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Fading dark spots. What is possible. What’s not.

Where are those dark spots (sunpots, liver spots, sunspots) coming from? From our skin “protesting” UV radiation, which contains more energy than the skin can cope with. The excess energy damages the sensitive mechanisms that control skin pigmentation, specifically, synthesis of melanin and its delivery to the keratinocytes. What is interesting (and annoying) is that the damage extends to fibroblasts deep in the dermis, so that superficial exfoliation can’t eliminate the sunspot.

Figure. The epidermis. The bottom row of cells is the basal layer and the cell with dendrites is the melanocyte. See how the dendrites reach into the keratinocytes in the next layer of cells, the spinous layer. The melanocyte also interacts with the dermal-epidermal membrane and has receptors for a number of factors produced in the epidermis. Melanosomes full of melanin will be transferred to the keratinocytes. UV light will stimulate the synthesis of melanin and its transfer to the keratinocytes, giving you that tanning you may want, plus the sunspots you don’t. Illustration by Magda Levy.

 

As you may have realized, those sunspots are very persistent. Even if you peel that area with a chemical peel, the new skin will eventually develop a sunspot almost as dark as the one you had before. This persistence could be due to a number of factors. The chemical peel killed the epidermis and even parts of the dermis, but the hyperpigmentation may persist. One possible explanation is that UV damaged, senescent fibroblasts in the dermis are producing messengers that influence the melanocytes in the epidermis. If this is true, then we may have to add senolytics to the mix of skin brightening actives. Quercetin and fisetin are senolytics, which “disarm” the mechanisms against cell death that the senescent fibroblasts use to persist.

It is also possible that lipofuscin, a non-melanin pigment made out of destroyed lipids, proteins and carbohydrates, also contributes to the spot.

Whatever the mechanism or composition of the sunspot,  UV is a deciding factor and prevention will do the trick. After the fact? Try some exfoliation, Vitamin A, UV repair cream, with a lot of patience. It took a lot of UV, ROS* and many years to age that skin to where it is now. Don’t try to rejuvenate it within days. Patience will help.

What to use

Senolytics: Quercetin, Fisetin

Actives that can help the dermal-epidermal junction: apocynin, ROS Terminator

Inhibitors of melanin synthesis and accumulation: many. Read more about the mechanism of pigmentation and how they are affected by UV here

Ready to use products: UV repair cream, Skin Brightening cream

Side effects: don’t go for “fast and furious” chemicals like hydroquinone, they will only make things worse, especially for dark skin.

 

References

Yoon JE, Kim Y, Kwon S, Kim M, Kim YH, Kim JH, Park TJ, Kang HY (2018). “Senescent fibroblasts drive ageing pigmentation: A potential therapeutic target for senile lentigo”. Theranostics. 8 (17): 4620–4632. doi:10.7150/thno.26975. PMC 6160768. PMID 30279727.

Toutfaire, M., Bauwens, E., & Debacq-Chainiaux, F. (2017). The impact of cellular senescence in skin ageing: A notion of mosaic and therapeutic strategies. Biochemical Pharmacology, 142, 1–12. doi:10.1016/j.bcp.2017.04.011

Kirkland, J. L., & Tchkonia, T. (2020). Senolytic Drugs: From Discovery to Translation. Journal of Internal Medicine. doi:10.1111/joim.13141 

 

 

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