Chronic exposure to cortisol (the stress hormone) increases cellular energy expenditure by 60% in the laboratory and accelerates cellular aging, but hair that turns gray under stress regains its color when stress subsides, suggesting that part of this process is reversible
Chronic exposure to cortisol (the stress hormone) increases cellular energy expenditure by 60% in the laboratory and accelerates cellular aging, but hair that turns gray under stress regains its color when stress subsides, suggesting that part of this process is reversible
These findings come from Martin Picard's laboratory of mitochondrial psychobiology at Columbia University. In 2021, the laboratory showed that gray hair spontaneously regains its color in some healthy people. In 2023, it showed that chronic cortisol exposure increases cellular energy expenditure by an average of 60%. Picard discussed these findings on October 11, 2026, in an interview with Modern Healthspan.
In 2021, Picard's laboratory published a method in eLife that turns an individual hair into a record of changes over time: its pigmentation pattern shows when the follicle lost and regained the ability to produce color. In one of the 14 participants, hairs regained their color after a vacation, during the month with the lowest reported stress that year. White segments of those same hairs contained more mitochondrial proteins than dark segments.
A broader concept, allostatic load, helps explain this connection. In 1988, physiologist Peter Sterling proposed that the body prepares for stress in advance, and that maintaining this readiness also consumes energy. Neuroendocrinologist Bruce McEwen identified stress hormone receptors in the brain and, in 1993, called this cost allostatic load: without periods of recovery, it accumulates as wear and tear.
Picard applied this concept to mitochondria: the cortisol receptor, known for its activity in the cell nucleus, also has a second target, the mitochondrion itself. In 2023, he measured the cost: in cultured skin cells continuously exposed to cortisol, energy expenditure increased by an average of 60%, and the cells aged faster, with shorter telomeres and a shorter lifespan in culture. A similar relationship was found in another species: corticosterone, the avian counterpart of cortisol, increased the biological age of zebra finch chicks by almost 38%. These findings show that stress hormones accelerate aging both in cultured cells and in a whole living organism.
Stress also affects mitochondria through blood glucose: anxiety raises glucose levels even without food intake, and excess glucose breaks their elongated network into small fragments, leaving the cell more likely to die when exposed to further stress. Picard describes the increased energy demand as a trade-off: “Cells divert that energy specifically from growth, maintenance, and repair, the very processes that protect against aging.” Under stress, a mitochondrion can leak, releasing its own DNA into the cell. Mitochondria originated as bacteria engulfed by a cell 1,5 billion years ago, so the immune system interprets this DNA as evidence of a bacterial infection and triggers inflammation, even though no infection is present.
In 2024, Picard and his coauthors brought these findings together in a model of the whole organism in Nature Aging. The model addresses a paradox: energy expenditure declines after age 70, even as damaged cells require more energy. It proposes that the brain allocates the body's overall energy budget: aging cells signal their growing demand, and the brain reduces spending on less urgent functions, leading to fatigue, reduced mobility, and immune dysfunction.
“If life never presents any challenges, it becomes boring. And boredom is one of the worst states a person can experience,” Picard says. The model suggests a practical approach: ensuring periods of recovery allows repair to begin. Some of the effects of the energy cost that ages cells may then be reversed, as illustrated by a hair regaining its color after a vacation.