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Archive for June, 2010

Sunlight and melanoma: doctors offer differing views on controversial topic

Posted by D3forU on June 26, 2010

Sunlight and melanoma: doctors offer differing views on controversial topic.

(Special Report) Dermatology Times May , 2008 National report —

Dermatology Times asks two leading dermatologists whether sun exposure triggers melanoma.

Bernard Ackerman. M.D., director emeritus of the Ackerman Academy of Dermatopathology in New York, and a professor of dermatology and pathology at Downstate University Medical Center in Brooklyn, N.Y., has challenged prevailing views about the relationship between sunlight and the development of melanoma.

James Spencer, M.D., a faculty member at Mount Sinai Hospital in New York who currently practices dermatology in Florida, has been actively involved in sun awareness campaigns and campaigns against indoor tanning, with the support of the American Academy of Dermatology.

Q: What is the cause of melanoma?

A: Dr. Ackerman: “I think that melanoma is genetically determined, and that the sun is not responsible for it. Sunscreens don’t prevent melanoma, and the sun itself does not cause melanoma.”

A: Dr. Spencer: “The best evidence is that melanoma is a result of sunlight exposure. The epidemiologic evidence is strong, including the observation of a dramatic increase in incidence as fair-skinned, sun-sensitive peoples move closer to the equator.

Certainly, the occurrence of melanoma in patients with xeroderma pigmentosum is compelling. These patients cannot repair ultraviolet-induced DNA damage and have a remarkable increase in skin cancer incidence, including melanoma.”

Q: Does early or intense I sun exposure play a role in the progression of this disease?

A: Dr. Ackerman: “The sun plays no role at all in initiating the disease. When melanoma occurs in Asians and Africans, it occurs on the soles, the palms, the nail unit and the mucous membranes. It is obvious that melanoma in Asians and African s is not induced by the sun. When the sun truly is responsible for lesions in skin of any color, there are two principles involved that are inviolate: The lesions only occur on sun-exposed sites and are multiple. There are several examples such as freckles, solar lentigines and solar keratoses. But when you look at melanoma, even in Caucasians. it occurs mostly on covered sites, not sun-exposed sites. In 90-plus percent of cases, melanoma is solitary.”

A: Dr. Spencer: “We are dependent on epidemiological studies for the data, and the epidemiological studies do suggest that early and intense exposure plays the great role. But the studies also suggest that adult exposure plays a role.”

Q: Can tanning booth exposure promote the development of melanoma?

A Dr. Ackerman: “There is no compelling evidence that sun tan parlors have induced a single melanoma. The industry should be controlled if, in fact. the industry induces cancers, but that should be predicated on evidence and not on accusation.”

Dr. Spencer: “We don’t have direct experimental evidence. The biggest and most recent studies that compare subjects to age-matched controls suggest that indoor tanning is an independent risk factor for the development of melanoma. No study has ever shown indoor tanners get less melanoma, as the vitamin D advocates would suggest.”

Q: Why is the incidence of melanoma wildly different in various parts of the world, with the highest incidence in sunny climates?

A: Dr. Ackerman: “This comes from epidemiological data. Some studies have shown that the closer to the equator, the higher the incidence of melanoma. That doesn’t mean the sun is responsible for the higher incidence. The Irish in Australia have a high incidence of melanoma, but so do the Irish in Ireland.”

A: Dr. Spencer: “If you compare people of English heritage in Australia to people of English heritage in England, the two groups are relatively genetically homogeneous. But Australia has the highest melanoma rate in the world. That is on e of the most compelling arguments that sun exposure causes melanoma.”

Q: Why does the location of the average melanoma differ from that of two sun-induced tumors, BCC and SCC, namely on the head and neck region?

A: Dr. Ackerman: “Solar keratoses occur only on sunexposed sites. It is established that the sun is the cause of solar keratoses. The opposite is true for melanoma. As for basal cell carcinoma, the evidence is far from compelling that the sun is the major cause of it.”

A: Dr. Spencer: “One explanation is that it’s a result of intermittent highest-intensity exposure. You are more likely to get sunburned on your back. You don’t expose your back much, and then men take their shirts off at the beach, and that is where the burn occurs. The back has the highest incidence of melanoma in men; the legs. in women. Another possibility is that the effects of the sun are systemic and not limited to areas of direct exposure. For example. ultraviolet light-inducing immunosuppression is systemic. Lastly, I think it will turn out that melanoma, like most things, is multifactorial, but ultraviolet radiation seems to be the major factor.”

Q: Why has the incidence of melanoma increased so dramatically in the past two decades?

A: Dr. Ackerman: “There has been no increase in the incidence of melanoma. An indication of that are the most recent figures from the American Cancer Society. We have far better surveillance and far better criteria clinically and histopathologically for diagnosis of melanoma. There has never been a true epidemic of a malignant neoplasm, and melanoma is no exception.”

A: Dr. Spencer: “There are two explanations. One explanation is that it’s overdiagnosed. The literature does not support that view. The other explanation is that susceptible populations are more exposed to ultraviolet light. In decades past, exposure to ultraviolet light was limited. Now people go to Jamaica or Hawaii for a vacation during winter break. They often burn their skin while on vacation.”

Q: Do severely dysplastic nevi progress to melanoma?

A: Dr. Ackerman: “The mantra at the Clark school is that the dysplastic nevus is the greatest risk factor for melanoma. How can that be if the sun is the cause of it? Most melanomas in Caucasians (85 percent) do not begin in association with a nevus of any kind. Moreover, the so-called dysplastic nevus actually is several different kinds of nevi.”

A: Dr. Spencer: “Dysplastic nevi are a marker of the high-risk individual. but I don’t think the evidence is there that they are literal precursors of melanoma. The kind of person who makes dysplastic nevi is the kind of person who makes melanoma, but dysplastic nevi are not pre-melanomas.”

Q: Do you believe sunlight exposure is necessary for vitamin D production, or can it be obtained more safely from multivitamin tablets?

A: Dr. Ackerman: “I think the best way to get vitamin D is through sun exposure. Vitamin D plays a role in immune responses and in prevention of cancer. It may prove to be that vitamin D that one gets through the sun is really crucial for a healthy life. I can’t believe that the artificial (multi-vitamin) is better than natural. If you burn, stay out of the sun. If you tan, a certain amount of daily sun is advantageous to your health.”

A: Dr. Spencer: “You can easily get the recommended daily allowance of vitamin D with a normal diet. Some people feel mega doses of vitamin D improve health. It would be hard to get that from your diet. The answer is to take a vitamin pill. You don’t need to jeopardize your health with intentional tanning to get vitamin D.”

BY LOUISE GAGNON STAFF CORRESPONDENT

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Sunlight and Artificial Ultraviolet B Radiation

Posted by D3forU on June 16, 2010

by Dr Michael Holick

Sensible sun exposure can provide an adequate amount of vitamin D3, which is stored in body fat and released during the winter, when vitamin D3 cannot be produced.7, 15, 85, 108, 109, 110

Exposure of arms and legs for 5 to 30 minutes (depending on time of day, season, latitude, and skin pigmentation) between the hours of 10 a.m. and 3 p.m. twice a week is often adequate. 2, 7, 108, 109, 110

Exposure to one minimal erythemal dose while wearing only a bathing suit is equivalent to ingestion of approximately 20,000 IU of vitamin D2. 1, 2, 7, 85

The skin has a great capacity to make vitamin D3, even in the elderly, to reduce the risk of fracture.109, 110, 111

Most tanning beds emit 2 to 6% ultraviolet B radiation and are a recommended source of vitamin D3 when used in moderation.111, 112, 113, 115

Tanners had robust levels of 25-hydroxyvitamin D (approximately 45 ng per milliliter [112 nmol per liter]) at the end of the winter and higher bone density as compared with nontanners (with levels of approximately 18 ng per milliliter [45 nmol per liter]). 112

For patients with fat malabsorption, exposure to a tanning bed for 30 to 50% of the time recommended for tanning (with sunscreen on the face) is an excellent means of treating and preventing vitamin D deficiency (Table 3). 113

This reduces the risk of skin cancers associated with ultraviolet B radiation.

http://www.uvadvantage.org/portals/0/pdf/NEJournalofMedicine.pdf

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Brighten Up Your Day with Mother Nature’s Sunshine

Posted by D3forU on June 14, 2010

Lack of sunshine can create up to 20 Times (2000%) the risk of many internal cancers, and actually increase the risk of melanoma. Many more lives are lost because of insufficient solar UVB and Vitamin D than from skin cancer and melanoma.51,115-117

http://xr.com/GrantVitDcanc

CDC Melanoma Mortality 30 years 1975-2005

CDC 30 Year Melanoma Mortality 1975-2005

Melanoma Mortality Rates have remained steady for Women for the past 30 years at a rate of 2/100,000 while Men have risen two-threefold in the same time frame. Women frequent tanning salons at a ratio of 4:1. shouldn’t the rate be reversed?

Indoor tanners have Vitamin D levels 90% higher than those who do not. They also have ~20% lowered Parathyroid (PTH) levels, and higher Bome Mass Density (BMD).

http://xr.com/TangVitD

SunScreen SALES vs Melanoma

Humans evolved under the sun. Mother Nature played a cruel joke in that the same UVB that produces vast amounts of Vitamin D in the skin can also burn and/or damage it with overexposure. Sunscreens have been in use for the past 40 years, and not surprisingly, by blocking Natures’ own protection, we may have caused many of the melanomas being seen.

Interestingly, the same sun that may cause melanoma may actually protect against the most serious cases.

A little bit of anything is usually good for us, but an overabundance may cause harm. Moderation is the key. Get regular sun exposure on as much body surface for a short period of time outdoors when you can, between the hours of 10A and 2P, when the sun is above 45°, typically between April and November at a line from Boston to Sacramento (40°N Lat).

If that’s not practical, Indoor tanning salons offer time controlled UV exposure that doesn’t vary with the time of day, season, cloud cover, ozone layer, or many other factors.

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Is the Sun Good for You?

Posted by D3forU on June 13, 2010

How do you feel about sunlight?

Does it cheer you up. Do you like to be tan? Does sun tan look good?

Of course we have to be aware of the possible risks and damages from sun, but we can’t be let to believe that sun doesn’t do anything good.

Sun is the reason we live! Because of sun this planet is alive! This is the reason you feel good about the Sun. Sun made all of us. For years we have been told to cover up in the sun to cut the risk of getting skin cancer.

But now it has come to light that sun is actually good for the body. Recent studies have shown that a sensible amount of UV light reduces your risk of several cancers and health conditions.

It’s all thanks to Vitamin D, which is made through our bodies through the action of UVB rays on our skin. Professor Michael Holick of Boston University School of Medicine is the author of “The UV Advantage” book. “We get about 90 to 95% of our vitamin D from the sun,” says Holick.

He advises people should get 5 to 15 minutes of sun exposure three times a week to boost vitamin D levels. Tanning controversy More recently, some researchers have advised that tanning in moderation may be healthier than is commonly believed.

Edward Giovannucci, professor of medicine and nutrition at Harvard states that according to his research, people who have sufficient vitamin D due to UV exposure, and other intake, may prevent 30 deaths for each one caused by skin cancer.

His research also suggests that diet accounts very little for vitamin D3 necessary for curbing cancer. Michael Holick, Boston professor of dermatology, claimed that moderate exposure to sunlight probably reduces risk to many forms of cancer, diabetes, seasonal affective disorder, and other diseases.

These researchers are vigorously opposed by most dermatologists, for example, Dr. Elewski, president of the American Academy of Dermatology, argued that minutes of exposure to sunlight can be dangerous, and that people can get all the vitamin D they need through supplements.

Large clinical studies have found vitamin D produced both through exposure to sunlight and through dietary supplements dramatically decreases cancer risk, and helps cancer recovery.

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Gene implicated in human pigment variation

Posted by D3forU on June 10, 2010

Ishani Ganguli

A pigmentation gene first identified in zebrafish helps explain skin color differences between human European and African populations, a new Science study shows. A derived variant of the slc24a5 gene, which is correlated with light skin color and differs from the ancestral allele by only one nucleotide, seems to have undergone strong natural selection in European populations.

While scientists had previously found pigmentation genes that contribute to variations within populations, said senior author Keith Cheng, “it’s been a complete mystery” as to what drives major variations in human skin color. “It’s remarkable that this difference in skin color that has historically been partly responsible for a great deal of problems in our civilization is due to this one nucleotide out of 3 billion,” Cheng told The Scientist.

“What these findings speak to is the molecular differences that explain differences in skin color. That is very different than what people refer to as race,” said Greg Barsh at Stanford University, who did not participate in this study. Cheng’s team at the Pennsylvania State University College of Medicine in Hershey was studying the golden mutation in zebrafish—characterized by lighter-colored stripes than the wild type—when the researchers noticed that the phenotypes were distinguished by differences in the number, size, and density of melanosomes (melanin-producing granules) in the stripes.

“That was to our amazement,” Cheng told The Scientist, “because those types of changes are the same types of changes that we see between darker and lighter human beings.” Using positional cloning, the researchers isolated slc24a5 as the gene responsible for the golden phenotype in zebrafish and pinpointed its mutation as a stop codon that truncates the translated protein by 40%.

BLAST searches confirmed their suspicion that this zebrafish gene has a closely related counterpart not only in many other vertebrates but in humans, with 69% sequence homology. When the researchers injected human slc24a5 mRNA into golden zebrafish embryos, the wild type stripes were restored.

The results showed that the gene’s function has been conserved over vertebrate evolution, what Barsh called a perfect demonstration “that nature doesn’t reinvent the wheel.”

The scientists found slc24a5 to be highly expressed in the melanin-producing cells of both zebrafish and mammals. In an effort to determine what role the previously uncharacterized protein might play in pigmentation, the team localized it to intracellular, membrane-bound structures—likely melanosomes.

Further observations based on structure and related proteins led them to conclude that SLC24A5 may be involved in organellar calcium uptake, though Cheng said that much remains to be determined about the protein’s mechanism.

The team then turned to genomics to see how the protein might be important in humans. When they consulted the recently published HapMap, they discovered that there were two primary alleles, varying at only one locus. And while nearly all East Asian and African genomes had a site containing alanine, the ancestral allele shared by other vertebrates, 99% of the Europeans had threonine, representing a derived allele.

This striking bifurcation, coupled with a marked decrease in heterozygosity in nearby genes within the European genomes, led the group to conclude that the threonine variant has been the target of strong natural or sexual selection in European populations.

As a functional test of their findings, Cheng’s group was able to correlate slc24a5 genotype to skin color—measured by reflectance—in 308 individuals with mixed African and European ancestry. Homozygotes for each allele tended to be either light-skinned or dark-skinned, respectively, with heterozygotes falling in the middle.

The researchers determined that the threonine (skin-lightening) allele is partially dominant to the alanine allele, and that the gene accounts for between 25% and 38% of European-African differences in melanin levels. While Cheng said they have “identified the probable largest impact gene explaining the difference between Europeans and Africans,” they are curious about other genes in play that would explain pigmentation differences between East Asian and African populations.

On a biochemical level, Barsh said, other proteins that have been implicated in pigmentation seem to have similar biochemical mechanisms to SLC24A5, highlighting the need to determine how SLC24A5 interacts with these proteins and with ones that have yet to be identified.

Cheng’s findings are consistent with what he said is the prevailing evolutionary wisdom: melanin blocks UV light, and while darker skin is advantageous under strong sunlight because it reduces the destructive effects of UV rays, lighter skin is adaptive in less sunny climates since it allows more sunlight absorption for the production of vitamin D.

References

1.  http://www.sciencemag.org

2.  http://www.the-scientist.com/2005/10/24/16/1

3.  http://www.hmc.psu.edu/pathology/residency/experimental/cheng.htm

4.  http://med.stanford.edu/profiles/Gregory_Barsh/

5.  http://www.the-scientist.com/news/20051026/01

link to Genome Biology

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