Slowing aging across all ages: from theory to practice
Abstract
Aging is a primary risk factor for multi-morbidity and declining quality of life. The geroscience hypothesis posits that targeting biological aging mechanisms may prevent or delay morbidity, yet translating theory into practice remains challenging. Unknown long-term risks and a lack of well-validated, responsive, and practical surrogate endpoints hinder the field’s preventive aspirations. This review addresses these obstacles by introducing the biological aging cycle and the regeneration model of aging—frameworks that summarize and distill the complexity of aging into a series of fundamental steps. These models provide insights into potential trade-offs of anti-aging interventions and can guide strategies to slow aging across diverse populations. Further, AMP-activated protein kinase (AMPK) and DNA damage are highlighted as master regulators of aging checkpoints and are promising surrogates for healthy and unhealthy aging, respectively. Altogether, these insights can transform geroscience, nutrition, and lifestyle medicine, paving the way for innovative approaches to extend healthspan.
The paper
Preprint, 24 Oct 2024, Open access, Preprint, not peer-reviewed



