Every industry has defining moments the ones that separate hype from principle and reveal who’s truly here for the long game. This is one of those moments for ours, and I want to be completely transparent about where we stand. Biomed Industries is the company credited with discovering Bioglutide (NA-931) and developing it as a next-generation GLP-based compound. Our raw materials came from the same supplier Biomed reportedly uses. Recently, serious accusations have surfaced against Biomed claims of fraudulent data, lack of publicly verifiable sequence information, and the absence of a disclosed CAS number or molecular structure. The accuser has raised valid scientific concerns that deserve to be addressed. At the same time, these allegations are new, and Biomed has not yet had the opportunity to publicly respond. That’s why we are pausing not panicking. Even in moments like this, our safeguards remain strong. We can fully document purity through HPLC and LC-MS, confirm sterility and endotoxin levels, and provide verified Certificates of Analysis. However, without a public reference structure or sequence, no lab including ours can confirm 100% molecular identity. We can verify that a compound is clean, sterile, and potent, but we can’t compare it to a molecule that’s never been fully published. To give some context, CB4211 is a great example of how innovation often moves faster than public documentation. This compound, developed for mitochondrial health and metabolic optimization, has been prescribed by physicians and compounded by pharmacies despite its structure, sequence, and CAS never being publicly released. That doesn’t make it ineffective or illegitimate it simply illustrates that, just like Bioglutide, the available data can only go so far. In both cases, these products are sourced, tested, and manufactured to the highest standards, with thorough purity and safety testing but without full structural transparency. That means identity and uniqueness are established through trust, testing, and outcomes rather than public disclosure. For all we know, CB4211 could be a more advanced form or reformulated analog of MOTS-c—or perhaps just a more expensive version under a new label. Until formal sequencing or patent releases are made public, no one can say for sure. This doesn’t discredit its value; it simply reminds us that in early-stage biotech, certainty often trails behind discovery. That’s why rigorous testing, ethical sourcing, and open communication about what is known and what isn’t are so vital.

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.

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.

For the last two nights, I’ve been blindsided by a headache that seems to materialize out of nowhere the kind that starts behind your temple and slowly tightens its grip until your whole body feels like it’s wound up like a steel cable. Naturally, I wanted answers. I don’t do “random.” Every symptom is data, every signal has a story. So I went digging the only way I know how through the lens of cellular medicine. And, as usual, when you zoom down to the molecular level, the mystery starts to make sense. What felt like a simple tension headache turned out to be a full-blown communication breakdown between redox balance, nitric oxide signaling, and the mitochondria running the show. When that dull pressure starts behind your temple and your whole body begins to feel like it’s turning to stone, what’s really happening is not a simple tension issue it’s a systems problem. Think of your body as an electrical city. By evening, you’ve run low on voltage, your wiring (the nerves) is misfiring, and the traffic lights controlling blood flow and muscle relaxation are blinking out of sync. The power grid your mitochondria is struggling to keep up with demand. Your mitochondria are the power plants in every cell. During the day they work hard generating energy by passing electrons down a chain of complexes that use oxygen to create ATP. When that process slows or becomes inefficient, electrons leak, forming reactive oxygen species sparks that can damage cell membranes and enzymes. Normally, a little of this “redox signaling” is good; it tells your body how to adapt. But when the load is heavy and recovery short, those sparks become wildfire. The result is a drop in cellular voltage, a buildup of oxidative stress, and an overall redox imbalance. This loss of balance directly affects nitric oxide, one of the body’s key signaling molecules for blood flow and nerve function. Under healthy conditions, nitric oxide synthase (NOS) takes arginine and, using a helper molecule called BH4, produces nitric oxide (NO). That NO tells blood vessels to relax and muscles to stay supple. But when oxidative stress rises, BH4 gets oxidized and NOS goes “rogue,” producing superoxide instead of NO. The rogue product reacts with what little NO is left, forming peroxynitrite an aggressive compound that damages mitochondrial membranes, DNA, and enzymes. It’s like sending both water and acid through your plumbing at once. The pipes the blood vessels swell, leak, and misbehave, creating the throbbing pain of a headache while starving muscles of oxygen and ATP.

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.