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Dietary Fish Oil Found to Deflect Sun Damage
8/1/2005
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Anti-inflammatory effect of omega-3s seen to reduce damage induced by UV rays

by Craig Weatherby



Readers of "Vital Choices" may recall that we ran two articles this summer, concerning the beneficial effects of vitamin D and the role of fish and sun in providing this essential anti-cancer nutrient.


Next to sun exposure, fish are the most significant sources of vitamin D. (Sun rays prompt certain bodily compounds in skin to change into vitamin D.)


In recent months, leading cancer and vitamin D researchers have voiced concerns about extreme sun avoidance. They calculate that more cancers may be caused by under-exposure to sun than by moderate exposure (20-30 minutes per day).


For example, Harvard’s Edward Giovannucci, M.D. told NPR recently that for every person who dies from skin cancers caused by excessive sun exposure, an estimated 30 people may die of non-skin cancers related to vitamin D deficiencies caused by insufficient sun exposure or dietary intake.


This seems to leave us on the horns of a dilemma. We need to get sufficient sun exposure to prevent cancer, but not so much that we will suffer sunburns or increase the risk of skin cancers.


Sunscreen offers some protection, but statistics suggest that its anti-cancer benefits may have been oversold. While typical sunscreens do a good job of blocking skin-burning UVB rays, they offer relatively weak protection against UVA rays, which penetrate much more deeply into skin, and appear to play a much larger role in cancer promotion and skin aging than we thought.


Omega-3s may help reduce sun damage

The omega-3s in fish (EPA and DHA) exert significant anti-inflammatory effects throughout the body, and the results of new research suggest that, as a consequence, omega-3s can help counteract the deleterious effects of solar radiation.


We were alerted to this new benefit by a press release from the Norwegian Seafood Export Council (NSEC), and, given the source, we were inclined to skepticism.


However, when we read the research that prompted the release, we were persuaded that Norwegian seafood trade group’s announcement contained much more than a grain of truth. They’d cited recent research by a team at Britain’s University of Manchester, which we found and examined in detail, and which led us to similar research by other groups.


The University of Manchester team, led by professor Lesley Rhodes, began publishing relevant research in 1994, starting with two small tests in human subjects, designed to examine the effects of dietary fish oil (10 grams per day, containing EPA and DHA) on skin inflammation induced by solar radiation.


Following the positive results of these preliminary investigations—which showed that people taking fish oil became increasingly resistant to sunburn over a three-month period—the Manchester team conducted two well-controlled clinical trials of omega-3s, whose results were published in 2003 and 2004.


The first trial involved 42 volunteers, and the second involved 28 people.  The participants in both studies took four grams of supplemental EPA (not DHA) or oleic acid (the monounsaturated fat abundant in olive oil) for three months.


Both double-blind, randomized studies produced positive results. As the Manchester team reported, “The subjects taking EPA, but not OA, showed a significant rise in their minimal erythemal dose... longer-term supplementation might reduce skin cancer in humans.”


In this context, “minimal erythemal dose” means the smallest dose of solar radiation required to produce the abnormal redness associated with sun burn. This redness, or erythema, results from inflammation: the immune response that occurs in response to tissue damage from solar radiation.  In other words, the skin of the volunteers who’d taken EPA supplements was significantly more resistant to sun-induced inflammation.


The results also showed that the groups taking EPA enjoyed reductions in several early markers of cancer risk in skin, including sunburn, UVR-induced p53 [a cancer-suppressing gene], and strand breaks in peripheral blood lymphocytes.  These positive changes indicate that EPA protects against the genetic damage in skin tissue associated with increased cancer risk.


How omega-3s diminish sun damage

Inflammation is the body’s response to infections, burns, and wounds.  While inflammation is generally a positive thing, chronic inflammation can be induced by dietary excesses or deficiencies, and become a source of secondary damage to the body’s cells. For example, inflammation promotes obesity and diabetes, raises the risk of heart attacks and Alzheimer’s, and promotes cancerous changes to prostate and other tissues.


While dietary EPA does not block the sun’s UVA or UVB rays, or reduce the amount of direct tissue damage those rays can cause, it reduces the excessive, cell-damaging inflammation produced by the body in response to UV-induced tissue damage. This is why it took more UV exposure to redden the skin of the University of Manchester study subjects who took supplemental EPA.


And EPA isn’t the only fish-derived omega-3 that reduces UV-induced inflammation in skin.  Previous studies by the Manchester team and other research groups has documented the similar anti-inflammatory effects of DHA in skin cells exposed to UV radiation.


Specifically, EPA and DHA reduce production of interleukin (IL)-8, the cytokine (chemical messenger) primarily responsible for the skin inflammation seen in epidermal and dermal cells exposed to UVB rays, as well as production of a pro-inflammatory prostaglandin (chemical messenger) called PGE-2.


The picture is not entirely one-sided, since dietary omega-3s raise the levels of omega-3s in skin cells, and omega-3s are more prone to oxidation by the free radicals generated in response to UV radiation. However, this hypothetical drawback to a diet rich in omega-3s appears to be far outweighed by the positive effects of a diet rich in omega-3s.


As the Manchester University team reported in their first article on this subject, “…omega-3 fatty acids produce a pronounced reduction in UVB-erythemal [sunburn] sensitivity, although susceptibility of skin to lipid peroxidation [damage to fatty acids caused by free radicals] is increased. Thus, omega-3 fatty acids may act as an oxidizable buffer, protecting more vital structures from free radical damage.”


In other words, dietary omega-3s create an environment in which UV radiation is less damaging, and where cancer is less likely to develop.



Sources

  • Storey A, McArdle F, Friedmann PS, Jackson MJ, Rhodes LE. Eicosapentaenoic acid and docosahexaenoic acid reduce UVB- and TNF-alpha-induced IL-8 secretion in keratinocytes and UVB-induced IL-8 in fibroblasts. J Invest Dermatol. 2005 Jan;124(1):248-55.
  • Shahbakhti H, Watson RE, Azurdia RM, Ferreira CZ, Garmyn M, Rhodes LE. Influence of eicosapentaenoic acid, an omega-3 fatty acid, on ultraviolet-B generation of prostaglandin-E2 and proinflammatory cytokines interleukin-1 beta, tumor necrosis factor-alpha, interleukin-6 and interleukin-8 in human skin in vivo. Photochem Photobiol. 2004 Sep-Oct;80(2):231-5.
  • Rhodes LE, Shahbakhti H, Azurdia RM, Moison RM, Steenwinkel MJ, Homburg MI, Dean MP, McArdle F, Beijersbergen van Henegouwen GM, Epe B, Vink AA. Effect of eicosapentaenoic acid, an omega-3 polyunsaturated fatty acid, on UVR-related cancer risk in humans. An assessment of early genotoxic markers. Carcinogenesis. 2003 May;24(5):919-25.
  • Jackson MJ, Jackson MJ, McArdle F, Storey A, Jones SA, McArdle A, Rhodes LE. Effects of micronutrient supplements on u.v.-induced skin damage. Proc Nutr Soc. 2002 May;61(2):187-9. Review.
  • Pupe A, Moison R, De Haes P, Beijersbergen van Henegouwen GMW, Rhodes LE, Degreef H, Garmyn M: Eicosapentaenoic acid, a n-3 polyunsaturated fatty acid, differentially modulates TNFa, IL-1a, IL-6 and PGE2 expression in UVB-irradiated human keratinocytes. J Invest Dermatol 2002; 118: 692-8
  • Rhodes LE, Durham BH, Fraser WD, Friedmann PS. Dietary fish oil reduces basal and ultraviolet B-generated PGE2 levels in skin and increases the threshold to provocation of polymorphic light eruption. J Invest Dermatol. 1995 Oct;105(4):532-5.
  • Rhodes LE, O'Farrell S, Jackson MJ, Friedmann PS. Epidermal lipid peroxidation. J Invest Dermatol. 1994 Aug;103(2):151-4.

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