r/DIYmicroneedling

I thought this might be helpful for visual learners, a lot of people want more info on what stamping means and there are not a lot of videos of close up videos on it.

I chopped up the video because it was about something totally different lol so I made it into various different looping gifs instead so you'd get different examples.

Happy Sunday! Hope everyone has had a lovely weekend.

Sharing some more resources on SPF

This video is from Chisom Ikeji, MD, although in the comments she did say she thought it made her look greasy so thought that might be helpful! Her post said:

>I’m on a mission to find the best tinted sunscreens for deep skin tones and I’m starting with EltaMD. Tinted sunscreens with iron oxides block visible light that worsens hyperpigmentation and melasma. But none of that matters if it’s not made for deeper skin.
So I tested it. Watch to see my honest first reaction. Not sponsored. 

I recently ordered dr pen M8. My main concern is post acne scars and hyperpigmentation and want to enhance the overall skin appearance and texture.
What serums should I use with microneedling sessions and for recovery?? Tell me your best regimen.

This review looks at what we keep seeing (Ozempic face) and investigates whether it's a result of rapid fat loss or could GLP-1 rector agonists directly accelerate aging. The authors actually conclude that both may be true. And ironically, they also have research showing they have anti-aging effects on other parts of the body by reducing inflammation and oxidative stress. They examine whether mechanisms beyond fat loss may contribute to skin aging during GLP-1 therapy. Skin aging is characterized by reduced mitotic activity, impaired skin barrier function, decreased collagen and elastin product, diminished cellular proliferation, increased apoptosis, and elevated oxidative stress. Increased production of reactive oxygen stress damages DNA and cellular membranes, activates signaling pathways that reduce pro collagen synthesis, and stimulates inflammatory pathways involved in collagen metabolism.

GLP-1s have proven research on type 2 diabetes, obesity, and weight loss, but they also have demonstrated anti-inflammatory effects have been investigated for skin diseases. As their use has increased, so has facial aging associated with significant weight loss been noticed. The change is usually connected to the loss of facial fat because it alters facial contours and results in excess skin, more visible wrinkles, and changes in facial proportions. The authors note that this phenomenon is not unique to GLP-1s though, and has also been described following bariatric surgery. Histological studies of patients with major weight loss have demonstrated alterations in dermal structure, including changes in collagen and elastic fiber density.

The authors describe evidence suggesting that GLP-1s may influence dermal white adipose tissue (DWAT) and adipose-derived stem cells (ADSCs). These both express GLP-1 receptors. DWAT contribute to skin maintenance and regeneration and reduced DWAT has been associated with aging skin, decreased collagen production, and increased activity of an enzyme involved in collagen degradation (matrix metalloproteinase-1.) Studies show that GLP-1 receptors on ASDCs may decrease the production of protective cytokines and growth factors, impair fibroblast migration and collagen synthesis, and increase oxidative stress within the cells. There's also a lot more interesting in the weeds findings, but don't want this to get crazy long. They touch on estrogen receptors, muscle loss, etc.

The authors ALSO found evidence suggesting that GLP-1RAs may have effects that support skin health too. It reduces chronic inflammation and lower concentrations of AGEs. They also associate this with reduction of blood glucose levels. There are various studies touching on this as well. The authors also found from other studies that GLP-1s improve endothelial function and increase microvascular perfusion within the skin and subcutaneous tissue. But they note that no published study has directly linked these effects to delay skin aging yet and state additional research is needed.

The point of this review is that it argues Ozempic face is way more complex than simply losing facial fat, but there is currently still not enough evidence that GLP-1s directly age the skin. Please do not take this as discouragement from using them or as fear mongering. I want people to know the science of what could be going on. Keep in mind that this is a mini review, not a clinical trial. A lot of the mechanisms come from biology research and inferences. But what I would offer from this is. If these mechanisms are happening and you are using them, what would theoretically protect against them? If you're worried about reduced collagen signaling, you would want things that support collagen production. If you're concerned on oxidative stress, you would want to reduce oxidative damage. If it's about the reduced stem cell activity, you want to support tissue repair and regeneration. If you're worried about the loss of dermal estrogen signaling, that is currently being studied in peri and postmenopausal research. This paper to me actually is something that can be used on future research on how to combat these things.

Paschou IA, Sali E, Paschou SA, Tsamis KI, Peppa M, Psaltopoulou T, Nicolaidou E, Stratigos AJ. GLP-1RA and the possible skin aging. Endocrine. 2025 Sep;89(3):680-685. doi: 10.1007/s12020-025-04293-w. Epub 2025 Jun 11. PMID: 40498168; PMCID: PMC12370548.

https://www.dropbox.com/scl/fi/xldxphuzqw86m7xqx5s20/GLP-1RA-and-the-possible-skin-aging.pdf?rlkey=iiqiobjnckzwu3zt4yqxm1djl&st=pato0lja&dl=0 (dropbox link is actually from Thriving Through Menopause by Chiza Westcarr)

Not microneedling related, but regenerative aesthetics related. And I think an actual interesting implication of this paper is about whether controlled skin injury itself can durable remodel the skin's epigenetic state. That's a way bigger biological idea.

The authors repeatedly argue that the methylation changes do't happen immediately after injury. Instead they emerge gradually over 1-6 months as healing transition into tissue remodeling. They specifically describe this as moving from an inflammatory phase to a regenerative phase. Microneedling follows a similar biological process so would microneedling also produce the same delayed epigenetic remodeling? Not sure, it hasn't been investigated yet. I think the biggest finding wasn't just that methylation changed, but that 83.9% of strongly responsive CpGs shifted in the opposite direction of normal aging, meaning laser treatment partially reversed age associated methylation patterns. So is epigenetic rejuvenation a general property of regenerative therapies? Researchers have been so stuck in an obsession with college, that they are not investigating more interesting things imo. Collagen is just a buzzword at this point. We know all these things stimulate collagen, but does the treatment move aged skin toward a younger molecular makeup? Microneedling has actually never been tested this way. Same with these booster molecules. Then this makes me wonder, is the laser doing something unique or is controlled injury the real mechanism here? Also makes me wonder if all collagen stimulators converge on the same pathways because the laser altered methylation in pathways involving WNT signaling, stem cell maintenance, epidermal differentiation, collagen organization, extracellular remodeling, wound healing, immune regulation, and Polycomb-regulated developmental genes. Most of these are already known to become activated during microneedling from transcriptomic and histologic studies. So do different rejuvenation procedures actually all activate these same pathways? So there could be a shared pathway independent of the device.

Then if you want to get more in the weeds. Microneedling is actually makes a lot of sense. Laser studies have various stimuli, there's heat, coagulation, mechanical disruption, inflammatory signaling, etc. Microneedling is mostly just mechanical injury. So if microneedling produced similar methylation changes, that would suggest that technical regeneration alone is enough to remodel the epigenome. If that's not the case, then thermal injury might be necessary, so this is definitely worth researching. And making sure they are taking biopsies during actual relevant timing. They should be doing this 3 months, 6 months, 8 months post treatments.

Also something interesting from the study, beyond a direct molecular link to reversing cellular aging and physical skin benefits, the study also points to a direct molecular link to skin cancer biology. The laser positively modulates DNA methylation at keratinocyte-regulating loci, including FGFR3, HOXB4, UBE2I, and PPP1R18/PPP1R26, genes tied to the pathogenesis of basal and squamous cell skin cancers.

>Here's the post copy from Dr. Sajic: Your laser may be doing more than making your skin look younger. A new study found that fractional laser treatment reversed nearly 84% of age-related epigenetic changes and remodeled pathways linked to skin aging, DNA repair, stem cells, and even cancer-related biology. ⚠️ This does NOT prove it prevents skin cancer. But it does suggest lasers may help shift your skin toward a healthier molecular profile. The question is… What should you be doing between treatments—or while you’re waiting? There are evidence-based strategies that may help support DNA repair, reduce UV damage, and improve overall skin health. 

Study: Schallen, K.P., Schomacker, K., Banila, C. et al. Non-ablative fractional laser 1940-nm treatment modulates epigenetic signatures associated with skin aging in a split-face investigation. Sci Rep 16, 17695 (2026). https://doi.org/10.1038/s41598-026-56604-4

(Updated to add this note: This study is on repigmentation and grey hair research, I realize the title is blind)

Sharing a study looking at repigmentation. That and hair treatments, hair follicle stimulation, and hair follicle microenvironments seem to be a common interest.

Melanocyte stem cells (McSCs) regenerate the pigment producing melanocytes that color hair during each hair cycle. As these stem cells become depleted or stop contributing to hair regeneration, hair gradually loses pigment and turns grey. Understanding why this stem cell population fails has been a long standing question in stem cell biology. The prevailing model proposed that McSCs remain undifferentiated within a specific region of the hair follicle called the bulge, while the cells they produce leave this region, become mature melanocytes, and never return to the stem cell population.

Background info that might help: Stem cells can either maintain their identity or begin differentiating. Differentiation is the process by which a stem cell gradually acquires the structure and function of a specialized cell. In the traditional model, this process moves in one direction. Once a stem cell begins differentiating, it is expected to continue towards becoming a mature cell and permanently lose the ability to function as a stem cell. This study asks whether melanocyte stem cells instead retain the ability to reverse this process.

Back to the paper. The authors found that melanocyte stem cells do not always follow a one way path toward differentiation. During each hair growth cycle, many melanocyte stem cells begin expressing genes associated with mature melanocytes and enter an intermediate stage of differentiation. Rather than continuing directly to become mature pigment producing cells, some later lose these differentiation markers and regain the characteristics and function of melanocyte stem cells. The authors conclude that this revertsal, called differentiation, is a normal mechanism used to maintain the melanocyte stem cell population.

The authors first examined where McSCs are located before hair growth begins. Previous studies suggested that these cells are primarily found in the bulge. However, 3d imaging showed that most McSCs are actually located in the neighboring hair germ. By tracking individual cells over time, the authors showed that McSCs in their hair germ both generated mature melanocytes and produced cells that remained in the stem cell population for future hair cycles. This demonstrated that the hair germ contains the main population responsible for both pigment regeneration and long term maintenance. The authors then ask whether McSCs change ad hair growth begins. They found that these cells changed shape and activated genes involved in pigment production before producing mature melanocytes. Single cell RNA sequencing confirmed that the cells occupied an intermediate molecular state between undifferentiated melanocyte stem cells and fully differentiated melanocytes. These changes occurred early in regeneration, showing that McSCs normally begin the differentiation process during each hair cycle.

To determine whether differentiating cells could return to the stem cell population, the actors permanently labeled McSCs expressing Oca2, a one that is activated late during differentiation. As expected, some of these labeled cells became mature melanocytes that produced pigment in the hair bulb. Unexpectedly, other labeled cells migrated to another region of the hair follicle, switched off pigmentation genes, and persisted as McSCs through multiple rounds of hair regeneration. This demonstrated that cells that had already progressed well into differentiation could reverse that process and regain stem cell function.

The authors showed that nearly all melanocyte stem cells can undergo reversible differentiation rather than maintaining a permanently undifferentiated population. This process is controlled by local signals within the hair follicle. WNT signaling promotes differentiation in the hair germ, whereas reduced WNT signaling in the bulge allows cells to dedifferentiate and regain stem cell function. During aging, many McSCs fail to return to the hair germ and instead remain in the bulge, reducing melanocyte regeneration and contributing to hair greying.

I find it odd that the study doesn't investigate why. Like okay it explains where the cells get stuck... but then doesn't go for more. So like several possibilities could be the cause. The ECM around the follicle stiffens with age, adhesion molecules change, epithelial cells stop producing guidance cues, McSCs themselves lose the migration capacity, or all of these things happen together. It's hard to actually figure out what the best intervention is without that being identified. I'll set aside that a successful repigmentation study does exist and come back to that in the comments so I can just separate ideas. But, restoring McSC movement is something to think about. If those cells are stranded in the bulge and still alive, but just in the wrong place, a treatment that would encourage them to migrate back into the hair germ before the next cycle could be a plan of attack. So manipulating cell adhesion molecules (how tightly cells stick to their surroundings), extracellular proteins, chemokine signaling (cellular communication that guide movement), cytoskeletal regulators (proteins that control the assembly, disassembly, and organization of a cell's structural network) that control migration, etc because these would restore the normal regenerative cycle not trying to force pigment production. The paper shows that McSC identity depends on local signals so another approach could be instead of targeting the stem cells directly, you could try restoring the signals of the aging hair germ (WNT signaling, TGF-β , endothelin, stem cell factor/c-Kit, or notch signaling. Navigating this seems easier said than done though as these pathways regulate many cell types so it would need really precise timing. Also grey hair has been difficult to reverse by changing one of these pathways alone is prob not likely to restore the normal regenerative cycle and this paper kind of reinforces that. Another treatment approach could be if you think about how some McSCs become stuck in a partially differentiated state, it may be possible to push them back toward a differentiated state. The difficult is that forcing cells backwards carries risks if control is lost (abnormal growth or cancer). A different approach to look at would be instead of reversing greying, preserve the normal cycle earlier in life. If the problem is that stem cells gradually lose mobility over decades, then maintaining extracellular matrix structure, preventing fibrosis, or reducing chronic inflammation around the follicle might delay greying. If you are actually interested in these topics and looking through them, these are all 3 common themes we keep seeing across all literature right now in various spaces btw, if you're new here and interested write those down lol. And then a possible treatment could be if you think how McSCs only regenerate pigment during the normal hair cycle, a treatment or therapy might work if it times up with several events. So you'd want to trigger a new hair cycle, restore the proper niche signals, allow stem cells to migrate, and then let pigment producing melanocytes regenerate naturally. But that's very complex.

>

Abstract

>For unknow reasons, the melanocyte stem cell (McSC) system fails earlier than other adult stem cell populations, which leads to hair greying in most humans and mice. Current dogma states that McSCs are reserved in an undifferentiated state in the hair follicle niche, physically segregated from differentiated progeny that migrate away following cues of regenerative stimuli. Here we show that most McSCs toggle between transit-amplifying and stem cell states for both self-renewal and generation of mature progeny, a mechanism fundamentally distinct from those of other self-renewing systems. Live imaging and single-cell RNA sequencing revealed that McSCs are mobile, translocating between hair follicle stem cell and transit-amplifying compartments where they reversibly enter distinct differentiation states governed by local microenvironmental cues (for example, WNT). Long-term lineage tracing demonstrated that the McSC system is maintained by reverted McSCs rather than by reserved stem cells inherently exempt from reversible changes. During ageing, there is accumulation of stranded McSCs that do not contribute to the regeneration of melanocyte progeny. These results identify a new model whereby dedifferentiation is integral to homeostatic stem cell maintenance and suggest that modulating McSC mobility may represent a new approach for the prevention of hair greying.

>Supplementary information The online version contains supplementary material available at: https://doi.org/10.1038/s41586-023-05960-6.

>Peer review information Nature thanks Nick Barker, Rui Yi and the other, anonymous, reviewer(s) for their contribution to the peer review of this work.

Happy 4th everybody!

Thank you! I am really curious about this and wanting to hear from people who’ve actually done it.

I always find these helpful so sharing!

Ultracol is a Korean biostimulator made from Polydioxanone (PDO) (the same biodegradable, absorbable material used in surgical sutures.) It's the world's first PDO filler and is the only PDO-based product approved by MFDS and CE. It's developed by Ultra V, Ultracol converts PDO threads into tiny, uniform microspheres, the particles naturally degrade into water and carbon dioxide within 4-6 months. One vial of Ultracol 200 is equivalent to the collagen stimulating effects produced by over 1,400pcs PDO mono threads.

(I will also be sharing more info on the particles and data behind this, but it's a lot of info at once.)

Ultracol is available at Wimpole Fillers (the Fillers website version not their Pharmacy version) and there is a discount with code SciencePls.

Another pinterest find for newbies

This study investigated whether skin color and ethnicity influence how long microneedle created micropores remain open after treatment. The duration that these micropores stay open is clinically important because it determines how long drugs can continue to diffuse through the skin and micropore lifetime determines the duration of transdermal drug absorption.

The key finding is that darker skin exhibits significantly longer micropore closure times, suggesting a longer potential drug delivery window following microneedling. Because darker skin tones remained permeable for approximately 15-20 hours longer on average than lighter skin tones, identical treatments could theoretically produce different results and different drug exposure between people. This is important for literal medical purposes of actual drug delivery, is relevant for diabetes treatment and glucose monitoring, injectable peptide and medical therapies, medical microneedling, and cosmetic microneedling.

Also objective skin color measurements predicted micropore closure better than self identified race or ethnicity. Which means measured skin pigmentation is a more informative predictor of micropore closure than self identification. This highlights the importance of objective skin characterization in developing microneedling protocols, studies, treatment plans, etc.

Also thought it was worth noting that darker skin tones also showed stronger baseline barrier properties compared to lighter skin. Darker skin generally had lower TEWL (indicating less passive water loss), higher electrical impedance (suggesting a stronger skin barrier), and skin hydration did not differ significantly between groups.

Average micropore closure times:

Group	Closure time
Asian	44.1 h
Bi-/multi-racial	48.0 h
White	50.2 h
Latino	61.1 h
Black	66.5 h

Some limitations to keep in mind. There was only one Native American/Hawaiian participant included. Micropore closure was inferred from TWEl and impedance rather than direct drug pharmacokinetic measurements. The study included only health adults so the data really shouldn't be generalized to skin conditions and older populations.

This paper is around micropore lifetime and mostly around the drug delivery window BUT the same finding is directly relevant to the safety window. While micropores are open the skim barrier is not fully restored, so there may be a longer period where contamination, non-sterile products, irritants, or microbes could more easily enter disrupted skin.

>Abstract: Microneedles (MNs) allow transdermal delivery of skin-impermeable drugs by creating transient epidermal micropores, and micropore lifetime directly affects drug diffusion timeframes. Healthy subjects (n = 111) completed the study, self-identifying as Asian (n = 32), Bi-/multi-racial (n = 10), Black (n = 22), White (n = 23), Latino (n = 23), and Native American/Hawaiian (n = 1). L* was measured with tristimulus colorimetry to objectively describe skin lightness/darkness. MNs were applied to the upper arm; impedance and transepidermal water loss (TEWL) were measured at baseline and post-MN to confirm micropore formation. Impedance was repeated for 4 days to determine micropore lifetime. Post-MN changes in TEWL and impedance were significant in all groups (p < 0.05), confirming micropore formation regardless of skin type. Micropore lifetime was significantly longer in Blacks (66.5 ± 19.5 h) versus Asians (44.1 ± 14.0 h), Bi-/multi-racial (48.0 ± 16.0 h), and Whites (50.2 ± 2.6 h). Latinos (61.1 ± 16.1 h) had significantly longer micropore closure time versus Asians (44.1 ± 14.0 h). When categorizing data according to L*, micropore lifetime was significantly longer in darker skin. We report for the first time that micropore lifetime differences are present in human subjects of different ethnic/racial backgrounds, with longer micropore lifetime in skin of color. These results also suggest that objectively measured skin color is a better predictor of micropore lifetime than self-identified race/ethnicity.

Ogunjimi AT, Carr J, Lawson C, Ferguson N, Brogden NK. Micropore closure time is longer following microneedle application to skin of color. Sci Rep. 2020 Nov 3;10(1):18963. doi: 10.1038/s41598-020-75246-8. PMID: 33144596; PMCID: PMC7609754. https://pubmed.ncbi.nlm.nih.gov/33144596/

I would recommend checking out Victoria's instagram and hearing her talk about the whole thing as her voice deserves to be heard.

Beyond this being good news and she's getting the justice she deserves. I'm also sharing this to show that "professionals" have messed up people's faces. Sonya Dakar is known as being a celebrity esthetician, still has over 100k followers on instagram, has her own skincare line, hundreds of influencers partner with her promoting product with zero care about what she has done. There are also experiences from other people that she has caused damages to, these people just want to remain anonymous. She somehow has not actually had to face the consequences of her actions. I don't think her surrounding her license is enough personally.

I think we should call it what it is, Sonya Dakar disfigured this poor woman. And then made her PAY to have her "fix" it. Also keep in mind that these scars are still there, she just wears makeup. In one of her videos she talks about the emotional experience of everyday waking up and looking in the mirror and seeing these marks on her face.

Sonya Dakar did not refer her to a burn unit or plastic surgeon after it happened. Victoria could have gotten an infection, lost a limb, or died from this incident. She also could have had better results if she would have gone to professionals. To this day, no one knows what she even used on Victoria's face. She should never have even had any of these supplies in the first place. And definitely should not have had an RF microneedling machine. She never had the license to. She also has a history of wild and inappropriate behavior with the board and investigators. Her license had even been suspended multiple times. She physically assaulted and bit one even. Victoria's civil suit case is still ongoing.

But, because someone is a professional, it does NOT mean they are actually educated or able to perform medical treatments on you. Whatever was used on Victoria was chemical, but that is still a medical treatment. Microneedling is a medical treatment. And RF microneedling is a medical treatment. If you don't want to do DIY, that is totally okay! If you're just here to learn love that. But, if you are going to go to professionals make sure you thoroughly vet them. And if you are going to do DIY make sure you do enough research beforehand.

Overview from Allure: In August 2025, Victoria Nelson posted a 13-minute video on social media claiming that her face was permanently damaged after a facial and chemical peel with celebrity aesthetician Sonya Dakar. The video racked up millions of views and nearly 19,000 comments, some from people who claimed to have had similar experiences with Dakar. A few months later, Nelson filed a lawsuit against Dakar and a formal complaint to the California Board of Barbering and Cosmetology, which made the public aware of more details from the facialist's past. The complaint noted, for example, that Dakar's license had been suspended twice before, including one time after she reportedly tried to bite an inspector from the board. Now, the California Board of Barbering and Cosmetology has confirmed to Allure that Dakar has surrendered her license, effective July 22. She has also surrendered the establishment license for the Sonya Dakar Skin Clinic in Beverly Hills. Allure spoke to Nelson about this new development and where she goes from here. At the link in bio, read what she had to say, plus everything we know so far about the case. Photos: Courtesy Victoria Nelson

Okay wanted to share more information on NAD+ because there are a couple of different NAD+ boosters and I feel like people don't fully understand them! Also thought repairing UV damage was timely given one of the busiest times of the year of being outside and in the sun.

This study provides mechanistic evidence that nicotinamide enhances the repair of UV-induced DNA damage rather than preventing its formation. By preserving cellular energy stores (NAD+ and ATP), nicotinamide accelerates repair of both direct UV-induced DNA lesions (CPDs) and oxidative damage (8oxoG), offering plausible explanation for its observed ability to reduce precancerous lesions and skin cancer risk in clinical studies.

They found that nicotinamide increased overall DNA repair. Compared with UV exposure alone more cells initiated DNA repair, individual cells repaired DNA more rapidly, DNA repair activity increased significantly, and it did not stimulate cell proliferation so that would indicate the increased DNA synthesis reflected repair rather than cell division.

The findings support that nicotinamide is a promising chemopreventive gent for non-melanoma skin cancer because it enhances repair of UV-induced DNA damage, reduces persistence of mutagenic lesions, is inexpensive, has a strong safety profile, and had already shown efficacy in earlier clinical trials reducing actinic keratoses and potentially non-melanoma skin cancers.

They used both cultured keratinocytes and human skin, increasing biological relevance. Measured multiple forms of DNA damage, demonstrated consistent effects using several independent DNA repair assays, and examined physiologically relevant UV exposure levels like daily sunlight. They also found that nicotinamide did not increase hOGG1 enzyme expression which suggests that repair enhancement results from improved cellular metabolism rather than increased product of repair proteins.

There are some obvious limitations here, given it's a lab and ex vivo study rather than an in vivo clinical trial. It ws a short observation, small number of human skin donors, and the mechanism needs studies directly measured. BUT I would look at this as preliminary research and something that is really interesting and useful.

>Overview: Nicotinamide (vitamin B3) protects from ultraviolet (UV) radiation-induced carcinogenesis in mice and from UV-induced immunosuppression in mice and humans. Recent double-blinded randomized controlled Phase 2 studies in heavily sun-damaged individuals have shown that oral nicotinamide significantly reduces premalignant actinic keratoses, and may reduce new non-melanoma skin cancers. Nicotinamide is a precursor of nicotinamide adenine dinucleotide (NAD+), an essential coenzyme in adenosine triphosphate (ATP) production. Previously, we showed that nicotinamide prevents UV-induced ATP decline in HaCaT keratinocytes. Energy-dependent DNA repair is a key determinant of cellular survival after exposure to DNA-damaging agents such as UV radiation. Hence, in this study we investigated whether nicotinamide protection from cellular energy loss influences DNA repair. We treated HaCaT keratinocytes with nicotinamide and exposed them to low-dose solar-simulated UV (ssUV). Excision repair was quantified using an assay of unscheduled DNA synthesis. Nicotinamide increased both the proportion of cells undergoing excision repair and the repair rate in each cell. We then investigated ssUV-induced cyclobutane pyrimidine dimers (CPDs) and 8-oxo-7,8-dihydro-2′-deoxyguanosine (8oxoG) formation and repair by comet assay in keratinocytes and with immunohistochemistry in human skin. Nicotinamide reduced CPDs and 8oxoG in both models and the reduction appeared to be due to enhancement of DNA repair. These results show that nicotinamide enhances two different pathways for repair of UV-induced photolesions, supporting nicotinamide’s potential as an inexpensive, convenient and non-toxic agent for skin cancer chemoprevention.

Surjana D, Halliday GM, Damian DL. Nicotinamide enhances repair of ultraviolet radiation-induced DNA damage in human keratinocytes and ex vivo skin. Carcinogenesis. 2013 May;34(5):1144-9. doi: 10.1093/carcin/bgt017. Epub 2013 Jan 24. PMID: 23349012.