TED HUTCHINSON

"Most people are idly curious about their vitamin D levels, get several levels done to confirm they really are that low and then do nothing about it," Kovacs writes on an Internet blog.

In case any of the readers here are quite that stupid to think the $15.70 for 250 days supply of 5000iu D3 is a big deal, here are a couple of abstracts that may encourage them to at least get some regular UVB exposure on their skin.

Progression of malignant melanoma is associated with reduced 25-hydroxyvitamin D serum levels Solar UV-exposure, particularly intensive short-time and recreational sun exposure, is considered to be the major etiologic factor for melanoma. But on the other hand 90% of all requisite vitamin D has to be formed in the skin through the action of the sun – a serious problem due to the fact that new scientific findings convincingly demonstrate vitamin D deficiency to be associated with a variety of severe diseases including various types of cancer (e.g. colon, prostate and breast cancer). According to recent reports sun exposure is associated with a relatively favorable prognosis and increased survival rate in various malignancies, including malignant melanoma. It has been speculated that these findings were related to UV exposure-induced relatively high serum levels of vitamin D which may lead to a more favorable course of melanoma. To prove this hypothesis the present study aimed to correlate the serum level of 25-hydroxyvitamin D (which represents the readily measurable 'storage' precursor form of vitamin D) with tumor thickness at time of diagnosis and course of disease in patients with melanoma. The study population consisted of 212 patients with histologically proven cutaneous melanomas of different stages: stage I (n = 50); stage II (n = 20); stage III (n = 20); stage IV (n = 122). Basal 25-hydroxyvitamin D levels were analyzed (DiaSorin LIAISON 25-OH Vitamin D-Assay) in those patients and compared with a control group (n = 80). Additionally, each participant was requested to fill out a questionnaire about the history of sun exposure. Interestingly, basal 25-hydroxyvitamin D levels were lower in melanoma patients as compared to the control group, although this difference was statistically not significant. Moreover, progression of malignant melanoma was associated with statistically significantly reduced 25-hydroxyvitamin D serum levels. In conclusion, our findings add to the growing body of evidence that 25-hydroxyvitamin D serum levels may be of importance for pathogenesis and progression of malignant melanoma.

And this
1,25-dihydroxy vitamin D3 regulates cutaneous innate immune function Hormonally active vitamin D3 – 1,25-dihydroxyvitamin D3 (1,25D3) – acts as a signalling molecule in cutaneous immunity. In this study we investigated if Toll-like-receptor (TLR) function and antimicrobial peptide (AMP) expression are controlled by 1,25D3 in keratinocytes. The AMP cathelicidin and TLR cofactor CD14 were known to be induced by 1,25D3, and analysis of TLR2 expression revealed this also was increased by 1,25D3. Topical 1,25D3 application to human skin confirmed these results, showing increased cathelicidin, CD14 and TLR2 by immunostaining. Furthermore, the presence of 1,25D3 enabled human keratinocytes to respond to Malp2 (a TLR2/6 ligand) with increased cathelicidin production which was inhibited by neutralizing antibody to TLR2. 1,25D3 also increased the ability of keratinocytes to kill Staphylococcus aureus. Interestingly, keratinocytes surrounding human skin wounds increased expression of CD14 and showed a previously known increase in cathelicidin AMP. Thus, we hypothesized that 1,25D3 was also a signalling molecule during skin injury. Supporting this, we found that CYP27B1, the enzyme that converts 25-hydroxy vitamin D3 (25D3) to active 1,25D3, was significantly increased in wounds and induced in response to factors in the wound micromilieu such as TGFβ1 or TLR stimulation. Blocking the vitamin D receptor, inhibiting CYP27B1 enzymatic activity, or limiting 25D3 in culture each prevented TGFβ1 from inducing cathelicidin, CD14 or TLR2. Furthermore, mice deficient in CYP27B1 failed to increase CD14 in vivo following injury. Thus, this investigation demonstrates how injury initiates the innate immune response; 25D3 is activated to 1,25D3 by enzymatic conversion, a process triggered by microbial products or host factors such as TGFβ1. The increase in 1,25D3 then directly increases cathelicidin release and enables responsiveness to microbial products through induction of TLR cofactor CD14.[/url]

For those who are not familiar with reading medical research abstracts these papers show that previous advice from Dermatologists to stay out of the sun to protect your skin have been too simplistic. Because we need higher levels of Vitamin D to protect from heart disease, cancer and diabetes it is more important to get sun exposure providing you never get sunburnt. (getting sunburnt destroys the vitamin D near the surface of the skin and thus leaves the damaged skin cells unprotected and liable to cancerous mutations. So regular short sun sessions improve your skins immune functions and may well reduce your chance of MRSA. The skin cancer that actually kills most people is melanoma and the first paper makes it quite clear the lower your vitamin d status the more likely you are to get melanoma and the more sun exposure those with Melanoma get the longer they lived and the better their prognosis.

So while it is important never to get burnt by UVB, it's really important not to keep your skin covered all the time, either with clothing or sunscreen.

For those using sunlight rather than tanning beds exposing as much skin as is practicable for a short period as this calculator works out is the best way of ensuring a high vitamin D status but if this isn't possible then do use EFFECTIVE STRENGTH D3 Cholecalciferol supplements.

I agree with this statement
"Many of the requests to test blood levels of the so-called sunshine vitamin are unnecessary, he said, advising that patients concerned about whether they are getting adequate amounts of the nutrient should take a vitamin D supplement for several months. " the dangers of Vitamin D toxicity are greatly overstated. Using 5000iu/daily even with regular full body sun exposure could not possibly cause toxicity. Even 10,000iu/daily D3 is considered a safe upper limit. You need to take 40,000iu/daily for many months to raise status to the 350nmol/l level at which adverse events occur.
So although it is interesting to be tested and this should motivate people to take action with supplements/sun exposure to correct the situation (that means raising your status to around 125-150nmol/l 50-60ng) it is absolutely totally safe to just take sufficient Vitamin D to meet your body's daily needs and rely on your body to use the vitamin D from sun exposure to build your stores for the winter period. That only happens after your daily needs have been met and a level of 50ng -125nmol/l is attained and maintained.

I hope Eileen will forgive me if she has already drawn your attention to these abstracts.

eileen

Nice to see you back Ted. We've missed your very informative posts.

I was just visiting your profile on here last week to see where you've been. I hope all is going well for you. I see you are still passionate about your research which I admire. :)

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"under exposure to UV rays is as dangerous as overexposure....this is D life" eileen

eileen

Ted I finally got time to read those articles closely and some others on the Igenta web site. Thanks for sharing, it takes me a bit longer to comprehend it all. Thanks again!! :)

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"under exposure to UV rays is as dangerous as overexposure....this is D life" eileen