• Corpus ID: 38425567

Eat Your Sunscreen : How the Food We Consume Can Protect Our Skin from the Sun ’ s Harmful Rays

  title={Eat Your Sunscreen : How the Food We Consume Can Protect Our Skin from the Sun ’ s Harmful Rays},
  author={Howard Murad and J E Murad},
Ultraviolet radiation from the sun, in countless laboratory and clinical studies, has been implicated to cause inflammation of the skin, oxidative stress and free-radical damage, among other problems. While sun-protecting topical products have been useful to assist in reducing sun damage, their protection alone is not adequate to prevent ultraviolet effects. Because of this, new skin protecting and cell-fortifying methods are needed to promote healthy skin and offer the highest available… 


Natural products as aids for protecting the skin's immune system against UV damage.
Animal and now human studies have shown that a class of agents known as oligosaccharins--complex carbohydrates found in plants--protect the cutaneous immune system from UVB-induced and UVA-induced immunomodulation, and these agents, particularly tamarind xyloglucan, may become important adjunctive ingredients to sunscreens.
Nutritional protection against skin damage from sunlight.
Dietary protection is provided by carotenoids, tocopherols, ascorbate, flavonoids, or n-3 fatty acids, contributing to maintenance resistance as part of lifelong protection.
Antioxidants: What is their significance in sun protection?
When antioxidant materials proven to be effective at preventing DNA damage and lipid peroxidation are incorporated into a sunscreen product, no effect is measurable on the sun protection factor (SPF) of the product.
Topical vitamin C protects porcine skin from ultraviolet radiation‐induced damage
Evidence is provided that the vitamin C levels of the skin can be severely depleted after UV irradiation, which would lower this organ's innate protective mechanism as well as leaving it at risk of impaired healing after photoinduced damage.
Dietary tomato paste protects against ultraviolet light-induced erythema in humans.
It is feasible to achieve protection against UV light-induced erythema by ingestion of a commonly consumed dietary source of lycopene, and no significant difference between groups was found at wk 4 of treatment.
UV photoprotection by combination topical antioxidants vitamin C and vitamin E.
Appreciable photoprotection can be obtained from the combination of topical vitamins C and E and it is suggested that these natural products may protect against skin cancer and photoaging.
Chemoprevention of photocarcinogenesis by selected dietary botanicals.
  • M. Baliga, S. Katiyar
  • Biology, Medicine
    Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology
  • 2006
This review summarizes chemopreventive effects of some selected botanicals, such as apigenin, curcumin, grape seed proanthocyanidins, resveratrol, silymarin, and green tea polyphenols, against photocarcinogenesis in in vitro and in vivo systems.
Green tea polyphenol (-)-epigallocatechin-3-gallate treatment of human skin inhibits ultraviolet radiation-induced oxidative stress.
Application of EGCG to human skin before a single UV exposure of 4x minimal erythema dose (MED) markedly decreases UV-induced production of hydrogen peroxide and nitric oxide in both epidermis and dermis and afforded protection to the antioxidant enzyme GPx.
Supplementation with beta-carotene or a similar amount of mixed carotenoids protects humans from UV-induced erythema.
Long-term supplementation for 12 wk with 24 mg/d of a carotenoid mix supplying similar amounts of beta-carotene, lutein and lycopene ameliorates UV-induced erythema in humans; the effect is comparable to daily treatment with 24mg of Beta- carotene alone.
Skin aging.
  • N. Puizina-Ivic
  • Medicine
    Acta dermatovenerologica Alpina, Pannonica, et Adriatica
  • 2008
There are two main processes that induce skin aging: intrinsic and extrinsic. A stochastic process that implies random cell damage as a result of mutations during metabolic processes due to the