Why do we age? For decades, one of the dominant explanations has been that cells and tissues gradually accumulate molecular damage until they can no longer function normally. DNA mutations, damaged proteins, mitochondrial dysfunction, epigenetic alterations, and other forms of cellular wear have all been proposed as major drivers of aging. But another theory offers a very different possibility: some aspects of aging may result not from biological systems breaking down, but from developmental programs continuing to operate after they are no longer beneficial.
A research perspective published in Volume 18 of Aging titled “A brief history of the hyperfunction theory of aging and future directions,” traces the development of this idea and examines where the field may go next.
The article was written by João Pedro de Magalhães from the Genomics of Ageing and Rejuvenation Lab, Department of Inflammation and Ageing, College of Medicine and Health, University of Birmingham, United Kingdom. Rather than presenting a new experiment, the paper combines historical analysis, evolutionary theory, experimental evidence, and the author’s own perspective on how programmatic models could reshape aging research.
Full blog post - https://aging-us.org/2026/09/developmental-programs-could-help-drive-the-aging-process/
DOI - https://doi.org/10.18632/aging.206403
Corresponding author - João Pedro de Magalhães - jp@senescence.info
Abstract video - https://www.youtube.com/watch?v=VwC6aJoUUQo
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Keywords - aging, antagonistic pleiotropy, longevity, programmatic aging, quasi-program
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