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Castore: Built to Adapt

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22 contributions to Castore: Built to Adapt
Jetlag
What protocol do you follow to minimize jet lag, avoid drops in HRV, and improve sleep after traveling to a different time zone? @Anthony Castore
0 likes • 22d
@Drew Wurst great!! Thank you
0 likes • 4d
@Robert Clarke thank you!!
DHA IS NOT JUST A FAT PART 3
DHA, PLASMALOGENS, AND MITOCHONDRIAL MEMBRANE POTENTIAL: POWER WITHOUT INSTABILITY At this point in the series, one thing should be clear: membranes are not passive. They are active regulators of signal timing, electron flow, and system stability. Nowhere is that more consequential than in the mitochondria. Most conversations about mitochondria focus on output. ATP. Energy. Fuel utilization. Fat versus glucose. Those discussions matter, but they start too late in the causal chain. Mitochondria do not fail because they lack fuel. They fail because electron flow becomes unstable. To understand why DHA and plasmalogens matter here, we need to talk about mitochondrial membrane potential, often abbreviated as ΔΨm. ΔΨm is usually described as voltage. A battery. A charge gradient across the inner mitochondrial membrane. That description is technically accurate, but conceptually incomplete. ΔΨm is not just how much charge exists. It is how controlled that charge is. A stable membrane potential means electrons move smoothly through the electron transport chain, protons are pumped predictably, and ATP synthase can operate efficiently. An unstable membrane potential means electrons back up, leak, and react with oxygen in places they shouldn’t. This is where most mitochondrial dysfunction actually begins. The inner mitochondrial membrane is not just a lipid barrier. It is a highly specialized electrical interface. It contains densely packed protein complexes, curved membrane structures, and unique lipid compositions. Its job is not to hold charge. Its job is to manage electron flow under load. DHA and plasmalogens directly influence how well it does that job. DHA alters the dielectric properties of the membrane. In practical terms, it changes how electric fields behave within the membrane. It reduces resistance to lateral electron movement and improves the probability that electrons move forward through the chain instead of backing up. This matters at Complex I and Complex III in particular, where electron congestion commonly occurs.
2 likes • 11d
I love your posts. That s why I am asking now - What happens to protein folding when membrane conductivity increases faster than redox buffering capacity?
1 like • 11d
@Anthony Castore do you find useful increased rdw as an early marker?
Carbs vs No Carbs on Retatrutide Here’s What Everyone’s Missing
This Retatrutide carbs vs no-carbs discussion is a perfect example of the kind of work we’ll be doing inside the Cellular Intelligence Circle. I am attaching a video so you guys can get a sense of what to expect. Not hot takes. Not protocols copied from the internet. Not arguing teams or tribes. Instead, I’ll show you how I actually think. How I zoom out, identify what system is really being affected, and trace decisions back to first principles like cellular energetics, redox balance, signaling hierarchy, and context. You’ll see how to move beyond surface-level debates and start asking better questions. The kind of questions that cut through hype, confusion, and false certainty. The goal of the Circle isn’t to tell you what to think. It’s to teach you how to think for yourself. If you’re tired of conflicting advice, overconfident influencers, and protocols that work in theory but fall apart in real humans, this community is built for you. We’ll break down topics like peptides, metabolism, training, recovery, fat loss, and longevity in a way that connects the dots instead of fragmenting them. We kick off in February, and each month will center around a focused agenda designed to build real understanding, not just information overload. Members will get long-form breakdowns, case studies, monthly live Q&A discussions, and practical frameworks they can actually apply. If this video made you stop and rethink the question instead of picking a side, you’re exactly who this was built for. More details coming soon…. The Cellular Intelligence Circle launches February.
Carbs vs No Carbs on Retatrutide Here’s What Everyone’s Missing
1 like • 11d
How this applies in ketogenic diets?
3 likes • 11d
@Anthony Castore thank you!! I fully agree. Also the microbiome changes are really clear - the microbes that increase degradation of carbs are very low - the microbiota is adapting .In parallel, taxa adapted to protein and fat fermentation become relatively more dominant.Without periodic carbohydrate exposure, both systems adapt toward efficiency within a constrained state, at the cost of resilience when conditions change.
Forget Calories Fat Loss Is a Symphony of Electrons, Enzymes, and Breath
Fat loss is one of those phrases that sounds simple eat less, move more but beneath the surface lies a molecular ballet that’s so intricate it borders on poetry. To really understand how fat leaves your body, you have to zoom in beyond the mirror, beyond the scale, all the way down to the molecules themselves. Fat loss isn’t burning; it’s transformation. It’s chemistry, communication, and coordination at the cellular level. Every drop of fat lost is a story of electrons, enzymes, and energy signals passing messages like runners in a relay race. Let’s start at the very beginning: the spark. Imagine you wake up and decide to go for a fasted morning walk. That first step is not just physical it’s molecular ignition. Movement sends a mechanical signal through muscle fibers that says, “Energy demand is rising.” Inside each muscle cell, this signal activates AMP-activated protein kinase, or AMPK. Think of AMPK as the body’s internal accountant. When it senses that the cellular energy balance is off too much AMP (spent energy) and not enough ATP (usable energy) it flips a switch from “store” to “spend.” AMPK begins turning off the enzymes that promote fat storage and turning on those that liberate energy. It tells fat cells to open their vaults. These vaults are made of triglycerides, which are three fatty acid chains attached to a glycerol backbone. To free energy, the bonds must be broken a process called lipolysis. Hormone-sensitive lipase (HSL) and adipose triglyceride lipase (ATGL) are the locksmiths here. They respond to signals from adrenaline and norepinephrine, which are released by the sympathetic nervous system when you start moving. These hormones dock onto beta-adrenergic receptors on fat cells, kicking off a cascade of cyclic AMP (cAMP) signaling. cAMP is like an internal text message that tells HSL: “Go to work.” Once the fatty acids are cleaved from glycerol, they’re released into the bloodstream, but they can’t just float around on their own they’re hydrophobic, meaning they repel water. So they hitch a ride on a protein taxi called albumin, which ferries them to tissues that can use them for energy, primarily muscle and liver. This is where the story gets electric literally.
2 likes • Nov '25
Amazing what you’ve said. I would add, in parallel, the correction of the hedonic - dopamine part— the motivation and reward circuitry that shapes behavior long before hormones act. Rebalancing dopamine tone restores drive, focus, and emotional stability, which makes the biochemical side of fat loss actually sustainable. Thank you for these posts ❤️
Fix the Grid, Not the Gauge: The Mitochondrial Root of Hot Flashes
Hot flashes can be seen not simply as a hormonal problem but as the visible sign of a deeper energy imbalance a flicker in the body’s power grid. Hormones aren’t useless they’re powerful messengers that often help restore balance when the system is struggling. But stopping at hormones is like patching a leak without checking the plumbing. We have to keep asking questions, digging deeper into why those hormones became imbalanced in the first place. Our goal isn’t to mask symptoms or apply temporary fixes; it’s to understand the root cause at the cellular and metabolic level so we can create true, lasting repair. The people who trust us with their health deserve that level of curiosity and commitment. We serve them best not by handing out patches, but by rebuilding the system underneath so it doesn’t keep breaking. At the foundation of that system is mitochondrial health. Mitochondria are the cell’s generators, producing energy in the form of ATP. When they falter, the hypothalamus the region that regulates temperature, sleep, and metabolism loses its steady rhythm. The result is the unpredictable heat surges we call hot flashes. The process unfolds in stages. In the earliest stage, subtle redox imbalances appear: the ratio of NAD⁺ to NADH drifts, and tiny sparks of superoxide begin to escape from the electron transport chain. You might imagine this as a dimming lightbulb the current still flows, but the wiring starts to hum. At this point, magnesium glycinate, niacinamide (vitamin B3), riboflavin (vitamin B2), and taurine help stabilize the system. Magnesium anchors ATP, keeping energy stored until it’s needed. Niacinamide and riboflavin recharge the batteries (NAD⁺ and FAD) that carry electrons through the mitochondrial turbines. Taurine acts as a shock absorber, buffering calcium shifts and protecting delicate membranes. Together they tighten the circuits so electrons can move smoothly again. Early signs that this is working are better sleep, fewer afternoon energy crashes, and steadier tolerance to stress or caffeine. On measurable levels, heart rate variability (HRV) improves, fasting glucose stabilizes, and body temperature becomes more consistent.
2 likes • Oct '25
Amazing like always. I would add the role of inhibiting the overactive KNDy neurons - for the effect on CGRP for symptom relief while working on mitochondria
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Miruna Muha
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@miruna-muha-2318
MD- dual specialization in endocrinology and andrology, advanced training in functional, longevity medicine

Active 4d ago
Joined Aug 2, 2025
Romania
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