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As diseases go, type 2 diabetes and epilepsy seem to have little in common. One is a metabolic disorder involving high blood glucose and failing insulin, the other a matter of neurons and electrical pulses. So it is odd that both often respond to fasting. Likewise, depression, obesity, Alzheimer’s, heart disease—all are wildly different diseases, yet all are influenced by diet. This shared vulnerability points to metabolism—the way we harvest energy from the food we eat and use it to power our cells.
One of the leading proponents of an energy-centric view of disease is Martin Picard, a biologist who directs the Mitochondrial Psychobiology Group at Columbia University. “Once we see ourselves as energetic processes,” he says, “many things make sense that didn’t make sense from a molecular perspective.”
Picard and a growing number of colleagues are making the big claim that many chronic diseases we treat as separate failures of separate organs may share one deeper problem: cells struggling to extract and use energy from food. If they are right, a common weakness runs beneath diseases now parceled out among different specialties, and medicine might have spent a century drawing boundaries in the wrong places.
At the heart of this argument lie mitochondria, the microscopic organelles that live in our cells and convert the energy stored in molecules of food into adenosine triphosphate, or ATP, the molecular power pack that drives virtually every reaction in the body, whether it’s moving, thinking or healing. We produce our body weight in ATP every day, and we burn just as much.
Any meltdown in our mitochondria will lead to a shortage of ATP, leaving cells with less energy to do their jobs. Picard believes many states of poor health start there, and his once unusual research focus is now mainstream. “Everybody agrees that mitochondrial dysfunction is part of aging biology,” says Matt Kaeberlein, former director of the Healthy Aging and Longevity Research Institute at the University of Washington. “It’s one of the hallmarks of aging. And I think you can make a pretty reasoned argument that mitochondrial dysfunction can precede and potentially drive many of the other hallmarks of aging.”“Mitochondrial dysfunction may contribute to the vast majority of common diseases.” —Matt Kaeberlein University of WashingtonCertainly, Kaeberlein says, health is about more than mitochondria. “If you’re going to argue that everything starts with mitochondrial dysfunction, I think most people would push back against that.” But the idea doesn’t need to explain all of aging to be worth chasing. “Mitochondrial dysfunction may contribute to the vast majority of common diseases,” he says. “Almost any disease you look at, you find a mitochondrial connection.”
That connection has gerontologists and biohackers alike racing to understand what makes mitochondria tick—and what we can do to keep them ticking as long as possible.Although mitochondria’s central role in our existence is often overlooked, scientists have understood their importance since the 1960s, when British biochemist Peter Mitchell proposed a then radical explanation for how mitochondria capture energy—work that earned him the Nobel Prize in Chemistry in 1978. The process, Mitchell showed, is fundamentally electrical. Electrons stripped from the atoms of our food are drawn toward atoms that will accept them. Among the elements biology has to work with, oxygen exerts the strongest pull.
Animals owe their existence to that attraction. We eat food, break it down into simpler molecules and send those to the mitochondria in our cells, which pry off electrons and let them flow through a string of molecules in their membranes known as the electron transport chain. At each step in this chain, a portion of the electrons’ energy is siphoned off to pump protons across a membrane—Mitchell’s great insight—and the pressure of those protons rushing back through a molecular turbine is what makes ATP. At the end of the chain, oxygen accepts the electrons and, together with protons, becomes water.
As many observers have noted, this flow of electrons through the body resembles the flow of electricity through the power grid. Power plants drive electricity through wires and into our homes, where our devices tap that energy to light our rooms and power our lives. The current has to meet the right amount of resistance in the right places. Too little, and the energy races past without doing any work, eventually damaging other components.
Something similar happens in our mitochondria. Under ideal conditions, electrons are slowed in their passage through the electron transport chain just enough that their energy can be transferred. But if the mitochondrial circuits are impaired or if there are simply more electrons from food pouring into the system than the mitochondria can handle, the flow can get bogged down. Electrons can then leak out of the chain, bonding with oxygen in the wrong parts of the mitochondria to form highly reactive free radicals that attack and deform neighboring molecules. These reactive oxygen species, or ROS, can do real damage to mitochondria, cells and organs.
No matter how smoothly electrons flow through mitochondria, a certain amount of ROS is unavoidable in everyday life. The classic free-radical theory of aging, first proposed in the 1950s, held that aging itself resulted from the relentless buildup of ROS in our cells, decade after decade, and the wear and tear this caused. Now we know the body is quite capable of repairing manageable amounts of ROS, which at lower levels can even act as signals, telling a cell to get to work. Only when the oxidative stress gets out of hand do mitochondria get dinged up, but when they do, they move electrons less efficiently, which leads to even more ROS and more damage. The brownouts spread. Eventually cells lose capacity, and the body follows.
Picard has written in this magazine about mitochondria’s role in health. In November 2025 he and Nirosha Murugan, a biophysicist at Wilfrid Laurier University in Ontario, codified this concept in the journal Cell Metabolism as the energy resistance principle. If a major cause of chronic disease is simply too many food-derived electrons frying the mitochondrial wires, then a major goal of medicine should be to reduce that overload. “The secret to longevity,” Picard says, “is to find ways to live at optimal energy resistance.”
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Noemi Fabra
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