8/21/09 The truth about tanning and cancer research from The International Agency for Research on Cancer- World Health Organization In early August, 2009, a story about the dangers of tanning beds based on an IARC report, stated tanning beds have been reclassified as a grade 1 carcinogen. This story, like so many other stories on this new report, went overboard in the characterization of the relative-risk of tanning beds. As proof, I direct you to recent comments made by Vincent Cogliano, head of the IARC Monographs program at the International Agency for Research on Cancer-- where the World Health Organization-sanction group's debate originated – where he admits the results on which many of the conclusions are based are "limited." He goes on to say that the reason the report highlighted tanning beds had nothing to do with the level of risk they present, but rather the rhetorical focus they wanted their report to have. He also admitted that a number of the studies in the report included European fair haired subjects (skin type I) who are naturally susceptible to melanoma. Please note, from the Whig Standard in Ontario, CA (http://www.thewhig.com/ArticleDisplay.aspx?e=1701381): "Most (of the 2009 position) is based on the 2006 working group report and we do not have the gold standard, double-blind type of research to work with," Cogliano said. When asked why tanning beds were made such a focus of this WHO/IARC position, Cogliano said: "It was our 100th year and we wanted to pick something that looked at the past and into the future. UV radiation and the sun is (from the) past, tanning beds (are linked to) the future." The IARC research working group of international experts on skin cancer and UV radiation conducted a "systemic review" of all literature and studies regarding UV radiation and skin cancer and sunbed use. The working group's review looked at 23 previously published studies that investigated the association between indoor tanning and melanoma risk in fair- skinned populations. But the studies included only fair-skinned people, who have been long proven to be more susceptible to melanoma. Cogliano said the use of fair-haired study subjects was natural since they are the ones who get the disease most often. Data from 19 of the studies was then used to determine that the relative risk associated with use of indoor tanning facilities could be projected to be 14% higher compared to those who never use indoor tanning facilities, in the test subjects reviewed. None of these was double-blind, placebo-controlled studies, as they simply looked back over other studies and tried as best they could to amalgamate all the results. When the analysis was restricted to just 10 specially selected studies, the risk of developing melanoma was projected to be 17% higher for those who engage indoor tanning than for people who did not. "The evidence gathered on sunbed use and skin cancer so far is limited by problems with the characterization of exposure and the potential confounding effect of sun exposure," the group's report said. Consider this information next time a story grossly exaggerates the dangers of tanning bed use. And the way the media, and the authors of the report, mischaracterized and exaggerated the dangers of tanning beds is truly irresponsible and has been very damaging to thousands of small business owners. We will continue to promote moderate and responsible use of our products so that our customers have access to all the benefits that UV light provides. With respect, John Overstreet Executive Director Indoor Tanning Association Also on the list with tanning beds: Besides the use of tanning beds, among other substances, behaviours, chemical combinations and drugs the World Health Organization ranks as Group 1 include: * Ethanol in alcoholic beverages, * Alcoholic beverages; * Solar radiation; the Sun * Wood dust; * Boot and shoe manufacturing; * Furniture and cabinet making; * Iron and steel founding; * Paving and roofing with coal-tar pitch; * Occupational exposure as a painter; * Rubber industry; * Estrogen-progestogen menopausal therapy (combined); * Estrogen-progestogen oral contraceptives (combined); * Estrogen therapy, postmenopausal; * Oral contraceptives; * Combined estrogen-progestogen oral contraceptives; * Coal-tar pitches; * Salted fish (Chinese-style). - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - Melanoma Myth is Based on F.E.A.R. by Patricia E. Reykdal and Donald L. Smith 07/29/2009 Make no mistake about it, cutaneous malignant melanoma (CMM) is not caused by exposure to ultraviolet radiation (UVR). Rather, the normal, natural and involuntary reaction to UVR exposure results in a signal sent by keratinocytes to the melanocytes, telling them to produce melanin that will be oxidized by UVA wavelengths to create a protective cap (i.e., a tan) that will protect the keratinocyte cells’ DNA from damage. But, if the UVR exposure is so intense or lasts so long that the existing melanocytes are not able to keep up with the demand for melanin, the following sequence takes place. 1. A signal is sent to the “mother” melanocyte cell, telling it to detach from the basement membrane, withdraw from the 36 keratinocytes in its epidermal melanin unit (EMU) and divide in order to form a new “daughter” melanocyte cell. 2. A signal is sent to the mother melanocyte cell, telling it to stop dividing. 3. A signal is sent to both the mother and daughter melanocyte cells, telling them to reattach themselves to the basement membrane, connect with 34 to 36 keratinocytes (in order to form two new EMUs) and to begin producing the melanin necessary to protect the nucleus of the keratinocytes from UVR damage. For reasons not presently understood, the signal telling the mother melanocyte cell to quit dividing sometimes gets scrambled, and the melanocyte continues dividing. When any cell loses the ability to quit dividing, it becomes a cancer. When the rapidly dividing (and out-of-control) cell is a melanocyte, the cancer formed is CMM. As you can see, the only link between UVR and CMM is a coincidental correlation—not a causal correlation. The failure of the public to understand this important distinction has made it possible for the dermatology community, the sunscreen industry and the various melanoma-related organizations to use F.E. A.R. (False Emanations Appearing Real) to promote their personal and professional interests. Just consider the following “inconvenient facts” that these groups choose to ignore even though they know, or reasonably ought to know, that the facts prove UVR is not the cause of CMM. There is no molecular signature. Several recent studies have confirmed the fact that there is a distinct and repeatable molecular signature showing that UVR overexposure can damage the DNA of keratinocytes which, in turn, can lead to basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). However, these same studies also confirm that there is no molecular signature showing that UVR damages the DNA of melanocytes. Sunscreens do not prevent CMM. If UVR was truly the cause of CMM, it would logically follow that sunscreen use over the past three decades should have prevented the increase in the incidence of CMM. But, study after study has shown that the use of sunscreen does not prevent the development of any form of skin cancer, including CMM. Authors’ Note: So, how did the dermatology community, the sunscreen industry and the various melanoma-related organizations react to this information? First, they blamed the messenger and attacked the authors of the studies. When this approach failed due to the sheer number of studies available, they next claimed that it was the failure of the public to apply enough sunscreen to prevent CMM. Whenthis approach also failed, the groups switched to their latest defense—saying that the longer UVA wavelengths are responsible for causing CMM and sunscreen did not previously contain UVA filters. If you study the timing, you will find that the decision to blame UVA coincides with the introduction of products containing UVA filters. Lucky coincidence? We don’t think so. And, of course, these groups have failed to acknowledge the several authors that have published scientific papers showing that UVA wavelengths do not cause CMM. CMM occurs most often on parts of the body not exposed to UVR. Researchers found that UVR exposure to one arm caused the number of melanocytes to increase in that arm (as expected) and also in the other arm, which was shielded from exposure (not expected). Further experiments showed that UVR exposure to one part of the body results in an increase in the number of melanocytes in the skin of the entire body. This explains how a melanocyte dividing in a part of the body not exposed to sunlight can be affected by a scrambled signal and become a CMM. This also explains why intense, intermittent UVR overexposure is more likely to result in a CMM—the person has more melanocytes dividing at the same time in an attempt to supply the necessary melanin. There is no world-wide epidemic of CMM. In an article titled, “Melanoma Epidemic: A Midsummer Night’s Dream?,” the authors concluded that the large increase in reported incidence of CMM is likely due to diagnostic drift, which classifies benign lesions as stage 1 melanoma. In other words, the so-called CMM epidemic is the result of the rapid increase in the number of dermatologists who are now removing a large number of lesions that were previously classified as benign and calling them a CMM. OK, now let’s tie all of this information together, using the following three examples. (In each example, the individuals work indoors, live in Boston and take a two-week summer vacation in a high-intensity UVR environment.) •Example 1: The individual utilizes a tanning salon on a regular basis in order to maintain a dark tan year-round. •Example 2: The individual only utilizes a tanning salon a few times in order to develop a “base tan” before going on the two-week holiday. •Example 3: The individual does not develop or maintain a tan. Some questions: Which individual will have the most “natural” protection from UVR damage? Which individual will be required to use more “artificial” sunscreen? Which individual will most likely have the highest vitamin D level? Obviously, the individual in Example 1 will have the most natural protection from UVR damage on the first day of the vacation and will only have to use a sunscreen when outside for a long period of time. Equally obvious is the fact that this individual is not likely to sunburn and is likely to have the highest blood level of vitamin D. Meanwhile, the individual in Example 2 will have some protection from UVR damage on the first day of the vacation, but will have to use sunscreen sooner than the individual in the first example. Similarly, this individual is likely to have a higher vitamin D level than the Example 3 individual but not as high as the Example 1 individual. The individual in Example 3 will only have the protection from UVR damage afforded by his or her constitutive (natural) pigmentation on the first day of the vacation and should start using a sunscreen immediately in order to prevent UVR damage. If this individual does not apply an adequate amount of sunscreen on day one (and continually reapply it), the stage is set for skin damage—the keratinocytes will signal the melanocytes to produce more and more melanin, and when the existing melanocytes cannot supply enough to keep up, they will start dividing. And, sooner or later, the signal to one of the “mother” melanocyte cells to stop dividing will get scrambled and result in a future CMM. Moreover, the overexposure will inevitably result in a painful sunburn. The bottom line is that, when UVR strikes the skin, a natural reaction occurs—unfortunately, that reaction has led to the erroneous belief that UVR causes CMM when, in actuality, there is only a coincidental relationship. Frankly, it is time to quit blaming UVR for causing CMM and start searching for the reason that the stop-dividing signal to the mother melanocyte gets scrambled. When the answer to that puzzle is found, we will be on the road to solving the CMM problem. The “Melanoma Epidemic” authors summed things nicely by stating that their finding indicated “ ... the need for a new direction in the search for the cause of melanoma” and for a “ ... re-evaluation in the role of ultraviolet radiation ... ” Patricia E. Reykdal and Donald L. Smith operate the Non-Ionizing Radiation Research Institute in Tucson, Ariz. They have written many articles promoting the benefits of controlled ultraviolet radiation exposure (CURE). You can e-mail comments or questions to reyksmith@aol.com. |


