If you’ve ever watched a great coach or a great clinician work, you’ll notice something they don’t stare harder; they see differently. They aren’t simply looking for more data; they’re trying to understand the rhythm beneath the data. Biology, especially mitochondrial biology, is a dance long before it becomes a number on a lab report. This article is about learning to see that dance. To understand how SS-31, methylene blue, ketone esters, and even your training decisions interact with real cellular dynamics, you need to know one thing above all else: Biology doesn’t run on quantity, it runs on phase. This is the part that confuses even very smart people. We’re trained to think that oxidative stress = bad, antioxidants = good, more oxygen = good, more ATP = good. But life is rhythmic, not linear. Your mitochondria aren’t furnaces they’re oscillators. They need to pulse. They need to switch between states. They need to signal, respond, tighten, release, and tighten again. This is why a supplement, a peptide, or a drug can work beautifully in one phase of physiology and completely derail things in another. To understand this, we need to talk about one of the most underrated molecules in all of human physiology: cardiolipin. CARDIOLIPIN: THE CONDUCTOR OF THE MITOCHONDRIAL ORCHESTRA Cardiolipin is a special lipid that lives almost exclusively in the inner mitochondrial membrane. If the mitochondrial membrane were a concert hall, cardiolipin would be the acoustic paneling that allows the orchestra to play in tune. It has four fatty acid tails, which is extremely rare most lipids have two. That design allows it to shape the membrane into cristae, those elegant folds where electron transport happens. These folds aren’t random architecture; they control the spacing, alignment, and speed of electron flow. Without cardiolipin, the ETC complexes would be like a bunch of musicians sitting in the wrong seats. Even more importantly, cardiolipin is both a sensor and a switch. When it is oxidized in the right way, it helps signal adaptation. When it is oxidized in the wrong way, it collapses mitochondrial membrane potential, releases cytochrome c, and pushes the cell toward apoptosis. This is why tools that interact with cardiolipin like SS-31 are profoundly powerful but profoundly phase-dependent. They’re not like taking creatine or magnesium; they actively alter the structural language of the mitochondria.

Day 12 – Transcendence: Becoming the Field Itself The final step in this progression isn’t about adding anything new; it’s about dissolving the separation between you and the systems you’ve been studying. Up to now, you’ve practiced coherence inside your own body learning how mitochondria, breath, mind, and rhythm all connect. Transcendence is the realization that those boundaries were never real. In biology, every cell lives within a field of communication: electromagnetic, biochemical, and informational. The moment a cell becomes coherent, it organizes the space around it. The same is true for you. When your internal state reaches harmony, you don’t just feel balanced—you become balance. Your presence shapes the field. This is why advanced biology and ancient philosophy meet at the same truth: everything is connected through resonance. When one node vibrates in order, others begin to entrain. A single coherent heartbeat can influence a room. A calm mind can redirect a conversation. A life lived in rhythm can ripple across generations. Transcendence is not an escape from the body; it’s the full expression of embodiment. It’s when your physiology becomes transparent enough for consciousness to move through it without distortion. You stop trying to manage your energy because you are energy self-organizing, self-aware, and endlessly renewing. At this stage, effort gives way to presence. You no longer need to force outcomes; you participate in them. Decision-making becomes intuition, training becomes meditation, conversation becomes transmission. The line between inner practice and outer world disappears. Quantum biology describes coherence fields extending beyond individual cells biophotons coordinating tissues through light. Social neuroscience shows that humans do the same thing through emotion, language, and body rhythm. When you are calm, others’ heart rates and brain waves synchronize with yours. When you live in coherence, you generate order in your environment without needing control.

🚀 Ketones = Game Changer. This is the thread where I’ll drop my go-to ketone protocols ⚡️ and YOU can fire away with any questions. 💬 Comment your experiences, hacks, and questions below—let’s build the ultimate ketone resource together. 👀 Webinar coming soon… stay tuned. Practical Dosing Blueprints 1.Pre-Workout Protocol (Performance & Focus) Goal: Elevate ketones, buffer acidosis, support hydration & glucose supply. - Hydration: 500–750ml water + electrolytes (sodium 500–1000mg, potassium 200–400mg). - Bicarbonate: 0.3 g/kg sodium bicarbonate (~20g for 70kg athlete), dissolved in water. Take 90–120 min before session to minimize GI upset. - Trehalose (Carbohydrate): 15–25g as slow-release carb for sustained glycogen supply. - Ketone Ester (D-BHB/1,3-BD): 15–25ml (~7–12g KE) 10–15 min pre-warmup. Effect: Dual-fuel system (glucose + BHB), reduced acidosis, enhanced mental focus . 2.Intra-Workout Endurance Protocol Goal: Sustain metabolic efficiency, prevent bonk, extend time-to-exhaustion. - Every 60 min: Trehalose or isomaltulose: 20–30g (slow carb). Ketone Ester: 10–15ml (~5–7g KE). - Optional: electrolyte top-up (sodium/potassium). Effect: Preserves glycogen, stabilizes glucose, sustains BHB 1–3 mM . 3.Post-Workout Recovery Protocol Goal: Accelerate glycogen resynthesis, repair, and inflammation control. - Protein: 20–30g whey or EAAs. - Carbs: 40–60g high-GI glucose or maltodextrin. - Ketone Ester: 20–30ml (~10–15g KE), taken 30–45 min post-exercise (separate from carb/protein drink for maximal signaling). - Trehalose: Add 10–15g if training volume is very high or glycogen depleted. Effect: 50% faster glycogen replenishment, stronger mTOR activation, reduced inflammation . 4.Sleep Recovery Protocol (Athletes) Goal: Deep recovery, improve next-day performance. - Ketone Ester: 2.5–10ml (~1–5g KE) immediately before bed. - Optional: Magnesium glycinate/threonate for additional relaxation.

After a long time, I’ll be in the US again as I’m heading to the Olympia. I also got a ticket for Olympia University, and I see that at least two members of the group will be speaking there – @Elizabeth Yurth and @Eric Fete. Can’t wait :) Will anyone else be there?

This whole “six-stage agonist” idea reads like a playground contest where six-year-olds are trying to one-up each other without thinking through the consequences. One kid says, “I can eat the most candy,” the next says, “Well I can stay up all night,” another brags, “I can ride my bike with no hands,” and pretty soon the game spirals into chaos everybody competing, nobody coordinating, and the end result is a bunch of sick, cranky kids. That’s exactly what happens when you try to bolt GLP-1, GIP, glucagon, IGF-1, Klotho, and myostatin inhibition together into a single product. Each of these signals has real, powerful effects on metabolism, growth, and cellular resilience, but they pull in opposite directions, act on different timelines, and demand very different dosing windows. Instead of synergy, you create noisy cross-talk that leaves the body trying to follow six conflicting orders at once. True optimization doesn’t come from piling on more levers or chasing the newest shiny receptor target it comes from respecting the intelligence of the cell, reducing signal noise, and using surgically precise interventions at the right time and in the right tissue. A “GLP-1 + GIP + glucagon + IGF-1 + Klotho + anti-myostatin” cocktail is mechanistically incoherent because it stacks pathways that biochemically push in opposite directions, on different clocks, in different tissues. GLP-1R and GIPR are Gs-coupled incretin receptors that raise cAMP/PKA and potentiate β-cell insulin secretion, slow gastric emptying (GLP-1), and alter CNS appetite; GCGR is also Gs-coupled but in hepatocytes it spikes cAMP/PKA to drive glycogenolysis and gluconeogenesis, directly opposing the glucose-lowering aim of the incretins and serine-phosphorylating IRS1 to blunt insulin signaling in liver. IGF-1R is an RTK that activates IRS→PI3K→AKT→mTORC1 and MAPK/ERK to promote hypertrophy and nutrient storage, while soluble Klotho evolved as a longevity brake: it partners with FGF23 for phosphate/Vit-D control and independently dampens IGF-1/insulin signaling and shifts cells toward FoxO-mediated stress resistance and autophagy i.e., the biochemical opposite of sustained mTORC1 drive. Myostatin inhibition removes SMAD2/3 repression at ActRIIB, disinhibiting satellite cells and mTORC1 in muscle; pair that with IGF-1 and you push strong anabolism in myofibers, but the liver is simultaneously being told by glucagon to export glucose and lipids while adipose receives a GIP signal that favors storage so partitioning gets noisy. Add hard constraints from pharmacology: receptor stoichiometry and PK don’t line up. IGF-1 (IGFBP-bound) has long half-life and broad tissue exposure; GLP-1/GIP need DPP-4 protection and act over minutes to hours; glucagon clears fast but hits liver immediately; Klotho’s effects are slow, endocrine, and context-dependent; anti-myostatin requires sustained exposure for weeks to remodel transcription. One fixed dose can’t simultaneously achieve the right receptor occupancy across these targets: the concentration that meaningfully engages IGF-1R will overshoot GLP-1R CNS effects; the dose that meaningfully inhibits myostatin in skeletal muscle will not “time-match” the brief hepatic cAMP bursts from glucagon; and any hepatic PKA surge will antagonize the insulin/IGF-1 signaling you need for clean glycogen and protein synthesis. Think of it like six foremen shouting conflicting orders on a construction site: IGF-1 and anti-myostatin demand “build muscle now,” Klotho says “slow growth and repair the scaffolding first,” GLP-1/GIP say “bring in insulin and store nutrients,” glucagon yells “ship the materials back out of the warehouse,” and the clock for each foreman runs at a different speed. The “peer-reviewed” reality is that the only reason GLP-1/GIP/GCGR tri-agonists can work in trials is because they are engineered single peptides with tuned receptor bias and potency ratios to achieve a net, phase-appropriate phenotype; bolting on IGF-1, Klotho, and anti-myostatin as separate levers breaks that balance and guarantees asynchronous, tissue-mismatched signaling. The likely story arc is predictable: week 1 you feel appetite suppression and see scale weight drop from GLP-1 physiology while hepatic glucagon spikes make glucose swing; by week 2–4 IGF-1 and anti-myostatin start pushing muscle protein synthesis but collide with hepatic PKA-mediated insulin resistance and GIP-biased adipose storage, so nutrient partitioning becomes erratic; by weeks 4–8 Klotho’s brake on IGF/insulin signaling and phosphate/Vit-D shifts muddy recovery and mitochondrial quality control, leaving you with jittery glycemia, inconsistent pumps, GI side effects, possible edema or mineral issues, and a plateau where fat isn’t reliably falling and muscle isn’t cleanly accruing. Instead of a symphony you get six instruments in different keys, different tempos, and different rooms the score reads “recomp,” but the sound is chaos.