🚀 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.

Mitochondria sit at the heart of long COVID, and their dysfunction explains why symptoms cut across so many systems. These organelles are more than energy factories; they are cellular sentinels that decide whether the body is in growth, defense, or repair mode. During acute infection, mitochondria deliberately shut down high-output energy production and switch into alarm signaling. They fragment, release ROS, and send out distress molecules to coordinate immune activity. In long COVID, that alarm mode never fully resets. Instead of resuming normal energy output, mitochondria remain locked in a fragmented, stressed state that drains vitality. One of the hallmarks is fission dominance. Normally, mitochondria exist in a dynamic balance between fusion and fission. Fusion allows mitochondria to share contents, repair damage, and optimize energy efficiency. Fission is used to isolate damaged segments and remove them through mitophagy. In long haulers, oxidative stress and cardiolipin damage tip the scale toward constant fission. The result is a population of small, inefficient mitochondria that can’t produce steady ATP. It is like breaking a power plant into dozens of tiny generators that each sputter and fail rather than pooling resources into one stable grid. Cardiolipin, the signature phospholipid of the inner mitochondrial membrane, plays a central role here. It stabilizes respiratory chain complexes and maintains cristae structure where ATP synthesis occurs. Viral infections, including COVID, generate excessive ROS that oxidize cardiolipin. Once cardiolipin is oxidized, it loses its ability to anchor electron transport complexes, causing electron leaks and more oxidative stress. This vicious cycle locks mitochondria into dysfunction. Imagine scaffolding inside a factory collapsing machines keep running but with sparks flying and energy leaking at every corner. The downstream effect is impaired electron transport. Complex I and Complex II become bottlenecks, leading to reduced oxidative phosphorylation and increased reliance on glycolysis. This metabolic shift produces excess lactate, explaining the exercise intolerance and post-exertional malaise many long haulers experience. Even mild activity can push lactate high because mitochondria can’t clear the workload efficiently. Patients feel as if their muscles are flooded with acid after the smallest effort, and in truth, their energy systems are behaving like an undertrained athlete running on fumes.

One of the best parts of this journey is having mentors who push me to keep learning and questioning. @Elizabeth Yurth has been that kind of mentor for me. She’s not only a brilliant mind in cellular medicine, she’s also someone who constantly reminds me to dig deeper, challenge assumptions, and ask better questions. It was actually Dr. Yurth who got me to revisit the research around Fatty15. Her guidance along with the incredible work she’s doing through the Boulder Longevity Institute and her Human Optimization Academy has been a game-changer for me and so many others. Having people like her in my corner makes me a better student, a better teacher, and hopefully of better service to all of you. With that in mind, I wanted to share some thoughts on Fatty15, the hype, the skepticism, and what we can really learn from it when we zoom out and ask deeper questions. Fatty 15 has become one of the most talked-about molecules in the wellness and longevity space, not because it is new to science, but because of the way it has been packaged and sold. Marketed as the first “essential” odd-chain saturated fatty acid, Fatty 15 (the supplement form of C15:0) promises to stabilize membranes, reduce inflammation, and extend healthspan. For many, the narrative is seductive: here is a nutrient that has been hiding in plain sight, maligned by decades of anti-saturated-fat dogma, finally rebranded as a cornerstone of cellular resilience. But step back from the marketing and look at the science, and the picture becomes more complex. Lipidologists and metabolic researchers, including Dr. Dayan Goodenowe, argue that high levels of pentadecanoic acid in the blood are not causal but correlative. In other words, elevated C15:0 is a marker of robust lipid metabolism, not the reason for it. To use an analogy, it’s like noticing that healthy cities all have clean street signs and then deciding that shipping in more street signs will fix a crumbling city. The signs are a marker of order; they are not the thing that creates it. Supplementing with C15:0 without repairing upstream dysfunction may not move the needle and in some cases, may even make things worse.