I am one of those people who on day one when I used Metashred (BAM/SLU combo) it sent me to the ER. Tried again a week later and although I was able to stay away from the ER it wasn't a pretty couple of hours. I decided instead to split up the two (SLU on training days and BAM on rest days). Been using SLU for a while at various dosages with no issues. For BAM, the capsules I have are 15mg. Took my first dosage yesterday on my rest day without issue. Is there a dosage I should be working up to?

I've been taking SLU for 6 weeks with no break. Is it advisable to now cycle off for 6 weeks? I've been taking CJC (no DAC)/Ipa for about 4 weeks now, Monday-Friday with a break on the weekend. Will I eventually need to cycle off or can I run this stack indefinitely? I also just started running retatrutide as well...0.5mg 3 times a week with the plan to titrate up to 1mg 3 times a week. What's the timeframe for taking this, and/or does anyone have a good protocol for this?

Last night, I woke up to something that shook me in a way I haven’t felt in a long time. My bulldog Jeter, who’s ten now and basically my shadow, was shivering on the inhale while he slept. At first I thought maybe he was cold, or dreaming. Bulldogs dream with their whole soul, so that wasn’t unusual. But something felt off. The tremor wasn’t rhythmic like dreaming. It was sharp, almost like a nerve misfiring. When he got up from bed to walk to another room, he seemed weak like his legs weren’t receiving the normal signals from his brain. His shoulders and legs trembled slightly, his paws looked unsure beneath him, and he kept repositioning like he couldn’t get comfortable. That’s when my stomach dropped. I scooped him up, put him in the car, and Julie and I drove straight to MedVet. If you’ve ever loved a dog deeply, you know that feeling where you go from half-asleep to wide awake with one single thought: “Please let him be okay.” At MedVet they gave him a ketamine and methadone shot for pain, and they suspected a disc issue in his spine. They didn’t run an MRI that night, so we were left with the kind of diagnosis most dog owners get at first: “Likely disc compression, monitor closely.” In other words, an entire universe of things could be happening under the surface. When we finally got back home, Jeter was sedated, wobbly, and tremoring. He was trying to be strong bulldogs have a level of pride that honestly rivals ours—but he was struggling. And in moments like that, both as a practitioner and as a dog dad, you are forced to sit between two worlds: the scientific understanding of what’s happening, and the emotional weight of watching someone you love suffer. That’s what inspired me to write this for you today not just to share the story, but to teach you what’s actually going on inside a dog’s body when a disc bulges, why the symptoms show up the way they do, and how targeted regenerative peptides like Pentosan, ARA-290, TB-500, BPC-157, and SS-31 can create a powerful recovery pathway when used correctly.

Redox is one of those concepts that everyone has heard of but very few people truly grasp, and yet almost everything in human physiology depends on it. For trainers and clinicians, redox is the hidden language that tells you why someone can train hard one day and crash the next, why fat loss stalls even with perfect macros, why motivation drops without a psychological trigger, why inflammation rises mysteriously, or why protocols that used to work suddenly stop producing results. Redox isn’t a supplement, a lab marker, or a buzzword. It is the most fundamental process life uses to create energy, repair damage, and adapt to stress. When redox flows, people adapt. When it gets stuck, people stagnate. Understanding redox at a deep level gives you the ability to see beneath symptoms, beneath lab markers, beneath surface-level physiology, and down into the actual physics and molecular dynamics that determine whether a person is moving toward resilience or toward dysfunction. This redox deep dive will walk through what redox is, why it matters, how it gets stuck, what “stuck” actually means at the molecular level, and how different stressors push the system into different dysfunctional patterns. Throughout this, I’ll use analogies and imagery that make the invisible world of electrons and membranes feel intuitive and concrete, allowing you to visualize exactly what is happening inside cells when energy is being made—or when the system jams. You’ll see how mitochondrial membranes behave like electrical waterfalls, how electrons move like crowds of people flowing through hallways, how redox imbalance can freeze a system the way traffic jams choke off a city, and how trainers and clinicians unintentionally worsen stuck redox by focusing on quantity of activity instead of the phase of the system. Redox is short for reduction and oxidation the transfer of electrons. To understand why this matters, imagine every cell in your body as a tiny city. Energy isn’t created in one burst; it’s created by passing electrons down a series of steps, like handing a baton from one runner to the next. Reduction is when a molecule gains electrons, oxidation is when it loses electrons. In biology, electrons fall down an energetic staircase inside mitochondria called the electron transport chain. As electrons move, they power tiny pumps that push protons across a membrane, building what can be imagined as a “pressure gradient” or electrical tension. This tension the mitochondrial membrane potential is like the charged battery that lets ATP synthase spin and generate ATP. Think of it like water flowing through a hydroelectric dam: the higher the water pressure behind the dam, the more electricity you can generate. If the water level drops too low, the turbine stops. If the dam wall gets blocked and pressure rises too high, the system becomes dangerous. Mitochondria work exactly the same way. Redox is the management of electron flow across the mitochondrial inner membrane. Everything hinges on whether electrons are moving, whether they have somewhere to go, whether the membrane potential is balanced, and whether the cell can match energy demand with supply.

Plasmalogens are one of the oldest, most fundamental molecules inside the human body, yet almost no one talks about them. If you imagine the cell as a city, plasmalogens are the shock-absorbing pavement, the insulation around every electrical wire, and the structural glue that determines how well the buildings hold up under stress. They make up a significant portion of the membranes around our cells, especially in the brain, heart, immune system, and mitochondria. They’re not used as fuel, they’re not signaling hormones, and they’re not vitamins they are architectural lipids, meaning their entire purpose is to create the “physical environment” inside which every biochemical reaction occurs. When this architecture is strong, cells communicate clearly, mitochondria keep up with energy demands, neurons fire smoothly, and tissues age more slowly. When plasmalogens decline as they do with aging, chronic inflammation, metabolic disease, and overtraining the whole system becomes more fragile. Surfaces become leaky. Signals get distorted. Energy becomes harder to make. And we see it clinically as brain fog, slower recovery, impaired metabolism, chronic fatigue, mood instability, and higher disease risk. To understand plasmalogens, you first need to understand the membrane. The membrane is the barrier between chaos and order. It keeps the inside of the cell different from the outside. But it’s not a hardened shell; it’s a flexible, dynamic, constantly-moving layer of phospholipids, cholesterol, proteins, and microdomains. Think of it like a high-tech trampoline. Every receptor sits in this trampoline. Every transporter is anchored to it. Every signal, from insulin binding to the NMDA receptor firing, depends on how stable and well-organized that trampoline is. Plasmalogens sit inside this membrane like reinforced beams with a special vinyl-ether bond. This bond is unique: it actually absorbs oxidative damage like a sacrificial shield. Instead of letting free radicals tear up the membrane, plasmalogens get hit first and protect the surrounding structure. This is why they are most concentrated in tissues with the highest oxidative stress—neurons, muscle, heart, immune cells, and mitochondria. When plasmalogens are low, cell membranes become thinner, more fragile, and more prone to dysfunction. Receptors do not cluster properly, inflammation becomes easier to trigger, and mitochondria lose their tight coupling between electron flow and ATP production. In other words, membranes lose intelligence.