When you train hard but feel like your body isn’t responding like it used to, it’s not just aging or bad luck. Deep inside your muscles, a type of cellular clutter starts to build up these are called senescent cells, often nicknamed zombie cells. They’re old, damaged cells that have stopped dividing but refuse to die. Instead, they hang around releasing inflammatory signals that disrupt everything around them. Over time, they block the very pathways that your training is supposed to activate. It’s like trying to grow a garden in soil full of toxins. Every cell in your body has a life cycle. Healthy cells divide, do their job, and when they become too damaged, they self-destruct through a process called apoptosis. Senescent cells are the exception. They survive by overriding that self-destruct button. These cells secrete inflammatory molecules, growth factors, and enzymes that damage neighboring cells a collection of signals known as the SASP, or senescence-associated secretory phenotype. In small doses, SASP can help heal wounds. But when it lingers, it becomes a chronic source of inflammation that weakens tissues. In muscle, SASP molecules like IL-6, IL-8, TNF-alpha, and TGF-beta disrupt how muscle stem cells, called satellite cells, communicate. These satellite cells are the key players in muscle repair and growth. When their environment is polluted by SASP, they stop responding to the normal anabolic cues from training, and muscle growth stalls. Senescent cells also drag down mitochondrial function. Mitochondria are your cells’ power plants, generating energy through respiration. In senescent cells, mitochondria become damaged and inefficient, leaking electrons that generate excessive reactive oxygen species, or ROS. This oxidative stress overwhelms the body’s antioxidant defenses and shifts the cell from a growth mode to a survival mode. Pathways like mTOR and IGF-1 that normally promote protein synthesis are suppressed, while stress pathways like NF-κB and p53 become chronically activated. The result is a body that’s inflamed, tired, and resistant to adaptation no matter how hard you train.

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.

One of the coolest things I’ve learned in this space came from Dr. Seeds. He is an extraordinary thinker and an exceptionally generous teacher, and this insight fundamentally changed how I understand inflammation. What makes it so powerful is not just the biochemistry, but the way it reframes old, familiar tools in an entirely new light. This concept connects aspirin, omega-3s, and resolution biology in a way that is both elegant and practical, and it’s a perfect example of Dr. Seeds’ ability to share deep, clinically meaningful knowledge with clarity and humility. At first glance, aspirin and fish oil look like simple, even old-fashioned tools. Aspirin has been around for more than a century, and fish consumption has been part of human diets far longer than supplements or pharmaceuticals. Yet when you zoom in to the molecular level, the interaction between aspirin and omega-3 fats reveals one of the clearest examples of how small biochemical changes can redirect entire inflammatory programs in the body. This is not about suppressing inflammation, but about teaching the body how to finish it. To understand why this matters, it helps to reframe inflammation itself. Inflammation is not a mistake or a flaw. It is a necessary biological response to injury, infection, or stress. The problem is not that inflammation turns on, but that in many modern contexts it does not properly turn off. The shutdown phase of inflammation is not passive. It is an active, enzyme-driven process governed by a class of signaling molecules called pro-resolving mediators, often abbreviated PRMs or SPMs. These molecules are the biochemical equivalent of a cleanup crew. They signal immune cells to stop recruiting reinforcements, clear debris, and restore tissue to normal function. The raw materials for these mediators come from fats stored in cell membranes. Specifically, long-chain fatty acids with 20 to 22 carbons. The most familiar of these are arachidonic acid, an omega-6 fat, and EPA and DHA, the omega-3 fats found in fish. These fats are not just calories. They are precursors to powerful signaling molecules. What determines whether they become inflammatory signals or resolving signals is the enzyme environment they encounter.

Hey friends, I’m reaching out because I’m walking through something really scary right now, and I would really appreciate your wisdom, experience, and prayers. About three weeks ago, I was hit with a really rough virus. I thought I was on the mend… and then about a week ago I suddenly started losing vision — first in my left eye, then in my right. I ended up in the hospital terrified and confused, not understanding what was happening to my body. While I was there, they ran a ton of tests — full blood panels, autoimmune workups, MRI, and even a lumbar puncture. Most of the autoimmune conditions they tested for have been ruled out, but I’m still waiting on a few more results that take longer, including the GFAP panel. Right now I’m sitting at about 50% vision loss in both eyes, which has been one of the most emotional and humbling experiences of my life. The neuro-ophthalmologist said ischemic optic neuropathy is still a possibility, but there are signs that make him hopeful it could instead be post-/para-infectious optic papillitis — inflammation of the optic nerve triggered by the virus I had. This is treatable, but recovery can be slow, sometimes taking a month or more before improvement begins. I’ve been on steroids for a week now with no major changes yet. I’m also feeling some nerve pain behind my right eye, which can happen during healing, but it’s hard not to worry when you’re living it. To support myself, I’ve been using: - Steroids - BPC-157 - Anti-inflammatory + gut support - Rest and as much calm as possible But this community has so much collective wisdom, especially around peptides, neuro repair, and post-viral healing — so I’m reaching out. If you have experience with optic nerve inflammation, optic neuritis, nerve repair, or post-infectious healing — what peptides, supplements, or approaches would you consider supportive right now? (ARA-290, TA-1, SS-31, MOTS-c, glutathione, SPMs, NAC, high-dose omega-3s, etc.) This whole situation has really tested me but I’m doing everything I can to support healing while staying safe. Any insight, personal experiences, or encouragement would mean the world to me right now.

June - August 2024 I was living in Portugal, lovely sun in the morning. Morning steps, cold plunge and sauna everyday. Super cool room on a night. I was on TRT and GH and RHR got down to about 48bpm. This year June 2025 I started reta, still on gh, trt......and I only went up to 3mg a week. My RHR has gone up to almost 70. Even when I stopped in for 4 weeks it didn't really move lower. Now I'm not sure why it's staying spiked, I was considering adding in a low dose Nebivolol but I know I shouldn't need to take something just to counteract that. We all know RETA increases RHR in a lot. But what else can I look at to see if anything else is causing this? Thanks