What happens to collagen with age?

What is collagen?

The word collagen comes from the Greek kólla ("glue") and genḗs ("forming") — that which forms glue. It was once described as biological glue holding cells in place, a loose metaphor for what we now understand about its structure and function.

Collagen is the most abundant protein in the body and is defined by researchers as "the major extracellular matrix (ECM) molecule that self-assembles into cross-striated fibrils, provides support for cell growth, and is responsible for the mechanical resilience of connective tissues." It is produced by a specialized cell called a fibroblast.

There are 28 types of collagen. Types I, II, and III make up the majority found in the body and in skin — 80% of skin collagen is type I, while type III makes up roughly 15%. Collagen has three distinct structural features: a repeating amino acid sequence (Gly–X–Y), with proline and hydroxyproline in the X and Y positions, and three chains wound into a tight triple helix.

What role does collagen play in skin?

The skin has three layers: the epidermis, dermis, and hypodermis. The dermis — the thickest, middle layer — is held together primarily by collagen with support from elastin. The dermis is especially rich in collagen fibers and is divided into two sublayers: the papillary (upper) dermis with thinner fibers, and the reticular (deep) dermis with dense, tightly woven fibers.

Collagen gives skin its mechanical and structural properties — its elasticity and viscoelasticity. Elasticity allows the skin to deform under force and return to its original form. Viscoelasticity, which collagen enables in combination with elastin, provides an additional degree of movement and recoil without injury. Beyond mechanical properties, collagen also regulates cell adhesion, directs tissue development, and signals chemotaxis — the migration of cells in response to growth factors.

What happens to collagen with age?

A reduction in collagen types I and III in the skin is a result of both chronological aging and sun exposure. Research has shown that collagen production in sun-protected skin of adults over 80 is 75% less than in young adults aged 18–29. The loss is driven by both increased collagen degradation and reduced collagen synthesis. The causes are multiple.

Reactive oxygen species (ROS)

ROS are the byproducts of normal cellular activity, but they increase with age. They consist of atoms or molecules with an unpaired electron — reactive and unstable, prone to stealing electrons from other molecules. In skin aging, ROS damage proteins, lipids, and DNA, and lead to the overexpression of matrix metalloproteinases (MMPs), which degrade collagen and inhibit its synthesis.

Cellular senescence

Senescent fibroblasts have an impaired ability to synthesize collagen. They also release a senescence-associated secretory phenotype (SASP) containing proinflammatory factors, which degrades the extracellular matrix and activates the same MMPs that degrade collagen.

Advanced glycation end products (AGEs)

AGEs are aging-related defects that form when collagen is exposed over time to ribose and glucose sugars. The resulting crosslinks cause reduced elasticity, increased stiffness, wrinkles, and skin discoloration. AGEs are also associated with high-sugar diets.

Hormonal changes

The decrease in estrogen that occurs during and after menopause is associated with a reduction in collagen of roughly 2% per post-menopausal year.

Sun exposure

UV radiation creates ROS, which activate the NF-kB pathway, increasing tumor necrosis factor alpha (TNF-α) and ultimately raising levels of MMPs that degrade the extracellular matrix and accelerate skin aging — prematurely. Nothing causes collagen degradation at the rate that unprotected sun exposure does.

Sleep loss, smoking, and stress

Sleep loss is associated with impaired collagen production and measurable increases in visible aging markers. Smoking increases MMP activity and substantially decreases synthesis of types I and III collagen. Chronic stress elevates glucocorticoids, which increase MMPs and decrease collagen synthesis.

What can you do about collagen aging?

Much can be accomplished by avoiding the accelerants above: consistent sun protection, limiting refined carbohydrates, adequate sleep, not smoking, and limiting chronic stress. For those who want to be proactive, the evidence supports several additional strategies.

Eat colorful fruits and vegetables

Carotenoids — the pigments that give fruits, flowers, and roots their vivid colors — are highly efficient antioxidants that protect against ROS-induced oxidative stress and collagen degradation. One study found that supplementation with a carotenoid-rich tomato extract reduced TNF-α, an inflammatory marker that stimulates MMP-1 expression. Another found that tomato-derived carotenoids down-regulated the MMP-1 gene. An in vitro study showed carotenoids increased pro-collagen levels in cultured human dermal fibroblasts exposed to oxidative stress.

Get the right nutrients

Collagen synthesis requires vitamin C, copper, zinc, and the amino acids glycine and proline. These are not optional cofactors — without them, collagen production stalls regardless of other interventions.

Use retinol

Retinol, a derivative of vitamin A available in topical form, has been shown to increase collagen in skin and decrease MMPs, improving texture and pigmentation, increasing epidermal thickness, decreasing wrinkling, and generally mitigating the effects of photoaging.

Supplement with collagen peptides

Collagen peptides — also called hydrolyzed collagen — are collagen broken down into smaller fragments through enzymatic reaction, primarily from bovine, marine, or porcine sources. A review and meta-analysis in the International Journal of Dermatology covering 19 studies and 1,125 participants found that collagen supplementation over 90 days led to improvements in skin hydration, elasticity, and wrinkles.

Collagen peptides provide building blocks for collagen synthesis and appear to act as signaling molecules that stimulate production of procollagen, elastin, and hyaluronic acid, while down-regulating collagen-degrading MMPs. Collagen production and maintenance, however, require healthy cells and an optimal cellular environment — which is why the broader NAD+ and cellular health picture matters alongside direct collagen supplementation.