Concern
6 plain-language articles on energy & mitochondria — the physiology, the compounds researched for it, and what the evidence actually shows.
6 articles
Mitochondrial fatigue: the energy problem doctors miss
You sleep eight hours and wake up flat. Coffee gets you to noon, then you crash. Workouts that used to feel good now feel like work for three days afterward. Labs come back normal — thyroid in range, ferritin fine, B12 fine, CBC unremarkable — and the verdict is some version of "everything looks good, try to manage your stress." If you've been told you're always tired for no reason, the reason is usually real. It just isn't on the standard panel.
NAD+ and cellular aging in plain English
If you've spent any time inside the longevity conversation, you've heard the term. NAD+ is on every supplement shelf, in every podcast, on the cover of every popular-science book about aging. What it isn't, in most of those places, is explained — what it actually does inside a cell, why levels drop with age, and why that drop matters for how you feel and how you age. Here's the plain-English version.
Elamipretide / Stegazo — the FDA approval for Barth syndrome and what it signals
The boy is maybe three years old and smaller than he should be. He tires quickly. His heart is enlarged on the echocardiogram — a dilated cardiomyopathy that the pediatric cardiologist has seen before in adults but rarely in a child this young. Blood work comes back with abnormally low neutrophil counts, which means infections will be harder to fight. His muscles are weak in ways that developmental milestones can't fully capture until he starts school and the gap becomes visible to everyone. The cause is a mutation on the X chromosome that his mother carried without knowing, and there is, when his family sits with the geneticist, no approved treatment to discuss. The name of what he has is Barth syndrome.
NAD+ and CD38 — why supplementing alone might not be enough
You start taking NMN. Your NAD+ levels come up, at least on a blood test. Three months later, maybe six, the effect seems to blunt. You're still taking it, the dose hasn't changed, but something about the initial lift has flattened. Maybe you increase the dose. Maybe it helps. Maybe it doesn't. You've entered a conversation that the supplement marketing doesn't prepare you for: that raising NAD+ levels is not just a question of what you put in, but of what's consuming it on the other end — and that consumption is running faster as you age.
SS-31 and cardiolipin — the mitochondrial membrane story
The 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.
SS-31 in mitochondrial myopathy and heart failure research
The 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.