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The Marshall Protocol Study Site > PROF. MARSHALL'S PERSPECTIVE > Prof. Marshall's Perspective > Skin Pigmentation does NOT affect Vit D production in skin


Skin Pigmentation does NOT affect Vit D production in skin
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Prof Trevor Marshall
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 Posted: Sat Oct 17th, 2009 17:26

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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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 Posted: Sun Oct 18th, 2009 16:28

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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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Prof Trevor Marshall
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 Posted: Sun Oct 18th, 2009 18:07

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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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 Posted: Sat Oct 24th, 2009 16:53

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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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Prof Trevor Marshall
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 Posted: Sat Oct 24th, 2009 23:16

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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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 Posted: Sun Oct 25th, 2009 18:31

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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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 Posted: Tue Mar 9th, 2010 19:30

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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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 Posted: Thu Mar 11th, 2010 17:07

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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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 Posted: Thu Mar 11th, 2010 18:14

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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 :D) 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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 Posted: Fri Mar 12th, 2010 06:51

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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 :D) 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...




:D, 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!?:P

 

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:D
 

 


Last edited on Fri Mar 12th, 2010 07:14 by Bane

Prof Trevor Marshall
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 Posted: Fri Mar 12th, 2010 07:55

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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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 Posted: Mon Mar 22nd, 2010 16:09

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Vitamin D Levels Have Different Effects on Atherosclerosis in Blacks and Whites, Study Finds

http://www.sciencedaily.com/releases/2010/03/100315091259.htm

 

ok??:P

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 Posted: Mon Mar 22nd, 2010 17:57

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Bane,

I read this yesterday and was going to post it but couldn't find it again.  I was actually going to make a comment that I was surprised that you had not posted it yet....:)

Very interesting study.

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 Posted: Mon Mar 22nd, 2010 20:50

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<<The study is the first to show a positive relationship between calcified plaque in large arteries, a measure of atherosclerosis or "hardening of the arteries," and circulating vitamin D levels in black patients. It appears in the March issue of the Journal of Clinical Endocrinology and Metabolism>>

Yes, very interesting -- the above is a quote from the article Bane posted a link to.  That would tie in with the finding of greater brain lesions with greater vitamin D intake by Payne et al...

Joyce Waterhouse



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 Posted: Wed Apr 7th, 2010 02:15

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The 1,25-dihydroxyvitamin D(3)-independent actions of the vitamin D receptor in skin.

http://www.ncbi.nlm.nih.gov/pubmed/20362670

The vitamin D endocrine system plays important but poorly understood roles in the skin and in hair follicle cycling. Rare, human genetic disorders and knockout mouse models highlight essential roles and potentially novel mechanisms of the vitamin D endocrine system in the skin. Vitamin D receptor knockout mice express a hair follicle cycling defect and a hyperproliferative phenotype resulting in disordered skin structure, epidermal thickening, and alopecia. In contrast, ligand knockout mice (i.e., mice with a disrupted CYP27B1 gene that encodes the 25-hydroxyvitamin-D(3) 1alpha-hydroxylase) have normal hair follicle function and a comparatively modest skin phenotype. These disparate models indicate that VDR may function independently of 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) in regulating hair follicle cycling and skin biology. Recent studies highlight this concept and provide key support for this hypothesis. While VDR knockout mice are highly susceptible to chemically-induced skin tumorigenesis, CYP27B1 knockouts are resistant. These studies reveal a second global physiological process in the skin that may be regulated by VDR in a 1,25(OH)(2)D(3)-independent fashion, namely, genoprotection against carcinogenic mutagens. Key cellular and molecular data supporting this mechanism were published recently showing a keratinocyte-selective transactivation activity mediated by VDR that is independent of the 1,25(OH)(2)D(3) ligand. Thus, evidence is building to support a potentially novel, 1,25(OH)(2)D(3)-independent mechanism through which VDR functions in keratinocytes and perhaps within stem cell populations in the follicle to regulate genoprotection and other key developmental processes in the skin.

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 Posted: Wed Apr 7th, 2010 16:05

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Bane wrote: The 1,25-dihydroxyvitamin D(3)-independent actions of the vitamin D receptor in skin.

http://www.ncbi.nlm.nih.gov/pubmed/20362670

The vitamin D endocrine system plays important but poorly understood roles in the skin and in hair follicle cycling. Rare, human genetic disorders and knockout mouse models highlight essential roles and potentially novel mechanisms of the vitamin D endocrine system in the skin. Vitamin D receptor knockout mice express a hair follicle cycling defect and a hyperproliferative phenotype resulting in disordered skin structure, epidermal thickening, and alopecia. In contrast, ligand knockout mice (i.e., mice with a disrupted CYP27B1 gene that encodes the 25-hydroxyvitamin-D(3) 1alpha-hydroxylase) have normal hair follicle function and a comparatively modest skin phenotype. These disparate models indicate that VDR may function independently of 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) in regulating hair follicle cycling and skin biology. Recent studies highlight this concept and provide key support for this hypothesis. While VDR knockout mice are highly susceptible to chemically-induced skin tumorigenesis, CYP27B1 knockouts are resistant. These studies reveal a second global physiological process in the skin that may be regulated by VDR in a 1,25(OH)(2)D(3)-independent fashion, namely, genoprotection against carcinogenic mutagens. Key cellular and molecular data supporting this mechanism were published recently showing a keratinocyte-selective transactivation activity mediated by VDR that is independent of the 1,25(OH)(2)D(3) ligand. Thus, evidence is building to support a potentially novel, 1,25(OH)(2)D(3)-independent mechanism through which VDR functions in keratinocytes and perhaps within stem cell populations in the follicle to regulate genoprotection and other key developmental processes in the skin.


Another thing that might be happening here is that there is another enzyme, apart from CYP27B1, that is capable of putting that second hydroxyl group in place ?

Just like there is, perhaps, an as yet unidentified enzyme that delivers the energy to break up 7-dehydrocholesterol into pre-vitamin D ?

Frans



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 Posted: Fri Apr 9th, 2010 00:56

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http://www.msrc.co.uk/index.cfm/fuseaction/show/pageid/1334

There is more going on in the skin hit by sunlight than just vitamin D production



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 Posted: Fri Apr 9th, 2010 09:42

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UV Exposure Has Increased Over the Last 30 Years, but Stabilized Since the Mid-1990s

http://www.sciencedaily.com/releases/2010/03/100316142529.htm

"In the tropics, the increase has been minimal, but in the mid-latitudes it has been more obvious. During the summer, for example, UV has increased by more than 20 percent in Patagonia and the southern portions of South America. It has risen by nearly 10 percent in Buenos Aires, a city that's about the same distance from the equator as Little Rock, Ark. At Washington, D.C.'s latitude -- about 35 degrees north -- UV has increased by about 9 percent since 1979."

As part of his study, Herman developed a mathematical technique to quantify the biological impacts of UV exposure. He examined and calculated how changing levels of ozone and ultraviolet irradiance affect life. For Greenbelt, Md., for example, he calculated that a 7 percent increase in UV yielded a 4.4 percent increase in the damage to skin, a 4.8 percent increase in damage to DNA, a 5 percent increase in Vitamin D production, and less than a percent of increase in plant growth.

"If you go to the beach these days, you're at slightly higher risk of getting skin cancer (without protection)," Herman said, though he noted the risk would have been even greater in the absence of regulations on ozone-depleting substances.

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 Posted: Fri Apr 9th, 2010 17:53

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Posted: Fri Mar 12th, 2010 11:07
Bane wrote: 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
"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."    ...................     suggests to me that we consider how Cro-magnon communities survived the Dryas ice sheets confined to caves in the south of France for many thousands of years.
At this time only the strongest and hardiest group members would go out to bring in their frozen meat or kill any predators about to rob the larder.

Someone whose liver and kidney were working harder (i.e. the darker skinned) would be using more energy during a devastating lack of access to resources, &
disadvantaged compared with the lighter skinned, who were not diverting much energy to a process which was no longer required during confinement away from sunlight.

Young men who were pale skinned mutants may have had more energy left to volunteer for a now dangerous trip to another cave for trade or to seek a bride.

Therefore pale skin gradually replaced the pre-dominant dark skins and a whole 'new look' appeared among humans.  As time went by and Europe was re-opened to immigration, the pale-skins had the established position and wealth and local know-how, so became a sort of aristocracy and were sort-after wives and husbands because of their rarity as well as their wealth.
Howzat?

PS anyone with cabin fever, just remember.... You wont have to do it for thousands of years :P



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 Posted: Mon Mar 5th, 2018 00:54

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Sallie Q wrote: Posted: Fri Mar 12th, 2010 11:07
Bane wrote: 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
"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."    ...................     suggests to me that we consider how Cro-magnon communities survived the Dryas ice sheets confined to caves in the south of France for many thousands of years.
At this time only the strongest and hardiest group members would go out to bring in their frozen meat or kill any predators about to rob the larder.

Someone whose liver and kidney were working harder (i.e. the darker skinned) would be using more energy during a devastating lack of access to resources, &
disadvantaged compared with the lighter skinned, who were not diverting much energy to a process which was no longer required during confinement away from sunlight.

Young men who were pale skinned mutants may have had more energy left to volunteer for a now dangerous trip to another cave for trade or to seek a bride.

Therefore pale skin gradually replaced the pre-dominant dark skins and a whole 'new look' appeared among humans.  As time went by and Europe was re-opened to immigration, the pale-skins had the established position and wealth and local know-how, so became a sort of aristocracy and were sort-after wives and husbands because of their rarity as well as their wealth.
Howzat?

PS anyone with cabin fever, just remember.... You wont have to do it for thousands of years :P

A high-coverage Neandertal genome from Vindija Cave in Croatia

Science.

2017 Nov 3;358(6363):655-658. doi: 10.1126/science.aao1887. Epub 2017 Oct 5.

Abstract

To date, the only Neandertal genome that has been sequenced to high quality is from

an individual found in Southern Siberia.

We sequenced the genome of a female Neandertal from ~50,000 years ago

from Vindija Cave, Croatia, to ~30-fold genomic coverage.

She carried 1.6 differences per 10,000 base pairs between the

two copies of her genome, fewer than present-day humans, suggesting

that Neandertal populations were of small size.

Our analyses indicate that she was

more closely related to the Neandertals that mixed with the ancestors of present-day

humans living outside of sub-Saharan Africa than the previously

sequenced Neandertal from Siberia, allowing 10 to 20% more Neandertal DNA to be

identified in present-day humans, including variants involved in low-density

lipoprotein cholesterol concentrations, schizophrenia, and other

diseases.

Last edited on Mon Mar 5th, 2018 00:58 by Markt9452



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