hallmarks-of-ageing
The Hallmarks of Ageing
Why do we age? Scientists describe it through a framework of "hallmarks" — the core biological processes that accumulate over time. Understanding them is the key to understanding the whole longevity field, including where ingredients like NMN, berberine and senolytics fit.
The hallmarks, one by one
Plain-English explanations of the core processes researchers point to. They overlap and interact rather than acting alone.
- 01 Genomic instability
- Damage to DNA accumulates over a lifetime — from radiation, chemicals and ordinary cellular wear. The body has repair systems, but they become less effective with age, allowing errors to build up.
- 02 Telomere attrition
- The protective caps on the ends of chromosomes — telomeres — shorten each time a cell divides. When they get too short, the cell can no longer divide safely.
- 03 Epigenetic alterations
- Changes to how genes are switched on and off (without changing the DNA code itself) drift over time, altering how cells behave. This is the basis of "epigenetic age" clocks.
- 04 Loss of proteostasis
- Cells normally keep proteins correctly folded and clear out damaged ones. With age this quality control falters, allowing faulty proteins to accumulate — closely tied to autophagy.
- 05 Deregulated nutrient sensing
- Pathways that sense energy and nutrients — including AMPK and mTOR — become dysregulated. This is the hallmark most directly linked to metabolism and to ingredients like berberine.
- 06 Mitochondrial dysfunction
- The cell's mitochondria generate less energy and more oxidative stress with age. Mitochondrial health connects to NAD+, CoQ10 and overall vitality.
- 07 Cellular senescence
- Cells that stop dividing but resist dying — senescent cells — accumulate and release inflammatory signals. Clearing them is the goal of senolytics such as fisetin and quercetin.
- 08 Stem cell exhaustion
- The pool of stem cells that repair and replenish tissues declines with age, reducing the body's ability to regenerate.
- 09 Altered intercellular communication
- The signals cells send each other shift with age — often toward chronic, low-grade inflammation (sometimes called "inflammaging"), which feeds back into the other hallmarks.
- + Newer additions
- More recent updates to the framework have proposed further hallmarks, including disabled macroautophagy, chronic inflammation and dysbiosis (an imbalanced gut microbiome) — reflecting how the science continues to evolve.
Where longevity ingredients fit
The hallmarks are why the longevity-supplement world looks the way it does. Most researched ingredients map onto one or more of them:
NMN and NAD+ relate to mitochondrial function and to sirtuins, which depend on NAD+. Berberine engages the nutrient-sensing pathway AMPK. Spermidine is studied for autophagy and proteostasis. Senolytics like fisetin and quercetin target cellular senescence. CoQ10 and glutathione relate to mitochondrial function and oxidative stress.
None of these is a cure for ageing, and the evidence varies hugely by ingredient — we're careful to describe what research has investigated rather than overstate it. But the framework explains the logic. Every term here is defined in our longevity glossary.
Hallmarks FAQ
The science, made clear
Every term here is defined in our glossary, and each mechanism links to a deeper, evidence-led guide. Explore the longevity library.
Open the glossary →About this guide. Written and reviewed by the Vitality Supplements Editorial Team, a UK supplement manufacturer, to our published editorial standards. Every batch we produce is independently tested by an ISO/IEC 17025-accredited laboratory, with a Certificate of Analysis available on request.
This is general educational information about the science of ageing and is not medical advice. The supplements referenced are sold as food supplements in the UK and carry no authorised health claims; no supplement is presented as treating, preventing or reversing ageing. Always consult a qualified healthcare professional before starting any supplement. References on our research references page.

