Vitamin D3, Cancer, Sun Exposure, Sunscreen and Addiction. 4/10

An, telling statistic that may confirm that sunscreens may be more of an issue then we thought is there was a 77% increase in incidence of skin cancer between 1994 and 2014. 9 Is this increase a result of our false belief that sunscreen was protecting us when it may in fact as I lay out above put us at greater risk.

Statistics can lie but food for thought. If you’re interested in more facts about skin cancer the http://www.skincancer.org site is loaded with them. So how do we know that more research in the future will not find similar issues with the current chemicals used in sun screens?

We don’t know and again not to be a fear monger we need to educate ourselves. Ok enough on sunscreens as I really didn’t intend to go so deep into them, but it is much worse than I believed. Like I always told my children don’t come to me with a problem if you haven’t thought about a solution.

I will not do that to you. What is the solution? For one optimal dosing of vitamin D3 in mine and others experience, offers some protection. Anecdotally I and others have found that increased blood levels of vitamin D3 appear to reduce sun burn.

As I will go on to explain in this blog post series optimal blood levels of vitamin D3 may help prevent cancer. The rest of the solution is moderate sun exposure. Yes, some of you want to be out of doors under full sun exposure for prolonged periods of time. I don’t have a great answer for you. As they say buyer beware.

Back to how our body coordinates responds to vitamin D3, sunlight to effect cancer and in a bit how it effects addiction. Sunscreens reduces pro-opiomelanocortin (POMC) production which means among other things less melanin production.

Thus, less melanin found in the skin and less protection from ultraviolet light when sun screen is not used. Thus, less protection from both UV-B but also UV-A. Greater risk of cancer. Less POMC production results in other negative effects.

With less POMC less adrenocorticotropic hormone (ACTH) is produced. ACTH has several functions in the body. It helps for example to maintain blood sugar levels by stimulating the release of cortisol, which also protects the body from stress and reduces inflammation.

Chronic inflammation is found is obese individuals and probably contributes all the diseases I associate with what I call winter syndrome and are mostly labeled as diseases of aging. Diseases that are more common as we age ones like hypertension, atherosclerosis, the “flu”, sleep apnea, autoimmune diseases and on and on.

There is a lot of evidence associating chronic inflammation with cancer. 1, 2, 3 In fact, at least 15% of cancers are started by infections. 4 As cells fighting infections release free radicals that form substances like peroxynitrate that can damage our DNA. 5 As during infection new cells are being created to replace damaged ones.

Thus, these new cells are more sensitive to DNA damage from substances like peroxynitrate. Resulting in P53 mutations-which I will explain in a bit, but these p53 mutations are similar in number in both cancer and autoimmune diseases. 6 Curiously one of the cancers associated with infections is colon cancer.7

Vitamin D3 benefits for cancer are perhaps most closely associated with reducing risk of, you guessed it colon cancer. 8 That was from a meta data study, which is a class of study I really don’t like and no I can’t have it both ways but food for thought.

I believe it reduces the risk of colon cancer is an improved quality of gut flora from increased blood levels of vitamin D3 and though I have no proof more likely to have increased benefit at optimal blood levels is the reason.

Like I wrote about in a previous blog posting (https://judsonsomerville.com/is-vitamin-d3-health-benefits-a-myth-1-8/) about the VITAL study, a meta data study which showed no benefit in taking at “high dose” vitamin D in reducing risk of cancer. I will not rehash that, but you can go to those postings to see my arguments. Which I still stand by.

1. Mohan SV, Chang AL. (2014) Advanced basal cell carcinoma: epidemiology and therapeutic innovations. Curr Dermatol Rep. 3(1): 40-45.
2. Macathur M, Hold GL, El-Omar EM. (2004). Inflammation and cancer II. Role of chronic inflammation and cytokine gene polymorphisms in the pathogenesis of gastrointestinal malignancy. J Physio. 286(4): G515-G520.

2. Coussens LM, Webb Z. (December 19-26, 2002). Inflammation and cancer. Nature. 420(6917):860-867.
3. Balkwill F, Mantovani A. (February 17, 2001). Inflammation and cancer: back to Virchow?. The Lancet. 357(9255):539-545.
4. Kuper H, Adami HO, Trichopoulos D. (2000). Infections as a major cause of human cancer. J Intern Med. 248:171-183.
5. Maeda H, Akaike T. (1998). Nitric oxide and oxygen radicals in infection, inflammation and cancer. 63:854-865.
6. Yamanishi Y, Boyle DL, Firestein, et al. (July 23, 2002). Regional analysis of p53 mutations in rheumatoid arthritis synovium. 99(15):10025-10030.
7. Kostic AD, Chun E, Meyerson M, Garrett WS. (September 2013). Microbes and inflammation in colorectal cancer. Cancer Immunol Res. 1(3):150-7.
8. McCullough ML, Zolstick ES, Smith-Warner SA, et al. (Feb 2019). Circulating vitamin D and colorectal cancer risk: An international pooling project of 17 cohorts. J Nat Cnacer Inst. 111(2):158-169.

*The information posted above is for educational purposes only. Always check with your doctor before initiating any changes in your medical treatment. If you do not, then The Two-Minute Health Fact, Dr. Judson Somerville, nor The Optimal Dose is responsible!