Collagen supplements are among the best-selling products in the women's health market. How they work, and where their efficacy ends, is almost never explained. Here's the complete picture and why NMN targets an area that collagen doesn't reach.
The collagen supplement market generates billions annually based on a simple, compelling promise: your skin, joints, and hair lose collagen with age—so you replace it by taking collagen.
The promise isn't entirely false. Collagen does indeed decline with age. But the mechanism by which ingested collagen is supposed to remedy this decline is more complicated than marketing suggests. And the gap between what collagen supplements do and what women hope for from them is wide enough to understand before making a purchase.
The more important question isn't whether collagen supplements work. It's whether they address the reason why collagen declines in the first place. And the answer to that is no.
Collagen supplements provide raw material. They do not change the cellular conditions that determine whether the body can produce, repair, and maintain its own collagen. And that is precisely the real problem. This 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 machinery that produces it. These are not the same, 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 forms the structural framework of skin, joints, bones, tendons, and connective tissue.
In the skin, it resides in the dermis—the layer beneath the surface where it's produced by cells called fibroblasts. The skin's firmness, elasticity, and thickness depend almost entirely on what these fibroblasts produce and how efficiently they maintain the underlying collagen framework.
From the mid-20s, collagen production decreases by about 1% per year. In the first five years after menopause, women lose up to 30% of their remaining skin collagen due to declining estrogen levels, which significantly weakens the signal that drives fibroblasts. By the time visible skin aging accelerates in the late 40s and early 50s, the decline has already accumulated over two decades.
The reason for this decline is not that the body runs out of building material. It's that the cells that produce and maintain collagen, the fibroblasts, work less efficiently because their cellular energy environment deteriorates.
Producing collagen is metabolically demanding. Keeping DNA repair systems intact, which protect collagen-forming cells, constantly requires energy. If this energy supply decreases—and it does, because NAD⁺ levels decline from the mid-20s—fibroblasts work more slowly.
So, collagen production doesn't decline because raw material is missing. Instead, it's because the cellular machinery that processes it runs out of fuel. This difference forms the entire argument for why collagen supplements and NMN address different things.
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.
Thus, the body does not receive intact collagen molecules from a supplement and transport them to the skin. It receives amino acids, primarily glycine, proline, and hydroxyproline in the case of collagen. These are distributed throughout the body wherever protein building blocks are needed.
There is no mechanism that preferentially directs these amino acids to the dermis or specifically to collagen production. They go where the body sends them according to its current priorities.
The research on ingested collagen is actually mixed. Some studies, particularly those with higher doses of hydrolyzed collagen peptides over longer periods, showed moderate improvements in skin elasticity and moisture.
The presumed mechanism is not that intact collagen reaches the skin. Rather, it's that hydrolyzed peptides may signal fibroblasts to increase their own collagen production. They act more as a stimulus than as a direct building material.
This is plausible, and the evidence is growing. But the effect sizes in most studies are moderate, and the research is by no means as conclusive as marketing suggests.
The industry's marketing is five steps ahead of science and the research yet to be done. It's an exciting field, but nutritional science has a history of getting enthusiastic too early and letting marketing dictate the message to consumers before large, long-term studies confirm the effects.
- Dr. Taylor C. Wallace, PhD
The problem collagen supplements cannot solve
Even assuming the most optimistic interpretation of the research—that hydrolyzed peptides do indeed stimulate fibroblasts—the supplement works on the surface of the problem.
It provides a stimulus to cells that are already struggling to respond efficiently because their cellular energy environment has been declining for years. A fibroblast with impaired mitochondrial function and insufficient NAD⁺ will respond less effectively to any stimulus, including that from collagen peptides, than a fibroblast in a healthy energy environment.
Providing a stimulus without restoring the ability to respond is like sending signals to a system that is running out of power to execute them.
NAD⁺ is needed for PARP enzymes that detect and repair DNA damage in skin cells. Fibroblasts divide frequently and accumulate DNA damage during normal cell turnover. If enough NAD⁺ is present, this damage is efficiently repaired, and fibroblasts continue to produce structural proteins consistently. 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, via epigenetic signals, how actively skin cells regenerate.
Collagen supplements touch none of these mechanisms. They address the outcome without changing the conditions that determine whether that outcome remains achievable at all.
Why the post-menopause window makes this difference urgent
The most significant collagen loss in a woman's life occurs in the five years directly after menopause. Up to 30% of remaining skin collagen can be lost during this time, as estrogen production sharply declines.
In the same timeframe, the NAD⁺ decline, which has been building since the mid-20s, reaches a level where its consequences for cellular energy production are most apparent.
Both processes reinforce each other. Fibroblasts receive fewer estrogen signals to produce collagen and have less NAD⁺ to drive the remaining production.
Adding more collagen raw material into this cellular environment is like providing material to a construction crew that lacks the strength to work.
Restoring NAD⁺ through NMN does not replace declining estrogen or hormone therapy where medically indicated. What it does is restore the cellular energy environment in which collagen-producing cells operate: It improves fibroblast efficiency, supports the DNA repair mechanisms that maintain their function, and dampens inflammatory conditions in skin tissue that accelerate collagen breakdown.
This addresses the power supply rather than the raw material. And in a system where cellular energy is the limiting factor, not material availability, it changes what that system is capable of at all.
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 the research on both sides shows
Research on ingested collagen is moderate but real for certain outcomes, 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 moisture 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 data basis is growing, but it does not match the certainty with which marketing operates.
Research on NMN and skin health is currently more mechanistic than clinical. Existing human studies measure metabolic and bodily 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. The clinical evidence in humans 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 postmenopausal women and found measurable improvements in metabolic function and cellular energy—precisely in the group where collagen loss is most accelerated. The connection between restored cellular energy and collagen production is biologically plausible. Direct clinical evidence specifically for the skin is still being built.
Are both better together?
There is no indication of harm from taking both products, and a plausible argument that they address complementary aspects of the same problem.
Collagen peptides can potentially provide a stimulus for fibroblast activity. NMN can restore the cellular energy environment that determines how efficiently fibroblasts respond to this stimulus.
If the research on ingested collagen is confirmed, and current data suggests moderate effects with correct dosing, 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 to 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 precisely the one that deteriorates with age. And it cannot be remedied with any amount of raw material.
This 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