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Dr Trevor Marshall
Foundation Staff
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Posted: Sun Oct 18th, 2009 01:26 |
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It is nice to see one's 'hypotheses' proven correct by others 
A study has just been published which shows that the amount of Vitamin D produced in the skin of people exposed to UVB radiation is not dependent on their skin pigmentation.
Further, those with low values of 25-D at the outset of the trial produced less 25-D from UVB radiation than those who were healthy at the outset.
http://www.nature.com/jid/journal/vaop/ncurrent/abs/jid2009323a.html
..Trevor..
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Jigsaw
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Posted: Mon Oct 19th, 2009 00:28 |
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"The increase in 25(OH)D level after UVB exposure was negatively correlated with baseline 25(OH)D level (P<0.001) and positively correlated with baseline total cholesterol level (P=0.005)"
I think this means those with a lower 25OH)D level increased it more.
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MP1.Arthritis30+yrs.3/98>3X50mgdoxy/wk.6/06 limitation.9/06:Noirs.11/06:25-D,15;1,25-D,29.4.20/07:25-D.7.
2/2/07:Beni40mg,Q6H.20/2:Mino25mg,Q2-3D.3/6:Beni40,Q8H.3/8Mino50Q2-3D.3/24Mino75Q2-3D.4/16Mino100Q2D.4/29,pH2.
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Dr Trevor Marshall
Foundation Staff
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Posted: Mon Oct 19th, 2009 02:07 |
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Oops - you win
I fell into the same trap as all the Vit D researchers fall into - we know the answer before we start
Anyway, the fulltext is on its way via inter-library loan so that I can double-check
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RobertTownsend
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Posted: Sun Oct 25th, 2009 00:53 |
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Trevor
Is it not the precursor D3 which is synthesised in the skin, rather than the mono-hydroxy 25OH-D3 - which is largely synthesised elsewhere in the body from precursor D3.
Don't most of the previous studies suggest that the only thing skin pigmentation effects is the exposure time needed before D3 levels in the skin reach their saturation level ?
RobertT
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CFS 4yrs,crippled knees;Oct05 Phase 1;Feb 06 Phase 2 ; Mar06 1,25D-61pMol/L 25D-23nMol/K;Jul06 Ph3 start ;July 08 dose tapering some abx,daytime fatigue much lower, skin still very light sensitive ;knee mobility very constrained with limited walking
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Dr Trevor Marshall
Foundation Staff
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Posted: Sun Oct 25th, 2009 07:16 |
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Ah, yes, the precursor step, from 7-dehydro-cholesterol to Vitamin D (mono-hydroxy 25OH-D3). Something about which I have not written a lot. But if you look at Figure 1 of my Bioessay, you can see that I show this step is shown as being catalyzed by "Energy - eg UVB"
http://TrevorMarshall.com/BioEssays-Feb08-Marshall-Preprint.pdf
The commonly accepted pragma is that this precursor is only synthesized in the keratinocytes of the skin under the influence of specific wavelengths in the UVB spectrum. I have been 'testing' this pragma this since these comprehensive papers written by Lehmann, et al, in 2001/2003:
UVB-induced conversion of 7-dehydrocholesterol to 1alpha,25-dihydroxyvitamin D3 in an in vitro human skin equivalent model
http://www.ncbi.nlm.nih.gov/pubmed/11710930
Demonstration of UVB-induced synthesis of 1 alpha,25-dihydroxyvitamin D3 (calcitriol) in human skin by microdialysis:
http://www.ncbi.nlm.nih.gov/pubmed/12709817
Recently, Lehmann wrote two good reviews which bring some of the early concepts up-to-date:
Role of the vitamin D3 pathway in healthy and diseased skin--facts, contradictions and hypotheses:
http://www.ncbi.nlm.nih.gov/pubmed/19146580
Wavelength-dependent induction of CYP24A1-mRNA after UVB-triggered calcitriol synthesis in cultured human keratinocytes:
http://www.ncbi.nlm.nih.gov/pubmed/16902422
The primary problem I have with the skin pragma is the lack of evidence supporting a keratinocyte-only role for the conversion of 7-dehydro-cholesterol, and also the paucity of good studies which have attempted to explore the pragma.
Like most of the pragma adopted surrounding the synthesis and actions of Vitamin D, I think this pragma (keratinocytes only) is incorrect. I look at the human body at the level of the proteins (and etc) within cells, not at the level of tissue. When I consider the level of activity within the cells, I find the concept that Vitamin D can only be formed in keratinocytes to be not at all convincing. IMO, the concentration gradient over the cell membranes is the factor that other researchers are failing to fully comprehend.
As support, I would first advance this study showing that UVB can induce Vitamin D in cells other than keratinocytes:
UVB-induced 1,25(OH)2D3 production and vitamin D activity in intestinal CaCo-2 cells and in THP-1 macrophages pretreated with a sterol Delta7-reductase inhibitor
http://www.ncbi.nlm.nih.gov/pubmed/16598763
But I find even more persuasive the anecdotal observation that nocturnal mammals do not need exposure to UVB to survive and flourish. Additionally, an elegant 1998 experiment with fish showed that neither exogenous Vitamin D nor UVB is necessary for fish to flourish. Indeed, it did not matter whether these fish were exposed to UVB, Vitamin D, or neither, - they lived identical lives in all cases:
"Vitamin D is not an essential nutrient for Rora (Labeo rohita) as a representative of freshwater fish"
http://www.ncbi.nlm.nih.gov/pubmed/9675700
I have advanced the hypothesis that the obvious, and probably accelerated, production of Vitamin D in the skin is a protective response to prevent damage to the skin produced by the UVB. I do not think it plays an essential role in human metabolism. I believe Homo sapiens functions perfectly well with enzymatic synthesis of Vitamin D in cells far away from the skin surface. This hypothesis would seem to be in line with the recent observation that the increased synthesis in keratinocytes correlates with apoptosis:
Lipidome of narrow-band ultraviolet B irradiated keratinocytes shows apoptotic hallmarks.
http://www.ncbi.nlm.nih.gov/pubmed/19845761
and is closely involved with the release of a key innate immunity cytokine:
Role for tumor necrosis factor-alpha in UVB-induced conversion of 7-dehydrocholesterol to 1alpha,25-dihydroxyvitamin D3 in cultured keratinocytes:
http://www.ncbi.nlm.nih.gov/pubmed/15225839
but more study is clearly needed. In the absence of such study I have rejected the pragma that UVB is necessary for normal Vitamin D metabolism in man. I suspect that more study will discover an enzyme which can provide the 'energy' for that stage of metabolic conversion. I have for 21 years myself lived without direct, conscious, exposure to daylight. A bone scan shows my own skeleton is right where it should be, regardless of the hideous disease I had to suffer during so many of those 21 years. Further I have seen no signs that an indoors lifestyle is harming anybody in our cohort (other than cabin sickness). So this is another pragma that I believe will fall, and along with it the concept that systemic "Vitamin D deficiency" is correlated in any way with skin pigmentation.
I hope that helps,
Trevor
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Perezt
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Posted: Mon Oct 26th, 2009 02:31 |
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Trevor,
What you have described makes allot of sense. Considering the importance of confirming the actual role of our skin in performing, or not, the conversion it amazes me that it has not been followed-up and done in humans. Then we can focus on the other alternatives.
Tom
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Dx Sarcoid 1989 / Oct05 1,25-D=126 & 25-D=30; Began: MP Dec2405 / P2 Mar2206 / P3 May2106 / P4 Feb0108
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Sallie Q
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Posted: Wed Mar 10th, 2010 03:30 |
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(and I notice one of the science articles I have made links to today also reproduces the idea that naturally dark skins are different)
this article is like the "curate's egg: good in parts"
http://www.sciencedaily.com/videos/2007/1108-sunscreen_in_a_pill.htm
"dermatologists say that Bio Astin, also know as Astaxanthin, acts like a sponge absorbing UV rays. It also reduces pain and inflammation from sunburn."
so I assume it is another red herring which will sell another dubious product
The good (useful) if true info is right at the end
"In the US, the UV index starts to increase in March and April, peaking every year in June. The ozone layer in the Earth’s upper stratosphere absorbs most of the sun’s UV radiation, but ongoing damage to that protective layer means that UV-related health risks continue to increase. NASA solar experts report that this year was the strongest and most active sun activity cycle in nearly 50 years, a state they expect to persist for the next 7-10 years. As a result, people will need more UV protection than ever before over the next decade."
Hang onto your hats, everyone
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stress57-83 b.cancer1990 20yrHotFlush SjogrensCFS 60%dysreg.vD 13.2 Sep08ph1 JanModPh2 May09Ph3 : 1,25D 30pg/mL Feb2010: 25D Jan5ng/mL lowLux must wear NoIR
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Bane
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Posted: Fri Mar 12th, 2010 01:07 |
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Where does white skin come from?
http://www.newscientist.com/article/mg20327222.500-where-does-white-skin-come-from.html
Robins also points to studies showing that while black volunteers have significantly lower blood levels of vitamin D than white volunteers after a whole-body dose of UVB, the difference narrowed and even disappeared when levels of metabolites derived from vitamin D were compared. This suggests that in darker-skinned people, enzymes from the liver and kidneys were working harder to keep the levels of the active metabolites the same, regardless of the skin pigmentation. "There seems to be a compensatory mechanism," says Robins. "That's another reason why the vitamin D hypothesis fails."
http://www.ncbi.nlm.nih.gov/pubmed/19425095
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Oral Lichen Planus(mild)/Clubbed Finger (digital clubbing)Last 25D 5.6ng/ml, phase3
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BIGDOG
Member in Phase 2
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Posted: Fri Mar 12th, 2010 02:14 |
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Dr Trevor Marshall wrote:
It is nice to see one's 'hypotheses' proven correct by others
A study has just been published which shows that the amount of Vitamin D produced in the skin of people exposed to UVB radiation is not dependent on their skin pigmentation.
Further, those with low values of 25-D at the outset of the trial produced less 25-D from UVB radiation than those who were healthy at the outset.
http://www.nature.com/jid/journal/vaop/ncurrent/abs/jid2009323a.html
..Trevor..
Further along the lines you are thinking with intracellular concentrations of D and/or its metabolites... I was just thinking we (or they ) can be just missing the forrest for the trees... high energy radiation has long been known to damage at the cellular level.
What if there are cells in the skin which are lysed with the radiation, causing the concentrations of intracellular D and/or metabolites to spill into the serum, where coincidentally the levels are measured?
Are we just seeing the insides of the 'egg' when it's dropped on the floor?
Fascinating...
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Diet changed AUG09 / PH1 NOV09 / PH2 FEB 09 /OLM 40MGq6h / M100mg48h / Z100mg10d / 25D 13ng NOV09 9ng DEC09 7ng FEB10 / 1,25D 18pg NOV09 20pg FEB10 / NO other meds /CFS-ME / LowLuxHome <30min sun weekly
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Bane
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Posted: Fri Mar 12th, 2010 14:51 |
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BIGDOG wrote: Dr Trevor Marshall wrote:
It is nice to see one's 'hypotheses' proven correct by others
A study has just been published which shows that the amount of Vitamin D produced in the skin of people exposed to UVB radiation is not dependent on their skin pigmentation.
Further, those with low values of 25-D at the outset of the trial produced less 25-D from UVB radiation than those who were healthy at the outset.
http://www.nature.com/jid/journal/vaop/ncurrent/abs/jid2009323a.html
..Trevor..
Further along the lines you are thinking with intracellular concentrations of D and/or its metabolites... I was just thinking we (or they ) can be just missing the forrest for the trees... high energy radiation has long been known to damage at the cellular level.
What if there are cells in the skin which are lysed with the radiation, causing the concentrations of intracellular D and/or metabolites to spill into the serum, where coincidentally the levels are measured?
Are we just seeing the insides of the 'egg' when it's dropped on the floor?
Fascinating...
, yea, what if there was a correlation between skin color and latitude? And that white skin could produce vitamin D more easily? Maybe that actually put them more at risk of getting immunosuppressed, especially in the summer months in these sunbathing sun loving times. Getting a tan might be a complementary system to protect us from to much hormone D? Could that explain the sudden rise in MS, and the more prevalence in northerly latitudes? Our sun loving culture!?
http://en.wikipedia.org/wiki/Sun_tanning
"Throughout history, tanning has seen several fluctuations in popularity. In early civilizations with a class system, social distinctions existed between those of tanned complexion and those without. This class system often separated those deemed to be high class and those who were not. This distinction was physically manifested in the color of one’s skin. Those who often spent long hours working in the sun were often grouped together as lower class. Women even went as far as to put lead-based cosmetics on their skin to artificially augment their appearance." However, these cosmetics slowly caused their death through lead poisoning. Achieving this light-skinned appearance was brought about in many other ways, including the use of arsenic to whiten skin, on to more modern methods such as full length clothes, powders, and parasols. This fair-skinned trend continued up until the end of the Victorian era. Niels Finsen was awarded the Nobel Prize in medicine in 1903 for his “Finsen Light Therapy”. This therapy was to cure infectious diseases such as lupus vulgaris and rickets. Vitamin D deficiency was found to be a cause of rickets disease, and exposure to the sun would allow Vitamin D to be produced in a person. Therefore, sun exposure was a remedy to curing several diseases, especially rickets. Shortly thereafter, in the 1920s, Coco Chanel accidentally got sunburnt while visiting the French Riviera. Her fans apparently liked the look and started to adopt darker skin tones themselves. Tanned skin became a trend partly because of Coco’s status and the longing for her lifestyle by other members of society."
AND SO IT WENT
Last edited on Fri Mar 12th, 2010 15:14 by Bane
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Oral Lichen Planus(mild)/Clubbed Finger (digital clubbing)Last 25D 5.6ng/ml, phase3
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Dr Trevor Marshall
Foundation Staff
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Posted: Fri Mar 12th, 2010 15:55 |
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You might like to edit that Wikipedia page about rickets to say it "was thought" to be due to Vit D. Citing this as the reference:
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=169216
"It is not due to vitamin D deficiency but is caused by not having enough calcium in the diet"
There are plenty of other studies, but this looks pretty authoritative, I think
..Trevor..
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