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How to Boost Your Skin’s Natural Sun Protection this Summer

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The link between UV rays from the sun and skin cancer has been well established, chronic sun exposure has also canoeing outdoorsbeen linked to photoaging of the skin. We also know that sun exposure is required for vitamin D production. Vitamin D is a complex fat soluble neuro-hormone involved in immune, bone, and even digestive function. Correcting deficiencies has been shown to improve immune function and even reduce risk factors for cancer development. Modified UV therapies have also been introduced as a treatment for autoimmune conditions such as vitiligo. So, how do we mitigate the risks of sun exposure in order to gain its benefits? The answer of course is in education and balance.

Let’s review the exact process of sun damage and key risk factors:

  1. Solar UV spectrum consists of UV-C ( wavelengths <280nm), UV-B (280-315nm), and UV-A ( 315-400nm.) Most UV-C and UV-B is absorbed by the atmosphere- hence the importance of maintaining atmospheric integrity. The UV-B and UV-A wavelengths that do penetrate the atmosphere will be absorbed by the skin. The depth to which these rays reach, will be determined by the length. For example, the shorter UV-B radiation will mostly be absorbed by the epidermis, or top layer of skin. While UV-A will reach the deeper dermal layer. Both wavelengths ranges can cause structural damage to DNA. However, UV-B tends to be more mutagenic and is related to the development of skin cancers. While, UV-A causes oxidative damage over time related to skin aging. Further, both UV-B and UV-A have some immunosuppressive properties, hence the application of UV for particular autoimmune conditions. Risks increase depending on the intensity of the UV exposure- related to latitude, time of day, and season and calculated by UV index. Further, risks are increased with length of exposure, greater area of exposure, and fair skin.
  2. The vitamin D conundrum: UV light is required for the activation of 7-dehydrocholesterol into cholecalciferol (vitamin D3) in the skin. Vitamin D3 ( which can also be digested from food or direct supplements) is then processed by the liver into calcidiol (25-hydroxy-vitamin D) and then sent to the kidney where it is converted into calcitriol (1,25-dihydroxy-vitamin D). Calcitriol is involved in a number of important functions: increasing immune function, improving growth of red blood cells, increasing insulin secretion, increasing absorption of calcium and phosphate for bone remineralisation and bone remodeling. Various forms of vitamin D have also been linked to inhibiting the growth of breast, colon, and prostate cells. Human clinical studies have also shown that vitamin D can also increase survival from metastases. Given our understanding of these pathways it is clear that the risk for vitamin D deficiency is linked with rigorous sun protection which can result in widespread negative health consequences.

Traditionally sun protection involves avoidance, physical barriers that block and reflect UV light, and chemicals that absorb UV light. Total avoidance of the sun is no longer recommended, nor is it particularly realistic. Sufficient vitamin D can be produced by exposure of approximately 18% of the body surface 2-3X/week to obtain “adequate” levels of vitamin D. Groups with high risk for vitamin D deficiency may need to increase this time or through supplementation. Avoiding high intensity prolonged exposure to the sun, that may result in burns will minimize risk. Further, diet and supplements can help minimise the risks associated with UV damage by absorbing UV radiation, providing antioxidant support for the resulting oxidative damage, repairing damage, and managing inflammation.

Internal UV damage protection requiring prolonged supplementation to account for skin turnover: Most internal treatments required 8-10 weeks of supplementation before benefits were seen.

  • Antioxidants such as quercetin have been shown to reduce the damaging effects of UV radiation in skin cells. Further, quercetin does not incur damage itself when exposed to UV light. Other antioxidants include carotenoids, tocopherols, vitamin E, flavonoids, vitamin C, and selenium.
  • Carotenoids- these pigments protect plants from photodamage and have demonstrated benefits in humans against UV damage as well.The carotenoid lycopene found in tomatoes, was shown to reduce to reduce the inflammation and redness that can result from sun exposure. Beta-carotene in carrots, was found to reduce the intensity of the redness due to sun damage.
  • Retinoids such as vitamin A, absorbs UV-B and UV-A by absorbing some of the light, preventing damage to the skin cells.
  • Polyphenols such as those found in green tea, are protective against damage, and inhibit the inflammatory cells. Further, these compounds have anti-tumor properties, aiding in cancer prevention.
  • Omega 3- studies linking fat consumption with the intake of omega-3 and omega-6 fatty acids, found that those who consumed a high ratio of omega-3:omega-6 had a lower incidence of squamous cell carcinoma. Human studies where individuals were given EPA also found that there were less markers of DNA toxicity after UV exposure, and reported less photosensitivity reactions than the control group.
  • Melatonin- Research published this month demonstrated that melatonin provides some photoprotective benefits due to its potent antioxidant, anti-inflammatory, and anti-carcinogenic activity.

What to look for in your natural topical sunscreen:

  • Zinc oxide- nanoparticle forms which has been investigated in the treatment of inflammatory diseases and has photoprotective effects. New research (January, 2016) has shown that zinc oxide works by absorbing the UV radiation rather than reflecting and scattering the light as previously thought.
  • As we discussed in a past blog post vitamin E can be beneficial topically as well as internally- it has been shown to provide some UV protection when applied topically to the skin in preventing cellular damage.
  • Some carrier oils such as coconut, jojoba, and shae have their own SPF capacities, though this is usually quite low.
  • Aloe vera latex resin acts as a barrier against UV sun damage.
  • Natural sunscreens may include cooling essential oils such as peppermint, camphor, wintergreen, and eucylaptus.

Image by: Jacob Lund via Adobe Stock

You may also be interested in:

Sun Damage Protection: The Power of Curcumin

References:

Buettner GR. The pecking order of free radicals and antioxidants: lipid peroxidation, alpha-tocopherol, and ascorbate. Arch Biochem Biophys. 1993 Feb 1;300(2):535-43.

Cole C, Shyr T, Ou-Yang H.Metal oxide sunscreens protect skin by absorption, not by reflection or scattering.Photodermatol Photoimmunol Photomed. 2016 Jan;32(1):5-10. doi: 10.1111/phpp.12214. Epub 2015 Nov .

Chowdhury et al.  Vitamin D and risk of cause specific death: systematic review and meta-analysis of observational cohort and randomised intervention studies. BMJ. 2014 Apr 1;348:g1903. doi: 10.1136/bmj.g1903.

Maini S, Fahlman BM, Krol ES. Flavonols Protect Against UV Radiation-Induced Thymine Dimer Formation in an Artificial Skin Mimic.J Pharm Pharm Sci. 2015;18(4):600-15.

Eberlein-Koning, B et al. Protective effect against sunburn of combined systemic ascorbic acid (vitamin C) and d-alpha-tocopherol (vitamin E). J. Am Acad Dermatol 1998;38:45-48.

Fuchs, J, Kern, H. Modulation of UV-light-induced skin inflammation by D-alpha-tocopherol and L-ascorbic acid: a clinical study using solar simulated radiation. Free Radic Biol Med 1998;25:1006-1012.

Havens et al.  Serum 25-hydroxyvitamin D response to vitamin D3 supplementation 50,000 IU monthly in youth with HIV-1 infection. J Clin Endocrinol Metab. 2012 Nov;97(11):4004-13. doi: 10.1210/jc.2012-2600. Epub 2012 Aug 29.

Kim, H.H., Cho S, Lee, S., Kim, K.H., Cho, K.H., Eun, H.C., & Chung, J.H. Photoprotective and anti-skin-aging effects of eicosapentaenoic acid in human skin in vivo.May 2006 The Journal of Lipid Research, 47, 921-930.doi: 10.1194/jlr.M500420-JLR200

Kim MH, Jeong HJ. Zinc Oxide Nanoparticles Suppress LPS-Induced NF-κB Activation by Inducing A20, a Negative Regulator of NF-κB, in RAW 264.7 Macrophages.J Nanosci Nanotechnol. 2015 Sep;15(9):6509-15

Marto J.,Ascenso A., M Gonçalves L.,Gouveia L.E., Manteigas P., Pinto P., Oliveira E., Almeida A.J., & Ribeiro H.M. Melatonin-based pickering emulsion for skin’s photoprotection.Drug Delivery. 2016. 23(5):1594-1607.  DOI: 10.3109/10717544.2015.1128496.

Middleton et al. Vitamin D deficiency: A simple algorithm employing weekly administration of 50,000IU of vitamin D. Am J Otolaryngol. 2014 Mar-Apr;35(2):85-8. doi: 10.1016/j.amjoto.2013.12.002. Epub 2013 Dec 12.

Schwartz, G.G., 2001. Vitamin D and the big three: cancers of colon, breast and prostate. In: Holick MF (editor). Biologic effects of light. Kluwer Academic Publishers (Boston, USA), pp. 255–266.

Sies, H & Stahl, W. Nutritional Protection Against Skin Damage from Sunlight. Annual Review of Nutrition. Vol. 24: 173-200. DOI: 10.1146/annurev.nutr.24.012003.132320

Theodoratou E1, Tzoulaki I, Zgaga L, Ioannidis JP. Vitamin D and multiple health outcomes: umbrella review of systematic reviews and meta-analyses of observational studies and randomised trials. BMJ. 2014 Apr 1;348:g2035. doi: 10.1136/bmj.g2035.

Valdivielso, J.M,, Cannata-Andía, J, Coll, B., Fernández, E. A new role for vitamin D receptor activation in chronic kidney disease. American Journal of Physiology – Renal Physiology Published 24 November 2009 Vol. 297 no. 6, F1502-F1509. DOI:10.1152/ajprenal.00130.2009

Wang X, Quinn PJ. Vitamin E and its function in membranes. Prog Lipid Res. 1999 Jul;38(4):309-36.

 

 

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