The Biology of Aging

Aging shouldn’t be viewed as a negative consequence of being alive—it means you’ve been fortunate enough to make it this far. The best way to celebrate aging is to understand how and why it happens, then support your biology so you age gracefully.

Aging Begins Within Our Cells

Microscopic image representing cells and aging

What we see at the surface is the culmination of aging at the cellular and molecular levels. Cellular aging—senescence—is a natural response to damage over time. As DNA damage accumulates, cells lose function and their capacity to replicate. Around mid-life, for example, dermal fibroblasts reduce collagen output, which contributes to decreased firmness and wrinkle formation. Senescence can be delayed or accelerated by environmental and genetic inputs.

Aging Can Be Examined at the Genetic Level

DNA compacted into chromosomes — DNA is so long it must be compacted into chromosomes to fit inside the nucleus.

DNA Is the Blueprint for Making You

DNA encodes proteins—the working materials of life across tissues from skin to muscle. A single cell’s DNA stretches ~2 meters (over 6 feet) and is densely packaged as chromosomes to fit into the nucleus. This packaging protects instructions cells need to maintain tissues like the extracellular matrix (ECM), which includes collagen, elastin, and hyaluronic acid.

Telomeres Protect Our DNA from Wear

Telomere diagram — Telomeres are like aglets on shoelaces—when they shorten too much, DNA frays and senescence follows.

Telomeres cap chromosome ends and preserve DNA integrity. With each cell division, telomeres shorten slightly; after ~50 divisions (the Hayflick limit), cells enter senescence. Stem cells and many cancer cells maintain telomere length and evade this limit, but most somatic skin cells do not—so minimizing unnecessary damage (and thus divisions) helps preserve youthful function longer.

Reactive Oxygen Species (ROS) and Skin

Antioxidants and ROS — Antioxidants help neutralize ROS before they disrupt cellular components.

ROS are reactive by-products of normal metabolism. In excess, they can oxidize lipids, proteins, and DNA, disrupting function and accelerating aging. Common ROS drivers include:

UV exposure (photo-oxidation)
Ionizing radiation (X-rays, gamma rays)
Certain drugs, pollutants, and chronic inflammation

UV-induced ROS — UV generates ROS that can damage cellular structures and ECM.

Excess ROS are implicated in visible hallmarks of aging (laxity, fine lines, uneven tone). Topical strategies that limit inflammation, maintain barrier function, and supply antioxidants can help counter UV-induced oxidative stress and support ECM integrity over time.

Practical Ways to Support Healthy Aging Skin

Preserve the barrier: keep skin slightly acidic (pH ~4.5–5.5) and fragrance-free to reduce inflammatory load.
Controlled renewal: use non-abrasive chemical exfoliation to encourage healthy turnover without mechanical injury (see No. 9).
Hydrate then seal: layer water-based, anti-inflammatory hydration (UV-R) under a lipid phase (Serum Bioluminelle).
Avoid micro-injury: skip dermarollers/abrasive scrubs; protect the ECM rather than puncturing it.
Daily photoprotection: consistent sunscreen to reduce ROS initiation at the source.

Deeper Reading — OUMERE Research Library

References

Campisi, J. & d’Adda di Fagagna, F. (2007). Cellular senescence. Nat Rev Mol Cell Biol, 8(9), 729–740.
Dreher, F. & Maibach, H. (2001). Protective effects of topical antioxidants in humans. In Oxidants and Antioxidants in Cutaneous Biology (Vol. 29), Karger.
Bowen, R. (2003). Free radicals and reactive oxygen. Colorado State University: vivo.colostate.edu.

Aging is universal; the rate and quality of aging are modifiable. Protect the barrier, minimize unnecessary damage, and let biology do what it does best—repair and renew.