Beta-carotene is perhaps the best known member of the carotenoid family, a group of highly pigmented (red, orange, yellow), lipid-soluble substances present in various fruits, grains, oils, and vegetables (including apricots, carrots, green peppers, spinach, squash, sweet potatoes, and tomatoes).
Like alpha- and gamma-carotene, beta-carotene is a provitamin because it can be converted into active vitamin A (retinol). In comparison to other carotenoid compounds, some of which have been shown to have potential in the dermatologic armamentarium (e.g., astaxanthin, lutein, lycopene, and zeaxanthin), beta-carotene has been demonstrated to contribute much more to human nutrition (Am. J. Clin. Nutr. 2001;73:853-64).
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Beta-carotene, found in carrots and other fruits and vegetables, has some beneficial dermatologic properties but its strong pitmentary component has so far limited its use in topical formulations.
The degree to which beta-carotene can be harnessed for dermatologic applications is debatable, with the aforementioned carotenoids displaying greater promise in this realm. In particular, the potent yellow/orange pigmentation delivered by beta-carotene poses significant challenges to topical formulation. That said, recent research has indicated that cutaneous benefits can be derived from the systemic use of beta-carotene. That is the focus of this column.
Mixed results for beta-carotene’s UV protective effects. Ten years ago, Obermüller-Jevic et al. observed that beta-carotene exerted pro-oxidant activity in cultured human skin fibroblasts by promoting UVA induction of heme oxygenase-1 (HO-1). The investigators subsequently showed in vitro that the provitamin A compound potently fosters the UVA induction of proinflammatory interleukin-6 in skin fibroblasts (FEBS Lett. 1999;460:212-6; FEBS Lett. 2001;509:186-90). Nevertheless, several experimental, but not clinical, studies have suggested that dietary beta-carotene yields protective effects against acute and chronic cutaneous photodamage (Arch. Biochem. Biophys. 2001;389:1-6).
In 2000, Frieling et al. reported on their large-scale (n = 22,071) randomized, double-blind, placebo-controlled 12-year primary-prevention trial of beta-carotene supplementation with follow-up, in which they found that supplementing with 50 mg of beta-carotene on alternate days in apparently healthy male physicians aged 40-84 years in 1982 did not affect the development of a first basal cell or squamous cell carcinoma (Arch Dermatol. 2000;136:179-84). Other studies published earlier or around the same time yielded similar results, indicating that oral beta-carotene exerted no influence in stemming, preventing, or promoting nonmelanoma skin cancers (N. Engl. J. Med. 1990;323:789-95; Lancet 1999;354:723-9; J. Am. Acad. Dermatol. 2006;54:933-46).
In a prospective study of 1,001 randomly selected adults in one Australian community, investigators sought to determine the relationships between consumption of antioxidant nutrients and the relative risk of cutaneous basal cell and squamous cell carcinomas. In 1996 antioxidant consumption was estimated, and histologically confirmed cancers were recorded between 1996 and 2004. Dietary consumption in the second tertile for beta-carotene and vitamin E was associated with a higher basal cell carcinoma risk, with no trend, in subjects with a skin cancer history or a specific BCC history at baseline (Eur. J. Cancer 2007;43:2707-16).
In 2006, Stahl and Krutmann found that the systemic use of beta-carotene in dosages of 15-30 mg/day over 10-12 weeks conferred protection against UV-induced erythema, but failed to provide full protection against UVR (Hautarzt. 2006;57:281-5.)
More recently, in a paper published in 2008, Köpcke and Krutmann reported on their literature review of supplementation studies of dietary beta-carotene as protection against sunburn. Their review included studies published up to June 2007 in PubMed, ISI Web of Science, and the EBM Cochrane Library. The meta-analysis netted seven studies on the subject and revealed that, indeed, beta-carotene supplementation imparted time-dependent protection against sunburn, with at least 10 weeks of supplementation necessary (Photochem. Photobiol. 2008;84:284-8).
In September 2007, Stahl and Sies clarified that dietary carotenoids, particularly beta-carotene and lycopene, as well as flavonoids, help prevent the emergence of UV-induced erythema after the nutrients are disseminated to light-exposed areas, including the skin and eyes. Specifically, the tested carotenoids and flavonoids diminished sensitivity to UV-induced erythema in volunteers after 10-12 weeks of dietary intervention. The investigators speculated that such micronutrients have the potential to impart protection against UVR throughout an individual’s lifetime (Mol. Biotechnol. 2007;37:26-30).
Although the data on the impact of beta-carotene on aging skin and photoaging remain sparse, Bayerl has noted that beta-carotene has been shown to protect against the phototoxic effects of porphyrins in the photohemolysis model, and that the provitamin A substance is indicated for erythropoietic protoporphyria, photosensitive diseases, and mitigating the side effects of phototoxic drugs (Acta Dermatovenerol. Alp. Panonica Adriat. 2008;17:160-2, 164-6).
In 2009, Camera et al. compared the effects of the carotenoids astaxanthin, canthaxanthin, and beta-carotene on UVA-induced damage to human dermal fibroblasts. The carotenoids were delivered to the fibroblasts 24 hours before UVA exposure. Astaxanthin displayed the strongest photoprotective effect, reversing all of the noted changes induced by UVA, whereas beta-carotene partially prevented the UVA-induced reduction in catalase and superoxide dismutase activities. Beta-carotene also increased membrane damage, provoked HO-1 expression, and dose-dependently induced caspase-3 activity. In addition, the greatest photostability among the tested carotenoids was associated with astaxanthin, and the least, with beta-carotene (Exp. Dermatol. 2009;18:222-31).