Hey everyone, I know @Anthony Castore is a fan of the Alpha Stim device. This past weekend I got the try the Nuropod (ear-electrode vagus nerve stimulator) for sleep/HRV/nervous system regulation. I know many of you use Alpha-Stim (cranial electrotherapy), from my understand the technology used by Nuropod has a more different influence on vagal tone because it uses transcutaneous auricular vagus nerve stimulation (taVNS) vs the Cranial Electrotherapy Stimulation (CES) used by Alpha Stim. Does anyone here use Nuropod? And for those who have tried both, how would you compare?

SLU-PP-332 is one of the most misunderstood compounds in the entire performance and longevity space, and nowhere is that misunderstanding more obvious than in the topic of water retention. People experience it, panic, and immediately assume “estrogen,” “bad purity,” “toxicity,” or “my body isn’t responding to SLU correctly.” But when you break down what’s actually happening at the cellular level, the explanation is far more interesting, far more predictable, and far more fixable than people realize. Water retention with SLU isn’t random. It’s not a flaw in the compound. It’s a message from your system saying, “Your signaling is mismatched.” In this article, we’re going to break down what that means, why it happens, how SLU interacts with AMPK, ERRα, and renal sodium handling, and what the body is actually trying to do. By the end, beginners will understand the big picture clearly, and advanced clinicians and coaches will be able to teach it to others. To understand SLU and water retention, you first need to understand what SLU is actually doing. SLU is not a fat burner. It is not a stimulant. It is not a thermogenic drug. SLU is a pan-ERR agonist meaning it activates estrogen-related receptors alpha, beta, and gamma. These receptors live inside the nucleus and act like metabolic switchboards. They determine which genes get turned on to burn fat, use oxygen, increase mitochondrial respiration, create new mitochondria, and shift fuel preference. ERRα in particular is a master regulator of mitochondrial function. It influences everything from oxidative phosphorylation to uncoupling protein expression to metabolic adaptation under stress. When SLU binds to these receptors, it triggers the same gene programs normally activated by aerobic exercise: DDIT4, which senses metabolic stress and tells the cell to adapt, and SLC25A25, which helps shuttle fuel across the inner mitochondrial membrane so you can produce energy more efficiently. These genes are not surface-level actors. They’re deep in the machinery. They’re the electricians rewiring the power grid.

Mitochondria are like cities within your cells each one packed with tiny power plants called cristae that convert oxygen and nutrients into energy. The denser and more intricately folded these cristae are, the more “real estate” your cell has for building ATP, the energy currency that runs everything from muscle contractions to hormone synthesis. A new human biopsy study found that after just eight weeks of high-intensity interval training, men with type 2 diabetes increased the density of their mitochondrial cristae by about seven percent. That’s not just more mitochondria it’s better mitochondria. The architecture itself became more efficient, which means their cells could produce more power per organelle. To visualize this, think of a wind farm. You can either add more turbines or improve the design of each blade so that every gust of wind generates more energy. HIIT acts like an engineer who sharpens the blades it triggers proteins such as OPA1, MICOS, and ATP-synthase dimers to fold the inner mitochondrial membrane into tighter, more efficient layers. These folds pack in more electron-transport chains, allowing smoother electron flow and higher ATP output. In people with insulin resistance, this remodeling ability (plasticity) remains intact; it’s just under-signaled. HIIT provides the metabolic stress that wakes it up, teaching the muscle to run on oxygen again instead of depending on inefficient glycolysis. You can think of HIIT as a controlled storm. The bursts of effort raise reactive oxygen species just enough to signal adaptation without causing damage if recovery and nutrition are right. Over time, the mitochondria respond by reorganizing their internal scaffolding to handle higher electron traffic with less “leakage.” This is why the right dose of intensity matters more than total volume. Too little stress and nothing changes; too much and the membranes buckle. The sweet spot builds resilience into both the structure and the signaling. In practical terms, here’s how you can use this insight to sculpt your own mitochondrial architecture.

From my own log here recently Wakeup 6am 1min Ice cold shower Fasted oral BPC-157, KPV, SLU-PP-332 on training days, fatty 15, 20g creatine, 10g L glutamine, Urolithin A, NR, R-ALA 32oz room temp water + LMNT 30min walk 3mg Zyn pouch (nicotine), 20g exogenous ketones, 0.2g psilocybin mushroom microdose. Crank out 2 hours hyper productive work and substantial uplift in mood (the mood part I largely credit to improvements in gut health, oral BPC/KPV and glutamine playing a role here) and the microdose of psilocybin.

I have what I believe to be an acute strain to the plantar fascia. (36 hours) Trying NOT to throw the kitchen sink at it. Readily available to me BPC-157, TB-500 GHK-CU, KPV Cartalax Red light - R+ | NIR+ wavelengths of 480nm, 630nm, 660nm, 810nm, 830nm, 850nm and 1060nm. I believe caused by increased overuse and chronic dehydration. Also fairly certain Pickleball was invented by orthopedists.