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

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.

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.

When most people hear the word “fats,” they think of calories or cholesterol. In cellular medicine, fats are far more than fuel they are the words and grammar of biological communication. Each lipid molecule is like a syllable that tells the cell when to inflame, when to repair, and when to rest. Two families sit at the heart of this conversation: plasmalogens and SPMs, or Specialized Pro-Resolving Mediators. Plasmalogens are ether-linked phospholipids that form part of every cell membrane and act as antioxidant shock absorbers. SPMs are signal molecules made from omega-3 fats that end inflammation once the threat has passed. When either group is depleted, the body can start an inflammatory “sentence” but forget how to end it. The result is chronic inflammation, autoimmunity, and neurodegeneration. Lipids are fat-like molecules that don’t dissolve in water. Inside the body, they serve three key roles: they build membranes, store energy, and act as messengers. You can imagine a cell membrane as a coral reef. The rigid corals are phospholipids that maintain structure, while cholesterol and glycolipids act like flexible anemones allowing movement and adaptability. Nutrients, ions, and hormones swim through this reef, and the condition of the lipids determines how well communication flows. Plasmalogens stand out because of their unique structure. Every phospholipid has three parts a glycerol backbone, two fatty acid tails, and a phosphate-based headgroup. Plasmalogens replace one fatty acid tail with a special vinyl-ether bond. This small chemical tweak gives them superpowers: they resist oxidation, store high-energy electrons, and can neutralize free radicals faster than most antioxidants. If a regular phospholipid is a car tire, a plasmalogen is a run-flat tire that can take damage and keep working. Plasmalogen production starts in the peroxisome, the cell’s detox and lipid-assembly center, and finishes in the endoplasmic reticulum, the folding factory. The process begins with DHAP (dihydroxyacetone phosphate), a byproduct of glucose metabolism. The enzyme GNPAT attaches the first fatty acid, then AGPS swaps that bond for an ether linkage using a long-chain alcohol. These steps need cofactors such as iron, magnesium, NADPH, and vitamin B5. The partially built molecule then travels to the ER, where desaturation forms the vinyl double bond, and the headgroup is added, completing the plasmenyl-phospholipid structure. The result is either plasmenylethanolamine or plasmenylcholine, depending on which headgroup is used.

When people first hear about mitochondrial peptides like SS31, MOTS-c, and Humanin, they often want to know which one is “best.” The truth is that each works on different levers inside the cell, and the right choice depends on what system is most stressed. Instead of guessing, we can use both objective markers and subjective markers to guide decisions. The key is to think of mitochondria as adaptable power plants. Each peptide teaches the plant a different skill SS31 strengthens the wiring, MOTS-c teaches it to use different fuels, and Humanin helps it resist damage signals. By paying attention to how our bodies respond, we can run small experiments and see what creates real improvements. The first place to start is redox stress. This is the balance between energy production and the “sparks” of free radicals that leak out. When sparks overwhelm the clean-up systems, we get fatigue, brain fog, and recovery issues. Labs like glutathione ratios or 8-OHdG give objective clues, but we can also use simple subjective markers. If someone feels like their workouts leave them drained for days, if their energy crashes mid-afternoon, or if their mood dips after training, redox stress may be the limiting factor. In that case, SS31 is often the best starting tool. SS31 binds to cardiolipin in the inner mitochondrial membrane, stabilizes the electron transport chain, and reduces the leakage of reactive oxygen species. In plain terms, it stops the wires from sparking and helps energy flow smoothly. Subjectively, people notice less soreness, steadier energy, and a calmer nervous system. HRV often improves, and the same training feels easier. If those markers shift in the right direction, SS31 is likely doing its job. The second area to evaluate is metabolic flexibility, which is the ability to switch between carbs and fats as needed. Poor flexibility shows up as high fasting insulin, high triglycerides, or simply the feeling that you “hit the wall” quickly without carbs. On a bike or during zone two cardio, if your heart rate climbs quickly and you feel like you cannot settle into a pace, that points to a problem in fuel choice. MOTS-c is the peptide that best addresses this. It activates AMPK, which signals the cell to clean up inefficient processes and shift toward fat oxidation. In practice, this means glucose uptake improves, fatty acid breakdown becomes more efficient, and new mitochondria are built. Subjective markers here include easier endurance work, steadier blood sugar, less hunger between meals, and a more even mood. On the performance side, lactate production during submaximal efforts goes down and zone two feels more sustainable. When those changes show up, MOTS-c is proving useful.