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High vitamin D a cancer dud?


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#1 FunkOdyssey

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Posted 26 June 2010 - 08:06 PM


"Ruh roh" -Scooby Doo

Am J Epidemiol. 2010 Jun 18. [Epub ahead of print]
Overview of the Cohort Consortium Vitamin D Pooling Project of Rarer Cancers.

Helzlsouer KJ; for the VDPP Steering Committee.
Abstract

The Cohort Consortium Vitamin D Pooling Project of Rarer Cancers (VDPP) brought together 10 cohorts to conduct a prospective study of the association between vitamin D status, measured as serum concentrations of 25-hydroxyvitamin D (25(OH)D), and the development of 7 rarer cancer sites: endometrial, esophageal, gastric, kidney, non-Hodgkin lymphoma, ovarian, and pancreatic cancers. The cohorts come from 3 continents, with participants from a wide range of latitude who are racially diverse. Across each cancer site, there was no evidence of a protective association between higher concentrations of 25-hydroxyvitamin D (>75 nmol/L) and cancer outcome. An increased risk at very high levels (>/=100 nmol/L) was noted for pancreatic cancer, confirming previous reports. The articles included in this issue detail the overall design and governance of the project, correlates of vitamin D status, and results from the cancer site-specific investigations. The Vitamin D Pooling Project realizes a major goal of consortium efforts, namely, to rigorously test hypotheses for rarer cancer outcomes that may not be adequately addressed in any one prospective cohort study. The results of this study have application for the planning and conduct of intervention trials, especially in determining potential risks.

PMID: 20562193


To rain on the high dose Vitamin D parade even more:

Tim Byers
Anticancer Vitamins du Jour-The ABCED's So Far
American Journal of Epidemiology Advance Access published on June 18, 2010
Am. J. Epidemiol. 2010 172: 1-3; doi:10.1093/aje/kwq112 [Extract] [FREE Full
Text]

It started 30 years ago with vitamin A: the idea that some cancers might be
caused by vitamin deficiencies. Animal experimental models led us to the
notion that cancer risk might be "materially" reduced by supplementation
with beta-carotene, a retinol precursor (1). Although that idea was
seductive, we were all disappointed when 2 large randomized controlled
trials that began in 1985 in Finland and the United States reported an 18%
increased risk of lung cancer caused by high-dose beta-carotene
supplementation and a 28% increased lung cancer risk caused by a combination
of beta-carotene and retinol (2, 3). The vitamin A era was over.

Next came the B vitamins. Again, based on animal experimental evidence and
supported by epidemiologic evidence of connections between diets low in B
vitamins and increased cancer risk, a large randomized controlled trial was
begun in 1985 in central China, where micronutrient deficiency was common
and where rates of cancers of the stomach and esophagus were extraordinarily
high. Nonetheless, several years of supplementation with a combination of
riboflavin (vitamin B2) and niacin (vitamin B3) had no effect on incidence
of upper gastrointestinal cancers (4). Interest in folic acid (vitamin B9)
persisted, though, in part because of its striking effect on neural tube
birth defects, coupled with speculation about possible benefits of food
fortification for diseases such as colorectal cancer that were inversely
associated with diets rich in folate-containing foods and supplements.
However, a 7-year randomized controlled trial found that high-dose folic
acid supplements actually increased risk of colorectal adenomas (5). The
vitamin B era was over.

Next came vitamin C, a popular charge led by none other than Linus Pauling,
the brilliant and charismatic 2-time Nobel laureate. Of all the cancers
thought to be related to vitamin C deficiency, gastric cancer led the way,
and of all the places on Earth where a vitamin C deficiency correction trial
might yield benefits for gastric cancer, Linxian, China, would be the best.
Indeed, vitamin C was tested in the Linxian trial, but just as for the B
vitamins, vitamin C produced no change in gastric cancer rates (6).

Next, slightly out of alphabetical order, came vitamin E. In 1993, we
launched headlong into a love affair with vitamin E fueled by compelling
observations that those who chose to take vitamin E supplements were at
lower risk of heart disease (7, 8). Vitamin E supplementation became the
rage as several large, randomized controlled trials were mounted. When those
results finally came in, the findings were again disappointing: vitamin E
supplementation offered no benefit for heart disease, and it slightly
increased overall mortality (9, 10). In the meantime, though, because of a
secondary observation that prostate cancer incidence was lower in the
vitamin E arm of the same Finnish trial that tested beta-carotene (vitamin E
had also been included as a factor) (11), a large factorial trial of vitamin
E (and selenium) was carried out for reducing prostate cancer incidence.
Disappointment again: there was no effect of either selenium or vitamin E on
incidence of prostate cancer (12). The vitamin E era ended in a whimper.

Over 2 decades of searching for an anticancer vitamin, we had seemed to skip
over vitamin D in its proper alphabetical sequence. In my role as a member
of the World Cancer Research Fund Expert Panel that considered the evidence
from commissioned meta-analyses of the world's literature on nutritional
epidemiology, I remember feeling concern as we finished our work that we
might have underestimated the importance of vitamin D because the bulk of
the evidence available at that time was derived from ecologic studies (13).
Subsequently, the International Agency for Research on Cancer conducted a
comprehensive review of the evidence for vitamin D and cancer prevention,
concluding that vitamin D may play a protective role in colorectal cancer,
but not for prostate cancer, and that the evidence is weak for breast cancer
(14). The conclusion by the International Agency for Research on Cancer
about the weakness of the evidence for breast cancer has been a source of
controversy among vitamin D protagonists (15, 16), but subsequent nested
cohort studies have found no relation between breast cancer risk and
circulating levels of vitamin D (17, 18).

Nonetheless, vitamin D remains the cancer-preventing vitamin du jour. Just
search the phrase "vitamin D and cancer" on the Internet to see what sorts
of information and products are now being marketed to the public. Vitamin D
is the new vitamin A, the new folic acid, the new vitamin C, the new vitamin
E.

An outstanding set of papers in this issue of the American Journal of
Epidemiology reports on findings about the relation between circulating
levels of vitamin D and subsequent cancer risk in a set of pooled cohort
studies conducted in the United States, Europe, and Asia. These studies
found no suggestion of an inverse association between vitamin D levels in
the circulation and later incidence of 6 types of cancers (upper
gastrointestinal, ovary, endometrial, pancreatic, kidney, and non-Hodgkin
lymphoma). Although these cancers are characterized as "rarer," this set of
sites collectively accounts for about a quarter of all deaths from cancer in
the United States. These studies offer compelling evidence against the
hypothesis that circulating levels of vitamin D are relevant to risk of
these cancers. This new information is important because an International
Agency for Research on Cancer review had decided that evidence was
previously insufficient to draw conclusions about these 6 cancer sites (14).

Whenever null findings are found, it is important to consider the usual
suspect reasons, and the authors of these papers have done an outstanding
job of that. The size of this pooled analysis is large enough to discount
concerns about low statistical power; there is a good level of internal
consistency in the previously documented associations between vitamin D
levels and factors such as seasonality, race, gender, diet, physical
activity, and body mass index; there was substantial interindividual
variation in these cohorts; and there did not seem to be confusion between
confounding factors or factors potentially in the causal pathway. The
question as to whether the time interval studied was the correct one remains
unanswered, however. If the geographic ecologic associations between sun
exposure and cancer risk are, in fact, due to long-term cumulative effects
of lifelong vitamin D exposures, then cohort studies in adulthood will not
be fully informative. However, it is important to note that this longer-term
ecologic possibility is not consistent with the other ecologic observation
of seasonal variation in cancer incidence that is often also attributed to
vitamin D levels in the circulation (19).

The only association observed in this set of 6 analyses was a troubling one:
that risk of pancreatic cancer was doubled for those in the highest quintile
of circulating vitamin D levels. This observation is disconcerting both
because pancreatic cancer is now the fourth leading cause of cancer death in
the United States and because the proponents of the vitamin D hypothesis are
now arguing that substantially elevating circulating blood concentrations
into that range should be a nutritional policy objective for the general
population (15, 16). As pointed out by Dr. Helzlsouer (20) in this issue of
the Journal, many ongoing randomized controlled trials are now using quite
high doses of vitamin D. As we await clearer evidence of benefits from those
trials, we will also need to be prepared to be vigilant about their
individual and collective power to assess any potential harms (21, 22).

It is timely for us to now reflect on the history of the past 25 years of
our alphabetical approach to studying single vitamin deficiency states as
causal factors for cancer. We have learned some hard lessons along the
alphabetical way. We now know that supernutritional levels of vitamins taken
as supplements do not emulate the apparent benefits of diets high in foods
that contain those vitamins (13), and we now know that taking vitamins in
supernutritional doses can cause serious harm. In short, we have found that
the reality of human biology is far more complex than is suggested by our
simple ideas.

Finally, it is important to recognize the efforts of the many Vitamin D
Pooling Project of Rarer Cancers collaborators who carried out such a
remarkable set of studies. As pointed out by the Institute of Medicine, we
are now in an era of "big science," in which definitive answers to big
questions will increasingly require massive efforts and large-scale
collaborations (23). Carrying out these types of collaborations requires
foresight, skill, and patience. Large-scale collaborations are critically
important, though, for our improved understanding of the true nature of the
determinants of human health. The dual problems of type 1 and type 2 errors
have best been exemplified in genetic epidemiology, but false discovery has
been a problem in nutritional epidemiology as well. Even though there was
consistency in the overall null observations across most of the cohorts in
this pooled analysis, there was some variation. It is easy to imagine that,
without this collaborative analysis, we might have been led down several
blind alleys derived from analyses of various subgroups and interactions. We
all should be grateful to the Vitamin D Pooling Project of Rarer Cancers
investigators for having saved us from years of false leads, as well as for
their vision and skill in carrying out this outstanding collaborative
project.


By the way, 100nmol/L = 40ng/mL, above which they describe as "very high levels" of Vitamin D.

Edited by FunkOdyssey, 26 June 2010 - 09:39 PM.

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#2 Blue

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Posted 26 June 2010 - 10:31 PM

Very interesting. But as they say, many ongoing clinical trial with vitamin D, so we will relatively soon know more.

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#3 health_nutty

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Posted 27 June 2010 - 01:46 AM

By the way, 100nmol/L = 40ng/mL, above which they describe as "very high levels" of Vitamin D.


Interesting, 40ng/mL is significantly lower than lower range of the vitamin D council recommendation (50-80ng/mL).

The plot thickens...

#4 niner

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Posted 27 June 2010 - 03:59 AM

If some's good, more's better, and too much is just right. --universal maxim.

Some would argue that seeing no improvement over 30ng/ml is not a surprise. On the other side of the coin, Melamed noted a broad minimum in all-cause mortality occurring at 50ng/ml. We discussed this at length last year some time. I've been shooting for around 50, but felt like it might be better to go over than under. This is the first report of a specific disease I've seen. The problem with these epidemiological studies (both this and Melamed) is all that we don't know much about the group with the high D levels. These were community-dwelling people who were by and large not supplementing. If they had high D levels, they probably spent a lot of time outdoors. The correlates of that are probably many. Also, there probably weren't that many people in the high D group, so statistics may be weak there.

#5 Sillewater

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Posted 27 June 2010 - 04:40 AM

So I guess all that research supporting the 30-40ng/mL range is the safest bet for now.
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#6 Jay

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Posted 27 June 2010 - 02:26 PM

There's no new data here - just new analysis of old data -- the type of "study" most susceptiple to bias.

With respect to the first "study," let me just give one example of why I think these authors are biased. They included esophageal cancer in their list of rare cancers supposedly not associated with vit D. Since I am at risk for esophageal cancer, I have made sure to be familiar with every vit D study in the area. Based on this background, I know that they have given great weight to a study conducted in China where all quintiles studies were deficient. That study found that people with higher levels of vit D (but still deficient levels) get more esophageal cancers than people with lower levels. The other studies in the area were conducted in Italy and found that the opposite -- higher vit D levels associated with less esophageal cancer. It just isn't relavent to the debate what happens at very low vit D levels in a poor province in China, but they included that data nonetheless. Why? In my opinion, they made sure to include this data simply because it is negative.

The second study framed vit D in the context of other vitamins, ignoring that vit D is backed by so much more evidence, including a randomized placebo controlled trial finding a 77% reduction in cancer rates among women taking 1100 IU of vit D + calcium. They failed to mention this trial, despite their apparent deference to the data from trials on other vitamins. That oversight reveals their bias.

It may well be the case that levels above 50ng/ml are not optimal. But, I don't think these studies provide remotely enough evidence to call vit D a dud.
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#7 FunkOdyssey

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Posted 27 June 2010 - 05:09 PM

But, I don't think these studies provide remotely enough evidence to call vit D a dud.


Correction: I'm posing the suggestion that HIGH vitamin D is a cancer dud, defined as any 25OHD value over 40ng/mL. Certainly a normal range of 30-40ng/mL offers amazing benefits compared to values lower than that (deficiency).

#8 nameless

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Posted 27 June 2010 - 06:26 PM

Did they happen to check vitamin A status in any of those studies? Or at least check it in the high percentile D people?

Just curious if their D levels were obtained from sunlight or something like cod liver. There is that 'Vitamin A negating D's benefit' theory as a possibility, while too much A could be the culprit if for some strange reason a large percentage of the high percentile D people were eating fish livers.

A bit troublesome though. I usually aim for a serum of 45-50 myself (and thought that was conservative), but <40 may be something to consider now.

#9 rwac

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Posted 27 June 2010 - 07:12 PM

Did they happen to check vitamin A status in any of those studies? Or at least check it in the high percentile D people?

Just curious if their D levels were obtained from sunlight or something like cod liver. There is that 'Vitamin A negating D's benefit' theory as a possibility, while too much A could be the culprit if for some strange reason a large percentage of the high percentile D people were eating fish livers.


Or the reverse. High vitamin D might be bad if it's not accompanied by adequate vitamin A.

#10 ramon25

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Posted 27 June 2010 - 11:45 PM

I wonder then why then why cultures who get alot of sunlight live the longest and are not dropping dead of pancreatic cancer..... These studies say nothing at all about wheter vitamin causes cancer. Maybe vitamin d used up other nutrients like (vitamin k, magnesium) which would support pancreas health. But in the end these studies dont prove ANYTHING remotley useful, fact of the matter is that being outdoors alot the way most of our ancestors did would supply a blood level higher the 40, more like 50-70. I swear and I mean this with all due respect people on this forum freak out about one study and start going back and forth between what is healthy and what is not, what is today and what is not tomorrow, its really impossible. Why would vitamin d seemingly prevent aging and cancer in so many fashions and then suddenly it causes cancder is this specific organ, why would any vitamin do this? if a certain range is helpful for alot of issues but specifically bad ofr one body part??? especially vitamin d which is a part of most of the cellular life on earth... Its like a weird neccesity to micro manage everything to perfection, its unrealistic people

#11 FunkOdyssey

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Posted 27 June 2010 - 11:57 PM

I wonder then why then why cultures who get alot of sunlight live the longest and are not dropping dead of pancreatic cancer.....


Probably because pancreatic cancer is rare and over 40ng/mL 25OHD doubled the risk which is still very low in absolute terms.

Edited by FunkOdyssey, 27 June 2010 - 11:59 PM.


#12 outsider

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Posted 28 June 2010 - 09:44 AM

There's no new data here - just new analysis of old data -- the type of "study" most susceptiple to bias.

With respect to the first "study," let me just give one example of why I think these authors are biased. They included esophageal cancer in their list of rare cancers supposedly not associated with vit D. Since I am at risk for esophageal cancer, I have made sure to be familiar with every vit D study in the area. Based on this background, I know that they have given great weight to a study conducted in China where all quintiles studies were deficient. That study found that people with higher levels of vit D (but still deficient levels) get more esophageal cancers than people with lower levels. The other studies in the area were conducted in Italy and found that the opposite -- higher vit D levels associated with less esophageal cancer. It just isn't relavent to the debate what happens at very low vit D levels in a poor province in China, but they included that data nonetheless. Why? In my opinion, they made sure to include this data simply because it is negative.

The second study framed vit D in the context of other vitamins, ignoring that vit D is backed by so much more evidence, including a randomized placebo controlled trial finding a 77% reduction in cancer rates among women taking 1100 IU of vit D + calcium. They failed to mention this trial, despite their apparent deference to the data from trials on other vitamins. That oversight reveals their bias.

It may well be the case that levels above 50ng/ml are not optimal. But, I don't think these studies provide remotely enough evidence to call vit D a dud.



Exactly, from the little I have seen, meta analysis are biased more than anything else. Thinking about it, it's a nice way to dilute the real findings.

#13 Blue

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Posted 28 June 2010 - 09:49 PM

I think this study is interesting:
http://www.medical-h...0717-1/abstract

Furthermore, the pancreas is the organ with highest concentration of vitamin K1 and mk4.
http://journals.camb...line&aid=877476

In addition, epidemiological studies have found low intake of cruciferous vegetables, but often not other vegetables, to increase the risk of pancreas cancer. They are rich in K1.

So as per the first study, is there a risk that a high dose of vitamin D will deplete vitamin K, and is the pancreas an organ particularly sensitive to such a depletion?

Edited by Blue, 28 June 2010 - 09:52 PM.


#14 ramon25

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Posted 29 June 2010 - 04:31 AM

My exact point. Also magnesium helps control insulin. high insulin CANNOT be good to pancreas. Vitamin D will deplete mag becuase it needs it. Most people dont get enough either way.

Edited by ramon25, 29 June 2010 - 04:33 AM.


#15 Blue

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Posted 29 June 2010 - 05:47 AM

Vitamin D will deplete mag becuase it needs it.

Source?

#16 mike250

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Posted 29 June 2010 - 06:10 AM

so it looks like supplementing with the whole vitamin K spectrum -- and not just k2--- is a good idea

#17 Blue

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Posted 29 June 2010 - 07:02 AM

so it looks like supplementing with the whole vitamin K spectrum -- and not just k2--- is a good idea

No one really knows which form is best. The above studies does not say which form is preferable. Sure, there is little mk7 in the pancreas but it may be that mk7 and k1 is converted to mk4 in humans (they do so in certain human caner cells). One could argue for going for mk4 directly but it seems to have a poor absorption, at least regarding blood values, compared to mk7 or K1. K1 is the only form having a double-blind study showing reduced cancer and severe disease. And so on, too few studies to draw any certain conclusions regarding best form.

Interesting to note that the above study regarding vitamn D and K also mentions vitmain A. But while the article argue for that both A and K can reduce vitamin D toxicity, that may be misleading. Vitamin A reduces the production by vitamin D of proteins dependent on vitamin K for proper function while vitamin K increases the number of functioning proteins. So it seems to me that this may argue for that a relatively low A and a relatively high D + K intake is optimal. Which may argued is what human studies also suggest.

Edited by Blue, 29 June 2010 - 07:10 AM.


#18 Blue

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Posted 29 June 2010 - 07:42 AM

Although one could possible argue that if vitamin K intake is very low, then a high vitamin A intake wculd be beneficial if this reduces less important vitamin K dependent proteins so that the little vitamin K available is used for more critical functions.

#19 Jay

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Posted 29 June 2010 - 10:17 PM

Blue, if you're not alrady aware of it, you might be interested in this study, discussed here by Chris Masterjohn.

Chinese researchers from Hong Kong recently published a paper in Stem Cell Reviews and Reports showing that vitamins A and D cooperate with one another to turn on neurogenin-3 in human pancreatic stem cells. They also provided a new mechanism for vitamin A and D interactions: they found that each vitamin increased the production of the other's receptor!



#20 Blue

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Posted 29 June 2010 - 10:56 PM

Blue, if you're not alrady aware of it, you might be interested in this study, discussed here by Chris Masterjohn.

Chinese researchers from Hong Kong recently published a paper in Stem Cell Reviews and Reports showing that vitamins A and D cooperate with one another to turn on neurogenin-3 in human pancreatic stem cells. They also provided a new mechanism for vitamin A and D interactions: they found that each vitamin increased the production of the other's receptor!

A cell study. Even if this occur in the buman body at achievable levels of A and D this does not mean that this is good. In increase in neurogenin-3 may well cause differentiation into islet cells but by doing so leave no steam cell left which will just cause a temporary improvement followed by complete diabetes. Maybe a high neurogenin-3 is what causes diabetes? Assuming steam cells are involved in diabetes in adult human at all. Cell studies are usually not worth much due to all the uncertainty. Is there at least an animal study showing that a combination of A and D is beneficial for something, anything?

Seems to me that that blog is rather desparately grasping at straws in order to defend a paleo diet high in vitamin A. I see no good reason there to ignore the human studies finding that high vitamin A decreases the efficieny of vitamin D.

#21 ramon25

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Posted 30 June 2010 - 12:01 AM

Vitamin D will deplete mag becuase it needs it.

Source?


If a nutrient needs another as a cofactor and there is a high intake of that nutrient and not its cofactor then there will likely be a reduction in that cofacor. that is smart supplementation 101,
as a matter of fact just google it, plenty of hits

Edited by ramon25, 30 June 2010 - 12:02 AM.


#22 health_nutty

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Posted 30 June 2010 - 02:07 AM

Vitamin D will deplete mag becuase it needs it.

Source?


If a nutrient needs another as a cofactor and there is a high intake of that nutrient and not its cofactor then there will likely be a reduction in that cofacor. that is smart supplementation 101,
as a matter of fact just google it, plenty of hits


He's asking you to post a link to the original research paper.

#23 Jay

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Posted 30 June 2010 - 02:14 AM

Blue, if you're not alrady aware of it, you might be interested in this study, discussed here by Chris Masterjohn.

Chinese researchers from Hong Kong recently published a paper in Stem Cell Reviews and Reports showing that vitamins A and D cooperate with one another to turn on neurogenin-3 in human pancreatic stem cells. They also provided a new mechanism for vitamin A and D interactions: they found that each vitamin increased the production of the other's receptor!

A cell study. Even if this occur in the buman body at achievable levels of A and D this does not mean that this is good. In increase in neurogenin-3 may well cause differentiation into islet cells but by doing so leave no steam cell left which will just cause a temporary improvement followed by complete diabetes. Maybe a high neurogenin-3 is what causes diabetes? Assuming steam cells are involved in diabetes in adult human at all. Cell studies are usually not worth much due to all the uncertainty. Is there at least an animal study showing that a combination of A and D is beneficial for something, anything?

Seems to me that that blog is rather desparately grasping at straws in order to defend a paleo diet high in vitamin A. I see no good reason there to ignore the human studies finding that high vitamin A decreases the efficieny of vitamin D.



I agree fully about the blog (and have made the point elsewhere on imminst). I just thought you'd be interested since you have separately expressed interest both in the interractions between fat soluble vitamins and the use of such vitamins in the pancreas. I thought it was interesting that vit D increases the number of RARs and vit A increases the number of VDRs in pancreas cells.

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#24 krillin

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Posted 30 June 2010 - 06:25 AM

A second study showing that > 40 ng/ml provides the lowest all-cause mortality. Unlike the first one, it didn't find increased risk above 50 ng/ml. Could be because the highest decile was only > 41.2 ng/ml (median 46 ng/ml). Free full text.

J Am Geriatr Soc. 2009 Sep;57(9):1595-603. Epub 2009 Jun 22.
Prospective study of serum 25-hydroxyvitamin D level, cardiovascular disease mortality, and all-cause mortality in older U.S. adults.
Ginde AA, Scragg R, Schwartz RS, Camargo CA Jr.
Department of Emergency Medicine, School of Medicine, University of Colorado Denver, 12401 E. 17th Avenue, B-215, Aurora, CO 80045. adit.ginde@ucdenver.edu
Abstract

OBJECTIVES: To evaluate the association between serum 25-hydroxyvitamin D (25(OH)D) levels and mortality in a representative U.S. sample of older adults. DESIGN: Prospective cohort from the Third National Health and Nutrition Examination Survey (NHANES III) and linked mortality files. SETTING: Noninstitutionalized U.S. civilian population. PARTICIPANTS: Three thousand four hundred eight NHANES III participants aged 65 and older enrolled from 1988 to 1994 and followed for mortality through 2000. MEASUREMENTS: Primary exposure was serum 25(OH)D level at enrollment. Primary and secondary outcomes were all-cause and cardiovascular disease (CVD) mortality, respectively. RESULTS: During the median 7.3 years of follow-up, there were 1,493 (44%) deaths, including 767 CVD-related deaths. Median 25(OH)D level was 66 nmol/L. Adjusting for demographics, season, and cardiovascular risk factors, baseline 25(OH)D levels were inversely associated with all-cause mortality risk (adjusted hazard ratio (HR)=0.95, 95% confidence interval (CI)=0.92-0.98, per 10 nmol/L 25[OH]D). Compared with subjects with 25(OH)D levels of 100 nmol/L or higher, the adjusted HR for subjects with levels less than 25.0 nmol/L was 1.83 (95% CI=1.14-2.94) and for levels of 25.0 to 49.9 nmol/L was 1.47 (95% CI=1.09-1.97). The association appeared stronger for CVD mortality (adjusted HR=2.36, 95% CI=1.17-4.75, for subjects with 25[OH]D levels<25.0 nmol/L vs those > or =100.0 nmol/L) than for non-CVD mortality (adjusted HR=1.42, 95% CI=0.73-2.79, for subjects with 25[OH]D levels<25.0 nmol/L vs those > or =100.0 nmol/L). CONCLUSION: In noninstitutionalized older adults, a group at high risk for all-cause mortality, serum 25(OH)D levels had an independent, inverse association with CVD and all-cause mortality. Randomized controlled trials of vitamin D supplementation in older adults are warranted to determine whether this association is causal and reversible.

PMID: 19549021




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