Is entropy the underlying factor driving aging?

New research from Gero suggests that aging may be driven by entropy, providing a fresh perspective on age-related disease and mortality.

In a recently published study in Aging Biology, researchers from the biotech Gero have proposed a pioneering model of aging that centers on entropy, the tendency of complex systems to move toward disorder. This model, based on the Second Law of Thermodynamics, posits that as humans age, a gradual accumulation of irreversible molecular changes – driven by entropy – increases the likelihood of age-related diseases and mortality. Gero’s findings offer a new lens on biological design, providing an interesting perspective on aging and understanding more about the role entropy plays in determining lifespan and aging may point toward promising avenues for therapeutic interventions that could significantly extend human healthspan.

My take on this: Entropy, a fundamental concept in thermodynamics, describes the irreversible tendency of systems to evolve from order to disorder over time. Applied to biological aging, entropy manifests as cumulative molecular damage, such as DNA methylation errors and mutations, that accumulates progressively in cells throughout life. This accumulation gradually impairs the body’s ability to maintain homeostasis, accelerating disease susceptibility and mortality risk. While cellular reprogramming and senolytic drugs can address some manifestations of aging, they do not reverse these entropy-driven changes, which is what sets Gero’s approach apart.

The study leverages data from extensive human datasets, including DNA methylation profiles and longitudinal medical records from the UK Biobank, to model how entropy impacts biological systems. The Gero team demonstrated that entropy-based aging accumulates in humans differently from short-lived organisms, such as mice, that tend to succumb to genetically programmed aging before substantial entropic damage builds up.

As Dr Peter Fedichev , Gero’s CEO, explains: “Our work offers a clear path forward to designing effective therapeutics aimed at the aging processes. We believe that within the lifetimes of those alive today, we could develop therapies to radically slow or stop aging.”

The research emphasizes the critical role of entropy in human aging by categorizing the underlying drivers of age-related decline into two distinct mechanisms. The first mechanism is age-related diseases – system failures such as hypertension – which are individually identifiable and often treatable. However, the second mechanism is microscopic damage that accumulates at the molecular level. This type of damage results from imperfect cellular repair processes, making it irreversible with current technology.

This model brings into question the efficacy of using mice as proxies for human aging research. Mice, which have short lifespans, primarily succumb to age-related diseases before entropic damage can significantly impact their longevity, but in contrast, humans have the capacity to control age-related diseases, allowing for the gradual buildup of entropy-driven molecular damage over a much longer timeframe. This insight, as Fedichev has noted, highlights why: “mouse studies are a poor way to understand human aging; mice and humans age in fundamentally different ways.”

Discover the potential of this new research and its impact on future therapies and more, straight from Dr Peter Fedichev right HERE .

Thanks for reading! If you’ve enjoyed this article, it would mean a lot to me if you could subscribe and share it on LinkedIn!