky enough to have access to a good clinic. Now there’s this growing tension emerging in the field between symptom management and regenerative signaling.That distinction matters. Biology does not really think in terms of pain versus no pain. Biology thinks in terms of stress, tissue integrity, signaling environment, energy availability, immune coordination, and mechanical loading. Pain is just one output of a much larger conversation. And once you start viewing osteoarthritis through that lens, a lot of things begin to make more sense. Take a dog with chronic joint degeneration. Most people imagine the cartilage as something that simply “wore out” like old tires. That analogy is incomplete. Tissues are alive. Cartilage is metabolically active. The synovial lining is active. Bone underneath the joint is active. Immune cells are active. Nerves are active. Mitochondria inside all of those tissues are constantly sensing stress and responding to the environment around them. The joint is less like a dead hinge and more like a neighborhood under chronic construction.Now think about what happens when the construction crew never gets coordinated instructions. Inflammation rises, but repair signaling is weak. Mechanical loading becomes abnormal because the dog moves differently to avoid discomfort. Muscle mass starts dropping because movement decreases. Mitochondrial energy production inside local tissues becomes less efficient. Oxidative stress rises. Synovial fluid quality changes. The immune system starts maintaining a low-grade inflammatory environment instead of resolving it.

For a long time we treated the microbiome like a side character in physiology. Digestion. Maybe immunity if someone was a little more advanced. But the deeper researchers have pushed into mitochondrial biology over the last few years, the harder it has become to draw a clean border between microbial behavior and cellular energy production. The border keeps dissolving. What is emerging now is less like a gut story and more like an orchestration story. Your mitochondria are not simply reacting to calorie intake or ATP demand in real time. They appear to be constantly receiving predictive information about the environment they are about to enter. Some of that information comes from hormones. Some from the nervous system. Some from immune signaling. But an increasingly important layer appears to come from microbes and the compounds they produce while metabolizing nutrients inside the gut. And honestly, this changes how we should think about recovery almost immediately. Because now recovery is no longer just about replacing depleted fuel or repairing tissue damage. It starts looking more like a coordination problem. A timing problem. A communication problem between systems trying to anticipate stress before it arrives. There is something strangely elegant about that. The old model of metabolism was mechanical. Food goes in. ATP comes out. More fuel equals more output. The newer model feels more ecological. Rhythmic. The cell is constantly interpreting its environment and making decisions based on incoming signals. What substrate should I prioritize? Should I become more oxidative or more glycolytic? Should I repair, expand, conserve, defend? Even mitochondria are not static little batteries sitting inside the cell waiting for instructions. They are adaptive sensory structures embedded inside a changing biochemical environment. That environment includes the microbiome. Take butyrate for example. One of the primary short chain fatty acids produced when microbes ferment fibers. Most people hear “fiber” and think bowel health. But butyrate reaches much further than that. It influences mitochondrial biogenesis, histone acetylation, inflammatory tone, oxidative stress handling, intestinal barrier integrity, and substrate selection. It changes the way mitochondria behave under stress. Not simply because it contains calories, but because it contains information.

Any personal experience with kisspeptin?