Topic
SS-31
Everything we've written on SS-31 — 6 articles covering the mechanism, the evidence, comparisons, and practical considerations.
6 articles
Mitochondrial healthNAD+ vs MOTS-c vs SS-31 vs Humanin — the mitochondrial peptide stack, decodedYou got your labs back and your biological age came out higher than your chronological age. Or the fatigue is real — not the kind that coffee fixes, not the kind that a good night's sleep fully resolves — a deeper, structural tiredness that has started to feel like a baseline rather than a symptom. Or you've been researching longevity seriously and you've arrived at the mitochondria, because the research keeps pointing there: cellular energy, oxidative stress, the gradual degradation of the organelles that power everything else. You've encountered four names being discussed — NAD+, MOTS-c, SS-31, Humanin — and you want to understand what each actually does, why they're being discussed together, and whether the combination logic holds up.7 min readMitochondrial healthMOTS-c in longevity stacks — what's being exploredThe longevity protocol world has a stacking problem. Not a problem in the sense that stacking is necessarily wrong — combining compounds that address different mechanisms is conceptually sound in medicine — but a problem in the sense that the reasoning often runs backward. The aspiration comes first. The compounds follow. The mechanism gets retrofitted to justify what was already going to happen. When you're dealing with compounds that have thin human evidence and strong preclinical data, this pattern matters enormously, because it's the difference between a rationally assembled protocol and an expensive bet dressed up in biological language.7 min readMitochondrial healthPeptides for energy and fatigue — what research has explored at the cellular and systemic levelYou don't feel stressed the way you feel hungry. Chronic fatigue doesn't go away when the stressful thing ends. It is there in the morning before anything has happened. It is there after a full night of sleep that didn't restore anything. The coffee works for an hour and then the tiredness reasserts itself, heavier than before. It is not dramatic — fatigue rarely is. It is a narrowing. The things you used to do without thinking about them now require decisions. You lie down in the afternoon not because you want to but because the alternative is worse.10 min readImmune modulationPeptides for kidney health — from microvascular protection to acute injury researchThe kidneys do their failing quietly for a very long time. A person can lose half of their functional kidney capacity before any symptoms appear — before they feel the fatigue, the fluid retention, the impaired sleep, the subtle cognitive dulling that characterizes advancing chronic kidney disease. The organ's reserve is substantial and its adaptation mechanisms are sophisticated. But this silence is also why chronic kidney disease often presents late, when the window for intervention has narrowed and the trajectory toward dialysis or transplant may already be set. An estimated 37 million Americans live with chronic kidney disease, and the majority don't know it.10 min readMitochondrial healthSS-31 and cardiolipin — the mitochondrial membrane storyThe power goes out and the neighborhood goes dark. You don't notice everything that ran on electricity until it stops running. The same logic applies to the mitochondria in your cells — not metaphorically, but mechanically. When the inner architecture of a mitochondrion begins to fail, it isn't one function that drops out. It's everything that electricity powers.8 min readMitochondrial healthSS-31 in mitochondrial myopathy and heart failure researchThe men who design drugs for heart failure have one of the more humbling jobs in medicine. Heart failure affects tens of millions of people worldwide. The field has produced real breakthroughs — ACE inhibitors, beta-blockers, SGLT2 inhibitors — and yet significant numbers of patients continue to progress toward transplant or death despite optimal medical therapy. When a new mechanism comes along, the desperation to apply it broadly is understandable. The history of cardiology is littered with compounds that worked brilliantly in animal models and failed in human trials. The cautionary lesson keeps being delivered and keeps being partially ignored.9 min read