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The melanoma epidemic

melanoma2The melanoma epidemic

With skin cancer rates quadrupling in the last 40 years, patient education and a daily prevention strategy could help to slow the incidence of malignant melanoma, write Dr Carl Thornfeldt and Dr Mervyn Patterson

 

At the age of 16, CB was a vibrant, champion track star when she went to spend a summer in California with her grandparents. As she dove into the swimming pool one day, her grandfather noticed a crusted black spot on her back. Her grandparents immediately called my office to arrange an appointment and flew her several hundred miles to see me.

The spot turned out to be a malignant melanoma (MM) skin cancer, 0.25mm thick. Despite being a young, healthy athlete with a university track scholarship prior to her diagnoses, after two radical surgical procedures including chemotherapy treatment, CB died before her 18th birthday from metastatic melanoma.

In 2010, around 12,800 people in the UK were diagnosed with malignant melanoma and in 2011, there were 2,209 deaths from the cancer. Melanoma is the fifth most common cancer in the UK, but lies 18th in the rankings for deaths from cancer reflecting high survival from the disease.

 

Melanoma incidence

Incidence rates have more than quadrupled since the mid-1970s. Age distribution differs from other cancers—there is a relatively high incidence in younger people—but 45% of cases are still diagnosed in the over-65s. The European age-standardised incident rates for males are significantly higher in Wales compared with England, Scotland and Northern Ireland. There is no such variation between the countries for females.

Malignant melanoma incidence in the UK is strongly inversely related to deprivation. It is one of the few cancers where incidence rates are lower for more deprived men and women and there is a clear trend of decreasing rates from the least to the most deprived. Lifetime risk of developing malignant melanoma is one in 55 for men and one in 56 for women.

The mortality rate per 100,000 is 2.9% in Wales, 2.6% in England, 2.4% in Scotland and 2% in Northern Ireland. Survival for melanoma is improving—in men, the five year age-standardised relative survival for malignant melanoma in England increased from 46% during the early 1970s to 84% between 2005–2009. In women, five year survival increased from 65% to 92% over the same time periods, respectively.

If lymph nodes are present and the MM thickness exceeds 4.0mm, the five-year survival rate drops to 40%. The death rate in darker skinned minorities is 250% higher than in Caucasians because 70% of those lesions involve palms, soles, genitalia and mucosal surfaces. When found in these sites, MM metastasises when the thickness of the lesion is smaller.

melanoma3When MM is discovered in Caucasians, 12% has already metastasised to other parts of the body while in African-Americans, 26.4% has metastasised and in Latinos, 17.6%. Only 0.5% of MM afflicts African-Americans and 3.1% afflicts Latinos.

One-third of those who survive a MM diagnosis will develop a second cancer, with another melanoma occurring in one in five melanoma survivors. Secondary cancers occurring to a greater degree include lymphoma, breast, thyroid, basal cell and squamous cell carcinomas.

The eleven major risk factors for MM each increase the risk by at least 200%. The highest risk factor increases MM to nearly 1000%. The risk of a second MM in one already afflicted has the greater risk of 6.5-fold.

Other factors include fair skin type (Fitzpatrick I), red hair and blue eyes, history of another type of skin cancer and having a sibling affected with a melanoma. If an individual experiences two or more blistering sunburns in childhood or uses a tanning bed—even only once—the risk of MM is doubled or higher.

 

Moles

There is a relationship between MM and nevi (moles), which are pigment cell growths. One to five atypical, or dysplastic, nevi increase melanoma risk by 3.8 times. Six or greater atypical nevi increase risk by 6.3. Twenty-five or greater number of even normal-looking nevi increase MM risk by 4.4 times and 100 or more increases the risk by 9.8 times.

It has been found microscopically that 22–50% of MMs have nevus cells indicating they arose in nevi. The nevus, also known as the “ugly duckling”, is the most sensitive marker for a risk of being an MM.

Invisible UVB induces nonmelanoma basal cell and squamous cell skin cancers. UVA not only induces wrinkles, but suppresses protective immunity, thereby increasing all types of skin cancers and it especially activates MM. Both UVA and UVB are linked to DNA damage and cell mutations even before a visible redness (erythema) or tan appears.

It is imperative to note that tanned skin is injured skin. In other words, there is no safe tan. In a convenience survey conducted on 100 random beachgoers in the summer of 2007, 87% of those polled believed that skin cancer, including MM, is linked to tanning. The study also noted that 81% of those asked still believe that tanned skin looks better than pale skin.

The Sun Exposure and Teen Study conducted by the American Academy of Dermatology reported in 2008 that 63% of teens believe they look better with a tan. One-third of teen respondents claimed to “always” use sun block, with nearly the same number of teens declaring that they “never” use sun block.

It’s not just on sunny, summer days that sunscreen application is needed. UVA rays penetrate though clouds and windows and are reflected off concrete, tarmac, snow and grass. These rays are present from sun up to sun down, all year round.

 

Tanning beds

Indoor tanning beds, also referred to as “fake-bakes” or “cancer-in-a-can” in the US, are considered the new nicotine—both the World Health Organization and the US Department of Health and Human Services designated UVA and UVB as proven carcinogens, equal to tobacco smoke.

Seventy-one percent of tanning salon patrons are females, aged between 16–29 years old. About one-fifith of American females have admitted to using a tanning bed, with a third claiming they use it to medicate anxiety and depression.

Additionally, about one-third of people who use tanning beds develop a psychological and psychiatric dependency, or addiction, to tanning. The majority of those suffer withdrawal symptoms when tanning is stopped. In my practice, only about 20% of melanoma patients who were using tanning beds prior to their diagnosis will actually stop this practice.

melanoma4The tanning bed industry touts “safer rays” in tanning beds, but any tan is a sign of damage to the skin. It was published in 2003 that 95% of tanning customers received more than the recommended dose of UV radiation, after studying people attending 50 tanning facilities. Tanning beds can expose an individual to four times the amount of UVA and two times the amount of UVB as a similar period of sunlight exposure.

We do not feel a sensation of the UVA rays on our skin, but they contribute most to skin ageing and skin cancer. UVA rays inhibit the function of the surveillance cells (Langerhans cells) which detect damaged cells and send white blood cells to destroy the damaged cells, usually before they move from premalignant dysplastic cells into cancer cells. These UV wavelengths also damage the protective skin barrier, while UVL and visible light stimulate skin barrier thickening to increase protection. These wavelengths are absent in tanning beds.

The table to the right lists the eight new criteria to diagnose MM, which have an accuracy rate of around 90%. It is especially effective in diagnosing early, thin MM that are considered to be the most curable. The previous A-B-C-D-E criteria allowed the MM diagnosis in about two-thirds of patients but many were advanced when these criteria were met.

A dermoscope is the dermatologist’s new weapon in the fight against MM. It is a hand-held cross-polarising microscope that increases accuracy in finding these cancers and their precursors by 82% for a trained user.

 

melanoma5Melanoma prevention

There are four components for an effective MM prevention strategy, beginning with daily use of sunscreen as the first line of defence.

Sunscreen use is as important as brushing your teeth. SPF 30 or higher is proven to reduce the number of MMs, premelanoma dysplastic nevi, actinic keratoses and squamous cell carcinomas. Men over the age of 60 report the lowest usage of sunscreen, yet have the highest incidence of MM. In this demographic, the rate of melanoma is increasing so fast that a man of this age diagnosed with a head or neck melanoma has twice the death rate of other demographics.

All colours of skin, regardless of race, should be using sunscreen. Naturally darker Fitzpatrick types have a lower incidence of skin cancer, but when MM is discovered in darker skin it is more advanced than on lighter skin, producing 2.5 times higher rates of death.

Sunscreen protection is measured by SPF for UVB and UPF for UVA. SPF is a multiple of the time UVB needs to induce skin erythema. For example, if one develops visible redness in five minutes of sun exposure without wearing sunscreen, a SPF 50 will provide 50 times five minutes of protection, or 250 minutes. SPF is not a percentage of blockade of the sun’s rays.

UPF is measured on a one to four star system, based on multiple criteria; including prolonging time for skin to increase pigmentation and the average, or critical, wavelength blockaded by the sunscreen. In order to be considered “broad-spectrum,” a sunscreen must have an SPF of at least 30 with UPF of three-stars, according to the US Federal Drug Administration (FDA). Only four ingredients are FDA-approved for broad-spectrum designation, including zinc oxide, titanium dioxide, Avobenzone (Parsol 1789) and Mexoryl SX (ecamsule), which are all available worldwide.

A clinical study published in 2011 showed that six or more anti-inflammatory and antioxidant ingredients added to marketed sunscreens do provide increased photo protection, while one to three added antioxidant ingredients show no increase photo protection.

 

Sunscreen application

It is important to keep in mind that the applied amount, or dose, of sunscreen to the protection ratio of sunscreen (SPF) is an exponential relationship. This means that the amount of sunscreen applied by the average person that has an SPF 16 actually provides a sun protection factor of two, while SPF 33 provides 4.4 protection factor.

So it is best to use SPF with 50 or higher, that contains multiple anti-inflammatory ingredients. Examples of sunscreens that meet these criteria include Banana Boat SPF115, Neutrogena Full Spectrum SPF100, Aveeno for Babies SPF60, Epionce Ultra Shield Lotion SPF50 and Thinksport Livestrong SPF50.

Sunscreens that maintain the labeled protection factor after 80 minutes’ submersion in a whirlpool are considered very water resistant, to which Epionce Ultra Shield Lotion SPF50 and Livestrong SPF50 comply. Regular usage of an SPF 30 or higher reduces the incidence of premalignant actinic keratoses and atypical nevi, as well as squamous cell carcinoma.

For best protection, apply sunscreen twice in the morning to cool, clean, dry skin, waiting at least 30 minutes between applications and at least 30 minutes prior to going outside, as recommended by worldwide dermatologist organisations. Sunscreen is always the last step before foundation make up, but applied after a barrier repair skin care product since sunscreen ingredients bind to the stratum corneum. This binding is prevented if one is already perspiring. Wearing make up with SPF does not provide adequate coverage, but it does, nonetheless, provide an extra layer of protection.

 

Skin barrier

The second line of defence against MM is a healthy, well-functioning skin barrier. The two major skin abnormalities known to induce skin cancer and visible ageing, as well as many common skin diseases, include:

Compromised stratum corneum barrier function due to excessive dryness, cold, wind, or having fair, sensitive skin, or suffering from hay fever and/or asthma.

Activation of damaging chronic inflammation due to exposure to pollutants, exfoliating skin care products and preservatives.

Truly healthy skin is characterised by optimum barrier function without chronic inflammation. A normal skin barrier is necessary to maximise epidermal defence. When the skin is injured, for example through sunburn or tanning, the first response after erythema is to increase the synthesis of three groups of specific oils (lipids) to repair the skin barrier permeability function. These three key physiological lipids include cholesterol, free fatty acids and ceramide.

The next event required for repair is to speed up the proliferation of epidermal cells. Chemical peels and microdermabrasion both accelerate this cell turnover.

The third line of defence against MM includes additional adjuncts, such as wearing clothing such as a UPF-rated cloth hat with a 3–5” brim, UV blocking sunglasses and/or sunshades, and UPF protective clothing. Mineral makeup also provides additional sun defence, as do sun protective laundry additives.

The fourth, and last, line of defence includes a healthy diet, incorporating anti-inflammatory foods, eating low-fat, low-sugar and low starch, with six or more daily servings of fruits and vegetables, oily fish and photoprotective foods. Green tea, pomegranate, grape seed and chocolate containing more than 55% cocoa (not including milk or white chocolate) are also very beneficial. Photoprotective supplements include golden fern (polypodium leucotomos), quercetin and melatonin.

Skincare professionals are often asked about spray tans and self-tanning agents. These options can provide minimal protection, with the active ingredient in spray tanning solutions giving a SPF value of around two. This is a service that my office provides. Dyhydroxyacetone is safe unless inhaled into the lungs, so avoid enclosed spray tanning booths.

 

Education

Not all is lost when educating your clients about MM, since it is documented that education does have impact. A study conducted in Dallas and Houston, Texas, involved 210 junior high and high school students aged between 12 to 18 and tested their general knowledge of sun exposure and MM.

After the first exam was completed, the students were then provided with correct answers with detailed explanations for each test item. The participants were then given a second exam to measure the effect of the educational piece on future sun exposure practices. It was concluded that students between 12 to 15 years old were significantly more likely to change future behaviour after learning about skin cancer, including MM prevention.

Skin care professionals are in a life and death battle for clients with the scourge of malignant melanoma. It has been documented in Australia—the country with the highest incidence of MM per capita—that education and protection can slow the increasing incidence of this colour blind killer.

Skin care professionals must seize this incredible opportunity to educate their client population about the dangers of sun exposure, and the importance of protecting their skin with the four lines of defence daily. Additionally, we must try to shift the attitude to that of pale skin, rather than tanned skin, is the real look of healthy beauty.

Dr Carl Thornfeldt is a dermatologist and founder of Episciences, W: epionce.com

References

1. June K, Robinson, Kim J, Rosenbaum S, Ortiz S. “Indoor Tanning Knowledge, Attitudes, and Behavior Among Young Adults From 1988-2007.” Arch Dermatol. 2008;144(4):484-488.

2. “Skin and Aging,” December 2008. p12

3. Whitworth L. “Legislators combat melanoma, restrict teen tanning.” Journal of the National Cancer Institute, Vol. 98, No. 22, November 15, 2006.

4. Wang SQ, Osterwalder U, Jung K. “Ex vivo evaluation of radical sun protection factor in popular sunscreens with antioxidants.” J Amer Acad Dermatol, 2011;65(3):525-530.

5. Thornfeldt C, Bourne K. “The New Ideal in Skin Health: Separating Fact from Fiction.” Allured Books, Carol Stream, Illinois; 2010, p149.

6. Lucci A, Watts Citro H, Wilson L, Debakey M. “Assessment of knowledge of melanoma risk factors, prevention, and detection principles in Texas teenagers.” Presented at the Annual Meeting of the Association for Academic Surgery, Tampa, Florida, November 2–4, 2000.

Author: bodylanguage

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