This study talks about overexposure to UVB. But keep in mind that Vitamin D is synthesized by the body in the presence of ultraviolet B; and Vitamin D is the likeliest mechanism for a protective effect of sunlight .
It could also be a major factor that vitamin D synthesis could shut down completely during winter since it’s much darker-thats why I would take cod liver oil, or another source of Vitamin D during the winter instead of the summer/spring. Another factor is the omega-6 to omega-3 fat ratio, which I believe is contributing to this problem as well. In fact, Cancer Res 2000 Aug 1;60(15):4139-45 states:
“Epidemiological, experimental, and mechanistic data implicate omega-6 fat as stimulators and long-chain omega-3 fats as inhibitors of development and progression of a range of human cancers, including melanoma.”
Last year, the prestigious National Academy of Sciences published a comprehensive review showing that the omega 6:3 ratio was the key to preventing skin cancer development. An Australian study done ten years ago, showed a 40% reduction in melanoma for those who were eating fish. And this was without any attention to lowering omega-6 fats.
Not many people get enough omega 3 fatty acids either- since Omega-3 fats help to normalize skin lipids and prevent dehydration in the cells-and half of America is probably deficient in omega 3’s.
I would love to see some studies done on people who have skin cancer and their consumption of omega 3’s and Vitamin D. I don’t think anyone is saying that overexposure to the sun can’t set you up for skin cancer later in life- thats nothing new, since too much of anything can be bad for you.
If you optimize your Vitamin D levels and eat enough omega 3’s and less omega 6’s, I don’t see how 30 minutes or even an hour of sun exposure will cause skin cancer.
It could be sunburn in conjunction with excess omega-6 fats that can increase your risk of skin cancer.
That would be pure ignorance on their part then, because the sun does not cause skin cancer. Overexposure MAY cause skin cancer, but there are other factors that play into this as well.
Really? I would love to hear more form you on this. As I understand it, UVB radiation causes serious damage to DNA which is a significant trigger for cancer.
Here’s a quote from a pubmed article: [b]"It is well known that chronic exposure to ultraviolet (UV) radiation present in sunlight is responsible for the induction of most nonmelanoma skin cancer (NMSC) in humans.
Wavelengths in the UV-B (290?320 nm) region of the solar spectrum are absorbed into the skin, producing erythema, burns, and eventually skin cancer. NMSC is the most common type of human cancer.
Recent surveys indicate that around one million new cases of skin cancer are diagnosed each year in the United States, about 70% of which result from repeated exposure of the skin to sunlight. Laboratory studies have shown that UV-B region of the solar spectrum is responsible for this effect.
The first step in UV skin carcinogenesis involves the induction of DNA damage. Occasional mistakes during the repair of this damage leads to the incorporation of wrong bases into the genetic material. The DNA damage that is left unrepaired may also disrupt cellular processes by obstructing the DNA and RNA synthesizing machineries and introduce wrong bases into the DNA.
These types of mistakes often result in mutation leading to loss or inappropriate expression of affected genes. Recent studies indicate that genetic alterations in the p53 tumor suppressor gene play an important role in the development of skin cancer.
The p53 protein is also involved in programmed cell death (apoptosis), and it has been proposed that p53 serves as a ?guardian of the genome? by aiding DNA repair or causing elimination of cells with excessive DNA damage. Unrepaired photoproducts in the p53 gene are transformed into mutations thereby initiating the process of carcinogenesis.
Following repeated exposures to UV, keratinocytes carrying p53 mutations acquire a growth advantage by virtue of their increased resistance to apoptosis. Recent studies have shown that UV-B damaged keratinocytes (sunburn cells) are eliminated by Fas/Fas-ligand interaction and that this pathway is dysregulated during UV skin carcinogenesis resulting in accumulation of p53 mutations in DNA damaged keratinocytes.
These results demonstrate a link between p53 pathway and Fas/Fas-ligand pathway and that dysregulation of both pathways can lead to the pathogenesis of UV-induced skin cancer."[/b] - J Biomed Biotechnol. 2001; 1(2): 49.