How collagen is lost and how to truly protect it

Almost everything you read about collagen is about how to stimulate its production. That's half the problem, and not the more urgent half.

Because collagen isn't lost only because less of it is produced: above all, it's lost because more of it is broken down. Anyone focusing entirely on synthesis is filling a bucket without noticing the hole in the bottom.

Article written by Elisa Avalle, founder of LeLang Skin Care and dermocosmetics specialist. Cover image generated with the support of artificial intelligence.

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Collagen is lost in two ways, not one

Collagen is the protein that gives the dermis its structure, and its amount depends on a balance between two processes that happen continuously.

On one side, fibroblasts produce new collagen. On the other, certain enzymes break it down to make room for new fibers: this is normal turnover, not a mistake.

The problem begins when the balance shifts. In your mid-twenties to early thirties, fibroblasts slow down; at the same time, accumulated exposure to UV rays, pollution, and smoke speeds up breakdown. The two curves move in opposite directions, and the gap between them is what you see in the mirror.

That's why a strategy focused only on stimulating production is too late: if degradation outpaces synthesis, producing more isn't enough to make up the difference.

Metalloproteinases: what breaks down collagen

The enzymes responsible are called matrix metalloproteinases, or MMPs. The one that acts directly on collagen is MMP-1, also known as collagenase.

MMP-1 is not an external enemy: the skin produces it itself. But its expression increases dramatically in the presence of free radicals, and this is the real mechanism by which the sun ages the skin. UV rays don't "burn" collagen: they prompt cells to produce the enzymes that cut it up.

That's also why daily sun protection is the first anti-aging treatment, long before any serum.

Collagen breakdown is one of the mechanisms of skin aging, but not the only one. Also at work are glycation, which stiffens the fibers already there; the degradation of elastin, which reduces elastic recoil; and chronic low-grade inflammation. These are distinct processes: acting on just one helps explain why certain treatments deliver less than they promise.

There’s a third change: not just how much, but what kind

This is the part that’s almost always missing from the discussion, and it explains something that seems contradictory to many people: why skin becomes less elastic even though it still has plenty of collagen.

There isn’t just one type of collagen in the dermis. The two main types are type I and type III, and they don’t do the same job. Type III is more elastic and less fibrous, and it predominates in young skin and tissue undergoing repair — which is why it’s called remodeling collagen. Type I is the supporting fiber, the one that provides strength.

The point is that the two work together: the abundant presence of type III is what allows type I to perform its elastic and supportive functions at its best.

With age, the balance shifts in two ways at once. Fibroblasts produce less and less type III collagen, while type I stiffens due to cross-links that form between the fibers, promoted by free radicals of oxygen. In adults, type I accounts for about 80% of dermal collagen, and type III just 15%; the remaining 5% is made up mainly of types IV and V.

The practical consequence is important. Even with the same total amount, dermis with little type III collagen and stiffened type I collagen behaves differently: it’s stiffer, less responsive, and slower to repair. It’s not just a matter of how much collagen there is, but what kind it is and what condition it’s in.

There’s also a useful takeaway about antioxidants, which are usually justified solely by their ability to reduce MMPs. If the cross-links that stiffen type I collagen are promoted by free radicals, then an antioxidant doesn’t just work upstream of collagen breakdown: it also helps slow the stiffening of fibers that are already there. These are two distinct benefits of the same action.

The three levers you can act on

Once you understand the mechanism, there are three distinct points at which a cosmetic product can act.

Most anti-aging products work only on the third lever. It’s the easiest to market — “stimulates collagen” — but on its own it’s the least effective, because it doesn’t address why collagen is disappearing.

What doesn’t work: collagen applied to the skin

It’s worth saying clearly, because it’s the most costly misconception.

Collagen applied to the skin as an ingredient does not rebuild the collagen in the dermis. The molecule is too large to cross the skin barrier: it stays on the surface, where it works as an excellent moisturizing film-former. That’s a real benefit, but it’s hydration, not rebuilding.

A “collagen” cream moisturizes well. If you’re looking for an effect on skin structure, what matters isn’t the word collagen on the label: it’s the actives that communicate with fibroblasts or inhibit enzymes.

Actives that really protect

The Gardenia meristem cell culture, a biotechnological active ingredient that acts on all three fronts at the same time, works on the first and second levers — the ones almost no one addresses.

The manufacturer’s in vitro tests on human fibroblasts, using an accelerated aging model, report statistically significant results for each mechanism.

These are in vitro tests conducted by the manufacturer, using cell cultures and not volunteers: they describe the mechanism and its relative intensity, not the result you’ll see in the mirror. We’re sharing them because they explain how the active ingredient works, and it’s right to know where the data comes from.

The responsible molecule is feruloyl-6-glucoside, a phenylpropanoid that the cell culture produces at a much higher concentration than the plant grown in the field.

Peptides work on the third lever, each in a different way. Matrixyl 3000 mimics the fragments produced by the dermis when collagen breaks down, and fibroblasts read it as a repair signal. A collagen fragment produced biotechnologically from a plant does something different: it doesn’t mimic a message; it provides an authentic fragment of the human sequence.

Why they’re needed together

Protecting and building are two distinct strategies, and neither one alone solves the equation.

In our serum, we chose to include all three in the same formula: Gardenia, which slows degradation; Matrixyl, which sends signals to fibroblasts; and the biotech fragment, which provides the authentic sequence. Alongside them are hyaluronic acid for immediate volume and grape polyphenols to fight the free radicals that trigger MMPs.

This isn’t a list of ingredients on a label: it’s a formula built around the mechanism, from cause to effect. You can find the rest of the anti-aging range in the LeLang selection of anti-aging treatments.

If you’re not sure where you are on the curve - whether the problem is already a loss of structure or still a matter of prevention - these are two different paths, and starting with the wrong one means waiting months to find out. At LeLang partner pharmacies, you can speak with a pharmacist who can help you figure out where to start.

What to do beyond cosmetics

Daily sun protection is the single most effective measure because it targets the main cause of increased MMPs. And this isn’t just theoretical: a four-and-a-half-year Australian randomized study measured significantly less skin aging in the group that used it every day.

Smoking also matters: it increases collagenase production and reduces tissue oxygenation, as does prolonged stress. Cortisol interferes with fibroblast activity, which is one reason skin looks duller and less firm during difficult periods.

For nutrition, you need the elements required for synthesis: vitamin C, which is essential for the enzyme that stabilizes the fibers, and enough protein to supply the amino acids.

Sources for this article

01 Fisher G.J., Kang S., Varani J., Bata-Csorgo Z., Wan Y., Datta S., Voorhees J.J., Mechanisms of photoaging and chronological skin aging, Archives of Dermatology, 2002; 138(11): 1462-1470.
02 Quan T., Qin Z., Xia W., Shao Y., Voorhees J.J., Fisher G.J., Matrix-degrading metalloproteinases in photoaging, Journal of Investigative Dermatology Symposium Proceedings, 2009; 14(1): 20-24.
03 Varani J., Dame M.K., Rittie L. et al., Decreased collagen production in chronologically aged skin, American Journal of Pathology, 2006; 168(6): 1861-1868.
04 Hughes M.C., Williams G.M., Baker P., Green A.C., Sunscreen and prevention of skin aging: a randomized trial, Annals of Internal Medicine, 2013; 158(11): 781-790.
05 In vitro tests by the manufacturer on Gardenia meristem cell cultures, conducted on human fibroblasts in an accelerated-aging model.

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