I was wondering if you have archives of your articles? I just read this article from the SR about VIP and I cannot tell if it is good or bad (after already placing an order). So looking for more clarity about using it.

I’m excited to announce I am planning an upcoming podcast with LVLUP Health’s founder, Kyal Van Der Leest. Kyal’s passion for innovation and integrity in formulation matches everything we value here! I am also thrilled to introduce a couple of members from their team: @Chuck G and @Jennifer Faye-Matthews. Chuck works with LVLUP’s practitioner accounts and Jen assists with their clinical education. They will be collecting our community's questions and feedback and are able to share product information and updates from LVLUP Health. LVLUP has offered us a group discount link here for 15% off - Castore Let’s use this as a place to ask questions, trade experiences, and grow together.

Diabetes and dementia are linked through a simple idea: the brain runs on energy, and diabetes disrupts the brain’s ability to use that energy. When the brain can’t make enough fuel, the neurons begin to slow their firing, mismanage inflammation, misfold proteins, lose membrane integrity, and eventually break down networks involved in memory, mood, coordination, and cognition. Dementia isn’t one event it’s a slow starvation paired with redox imbalance and membrane breakdown. Think of the brain like a city that runs on electricity. Glucose is the main power source. Insulin is the key that lets glucose into the cell. In diabetes especially Type 2 the key doesn’t work well. This creates “brain energy scarcity.” When neurons can’t pull glucose in effectively, they start producing large amounts of reactive oxygen species, shift into survival mode, and stop repairing themselves. Over time, this energetic bottleneck causes synapses to weaken, mitochondria to swell and fragment, and microglia to become overactive. This is why many experts call Alzheimer’s “Type 3 diabetes.” On a molecular level, poor glucose utilization collapses mitochondrial membrane potential, the voltage that drives ATP production. This voltage is the “life force” of the neuron. When it drops, the brain’s ability to manage calcium, recycle damaged proteins (autophagy), and maintain neurotransmitter balance all fall apart. Insulin signaling also regulates synaptic plasticity, serotonin production, acetylcholine balance, and BDNF. So poor metabolic signaling doesn’t only starve neurons it also makes them “forget how to learn.” Diabetes also increases levels of advanced glycation end products (AGEs), which are like sticky caramelized proteins that physically gunk up receptors, stiffen membranes, and activate inflammation. Blood vessel health declines, reducing oxygen delivery. Redox balance swings toward chronic oxidative stress. Over years, this combination erodes the frontal lobe, hippocampus, and basal ganglia structures tightly tied to memory, motivation, movement, and personality.

Join me for our October Live Q&A on Saturday, October 25 at 12:00 p.m. EST. We’ll dig into peptides, mitochondrial medicine, training and recovery design, and real-world protocol troubleshooting. Bring your questions (big or small), wins, sticking points, and labs or metrics you want decoded. Come ready to learn, take notes, and leave with clear next steps you can use the same day. To submit a question in advance, reply to this post with “Q&A” at the top and a concise summary of your question; live questions will be taken in order after pre-submissions. Save the date, invite a friend who’d benefit, and I’ll see you Saturday at noon. Here is the link to watch the replay of the Q&A thank you everone for joining and thank you for sending your questions in! https://us06web.zoom.us/rec/share/pcj7EkP9JA9hgj2SIcHeiFFgml4klErn_CRj33Nbb10OM0gmzh7itR_vKyHGXXwd.Cs3mioaqFw2jbYHe?startTime=1761407862000 Passcode: e4T2tR!l

Why are we (the collective “we”) not talking about Cardarine more? It’s effective, and it’s cheap as hell, win win IMO. I get that these peptides, small molecules and whatnot are the hot topic nowadays, rightfully so, but why isn’t Cardarine in that discussion? I’ve personally seen good results with using carnitine and Cardarine together, and now I’m looking at bringing in SLU and the other mitochondrial players. How would I use Cardarine along with carnitine, SLU, mots c, etc.? I’ve used carnitine and Cardarine pre training with good success, but like all of us here, I want to keep improving Like I mentioned, I’ve used carnitine and cardarine pre training (substrate session) thinking that I’ll spare muscle glycogen, therefore improving performance, by enhancing fat usage and stimulating PGC-1 in a training environment would help make sure those new mitochondria are exposed to that environment. But if I’m looking to build my glycolytic system, maybe that’s not the best approach, and keep those players on more metabolic days? @Anthony Castore