VISION, POSTURE, COGNITION, AND PERFORMANCE: HOW MEMBRANES GOVERN THE WHOLE ORGANISM Up to this point, we’ve stayed mostly at the cellular and membrane level. Conductors, buffers, mitochondria, failure modes. That work matters, but if it stays abstract it risks feeling disconnected from lived experience. So in this part, we zoom out. Membrane health doesn’t just determine what happens inside cells. It determines how an organism perceives the world, organizes its body, and decides how much stress it can tolerate. This is where DHA stops being a biochemical curiosity and becomes something you can see in posture, feel in cognition, and observe in performance. Let’s start with vision. Vision is often treated as a sensory add-on. Something that delivers information to the brain, where the “real work” happens. That framing is backwards. Vision is a primary regulator of autonomic tone. The retina is not just detecting light. It is converting photons into electron movement. That electron movement sets timing signals that propagate through the nervous system. These signals influence circadian rhythm, arousal state, muscle tone, and spatial orientation. The retina is one of the most DHA-dense tissues in the human body for a reason. Phototransduction is a high-frequency, high-precision process. Light hits photoreceptors, electrons move, ion channels open, and signals propagate in milliseconds. The system must respond quickly and reset just as fast. Any noise or delay degrades perception and increases stress. DHA allows retinal membranes to maintain signal fidelity under constant flux. It improves signal-to-noise and shortens recovery time between inputs. When DHA is insufficient, or when membranes are oxidatively unstable, the retina becomes noisy. The system compensates by increasing sympathetic tone. The body becomes more vigilant, more guarded, less adaptable. This is not psychological. It is electrical. From the retina, this tone propagates. Visual instability increases neck and jaw tone.

By now, the core idea should be clear. DHA is not nutrition. Plasmalogens are not optional add-ons. Mitochondria are not broken engines waiting for more fuel. And inflammation is not the enemy. Across fatigue, poor recovery, cognitive decline, chronic inflammation, burnout, and early aging, the common thread is a loss of signal integrity at the membrane level. This final section exists for one reason: to turn that understanding into a way of thinking that prevents overcorrection, overstimulation, and endless symptom chasing. This is not a protocol. It’s an operating system. The first principle of a membrane-first approach is order. Biology always restores structure before increasing output. When we reverse that order, systems become fragile. When we respect it, systems organize themselves naturally. So the most important question is not, “What should I add?” It’s, “What is the membrane currently capable of handling?” That single question eliminates most mistakes. The first step in this hierarchy is de-noising. Before trying to improve energy or performance, sources of chronic membrane instability need to be reduced. Excessive omega-6 intake, oxidized fats, environmental stressors, poor sleep, and unmanaged psychological stress all increase background electron noise. Adding conduction or stimulation into an already noisy system only amplifies chaos. This is why people sometimes feel worse when adding DHA, mitochondrial supplements, or aggressive training. The system was already loud, and better wiring simply exposes the problem. De-noising isn’t exciting, but it’s foundational. The second step is buffering. Once noise is reduced, the system needs protection before speed. This is where plasmalogens matter. Buffering increases membrane capacitance and allows electrons to move without damaging surrounding structures. This phase often feels calming rather than stimulating, and that’s not a failure. Calm means signal coherence is improving. Better sleep, feeling more grounded, and reduced reactivity without an immediate surge in energy are signs this stage is working. It’s important not to rush past it.

WHEN OMEGA-6 BREAKS THE CIRCUIT: INFLAMMATION AS CORRUPTED ELECTRON SIGNALING By now, we’ve reframed DHA as a conductor, plasmalogens as buffers, and mitochondrial membranes as electrical control surfaces. With that framework in place, we can finally talk about inflammation in a way that makes sense. This part may challenge some deeply held assumptions. Inflammation is rarely the primary problem. It is usually the visible consequence of corrupted electron flow. Omega-6 fatty acids sit at the center of this misunderstanding. Omega-6 fats are often described as “pro-inflammatory,” while omega-3s are described as “anti-inflammatory.” That language is convenient, but it hides the real issue. Omega-6 fats are not inherently inflammatory. They are chemically reactive and electronically unstable under modern conditions. That distinction matters. Arachidonic acid, the most discussed omega-6 fatty acid, is highly unsaturated. Like DHA, it contains multiple double bonds. But the pattern of those bonds, their spatial organization, and their interaction with the surrounding membrane environment lead to very different behavior. DHA supports long-range, smooth electron movement along membranes. Omega-6 fats tend to produce short-range, burst-like electron reactions. In practical terms, DHA behaves like a controlled transmission line. Omega-6 dominance behaves like a spark generator. This is not a moral judgment. It is physics. When omega-6 fatty acids dominate membrane composition, especially in the absence of sufficient plasmalogens and DHA, electron movement becomes fragmented. Instead of electrons moving coherently across the membrane surface, they jump, react, and terminate prematurely. These reactions generate lipid peroxides. Lipid peroxidation is not random damage. It is electron flow gone wrong. The system attempts to move charge, fails to control it, and produces reactive intermediates as a result. Those intermediates are what the immune system responds to. This is where the confusion begins.

Over the past few years, I’ve been using GH fairly regularly. I have access to high-quality pharmaceutical-grade GH, so I didn’t overthink it. At my age (54), the difference in how I feel, recover, and sleep is definitely noticeable. That’s always been the main reason I’ve used it, and 2 - 3 IU per day was enough for me. I only increased the dose before a competition to enhance fat burning. However, after listening to and reading content from Antony and Dr. Seeds, I came to understand that constant activation of mTOR and supraphysiological levels of IGF might improve well-being and appearance as we age — but they can also accelerate aging. That said, I used GH mostly while on a ketogenic diet, where GH doesn’t significantly elevate IGF, so that likely minimized the effect. Now I’ve been off GH for two months, and I’d like to test a protocol using GHRH and GHRP, aiming for more pulsatile GH release, and therefore potentially fewer negative effects on long-term health. I have access to the following peptides: Ipamorelin Sermorelin Fragment 176–191 IGF-1 DES MK-677 PEG-MGF MOD-GRF 1-29 CJC-1295 + DAC IGF-1 LR3 What would be the best combinations for: 1. Long-term health 2. Optimal anabolism 3. Fat loss pre-competition Thanks!

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.