Low energy is one of the most common complaints in medicine, coaching, and everyday life, yet it is one of the least precisely understood. People describe it as fatigue, burnout, brain fog, weakness, lack of motivation, or feeling “offline.” Athletes feel it when they cannot train. Patients feel it when they cannot work. High performers feel it when discipline no longer works. The problem is that “low energy” is not a diagnosis. It is a surface description of a system-level failure, and two people can experience nearly identical symptoms while the underlying biology is completely different. Treating them the same way helps one person and harms the other. To understand low energy correctly, you have to stop asking how to boost energy and start asking why energy is being limited in the first place. At the deepest level, there are two dominant failure modes. In one, the body cannot produce enough energy. In the other, the body is deliberately suppressing energy production. The first is mitochondrial damage, a capacity problem. The second is inflammatory inhibition, a regulatory decision. One is a broken engine. The other is a functioning engine with the brakes applied. Subjectively they feel similar. Biologically they are opposites. Everything that follows depends on recognizing which one you are dealing with. A simple model helps. Imagine the body as a car. The mitochondria are the engine. They take fuel and oxygen and convert them into usable energy in the form of ATP. Inflammation acts like the central control computer, deciding how much power the engine is allowed to produce. If the engine is damaged, pressing the accelerator does little. If the computer is limiting output, the engine could perform, but is being intentionally restrained. In both cases the car goes slow. Only one responds to pushing harder. Mitochondria exist inside nearly every cell and are responsible for producing ATP, the molecule that powers muscle contraction, nerve signaling, hormone synthesis, immune regulation, tissue repair, and cognition. Without adequate ATP, nothing in the body functions well. Energy production depends on intact mitochondrial membranes, functioning enzymes, proper redox balance, sufficient oxygen delivery, and a steady supply of micronutrients. When any part of this system is damaged, the maximum amount of energy the body can generate drops. This is not a motivational issue. It is a hard ceiling.

Let me tell you a story about the most important muscle in your body that almost nobody trains, almost nobody understands, and almost everybody is slowly losing. The diaphragm is not just a breathing muscle. That description is like calling the brain a “thinking organ.” It’s technically true, but it misses the point so badly that it becomes misleading. The diaphragm is a living interface between structure and signal, between chemistry and physics, between voluntary and involuntary control. It is a biological transistor. A gatekeeper. A conductor that coordinates pressure, charge, rhythm, and information across the entire organism. If you understand the diaphragm, you understand how the body integrates itself. If you lose the diaphragm, the body fragments. Let’s start simply, then go deep very deep. At the most basic level, the diaphragm is a dome-shaped sheet of muscle that separates the thoracic cavity from the abdominal cavity. When it contracts, it descends. When it relaxes, it recoils upward. This movement changes pressure in the chest and abdomen and drives airflow in and out of the lungs. That’s the textbook version. It’s also the least interesting. The diaphragm is the only skeletal muscle in the body that is both voluntary and involuntary. You can control it, but it doesn’t need you. That alone should make you suspicious that it sits at a crossroads no other muscle occupies. Embedded in and passing through the diaphragm are some of the most important structures in the body: the inferior vena cava, the esophagus, the aorta, lymphatic channels, and dense autonomic nerve plexuses. Every breath mechanically massages blood, lymph, and nerves. This is not a side effect. This is the design. Each diaphragmatic contraction creates a pressure wave. That wave propagates through fluid-filled tissues, fascia, and organs. Pressure waves in biological tissue are not just mechanical events. They are information-bearing phenomena. They alter ion channel behavior, membrane tension, protein conformation, and mitochondrial function.

This article is about one simple but deeply misunderstood idea: before you try to make mitochondria faster, stronger, or more powerful, you have to make them stable. And mitochondrial stability is not primarily about enzymes, supplements, peptides, or signaling molecules. It is about structure. Specifically, it is about membranes, and at the center of those membranes sits a phospholipid called cardiolipin. Most people think of mitochondria as engines. Engines burn fuel and make energy. When energy feels low, the instinct is to add more fuel or push the engine harder. But mitochondria are not engines in the mechanical sense. They are closer to power plants built out of flexible walls, electrical gradients, and flowing electrons. If the walls of the power plant are damaged, leaky, or poorly organized, no amount of fuel will restore output. In fact, pushing fuel through a damaged system often makes things worse. To understand why, we need to go down to the molecular level and build back up. Mitochondria are double-membrane organelles. The outer membrane is relatively smooth and permissive. The inner membrane is where the magic happens. It folds inward into structures called cristae. These folds massively increase surface area, and that surface area is packed with the electron transport chain. The electron transport chain is not a single thing; it is a series of protein complexes embedded in the inner membrane that pass electrons from one to the next, ultimately creating a proton gradient that drives ATP synthesis. This system is not rigid. It is dynamic, fluid, and responsive to stress, fuel availability, redox state, and training load. The inner membrane has to be both strong and flexible at the same time. That balance is determined by its lipid composition. This is where cardiolipin enters the picture. Cardiolipin is a unique phospholipid found almost exclusively in the inner mitochondrial membrane. Unlike most phospholipids, which have two fatty acid tails, cardiolipin has four. This gives it a distinctive shape that allows it to curve membranes, stabilize protein complexes, and act like molecular glue holding the respiratory chain together.

Let’s begin by looking at aging and longevity through the lens of neuron survival. Most conversations about aging revolve around damage. Oxidative damage. DNA damage. Protein damage. The story we are usually told is that aging is the slow accumulation of wear and tear until the system finally breaks. That framing sounds intuitive, but it is incomplete. Cells do not usually fail because damage suddenly appears. They fail because their ability to repair damage, buffer stress, and maintain energy quietly erodes over time. Aging, at its core, is better understood as a progressive loss of energy resilience. Neurons are one of the earliest and clearest indicators of this process. They are among the most energy-demanding cells in the body, and unlike many other tissues, they cannot easily be replaced. They must maintain electrical gradients every second, transmit signals across long distances, repair DNA continuously, and coordinate complex networks that never truly shut off. This means neurons live very close to their energetic limits even under normal conditions. As NAD+ availability declines with age, neurons become less capable of surviving inflammatory stress, metabolic stress, and excitotoxic stress. Long before neurons actually die, this loss of resilience shows up as slower processing speed, poorer stress tolerance, impaired memory consolidation, reduced emotional regulation, and diminished adaptability. People feel “off” years or decades before anything that would qualify as neurodegeneration appears on a scan. From a longevity perspective, this reframes the goal entirely. Longevity is not primarily about adding years at the very end of life. It is about preserving cognitive, emotional, and functional capacity across the middle decades where most people actually live. Strategies that stabilize energy metabolism and reduce unnecessary NAD+ depletion are therefore plausibly longevity-aligned even if they do not regenerate tissue or reverse existing damage. The key shift is this: longevity is less about creating new cells and more about preventing avoidable cell loss.

Creating this space has genuinely been a dream come true. Being able to have thoughtful conversations, challenge ideas, learn out loud, and walk alongside people as they navigate their health has been incredibly meaningful to me. I don’t take it lightly that you choose to spend your time here, ask questions, give feedback, and share your experiences. That trust matters. What excites me most isn’t just protocols or tools it’s the mindset I see here. People being proactive instead of reactive. People choosing to learn, to stay curious, and to take ownership of their health. That kind of curiosity is powerful, and honestly, it makes this work fun. Health should feel empowering, not overwhelming, and learning should feel like an invitation, not a burden. I’m deeply grateful for the support, the conversations, the respectful disagreements, and the encouragement. This community pushes me to think more clearly, teach better, and keep refining my own understanding. I’m committed to continuing to learn, to get better, and to show up fully as part of this process alongside you, not above it. Looking ahead, I’m really excited about what’s coming next year. I’ll be expanding ways to work together more closely beyond one-off consults, for those who want deeper guidance and continuity. That said, this space will always be rooted in generosity, shared learning, and mutual respect. If you’re enjoying the conversations here, know that I care just as much about this community as I do about any one-on-one work. Thank you for being here, for being curious, and for being part of something that feels genuinely special. I’m grateful for every one of you, and I’m looking forward to continuing this journey together.