But before getting too far into the details of sensible sunning, let’s tackle the issue of skin cancer and premature aging caused by the sun.
Sunburn versus Suntan
One of the most important jobs of the epidermis—especially in light-skinned people—is to adapt quickly to protect skin cells from the sun’s radiation. The defense mechanism the skin uses against sunburn is what we call tanning, which is an ingenious process. In response to sun exposure, the melanocytes produce melanin that makes the skin darker. The production of more melanin is triggered through an increase in the activity of an enzyme called tyrosinase. Melanin protects the skin by absorbing UV radiation. Even short bursts of sun exposure will trigger the melanocytes to produce more melanin.
Dark-skinned people do not have more melanocytes, but their melanocytes are more active, which explains why their skin is always pigmented. It also explains why the risk of all forms of skin cancer is lower for dark-skinned people—the cells of their skin are always more protected from damaging UVB and UVA by the presence of melanin, which acts like an umbrella, shielding the cell’s vulnerable DNA and proteins from UV damage due to sun exposure. Melanin actually migrates upward and, like an umbrella, shades the nucleus of the cell from damaging UV radiation.
Sunburn is quite different from a suntan. When you get a sunburn, your skin turns red and can sometimes blister and peel. This redness, known in scientific terms as erythema, is actually caused by increased blood flow to the skin. This begins approximately four hours after the sun exposure and reaches its peak between eight and twenty-four hours after exposure. Blood is being sent to the skin to attend to cells that have been damaged by the sun. When severely damaged squamous and basal cells cannot repair themselves, they “commit suicide” so they won’t replicate in a mutated state and cause cancer (this results in peeling). This form of cell suicide is known as apoptosis, or programmed cell death.
Fear of skin cancer is one of the main reasons for the hysteria over sun exposure. As is the case with so many health axioms, the relationship between sunshine and cancer isn’t as straightforward as most people think. There are a number of myths associated with what causes skin cancer.
Myths Exposed
Many myths are associated with skin cancer, thanks to the barrage of public
misinformation on this topic. Here are some of them. (I’ve touched upon many of these already, but they bear repeating.)
Any and all sun exposure causes skin cancer. Because UVB exposure is the easiest way to increase levels of 25-vitamin D, which humans can’t live without, this statement needs to be questioned. While it’s true that UVB radiation from sunlight—especially chronic overexposure to sunlight—is thought to be one of the causes of nonmelanoma skin cancer, virtually all nonmelanoma skin cancers are treatable and curable when detected early, and sunlight is proven to have protective benefits over the more deadly internal cancers. The trade-off between the risk of basal-cell carcinoma, for example, and the risk of stage 4 breast cancer cannot be understated. And you’ll hear me state this more than once:
there is no data to suggest that sensible sun exposure increases the risk of nonmelanoma skin cancer.
Sun exposure is the main cause of melanoma. There is no scientific evidence that regular, moderate sun exposure causes melanoma. As the FDA observed after a 1995 conference on melanoma, the relationship between melanoma and sunlight is baffling. Melanoma is seen more often in people who do not receive regular, moderate sun exposure than in those who regularly spend time in the sun. Most melanomas also occur on parts of the body that receive little or no sun exposure. This suggests that genetics plays a much more important role in the development of skin cancer than does regular, moderate sun exposure. There is also evidence that UVB-protection-only sunscreens may distort the UVB/UVA ratio that penetrates into the skin, thus contributing to melanoma development.
Remember, UVA penetrates much more deeply than UVB, bombarding melanocytes and immune cells. Sunburns as a child or young adult increase a person’s risk of melanoma, especially in areas least exposed to sunlight. A possible explanation for this is that sunburns may damage some melanocytes.
Normally, this would trigger the immune system to jump into action to attack and kill the defective melanocytes. (This is known as immuno-surveillance and is a very good thing for keeping defective cells in check so they don’t lead to cancer.) However, if the immune system is also affected by excessive UVB or UVA exposure, this immuno-surveillance system can become compromised. It then may no longer identify damaged melanocytes, and a major mechanism for preventing out-of-control melanocytes from growing into a deadly cancer is all but lost.
We are in the midst of a skin cancer “epidemic.” It is inaccurate to call the increasing incidence of skin cancer an epidemic. Skin cancer rates have been
rising steadily since the early twentieth century. Skin cancer rates are going up solely because more people are excessively sunbathing. Although skin cancer rates have been rising steadily since the early twentieth century, it wasn’t until the 1960s that a tanned skin was considered desirable. Present-day people actually spend less time outdoors than did our forebears, most of whom worked the land before the Industrial Revolution. Working outdoors throughout the year probably helped previous generations build a resistance to sunburn in the form of tanned skin.
More recently—especially in the 1970s and 1980s, when a severe sunburn was considered a prerequisite for an eventual summer tan—people have become more likely to get sunburned. Adding insult to injury, the use of UVB-protection-only sunscreens probably contributed to the rise of melanoma because they promoted massive exposure to deeply-penetrating UVA. There’s one hundred to one thousand times more UVA than UVB in sunlight. What’s more, it helps to bear in mind that nonmelanoma skin cancer has an extremely low death rate. In the United States, it claims about 1,200 lives a year.
If you get regular, moderate sun exposure, you have less chance of developing malignant melanoma. New research shows that melanoma is more prevalent in Europe and North America than in the equatorial latitudes, which again suggests that regular sun exposure may prevent melanoma. At the very least, moderate sun exposure will not increase the risk of melanoma.
There’s no such thing as a safe tan. Tanned skin protects you against sunburn, thought to be the main cause of melanoma. Also, it’s more dangerous to avoid sun exposure completely than it is to get regular, moderate sun exposure.
If you avoid getting sunburned, the benefits of sun exposure will far outweigh the possible dangers. Independent scientific research has shown that if you live in a sunny climate, or if you live in a not-so-sunny climate but expose yourself to sun, then your increased production of vitamin D due to UVB radiation will help lower risk of a host of debilitating and fatal diseases. Colon, prostate, and breast cancer—which together claim more than 115,000 lives each year—can in some cases be prevented by regular, moderate sun exposure. People who get regular, moderate sun exposure are less likely to get a malignant melanoma than those
who don’t. And don’t forget about all the research backing sunlight’s effect on a multitude of common illnesses and diseases, including internal cancers.
Tanning is like smoking to your skin. Wrong. Tanning is natural. It is your body’s natural defense against sunburn. Smoking is an unnatural habit that your body rejects by becoming ill.
So What Is Skin Cancer?
Our bodies function normally when the cells that make up the different tissues
—such as the prostate, breast, and colon—grow, divide, and replace themselves in an orderly fashion. Occasionally, cells divide too rapidly and multiply out of control; this can lead to cancer. Skin cancer results when this process occurs in the cells of the skin. There are several forms of skin cancer, but all of them fit into two broad categories: nonmelanoma skin cancer and melanoma.
Nonmelanoma Skin Cancer. By far the most common forms of nonmelanoma skin cancer are basal-cell carcinoma and squamous cell carcinoma (carcinoma is the medical term for cancer). Basal-cell carcinoma (BCC) affects the basal cells in the epidermis and is the most common form of nonmelanoma skin cancer.
BCC usually occurs on areas of your skin that are most exposed to the sun and that are most likely to have been sunburned, such as the nose, face, tops of the ears, and backs of the hands. Often BCC appears as a small, raised bump that has a smooth, “pearly” appearance. Sometimes BCC looks like a scar and feels firm when you press on it. BCC may expand in size and spread to tissues around it, but these cells rarely spread to other parts of the body.
Squamous cell carcinoma (SCC) also occurs on areas of the epidermis that are most often exposed to excessive amounts of sun. Often SCC appears as a firm, red bump. The tumor may feel dry, itchy, and scaly, may bleed, or may develop a crust. SCC very occasionally spreads to nearby lymph nodes (lymph nodes produce and store infection-and cancer-fighting immune cells). SCC may also appear on parts of your skin that have been burned, exposed to chemicals, or had X-ray therapy.
Both types of nonmelanoma skin cancer are thought to be caused by long-term exposure to sunshine. Such exposure over many years may cause damage to the skin cells themselves so that they eventually start replicating out of control. Sun exposure over many years may also desensitize the skin’s immune system in such a way that it will not recognize and act against cancerous skin cells.
Finally, researchers have been looking at the p53 gene, a “quality-control”
gene that is responsible for fixing a damaged cell or causing it to kill itself (apoptosis). There is mounting evidence that the p53 gene system may be damaged by excessive, long-term sun exposure. Each person has two p53 genes
—one from each parent. When one p53 gene is damaged, the skin cell becomes sick and multiplies abnormally to form a precancerous, scaly lesion known as an actinic keratosis. When both p53 genes are damaged and can no longer function properly, the skin cell may start replicating out of control and become a nonmelanoma skin cancer. The p53 gene is so important that it was declared the molecule of the year by the editors of the journal Science and appeared on the cover of Newsweek.
The likelihood that you will develop nonmelanoma skin cancer is greater if your exposure to sunshine began when you were a child, adolescent, or young adult. During these early years, the skin is especially vulnerable to sunburning.
There is also the simple fact that the earlier in life that skin cells are damaged, the longer the chance they have to replicate in a mutated state. There’s also more time to damage that second p53 gene.
Remember, not everyone who is exposed to strong sunshine from a young age is going to develop nonmelanoma skin cancer. Some people are genetically predisposed to this disease. This explains why certain people get nonmelanoma skin cancer while others don’t—even when they have the same skin type and are exposed to just about the same amount of sun. It’s also believed that a fatty diet may predispose you to a variety of cancers, including nonmelanoma skin cancer.
People who suffer from DNA-repair-enzyme diseases such as a xeroderma pigmentosum (XP) also experience a much higher risk of skin cancer. XP is an extremely rare skin disorder whose sufferers are highly sensitive to sun exposure. The cause of XP is hypersensitivity of the skin cells to UV radiation due to a defect in the gene’s DNA repair system. People with XP experience premature aging of the skin and multiple skin cancers. The disease is usually diagnosed in infancy when the child with XP exhibits severe skin problems, including skin reddening, scaling, and freckling. Skin cancers usually appear in early childhood, as do chronic eye problems. There is no cure for this disease, and the only course of action is to stay out of the sun.
Melanoma. Melanoma is a different story. Although rare, melanoma is much more deadly than nonmelanoma skin cancer. Comprising less than 5 percent of all skin cancers, melanomas are responsible for the majority of skin-cancer deaths, killing about 8,600 Americans annually. The number of new cases of
melanoma in the United States has not changed much in the last eight years.
Overall, the lifetime risk of getting melanoma is about one in fifty for whites, one in one thousand for blacks, and one in two hundred for Hispanics.
Melanomas occur in the deeper pigment-producing cells located between the dermis and epidermis, known as the melanocytes. When melanocytes become cancerous, or malignant, these cells grow uncontrollably and aggressively invade surrounding healthy tissues. Melanoma may stay in the skin, but more often it spreads, or metastasizes, through the blood or lymph system to the bones and organs, including the brain, lungs, and liver. Melanoma sometimes occurs in an existing mole or other skin blemish such as a dysplastic nevus (pronounced dis-PLAS-tik NEE-vus), but it often develops in otherwise unmarked skin. In men, melanoma develops most often on the upper back, and in women it is usually seen on the legs, although it may occur anywhere.
Melanoma is most common in people with fair skin and those who have a large number of moles, although it affects people of all races. Melanoma usually resembles a flat brown or black mole with an irregular, uneven border. Usually the blemish is not symmetrical. Melanoma lesions are often 6 millimeters (0.24 inches) or more in diameter. Any change in the shape, size, or color of a mole may indicate melanoma. A melanoma may be lumpy or rounded, change color, become crusty, ooze, or bleed.
There are numerous risk factors for melanoma. Excessive exposure to the sun is but one. But as you already know, melanomas occur in people who don’t spend time in the sun and are often seen on parts of the body that aren’t much exposed to the sun. Some of the nonradiation risk factors include the following:
• Heredity. If two or more of your family members have had a melanoma, you are much more likely to get one.
• Dysplastic nevi. These kinds of moles are more likely than normal moles to become melanomas.
• Many normal moles. If you have more than fifty moles on your body, this increases your chance of developing a melanoma because melanoma usually begins in the melanocytes of a normal mole.
• Weakened immune system. People whose immune system is weakened by certain other forms of cancer, certain drugs (such as cyclosporine) prescribed after organ transplants, or AIDS have a greater risk of developing melanoma.
• Previous melanoma. People who have already had a melanoma are at a high risk of developing another.
• Defective DNA repair system. People with the extremely rare skin disorder xeroderma pigmentosum (XP), described above, tend to have a defective DNA repair system and are at a higher risk of melanoma.
This brings us to the relationship between sun exposure and melanoma.
Normal sun exposure of the type that builds a tan doesn’t seem to be responsible for melanoma. Numerous studies pioneered by Drs. Cedric and Frank Garland, and Dr. Ed Gorham show that people who work outside have a lower incidence of melanoma than do people who work inside. Despite the fact that the United States was for several centuries a rural, agriculture-based nation whose citizens were outdoors much of the time, melanoma was so rare then that separate statistics weren’t kept on the disease until the 1950s.
So what’s going on? Why are melanoma rates increasing rapidly and have been doing so at a rate of 2 percent per year for more than thirty years? The answer is surprising—it may be because people are exposed to sunshine less during their working hours. Sunburns are a risk factor for melanoma. Because people these days—young and old alike—work outside less and therefore get less regular sun exposure than did previous generations, they are at increased risk of getting sunburned rather than suntanned when they do go out in the sun.
Another explanation for the rise in melanoma may surprise you even more:
the use of sunscreens starting in the 1950s. Before any of you heave your sunscreen into the trash, let me make the point that the type of sunscreen that probably contributed to the rise of melanoma is the kind that protected only against UVB radiation. As I detailed earlier, until the late 1990s, UVB-protection-only sunscreen was all that was available, and this had been the case since the 1940s. In the past few years, this type of sunscreen has been phased out in favor of sunscreens that protect against both UVB and UVA radiation.
Recall when I explained that sunscreen was first developed to enable people to avoid sunburn and thereby spend more time in the sun, either tanning or participating in outdoor recreation. Although these early sunscreens protected against the burning radiation of UVB, they did not protect against UVA radiation. At the time, UVA radiation was not thought to be harmful because it didn’t cause the obvious symptoms of sunburn. The increase in melanoma may be partially due to the fact that by protecting people against UVB, UVB-only sunscreen use enabled people to receive massive doses of UVA, which penetrates deep into the epidermis and dermis to damage the melanocytes and cause immune tolerance. We now know that UVA is partially responsible for melanoma, and the cosmeceutical industry has introduced sunscreens that protect
against both UVB and UVA radiation—so-called broad-spectrum sunscreens.
You should always use broad-spectrum sunscreen when trying to prevent sunburn. Look for sunscreens that clearly state they protect against both UVA and UVB, because discrepancies still exist in the market. Be aware, too, that no sunscreen can fully protect you.
With all this in mind, it is important to repeat that melanoma usually occurs in parts of the body that are not exposed to the sun and is seen in people who do not spend much time in the sun, two factors that indicate that sun exposure may not be a risk factor for this serious disease.