In the previous article, we discussed a common sense approach to getting enough sun to stimulate vitamin D production whilst reducing the risks of skin cancer. However, there are times when we get a little bit too much sun and end up with sunburn. Many of us have suffered from this very uncomfortable and often painful condition. Perhaps you’ve been on the beach, the sun is shining, and there is a cool breeze so it doesn’t feel that hot. Later in the day, your skin starts to look very red and you feel sore.
Millions of people are affected by sunburn each year. In fact, the US Centers for Disease Control and Prevention (CDC) reported in 2012 that just over 50% of all adults reported at least one sunburn in the previous 12 months. In this article, we’ll take a look at sunburn and what is actually going on under the skin. Sunburn is usually mild and short-lived, but more intense reactions can be very painful and result in blistering. Generally, the intensity of the sunburn is determined by the total ultraviolet radiation (UVR) absorbed by the skin and thus, low doses over longer periods of time will lead to the same degree of sunburn as high doses over a short period. Research shows that frequent episodes of serious sunburn can increase your risk of developing skin problems in later life, such as ageing (wrinkling) and skin cancer.
Sunburn is an acute inflammatory reaction that follows excessive exposure of the skin to ultraviolet UVR which can be from too much sun or from tanning beds. Most sunburns are classified as superficial or first-degree burns and it is a sure sign that there has been direct damage to DNA caused by excessive exposure to UVR and this results in inflammation and apoptosis of skin cells. What is apoptosis? In this context, apoptosis is the death of skin cells.
DNA absorbs UV light, and the absorbed energy can result in damage to DNA – our genetic material. What happens is that excessive UVR exposure can break bonds in the DNA. Most of the DNA breakages are repaired by proteins present in the cell, but if the amount of damage is too great, the alterations to the DNA may remain as permanent mutations. The unrepaired genetic damage of the DNA can lead to skin cancers.
The characteristic reddening of the skin that comes with sunburn is called erythema. This is the result of skin damage causing dilatation of the blood capillaries. When the melanin in our skin can no longer absorb the UVR, the damage to DNA starts to occur and the inflammatory response is initiated. This is when leukocytes start to infiltrate the inflamed area to remove sun-damaged cells. During the sunburn response, expression of cyclooxygenase 2 (COX-2) in the epidermis and dermis increases significantly.
COX-2 is involved in the production of prostaglandins. These are made at sites of tissue damage or infection, where they cause inflammation as part of the inflammatory response. Blocking COX-2 impedes the production of prostaglandins and therefore reduces inflammation and pain. Non steroid anti-inflammatory drugs (NSAIDs) block the COX enzymes which reduces pain and inflammation, however, they have a number of undesirable side effects. There are natural alternatives to NSAIDs that can inhibit COX-2 and therefore reduce pain and inflammation. The gingerols in ginger root are a good example of a potent anti-inflammatory that inhibits COX-2 and also Nuclear Factor kappa-B (NF-kB) which is essentially the master switch for inflammation.
Types of UVR.
UVR consists of both UVA and UVB radiation. It is UVB that is primarily responsible for producing sunburn but because the solar energy reaching the earth is primarily UVA, it also contributes to sunburn and other harmful effects of UV radiation. Most of us are exposed to large amounts of UVA throughout our lifetime. UVA rays account for up to 95 percent of the UV radiation reaching the Earth's surface. Although they are less intense than UVB, UVA rays are 30 to 50 times more prevalent. They are present with relatively equal intensity during all daylight hours throughout the year, and can penetrate clouds and glass.
UVA, which penetrates the skin more deeply than UVB, has long been known to play a major part in skin aging and wrinkling (photoaging), but until recently scientists believed it didn’t cause significant damage in areas of the epidermis (outermost skin layer) where most skin cancers occur. Studies over the past two decades, however, show that UVA does indeed damage skin cells in the basal layer of the epidermis, where most skin cancers occur. UVA contributes to, and may even initiate the development of skin cancers. UVA is the dominant ray in giving us a tan, however, tanning causes cumulative damage over time.
A tan results from injury to the skin's DNA; the skin darkens in an imperfect attempt to prevent further DNA damage. These imperfections, or mutations, can lead to skin cancer. UVB, the chief cause of skin reddening and sunburn, tends to damage the skin's more superficial epidermal layers. It plays a key role in the development of skin cancer and a contributory role in tanning and photoaging. Its intensity varies by season, location, and time of day. UVB rays can burn and damage your skin year-round, especially at high altitudes and on reflective surfaces such as snow or ice, which bounce back up to 80 percent of the rays so that they hit the skin twice. UVB rays do not significantly penetrate glass.
Skin Types and Sunburn
Although sunburn can occur in both fairly and darkly pigmented individuals, skin type determines how susceptible an individual is to sunburn. Moderately pigmented skin requires 3-5 times the exposure, and darkly pigmented skin up to 30 times the exposure, compared with the amount of time required to induce sunburn in those with fair pigmentation.(1) As defined by the Fitzpatrick skin phototype classification (see Table 1), skin types IV-VI are unlikely to experience sunburn following excess UV radiation exposure.(2)
Table 1. The Fitzpatrick skin phototypes
Sunburn duration is also a function of skin type. Immediate UVB-induced sunburn can occur in individuals with skin types I and II, but usually the sunburn response is delayed until six to 24 hours after exposure. UVB-induced sunburn may last for one to two weeks for fair skin types I and II, while for skin type V individuals it may disappear as soon as three days after exposure.
Antioxidants and Sunburn
Our skins has several internal defense mechanisms against UVR. These include melanin and antioxidants. Melanin, the pigment deposited by melanocytes, is the first line of defense against DNA damage at the surface of the skin. It’ job is to scatter and absorb UVR but it cannot totally prevent skin damage.
UVR exposure causes DNA oxidation and the generation of Reactive Oxygen Species (ROS) or free radicals. When these free radicals exceed our capacity to combat them, we get oxidative stress. The reduction of oxidative stress can be achieved on two levels: by lowering exposure to UVR and/or by increasing levels of antioxidant defense in order to scavenge these free radicals. Antioxidants combat oxidative stress and attenuate the damaging effects of reactive oxygen species (ROS). They impair and even reverse many of the events that contribute to toxicity or disease in the skin. However, chronic exposure to UVR can overwhelm the skin;s antioxidant capacity, leading to oxidative damage, premature skin aging and skin cancer. There are numerous antioxidants in the skin as follows:
Dietary antioxidants play a major role in maintaining the homeostasis of the oxidative balance and we get most of our antioxidants through diet, however, UVR exposure affects the skin antioxidants. Vitamin E, GSH, SOD, catalase, and ubiquinol are all depleted in both the dermis and epidermis layers of the skin when exposed to UVR. Research shows that the oxidation caused by UVR exposure can be prevented to a large degree by prior antioxidant treatment. There have been many studies performed with different antioxidants or combinations of antioxidants and phytochemicals that have found evidence that free radical damage can be prevented to a significant degree. Lets take a closer look.
Vitamin C is a potent antioxidant and protects cells from free radical damage. Foods rich in vitamin C are citric, red and green paprika, and fruits and vegetables in general. Your body does not make vitamin C on its own, and it does not store it either, so it is important that you include plenty of fruits and vegetables in your daily diet.
In one study, vitamin C supplements (500 mg/day) were taken by 12 volunteers for 8 weeks.
The results showed significant rises in plasma and skin vitamin C content (3). But it did not have any effect on the UVR-induced sunburn or the erythemal response. However, many other studies have found that vitamin C can increase collagen production, protect against damage from UVA and UVB rays, correct pigmentation problems, and improve inflammatory skin conditions.(4)
Vitamin E is is one of the main biological defenders of membranes and a potent antioxidant. It is found in spinach, almonds, sunflower seeds, avocados and broccoli. There are different forms of vitamin E that include isomers known as tocopherols and tocotrienols. Skin exposure to UVR results in significant depletion of vitamin E which means that vitamin E is being used to fight free radicals and 'quench' Reactive Oxygen Species (ROS) during UVR skin exposure.(5) Depletion of vitamin E is one of the earliest oxidative stress markers in human skin exposed to UVR and other environmental stress.(6) One study showed that the number of sunburn cells was decreased by treatment with the antioxidant alpha-tocopherol and may result from both direct protection from free radicals and indirect protection by means of increased epidermal thickness.(7) Vitamin E provides protection against UV-induced skin photodamage through a combination of antioxidant and UV absorptive properties.
Beta-carotene is a pigment found in plants that gives them their color. The name beta-carotene is derived from the Latin name for carrot. Foods that are rich in beta-carotene are sweet potato, carrots, spinach, melon, sweet red peppers, peas and broccoli. Carotene supplements are frequently used as so-called oral sun protectants, but studies proving a protective effect of oral treatment with carotene against skin responses to sun exposure are scarce and conflicting results have been reported.
Studies on the systemic use of carotene provide evidence that 15–30 mg/d over a period of about 10–12 weeks produces a protective effect against sunburn.(8) Similar effects have been attributed to mixtures of carotenoids or after long-term intake of foods rich in carotenoids. Supplementation with carotenoids contributes to basal protection of the skin but is not sufficient to obtain complete protection against severe UVR. Studies showed that the efficacy of beta carotene in systemic photoprotection depends on the duration of treatment and on the dose. (8) For successful intervention, treatment with carotenoids is needed for a period of at least ten weeks.(9) Research published in 2000 investigated the effects of the antioxidant effect of carotenoids and tocopherols against scavenging of Reactive Oxygen Species (ROS) generated during UVR oxidative stress.(10) Basically, the researchers were looking to see if supplementation with antioxidants could protect the skin from sunburn or UV-induced erythema. The results showed that the antioxidants used in this study provided protection against sunburn and may be useful for diminishing sensitivity to UV light.
Astaxanthin, pronounced asta-zan-thin, is a naturally occurring carotenoid or pigment primarily found in marine organisms such as salmon, krill and shrimp, as well as in micro-algae. This carotenoid is the pigment that gives salmon their pink colour. Astaxanthin is a very potent anti-oxidant and anti-inflammatory. In fact, it is the strongest anti-oxidant known and has many other health benefits for the eyes, central nervous system, brain, skin and immune system.
In a study on carotenoids and UVA exposure, astaxanthin was shown to exhibit a pronounced photoprotective effect and counteracted UVA-induced alterations to a significant extent.(11) Another study published in 2010 showed that astaxanthin has significant benefit on protecting against UVA-induced skin photo-aging such as sagging and wrinkles.(12) Research published in 2012 showed that taking astaxanthin leads to a reduction in Nuclear Factor kappa-B (NF-kB) DNA binding activity. This is a good thing because it down-regulates the expression of COX-2 and therefore suppresses inflammatory prostaglandins (PGE2) and other inflammatory mediators.(13)
Co-enzyme Q10 (CoQ10) is often called the ‘biochemical spark plug’ because of its important role in the production of energy. It is also a potent antioxidant and there is evidence that CoQ10 also has anti-inflammatory properties. It is made naturally in the body, as well as obtained from our diet, however, as we get older, CoQ10 levels decline and if we don’t get enough from our diet, a deficiency can occur. It was recently reported that CoQ10 protects against oxidative stress-induced cell death and enhances the synthesis of basement membrane components in dermal and epidermal cells.(14) CoQ10 has also been shown to reduce free radical production and DNA damage triggered by UVA radiation.(15) Studies show that CoQ10 appears to have also a healing effect on the skin.(16)
Glutathione, pronounced “gloota-thigh-own,” is a very potent antioxidant that is getting a lot of attention in the scientific community. However, research is showing that an increasing amount of people have deficiency because of poor diet, chronic stress, infections, overuse of anti-biotics, environmental toxins and so on. In cell culture models using human skin cells, it has been clearly shown that glutathione depletion leads to a large sensitization to UVA and UVB. There is a direct correlation between the levels of sensitisation and cellular glutathione content. Research also shows that glutathione is a photoprotective agent in skin cells with studies showing that glutathione levels in both dermis and epidermis are depleted by UVA treatment (17)
Recently, there has been a lot of interest in green tea because of its reported health benefits. Tea leaves contain varying amounts of polyphenols, particularly flavonoids. Research suggests that green tea polyphenols are photoprotective in nature and can be used as pharmacological agents for the prevention of solar UVB light-induced skin disorders including photoaging, melanoma, and nonmelanoma skin cancers.
Studies show that topical treatment or oral consumption of green tea polyphenols (GTP) inhibits chemical carcinogen or UV radiation-induced skin carcinogenesis. Topical application of GTP prior to exposure of UVB protects against UVB-induced immune system suppression, which was associated with the inhibition of UVB-induced infiltration of inflammatory leukocytes.(18) Another study demonstrated that topical application of green tea polyphenols reduced UVB-induced oxidation of lipids and proteins and depletion of antioxidant enzymes.(19)
Summary on Antioxidants
The DNA molecules in our skin are constantly “bombarded” by free radicals originating from UVR as well as internal processes. Antioxidants scavenge free radicals and also enhance the DNA enzyme repair systems. The research shows that antioxidants can help to reduce oxidative stress and free radical formation and thereby slow down the skin damage process. Antioxidants like vitamins C and E and many others cannot be synthesized by the human body and must be obtained through our diet. As we age, the effectiveness of our antioxidant system diminishes, making supplementation with antioxidants more important. This may well be an excellent protective strategy against age-associated skin oxidative damage. However, it is important for all ages to get adequate antioxidants through diet and supplementation given the importance they play in reducing oxidative damage.
It can also be helpful to apply topical antioxidant preparations before going out in the sun. Studies have demonstrated significant photo-protective effects of “natural” and synthetic antioxidants when applied topically before UVR exposure. It's worth noting that no significant protective effects were obtained when antioxidants were applied after UVR exposure. UVR-induced skin damage is a rapid event, and antioxidants can only prevent damage to the skin when they are present in the body and skin, in enough concentration, before we head off to the beach this summer.
So its clear that eating your fruit and veg as well as taking supplements such as astaxanthin and CoQ10 can help prevent skin damage from sun exposure. Its not a a panacea though because no amount of antioxidants will help if sun exposure is excessive. When the antioxidant system is depleted, then oxidative stress is going to occur, and when it does, we know that there may well be some DNA damage and sunburn follows. Of course, the best cure is prevention and being sensible about how much UVR we expose ourselves to. In the next article on this topic, we'll take a look at sun cream protection and the research for and against it, as well as the wider environmental impact.
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