Thailand Medical Researchers Find That Anti-Aging NMN Cream May Worsen Sun-Damaged Skin
Nikhil Prasad Fact checked by:Thailand Medical News Team Nov 01, 2026 59 minutes ago
A new study by medical researchers in Thailand has raised concerns about nicotinamide mononucleotide (NMN), a compound increasingly promoted for its potential anti-aging benefits. Researchers discovered that prolonged application of NMN cream failed to protect mouse skin against ultraviolet B (UVB) radiation and was associated with worsening cellular abnormalities linked to chronic sun damage.
Thai researchers found that prolonged use of NMN cream failed to protect UVB-exposed mouse skin and was associated with worsening microscopic damage and inflammatory changes
The findings challenge assumptions that boosting cellular energy metabolism necessarily protects aging skin, particularly when that skin experiences repeated ultraviolet exposure.
Researchers from the following institutions conducted the study:
-Division of Dermatology, Chulabhorn International College of Medicine, Thammasat University, Pathum Thani, Thailand.
-Department of Pathology, Faculty of Medicine, Thammasat University, Pathum Thani, Thailand.
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Why NMN Has Attracted Attention in Anti-Aging Skincare
NMN is a precursor of nicotinamide adenine dinucleotide (NAD+), a molecule essential for cellular energy production, DNA repair, and responses to environmental stress.
Because NAD+ levels influence several biological processes associated with aging, NMN has attracted interest as a possible ingredient in anti-aging treatments.
However, researchers questioned whether continuously supplying NMN to already damaged skin might produce unintended consequences.
This
Thailand Medical News report examines their findings and the implications for skincare products containing NMN.
How Researchers Investigated Long-Term NMN Exposure
The investigation involved 24 female mice divided into four groups of six animals.
One group received no ultraviolet exposure. Another received UVB radiation alone. A third received UVB followed by an inactive cream, while the fourth received UVB followed by cream containing 5% NMN.
UVB radiation was administered three times weekly at 120 millijoules per square centimeter for 25 weeks.
Cream was applied within 20 minutes after irradiation to investigate its effects on skin recovery rather than sunscreen protection.
Researchers monitored visible skin deterioration, epidermal thickness, abnormal cellular development, and genes involved in inflammation and DNA repair.
NMN-Treated Skin Showed Increasing Damage
All UVB-exposed groups developed progressive skin damage. However, an important difference emerged during prolonged treatment.
After approximately 12 weeks, skin da
mage in mice receiving UVB alone or inactive cream stabilized or slightly declined.
In contrast, deterioration continued in NMN-treated mice after week 16. By week 25, the NMN group showed greater average clinical severity than the UVB-only group, although this difference did not reach statistical significance (p=0.08).
The researchers therefore could not establish that NMN caused worse visible damage.
Microscopic Examination Revealed Concerning Changes
More striking findings emerged when researchers examined skin tissue. Between weeks 12 and 25, epidermal thickness increased significantly only in the NMN-treated group.
The proportion of dysplastic lesions also increased significantly in this group (p<0.01).
Dysplasia describes abnormal cellular organization and development. Although it does not automatically indicate cancer, it can occur in tissues experiencing prolonged injury and may represent precancerous changes.
Interestingly, NMN-treated mice initially showed relatively mild microscopic abnormalities at week 12 before experiencing substantial deterioration.
Other UVB-exposed groups already demonstrated considerable abnormalities earlier, but did not show statistically significant worsening between these measurement points.
Gene Activity Suggested Persistent Cellular Stress
Molecular testing revealed additional warning signs. Three genes associated with abnormal epidermal activity increased significantly in NMN-treated skin:
-Krt6: Increased significantly (p<0.01), indicating heightened cellular stress and abnormal skin-cell proliferation.
-Krt16: Increased substantially (p<0.001), suggesting sustained epidermal injury responses.
-S100a8: Increased significantly (p<0.001), indicating inflammatory activity and disrupted skin regulation.
Meanwhile, Krt1, associated with normal skin-cell differentiation, showed no significant increase.
Together, these findings suggested that NMN-treated skin experienced persistent inflammatory stress rather than restoration of normal epidermal function.
DNA Repair-Related Genes Responded Differently
Researchers also examined Parp1 and Sirt1, genes associated with NAD+-dependent cellular repair and stress responses.
Both increased significantly over time in mice receiving UVB alone or inactive cream.
Surprisingly, neither showed significant increases in NMN-treated mice. However, gene-expression measurements cannot establish whether actual DNA repair activity was impaired.
Researchers also did not measure skin NAD+ concentrations, leaving the underlying biological mechanism uncertain.
Conclusions and Implications for Human Skincare
The findings raise important questions about prolonged NMN application to chronically sun-damaged skin. Although significant tissue abnormalities developed during treatment, the small animal study cannot establish that NMN directly caused deterioration or increases skin cancer risk. Larger investigations involving different concentrations, direct biochemical measurements, and human skin are necessary before definitive safety conclusions can be reached.
The study findings were published in the peer reviewed journal: International Journal of Molecular Sciences.
https://www.mdpi.com/1422-0067/27/21/9807
Read Also:
https://www.thailandmedical.news/articles/thailand-medical
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