Collagen supplements are among the best-selling products in the women's health market. How they work, and where they stop working, is almost never explained. Here is the full picture and the reason why NMN addresses a point that collagen cannot reach.
The market for collagen supplements generates billions annually based on a simple and plausible promise: your skin, joints, and hair lose collagen with age - so you replace it by taking collagen.
The promise is not entirely false. Collagen does indeed decrease with age. But the mechanism by which ingested collagen is supposed to correct this decline is more complicated than marketing suggests. And the gap between what collagen supplements do and what women hope to achieve with them is large enough to warrant understanding before buying.
The more important question is not whether collagen supplements work. It is whether they address the reason why collagen decreases in the first place. And the answer to that is no.
Collagen supplements provide raw material. They do not alter the cellular conditions that determine whether the body can produce, repair, and maintain its own collagen. And that is the actual problem. That is where NMN comes in—at a fundamentally different level and with a fundamentally different approach.
Collagen supplements provide the material. NMN restores the cellular apparatus that produces it. These are not the same thing, and they do not lead to the same results.
What collagen is and why it declines
Collagen is the most abundant protein in the human body. It is the structural framework of skin, joints, bones, tendons, and connective tissue.
In the skin, it is located in the dermis—the layer beneath the surface, where it is produced by cells called fibroblasts. The firmness, elasticity, and thickness of the skin depend almost entirely on what these fibroblasts produce and how efficiently they maintain the collagen framework underneath.
From the mid-20s, collagen production drops by about 1% per year. In the first five years after menopause, women lose up to 30% of their remaining skin collagen because estrogen levels drop, significantly weakening the signal that drives the fibroblasts. By the time visible skin aging gains momentum in the late 40s and early 50s, the decline has been building for two decades.
The reason for this decline is not that the body is running out of building material. It is that the cells that produce and maintain collagen, the fibroblasts, are working less efficiently because their cellular energy environment is deteriorating.
Producing collagen is metabolically expensive. Keeping the DNA repair systems that protect collagen-producing cells intact constantly costs energy. When this energy supply drops—and it does, because NAD⁺ levels decline from the mid-20s—fibroblasts work more slowly.
Therefore, collagen production does not decline because raw material is missing. It declines because the cellular apparatus that processes it is running out of fuel. The entire argument for why collagen supplements and NMN address different things is based on this difference.
What happens to ingested collagen in the body
Collagen is a protein. When swallowed, the digestive system breaks it down into amino acids and peptides—just like any other dietary protein.
The body does not receive intact collagen molecules from a supplement and route them to the skin. It receives amino acids, in the case of collagen primarily glycine, proline, and hydroxyproline. These are distributed throughout the body wherever protein building blocks are needed.
There is no mechanism that directs these amino acids preferentially to the dermis or specifically into collagen production. They go wherever the body sends them according to its current priorities.
The state of research on ingested collagen is actually mixed. Some studies, particularly those with hydrolyzed collagen peptides in higher doses over longer periods, have shown moderate improvements in skin elasticity and hydration.
The presumed mechanism is not that intact collagen reaches the skin. Rather, it is that hydrolyzed peptides may signal fibroblasts to increase their own collagen production. Thus, they act more as a stimulus than as direct building material.
This is plausible and the evidence is growing. But the effect sizes in most studies are moderate, and the research is far from as clear-cut as the marketing suggests.
The industry's marketing is five steps ahead of science and the research that is still pending. It is an exciting field, but nutritional science has a history of getting excited too early and letting marketing determine the message to consumers before major long-term studies confirm the effects.
- Dr. Taylor C. Wallace, PhD
The problem that collagen supplements cannot solve
Even if you accept the most optimistic interpretation of the research—that hydrolyzed peptides actually stimulate fibroblasts—the supplement works on the surface of the problem.
It provides a stimulus to cells that are struggling to react efficiently anyway because their cellular energy environment has been declining for years. A fibroblast with declining mitochondrial function and too little NAD⁺ is less capable of responding to any stimulus, including the one from collagen peptides, than a fibroblast in a healthy energy environment.
Providing a stimulus without restoring the ability to react to it is like sending signals to a system that is running out of electricity to carry them out.
NAD⁺ is required for the PARP enzymes that identify and repair DNA damage in skin cells. Fibroblasts divide frequently, accumulating DNA damage during normal cell turnover. If enough NAD⁺ is present, this damage is repaired efficiently, and fibroblasts continue to consistently produce structural proteins. If NAD⁺ levels are low, repair slows down, damage accumulates, and fibroblast function gradually declines.
NAD⁺ also activates sirtuins, which regulate the inflammatory response in skin tissue and control how actively skin cells renew themselves via epigenetic signals.
Collagen supplements do not touch any of these mechanisms. They address the result without changing the conditions that determine whether that result remains achievable at all.
Why the post-menopausal window makes this difference urgent
The strongest collagen loss in a woman's life occurs in the five years immediately following menopause. Up to 30% of remaining skin collagen can be lost during this time as estrogen production drops sharply.
In this same window, the decline in NAD⁺ that has been building since the mid-20s reaches a level where its consequences for cellular energy production are most pronounced.
Both processes reinforce each other. Fibroblasts receive fewer estrogen signals to produce collagen and have less NAD⁺ to fuel the remaining production.
Adding more raw collagen material to this cellular environment is like delivering supplies to a construction crew that lacks the energy to work.
Restoring NAD⁺ via NMN does not replace declining estrogen or hormone therapy where it is medically indicated. What it does is restore the cellular energy environment in which collagen-producing cells work: it improves fibroblast efficiency, supports the DNA repair mechanisms that maintain their function, and dampens the inflammatory conditions in skin tissue that accelerate collagen degradation.
This targets the power supply rather than the raw material. And in a system where cellular energy is the limiting factor rather than material availability, that changes what this system is even capable of.
Collagen production is not limited by the availability of raw materials. It is limited by available cellular energy. NMN addresses this limit. Collagen supplements do not.
What research confirms on both sides
Research on ingested collagen is moderate, but real for certain results, in certain groups, at certain dosages.
Studies with hydrolyzed collagen peptides in doses of 2.5 to 10 grams daily over eight to twelve weeks showed improvements in skin elasticity and hydration in some cases. The effects were most pronounced in older women with lower baseline values. The mechanism is debated, and the effect sizes are not large. The database is growing, but it does not match the certainty with which marketing is presented.
Research on NMN and skin health is currently more mechanistic than clinical. The existing human studies measure metabolic and body functions, not skin-specific endpoints.
The mechanistic evidence linking NAD⁺ to fibroblast function, collagen synthesis, DNA repair in skin cells, and inflammation regulation in skin tissue is well established. Clinical human evidence that NMN specifically improves skin is building, but not yet as mature as the evidence for energy, sleep, and metabolism.
The most cited human study on NMN, Yoshino et al. (2021), was conducted with post-menopausal women and found measurable improvements in metabolic function and cellular energy—exactly in the group where collagen loss is most accelerated. The link between restored cellular energy and collagen production is biologically sound. Direct clinical evidence specifically for the skin is still being developed.
Are both better together?
There is no evidence of harm from taking both products, and a plausible argument that they address complementary sides of the same problem.
Collagen peptides may potentially provide a stimulus for fibroblast activity. NMN can restore the cellular energy environment that determines how efficiently fibroblasts react to that stimulus.
If the research on ingested collagen is confirmed, and the current data points to moderate effects at the right dosage, then the combination of a stimulus and the restored energy to follow it is a more complete approach than either product alone.
The honest caveat remains: neither replaces the other. And neither replaces the broader cellular and hormonal support upon which skin health depends during the aging process.
Collagen supplements are not a scam. They are a partial solution for a multi-dimensional problem. The dimension they do not address—the cellular energy environment that determines whether collagen can be efficiently produced, maintained, and repaired—is exactly the one that worsens with age. And which cannot be fixed with any amount of raw material.
That is where NMN comes in. And that is the difference worth understanding before you decide what your money is better spent on, or if the answer is both.
Sources
- Brincat, M. P., Baron, Y. M., & Galea, R. (2005). Effect of menopause on the skin. Climacteric, 8(Suppl 1), 11–23. https://doi.org/10.1080/13697130500161963
- Shuster, S., Black, M. M., & McVitie, E. (1975). The influence of age and sex on skin thickness, skin collagen and density. British Journal of Dermatology, 93(6), 639–643. https://doi.org/10.1111/j.1365-2133.1975.tb05100.x
- Covarrubias, A. J., Perrone, R., Grozio, A., & Verdin, E. (2021). NAD+ metabolism and its roles in cellular processes during ageing. Nature Reviews Molecular Cell Biology, 22(2), 119–141. https://doi.org/10.1038/s41580-020-00313-x
- Yoshino, M., Yoshino, J., Kayser, B. D., et al. (2021). Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. Science, 372(6547), 1224–1229. https://doi.org/10.1126/science.abe9985
- Imai, S. I., & Guarente, L. (2014). NAD+ and sirtuins in aging and disease. Trends in Cell Biology, 24(8), 464–471. https://doi.org/10.1016/j.tcb.2014.04.002
- Massudi, H., Grant, R., Braidy, N., et al. (2012). Age-associated changes in oxidative stress and NAD+ metabolism in human tissue. PLOS ONE, 7(7), e42357. https://doi.org/10.1371/journal.pone.0042357