Does drinking coffee have consequences on the skin?

In a study conducted by Eisuke F. SATO, researchers aimed to verify the impact of oral administration of polyphenols derived from coffee (caffeic acid and chlorogenic acid) on mice with UVB-induced skin dermatitis. After oral administration of caffeic acid at 100 mg/day, or chlorogenic acid at 100 mg/day for eight days, only caffeic acid was found to inhibit dermatitis. More specifically, a significant reduction in inflammatory markers such as the degree of erythema and skin oedema was observed.

UVB irradiation is known to activate several signalling pathways, including the mitogen-activated protein kinases (MAPK) pathway, which has been implicated in UVB-induced skin inflammation and carcinogenesis. MAPKs, which belong to a family of serine/threonine protein kinases, are activated by UVB. They play an important role in cellular functions such as proliferation, differentiation, and inflammation. The pathway by which caffeic acid inhibits dermatitis is therefore possibly linked to this pathway, by decreasing MAPK levels.

In the previously mentioned study, the researchers also aimed to verify the effect of oral administration of caffeic acid (100 mg/day) and chlorogenic acid (100 mg/day) for eight days on mice with hyperpigmentation induced by UVB rays. Similar to the last result, only caffeic acid was able to inhibit skin hyperpigmentation.

Pigmentation is a protective response of the skin against UV damage, achieved through the production of melanin in melanocytes. The production of melanin induced by UV irradiation is regulated by α-MSH. α-MSH binds to the MC1 receptor on melanocytes, leading to an increase in cAMP, which stimulates the expression of the microphthalmia-associated transcription factor (MITF). MITF then activates the expression of enzymes such as tyrosinase, which is essential for melanin synthesis.

In this study, the oral administration of caffeic acid induced an increase in β-endorphin levels. β-Endorphin is an opioid peptide that is believed to participate in the inhibitory action on UVB-induced melanocyte activation by reducing the accumulation of cAMP generated by α-MSH. Given these results, we can consider that the inhibitory effect on pigmentation by the oral administration of caffeic acid might have been exerted through a β-endorphin pathway.

This could explain a potentially anti-pigmentary effect of coffee consumption. However, further studies are needed to confirm these results.

Michael KRUGER and his colleagues aimed to evaluate the relationship between daily coffee consumption and skin carcinoma. This study is a cross-sectional analysis of Caucasian women (n = 93,676). Compared to non-drinkers, women who drank only caffeinated coffee daily had a 10.8% reduced prevalence of non-melanoma skin cancer. Consuming six or more cups of caffeinated coffee per day was associated with a 36% reduction in non-melanoma skin cancer. Unlike caffeinated coffee, daily consumption of decaffeinated coffee was not associated with a significant change in non-melanoma skin cancer reports among women.

Daily consumption of caffeinated coffee has thus been associated with a dose-dependent decrease in the prevalence of non-melanoma skin cancer in women.

Caffeine is one of the most studied compounds in the context of the chemopreventive power of coffee. Caffeine exerts its antiproliferative action and anticarcinogenic effects by regulating the growth, development, and apoptosis of tumour cells. It has been demonstrated that caffeine inhibits UV-induced carcinogenesis by suppressing the formation of thymine dimers, which are DNA lesions. However, the anti-carcinogenic potential of coffee in skin cancer is not solely attributed to caffeine. The polyphenols contained in coffee are known to inhibit carcinogenesis as they possess antioxidant properties by scavenging free radicals, and anti-inflammatory properties. Besides their antioxidant activity, polyphenols are known to prevent carcinogenesis by inhibiting cyclooxygenase-2 (COX-2).