70 replies to this topic

[mikey]

Well, since I've been taking 11,000 IU, which renders an OH-vitamin D blood level of 60 ng/mL I've had a tremendous reduction in herpes cold sore outbreaks - only two small pimple-sized lesions in three years, that each disappeared in less than a week. It used to be much worse and I get no colds or flu.

I'm sorry that there's a big pharma war against vitamins, where studies are set up to make useful nutrients look ineffective.

But that's probably the major thing to watch out for - the strategic creation of negative publications to keep consumers from attaining optimal health.

I've devoted an entire section of my web site to correcting studies that were obviously designed to make safe, effective nutrients look like they either don't work or might harm you. To see it, click here.

[Mind]

I think most of the vitamin D promotion relies on misidentifying association as causation. Higher vitamin D levels are probably in most cases simply an accidental by-product of a healthy (physically active, outside) lifestyle, not a cause. It is the (outside) physical activity that causes improved health, not the vitamin D, and also the better health that allows outside physical activity, causing higher vitamin D levels as a by-product.

This is a good quote because it applies to almost every substance life-extensionists take in order to stay healthy. It should be pretty obvious to everyone who reads the forums here and is vaguely familiar with aging theories, that levels of hormones (like vitamin D) and other markers for youth and vigor decline with age. There is nothing we can do about it. Supplementing is like a bandaid approach, but it is the best we got. From what I have read, exogenous supplementation, while not being anything remotely close to real rejuvenation, probably helps slow aging a little.

I disagree. There are too many cases where physical activity has been controlled for to blame all (or even most) of vitamin D's effects on it. This hormonal substance has been studied to death, and frankly, the physical activity argument is pretty simplistic.

If for some dietary or lifestyle reason you are not getting enough of a critical nutrient, you have to supplement. Either that or change your diet or lifestyle. There's simply no question that remediation of deficiencies improves health. I don't think that life extensionists particularly suffer from in inability to distinguish correlation from causation; I do think that they suffer from an inability to distinguish between a crappy in vitro study and a decent study in a mammal, but that's another story.

I take your point Niner. Maybe I didn't word things as optimal as possible. Some people think that supps and hormones are magic bullets against aging and will automatically make them super healthy. There is a lot hype. Correcting deficiencies will certainly keep people healthier for longer, but eventually we will have to get to the root of the problem. That is my point(s).

[Kevnzworld]

I think most of the vitamin D promotion relies on misidentifying association as causation. Higher vitamin D levels are probably in most cases simply an accidental by-product of a healthy (physically active, outside) lifestyle, not a cause. It is the (outside) physical activity that causes improved health, not the vitamin D, and also the better health that allows outside physical activity, causing higher vitamin D levels as a by-product.

This is a good quote because it applies to almost every substance life-extensionists take in order to stay healthy. It should be pretty obvious to everyone who reads the forums here and is vaguely familiar with aging theories, that levels of hormones (like vitamin D) and other markers for youth and vigor decline with age. There is nothing we can do about it. Supplementing is like a bandaid approach, but it is the best we got. From what I have read, exogenous supplementation, while not being anything remotely close to real rejuvenation, probably helps slow aging a little.

I disagree. There are too many cases where physical activity has been controlled for to blame all (or even most) of vitamin D's effects on it. This hormonal substance has been studied to death, and frankly, the physical activity argument is pretty simplistic.

If for some dietary or lifestyle reason you are not getting enough of a critical nutrient, you have to supplement. Either that or change your diet or lifestyle. There's simply no question that remediation of deficiencies improves health. I don't think that life extensionists particularly suffer from in inability to distinguish correlation from causation; I do think that they suffer from an inability to distinguish between a crappy in vitro study and a decent study in a mammal, but that's another story.

I take your point Niner. Maybe I didn't word things as optimal as possible. Some people think that supps and hormones are magic bullets against aging and will automatically make them super healthy. There is a lot hype. Correcting deficiencies will certainly keep people healthier for longer, but eventually we will have to get to the root of the problem. That is my point(s).

Some would argue ( me ) that uncorrected deficiencies are the root of the problem. That is the heart of orthomolecular medical thought.

[nowayout]

I think most of the vitamin D promotion relies on misidentifying association as causation. Higher vitamin D levels are probably in most cases simply an accidental by-product of a healthy (physically active, outside) lifestyle, not a cause. It is the (outside) physical activity that causes improved health, not the vitamin D, and also the better health that allows outside physical activity, causing higher vitamin D levels as a by-product.

This is a good quote because it applies to almost every substance life-extensionists take in order to stay healthy. It should be pretty obvious to everyone who reads the forums here and is vaguely familiar with aging theories, that levels of hormones (like vitamin D) and other markers for youth and vigor decline with age. There is nothing we can do about it. Supplementing is like a bandaid approach, but it is the best we got. From what I have read, exogenous supplementation, while not being anything remotely close to real rejuvenation, probably helps slow aging a little.

I disagree. There are too many cases where physical activity has been controlled for to blame all (or even most) of vitamin D's effects on it. This hormonal substance has been studied to death, and frankly, the physical activity argument is pretty simplistic.

If for some dietary or lifestyle reason you are not getting enough of a critical nutrient, you have to supplement. Either that or change your diet or lifestyle. There's simply no question that remediation of deficiencies improves health. I don't think that life extensionists particularly suffer from in inability to distinguish correlation from causation; I do think that they suffer from an inability to distinguish between a crappy in vitro study and a decent study in a mammal, but that's another story.

I don't dispute that deficiencies need to be corrected, but the issue under discussion is what should count as a deficiency. The IoM report convincingly argues, based on almost all the available research studies of any quality available as of 2010-11, that most Americans are not deficient in vitamin D, that deficiency should be defied as blood levels under 20 ng/ml, not 30 ng/ml as many of the test companies arbitrarily decided, and that much of the vitamin D boosterism of late is unjustified and false optimism.

Also, researchers putting on paper the standard incantations that they controlled for this or that parameter doesn't make it credibly true. I sincerely doubt the ability of researchers in most instances to truly control for levels of physical activity (in the minority of cases where they have even made an attempt to do so) given that subjective self-reports are notorious for lacking in credibility, and I don't see any studies where subjects were required to wear pedometers, for example, or were tested for objective measures of endurance or strength, over the period of the study during which the primary outcome was measured.

Edited by viveutvivas, 26 October 2012 - 10:33 PM.

[niner]

I disagree. There are too many cases where physical activity has been controlled for to blame all (or even most) of vitamin D's effects on it. This hormonal substance has been studied to death, and frankly, the physical activity argument is pretty simplistic.

If for some dietary or lifestyle reason you are not getting enough of a critical nutrient, you have to supplement. Either that or change your diet or lifestyle. There's simply no question that remediation of deficiencies improves health. I don't think that life extensionists particularly suffer from in inability to distinguish correlation from causation; I do think that they suffer from an inability to distinguish between a crappy in vitro study and a decent study in a mammal, but that's another story.

I don't dispute that deficiencies need to be corrected, but the issue under discussion is what should count as a deficiency. The IoM report convincingly argues, based on almost all the available research studies of any quality available as of 2010-11, that most Americans are not deficient in vitamin D, that deficiency should be defied as blood levels under 20 ng/ml, not 30 ng/ml as many of the test companies arbitrarily decided, and that much of the vitamin D boosterism of late is unjustified and false optimism.

Also, researchers putting on paper the standard incantations that they controlled for this or that parameter doesn't make it credibly true. I sincerely doubt the ability of researchers in most instances to truly control for levels of physical activity (in the minority of cases where they have even made an attempt to do so) given that subjective self-reports are notorious for lacking in credibility, and I don't see any studies where subjects were required to wear pedometers, for example, or were tested for objective measures of endurance or strength, over the period of the study during which the primary outcome was measured.

Aren't there any studies that correct for BMI? Just being outside doesn't necessarily make you healthy, if you are just lying around in the sun. BMI is a simple metric that says something about physical condition. Some of the vitamin D boosterism is unjustified hype, I would agree with that. That doesn't mean that all the studies are crap though, or that vitamin D is useless.

[mikey]

I think most of the vitamin D promotion relies on misidentifying association as causation. Higher vitamin D levels are probably in most cases simply an accidental by-product of a healthy (physically active, outside) lifestyle, not a cause. It is the (outside) physical activity that causes improved health, not the vitamin D, and also the better health that allows outside physical activity, causing higher vitamin D levels as a by-product.

This is a good quote because it applies to almost every substance life-extensionists take in order to stay healthy. It should be pretty obvious to everyone who reads the forums here and is vaguely familiar with aging theories, that levels of hormones (like vitamin D) and other markers for youth and vigor decline with age. There is nothing we can do about it. Supplementing is like a bandaid approach, but it is the best we got. From what I have read, exogenous supplementation, while not being anything remotely close to real rejuvenation, probably helps slow aging a little.

I disagree. There are too many cases where physical activity has been controlled for to blame all (or even most) of vitamin D's effects on it. This hormonal substance has been studied to death, and frankly, the physical activity argument is pretty simplistic.

If for some dietary or lifestyle reason you are not getting enough of a critical nutrient, you have to supplement. Either that or change your diet or lifestyle. There's simply no question that remediation of deficiencies improves health. I don't think that life extensionists particularly suffer from in inability to distinguish correlation from causation; I do think that they suffer from an inability to distinguish between a crappy in vitro study and a decent study in a mammal, but that's another story.

I don't dispute that deficiencies need to be corrected, but the issue under discussion is what should count as a deficiency. The IoM report convincingly argues, based on almost all the available research studies of any quality available as of 2010-11, that most Americans are not deficient in vitamin D, that deficiency should be defied as blood levels under 20 ng/ml, not 30 ng/ml as many of the test companies arbitrarily decided, and that much of the vitamin D boosterism of late is unjustified and false optimism.

Also, researchers putting on paper the standard incantations that they controlled for this or that parameter doesn't make it credibly true. I sincerely doubt the ability of researchers in most instances to truly control for levels of physical activity (in the minority of cases where they have even made an attempt to do so) given that subjective self-reports are notorious for lacking in credibility, and I don't see any studies where subjects were required to wear pedometers, for example, or were tested for objective measures of endurance or strength, over the period of the study during which the primary outcome was measured.

The IOM ignored the many studies put forth by true day-to-day vitamin D research scientists who they consulted, but did not include their suggestions. Their report was sadly lacking, as stated by noted and highly respected world authority vitamin D researchers - because it DID NOT include all the available research. It's conclusions were dismissed by the world's leading vitamin D researchers.

Addressing deficiencies is paramount to life extension. As Bruce Ames says, "Insufficiency boosts age-related diseases.

Further, Ames' study Micronutrient Deficiencies A Major Cause of DNA Damage stated that, "Eighty percent of American children and adolescents and 68% of adults do not eat five portions [of fruits and vegetables] a day" which might supply them with the necessary RDA of vitamins and minerals.

So who should supplement their diet? Who knows that their diet is inadequate?

These questions are why orthomolecular nutrition should be considered, especially for life extensionists.

[kismet]

Yes, only a few epidemiologic studies with *hard* outcomes, esp. all-cause mortality, were available back then. Two current meta-analyses contradict the IOM report on this. None of this is the really strong kind of evidence that we would like to see, but there is no doubt the IOM report is outdated. Now, there could be a reason to prefer the report due to its methodology...

The IOM included 100s of studies on surrogate and other outcomes that could have been of importance, that is how they get to 1000 refs.


Start in this thread: http://www.longecity..._30#entry519487

[mikey]

Yes, only a few epidemiologic studies with *hard* outcomes, esp. all-cause mortality, were available back then. Two current meta-analyses contradict the IOM report on this. None of this is the really strong kind of evidence that we would like to see, but there is no doubt the IOM report is outdated. Now, there could be a reason to prefer the report due to its methodology...

The IOM included 100s of studies on surrogate and other outcomes that could have been of importance, that is how they get to 1000 refs.


Start in this thread: http://www.longecity..._30#entry519487

I looked through that thread - http://www.longecity..._30#entry519487 - and I'm sorry, but their primary notion doesn't pass the smell test - thinking that vitamin D at dosing higher than 40 ng/mL is overdosing and causing cancers and CVD.
I take 11,000 IU/day. My blood level is 60 ng/mL. My blood level has been above 40 ng/mL for about six years.
I just took the BIOPHYSICAL250.
My cancer markers are all low to very low.
My CVD markers are healthy.

If one looks for studies to find optimal doses of nutrients, there is always a lowest dose where optimal effects begin to occur and a dose for most nutrients that are relatively non-toxic - where the cost of taking more isn't equitable because of diminishing returns OR, as with some nutrients - there is some kind of toxicity.

But to get optimal anti-aging effects one needs to take optimal doses, first to make sure that one doesn't suffer deficiencies that compromise cell health. And then to elicit the optimal beneficial effects, which tend to occur with higher doses.

I have a friend, an authority on vitamin D, who taught Dr. Mercola what he knows about vitamin D who wrote a 275-page paper on vitamin D.

Among her citations is a study that showed that about 5% of the population will experience hypercalcemia at 70 ng/mL. (I'd have to search through her paper to find the reference.)

She prefers her clients to have levels of 40 to 60 ng/mL. Many of the progressive vitamin D researchers state that 50 ng/mL is optimal and some go higher.

After multiple tests over the last six years I find that I need to take 11,000 IU to get a "supposed" optimal blood level of 60 ng/mL.

So I found that thread to be almost completely lacking, as I tend towards progressive orthomolecular nutrition, which I think has served me well for life-extension purposes.

I'm surprised that there is a vitamin D controversy, but then I'm surprised that there are politicians who think that the child of a rape is God's will.

[Hebbeh]

http://www.scienceda...21105130355.htm

Low Vitamin D Levels Linked to Longevity, Surprising Study Shows


ScienceDaily (Nov. 5, 2012) — Low levels of vitamin D may be associated with longevity, according to a study involving middle-aged children of people in their 90s published in CMAJ (Canadian Medical Association Journal).

"We found that familial longevity was associated with lower levels of vitamin D and a lower frequency of allelic variation in the CYP2R1 gene, which was associated with higher levels of vitamin D," writes Dr. Diana van Heemst, Department of Gerontology and Geriatrics, Leiden University Medical Center, Leiden, the Netherlands, with coauthors.

Previous studies have shown that low levels of vitamin D are associated with increased rates of death, heart disease, diabetes, cancer, allergies, mental illness and other afflictions. However, it is not known whether low levels are the cause of these diseases or if they are a consequence.

To determine whether there was an association between vitamin D levels and longevity, Dutch researchers looked at data from 380 white families with at least 2 siblings over age 90 (89 years or older for men and 91 year or older for women) in the Leiden Longevity Study. The study involved the siblings, their offspring and their offsprings' partners for a total of 1038 offspring and 461 controls. The children of the nonagenarians were included because it is difficult to include controls for the older age group. The partners were included because they were of a similar age and shared similar environmental factors that might influence vitamin D levels.

The researchers measured levels of 25(OH) vitamin D and categorized levels by month as they varied according to season. Tanning bed use, which can affect vitamin D levels, was categorized as never, 1 times per year and 6 times per year. The researchers controlled for age, sex, BMI (body mass index), time of year, vitamin supplementation and kidney function, all factors that can influence vitamin D levels. They also looked at the influence of genetic variation in 3 genes associated with vitamin D levels.

"We found that the offspring of nonagenarians who had at least 1 nonagenarian sibling had lower levels of vitamin D than controls, independent of possible confounding factors and SNPs [single nucleotide polymorphisms] associated with vitamin D levels," write the authors. "We also found that the offspring had a lower frequency of common genetic variants in the CYP2R1 gene; a common genetic variant of this gene predisposes people to high vitamin D levels.

These findings support an association between low vitamin D levels and familial longevity." They postulate that offspring of nonagenarians might have more of a protein that is hypothesized to be an "aging suppressor" protein. More research is needed to understand the link between lower vitamin D levels, genetic variants and familial longevity.
Story Source:

The above story is reprinted from materials provided by Canadian Medical Association Journal, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

• Raymond Noordam, Anton J.M. de Craen, Pardis Pedram, Andrea B. Maier, Simon P. Mooijaart, Johannes van Pelt, Edith J. Feskens, Martinette T. Streppel, P. Eline Slagboom, Rudi G.J. Westendorp, Marian Beekman, Diana van Heemst. Levels of 25-hydroxyvitamin D in familial longevity: the Leiden Longevity Study. CMAJ, 2012 DOI: 10.1503/cmaj.120233

[centagen]

I've been taking 5000 IU vitamin D3 for about 5 years and have had regular vitamin D blood tests. My level has never been above the middle of the normal range. Before taking D3 it was below normal.

[Kevnzworld]

Interesting study. There is so much we don't yet know about the biological functions of this vitamin/ hormone.
Dr Lyle Dennis of Extreme Longevity's comment on the study:

"This research may not lead to the conclusion that vitamin D levels per se leads to longevity.  Rather it may mean that people genetically predisposed to longevity are less likely to have genes leading to higher vitamin D levels as part of a network of genes.  That genetic network may reduce aging."

[Mind]

When I saw the D3 longevity study it made me think about other hormones as well. Hasn't it also been shown that supercentenarians (or other long-lived humans/mammals) have lower HGH and IGF-1 throughout their life (which would support the CR-type thinking, lower metabolism/less calories burned/less growth=less accumulated metabolic damage=longer life)?

The D3 Longevity study is an interesting data point to consider and add to the mix, but so far it seems the majority of studies point toward D3 as being health-promoting. It is definitely a hormone that declines with age (like every other youth/health marker), so if one is to remain a natural carbon-based human and wants to return/rejuvenate to an optimum youthful age (say 20), then you are going to need get those hormone levels back to youthful - post-puberty - norms.

[joelcairo]

I feel that study says more about the impact of the CYP2R1 gene than it does about vitamin D. The long-lived population is genetically programmed to have lower levels of vitamin D, even though they likely consume similar amounts of same and get similar levels of sun exposure, so why is that? I haven't read the full study, but for all I know they might have higher levels of vitamin D receptors or supporting proteins and metabolize it more efficiently.

Edited by joelcairo, 06 November 2012 - 07:37 PM.

[Hebbeh]

D2 may play a bigger role than D3.....

http://www.scienceda...21108131452.htm

Vitamin D Could Hold Vital Key to Arresting Development of Alzheimer’s Disease

ScienceDaily (Nov. 8, 2012) — Scientists at London's Kingston University have uncovered evidence that lack of a particular form of vitamin D is associated with Alzheimer's disease.

Working in collaboration with researchers from Brighton and Sussex Medical School and the Sussex Partnership NHS Foundation, the Kingston researchers spent six months analysing blood samples from patients with Alzheimer's. They compared test results from those not being treated with any drugs to those from people on medication and a further group who did not have the condition.

Lead researcher Professor Declan Naughton, from Kingston University's School of Life Sciences, said the results had revealed some important facts. Alzheimer's patients who were not using medication had very poor stores of vitamin D2 -- the type originating from food such as oily fish, rather than that obtained from exposure to the sun. "The vitamin was either non-existent or in such low quantities that it could barely be measured," he explained. "In comparison, people in the study who were either being treated with drugs to control their Alzheimer's or who didn't have the condition at all showed far higher levels."

In a further twist, the scientists found indications that Acetylcholinesterase inhibitors -- used to treat the early stages of Alzheimer's -- might play a role in actually "switching on" the body's absorption of vitamin D2.

"There are several different types of vitamin D that can be active in the body," Professor Naughton explained. "The key point in this study was that a blood test, which we developed at Kingston University, was for the first time able to accurately measure which, if any, of the different variations of vitamin D were present in Alzheimer's patients."

There had been speculation in the scientific community in the past that vitamin D, or a lack of it, might have a role to play in the development of Alzheimer's. However, this was believed to be the first time scientists had pinpointed the connection with the vitamin D2 metabolite, Professor Naughton said.

Although more research was still needed, the findings could eventually pave the way for medical intervention to restore levels of that particular strand of vitamin D, he added. Such an approach had the potential to have a marked impact on the devastating condition, which currently affects almost half a million people in the United Kingdom alone. "Further investigations are now needed to determine whether simple dietary advice or giving a specific supplement could restore beneficial levels in Alzheimer's patients," Professor Naughton said.

Vitamin D plays a key role in the development of healthy bodies. It helps to form and maintain strong teeth and bones and is thought to protect against a number of diseases such as cancers, cardiovascular conditions and neurological problems. "Most people associate vitamin D with exposure to the sun. The idea that a lack of the storage form originating from foods such as oily fish and egg yolks might be implicated in the development and progression of Alzheimer's definitely merits further research," Professor Naughton said.

The scientists' study, entitled Low 25OH Vitamin D2 Levels Found in Untreated Alzheimer's Patients Compared to Acetylcholinesterase Inhibitor Treated and Controls, has been published in international journal Current Alzheimer Research.
Story Source:
The above story is reprinted from materials provided by Kingston University.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
Iltaf Shah, Andrea Petroczi, Naji Tabet, Anthony Klugman, Mokhtar Isaac, Declan P. Naughton. Low 25OH Vitamin D2 Levels Found in Untreated Alzheimer’s Patients, Compared to Acetylcholinesterase-Inhibitor Treated and Controls. Current Alzheimer Research, 2012; 9 (9): 1069-1076 [link]

Edited by Hebbeh, 09 November 2012 - 01:56 AM.

[mikey]

http://www.scienceda...21105130355.htm

Low Vitamin D Levels Linked to Longevity, Surprising Study Shows


ScienceDaily (Nov. 5, 2012) — Low levels of vitamin D may be associated with longevity, according to a study involving middle-aged children of people in their 90s published in CMAJ (Canadian Medical Association Journal).

"We found that familial longevity was associated with lower levels of vitamin D and a lower frequency of allelic variation in the CYP2R1 gene, which was associated with higher levels of vitamin D," writes Dr. Diana van Heemst, Department of Gerontology and Geriatrics, Leiden University Medical Center, Leiden, the Netherlands, with coauthors.

Previous studies have shown that low levels of vitamin D are associated with increased rates of death, heart disease, diabetes, cancer, allergies, mental illness and other afflictions. However, it is not known whether low levels are the cause of these diseases or if they are a consequence.

To determine whether there was an association between vitamin D levels and longevity, Dutch researchers looked at data from 380 white families with at least 2 siblings over age 90 (89 years or older for men and 91 year or older for women) in the Leiden Longevity Study. The study involved the siblings, their offspring and their offsprings' partners for a total of 1038 offspring and 461 controls. The children of the nonagenarians were included because it is difficult to include controls for the older age group. The partners were included because they were of a similar age and shared similar environmental factors that might influence vitamin D levels.

The researchers measured levels of 25(OH) vitamin D and categorized levels by month as they varied according to season. Tanning bed use, which can affect vitamin D levels, was categorized as never, 1 times per year and 6 times per year. The researchers controlled for age, sex, BMI (body mass index), time of year, vitamin supplementation and kidney function, all factors that can influence vitamin D levels. They also looked at the influence of genetic variation in 3 genes associated with vitamin D levels.

"We found that the offspring of nonagenarians who had at least 1 nonagenarian sibling had lower levels of vitamin D than controls, independent of possible confounding factors and SNPs [single nucleotide polymorphisms] associated with vitamin D levels," write the authors. "We also found that the offspring had a lower frequency of common genetic variants in the CYP2R1 gene; a common genetic variant of this gene predisposes people to high vitamin D levels.

These findings support an association between low vitamin D levels and familial longevity." They postulate that offspring of nonagenarians might have more of a protein that is hypothesized to be an "aging suppressor" protein. More research is needed to understand the link between lower vitamin D levels, genetic variants and familial longevity.
Story Source:

The above story is reprinted from materials provided by Canadian Medical Association Journal, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

• Raymond Noordam, Anton J.M. de Craen, Pardis Pedram, Andrea B. Maier, Simon P. Mooijaart, Johannes van Pelt, Edith J. Feskens, Martinette T. Streppel, P. Eline Slagboom, Rudi G.J. Westendorp, Marian Beekman, Diana van Heemst. Levels of 25-hydroxyvitamin D in familial longevity: the Leiden Longevity Study. CMAJ, 2012 DOI: 10.1503/cmaj.120233

This exemplifies the difference between "signal" and "noise."
This is garbage science at its core.

Vitamin D2 has been shown in multiple studies to be ~1/3 as well utilized (converted) into active vitamin D in the blood stream as vitamin D3.
http://www.ncbi.nlm....pubmed/21177785
http://ajcn.nutritio...t/84/4/694.full
http://ajcn.nutritio...ontent/68/4/854

Further, more vitamin D delivers benefits that less vitamin D does not.
Anti-cancer, better mood, http://www.ncbi.nlm....pubmed/17138809, immune function and on and on.

Any effort to state the opposite is equal to Orwellian double-speak = non-science.

If you're confused enough to believe this garbage science, then there is little hope that you'll be able to reason your way through this. Dog bless you.

[Hebbeh]

This exemplifies the difference between "signal" and "noise."
This is garbage science at its core.

Vitamin D2 has been shown in multiple studies to be ~1/3 as well utilized (converted) into active vitamin D in the blood stream as vitamin D3.
http://www.ncbi.nlm....pubmed/21177785
http://ajcn.nutritio...t/84/4/694.full
http://ajcn.nutritio...ontent/68/4/854

Further, more vitamin D delivers benefits that less vitamin D does not.
Anti-cancer, better mood, http://www.ncbi.nlm....pubmed/17138809, immune function and on and on.

Any effort to state the opposite is equal to Orwellian double-speak = non-science.

If you're confused enough to believe this garbage science, then there is little hope that you'll be able to reason your way through this. Dog bless you.

Haha.

You're making a lot of assumptions. D2 obviously serves a purpose beyond D3 so how well it is converted to D3 is very well irrelevant. There are a lot of things we don't know yet but you seem to think you have all the answers already. Actually there is little hope for you with your closed mindedness to science that disagrees with your opinions. I think you need a little more tocotrienols.

Edited by Hebbeh, 09 November 2012 - 03:51 AM.

[mikey]

The article makes wrong statements.
"Lead researcher Professor Declan Naughton, from Kingston University's School of Life Sciences, said the results had revealed some important facts.Alzheimer's patients who were not using medication had very poor stores of vitamin D2 -- the type originating from food such as oily fish, rather than that obtained from exposure to the sun.

Wrong. Vitamin D2 does not come from animal or fish fats. It comes from the ergot fungus hence, ergocalciferol
D3 is cholecalciferol, from cholesterol, which only come from animal fats.

Quote: "Although sunshine exposure and fish consumption provide vitamin D in the form of D₃, a different bioactive, plant-derived form of vitamin D, named vitamin D₂, was produced in the early 1920s through ultraviolet exposure of foods."

The production and use of vitamin D2 was more a scientific blunder than anything else.

Vitamin D2 is well-known as not performing well in primate metabolism.

It doesn't raise serum 25-Hydroxyvitamin D adequately, exhibits poor binding to vitamin D binding proteins in plasma and vitamin D scientists say that it isn't suitable for normal physiologic metabolism. It's like it's a foreign entity, unnatural to human metabolism.

On the other hand, vitamin D3 is produced in the skin from UV irradiation and if you take a vitamin D3 supplement it converts about three times better into the active form of vitamin D in the bloodstream as supplemental vitamin D2.

Edited by mikey, 09 November 2012 - 06:32 AM.

[Hebbeh]

The article makes wrong statements.
"Lead researcher Professor Declan Naughton, from Kingston University's School of Life Sciences, said the results had revealed some important facts.Alzheimer's patients who were not using medication had very poor stores of vitamin D2 -- the type originating from food such as oily fish, rather than that obtained from exposure to the sun.

Wrong. Vitamin D2 does not come from animal or fish fats. It comes from the ergot fungus hence, ergocalciferol
D3 is cholecalciferol, from cholesterol, which only come from animal fats.

Quote: "Although sunshine exposure and fish consumption provide vitamin D in the form of D₃, a different bioactive, plant-derived form of vitamin D, named vitamin D₂, was produced in the early 1920s through ultraviolet exposure of foods."

The production and use of vitamin D2 was more a scientific blunder than anything else.

Vitamin D2 is well-known as not performing well in primate metabolism.

It doesn't raise serum 25-Hydroxyvitamin D adequately, exhibits poor binding to vitamin D binding proteins in plasma and vitamin D scientists say that it isn't suitable for normal physiologic metabolism. It's like it's a foreign entity, unnatural to human metabolism.

On the other hand, vitamin D3 is produced in the skin from UV irradiation and if you take a vitamin D3 supplement it converts about three times better into the active form of vitamin D in the bloodstream as supplemental vitamin D2.

It seems you are not entirely correct.

http://www.livestron...-of-vitamin-d2/

Animal Sources

Very few natural foods contain vitamin D, making it difficult to attain recommended levels without sunlight exposure. According to the National Institutes of Health, the flesh of fish, especially salmon, mackerel, sardines, cod and tuna are the best food sources of vitamin D in general, although the D3 form is more prevalent in these foods. Fish oils, such as cod liver oil, are also very rich in both vitamins D2 and D3. Smaller amounts of vitamin D2 are found in beef liver, shrimp, Swiss cheese and egg yolks.





Sponsored Links

http://www.livestron.../#ixzz2BjLc0KPL

[mikey]

The article makes wrong statements.
"Lead researcher Professor Declan Naughton, from Kingston University's School of Life Sciences, said the results had revealed some important facts.Alzheimer's patients who were not using medication had very poor stores of vitamin D2 -- the type originating from food such as oily fish, rather than that obtained from exposure to the sun.

Wrong. Vitamin D2 does not come from animal or fish fats. It comes from the ergot fungus hence, ergocalciferol
D3 is cholecalciferol, from cholesterol, which only come from animal fats.

Quote: "Although sunshine exposure and fish consumption provide vitamin D in the form of D₃, a different bioactive, plant-derived form of vitamin D, named vitamin D₂, was produced in the early 1920s through ultraviolet exposure of foods."

The production and use of vitamin D2 was more a scientific blunder than anything else.

Vitamin D2 is well-known as not performing well in primate metabolism.

It doesn't raise serum 25-Hydroxyvitamin D adequately, exhibits poor binding to vitamin D binding proteins in plasma and vitamin D scientists say that it isn't suitable for normal physiologic metabolism. It's like it's a foreign entity, unnatural to human metabolism.

On the other hand, vitamin D3 is produced in the skin from UV irradiation and if you take a vitamin D3 supplement it converts about three times better into the active form of vitamin D in the bloodstream as supplemental vitamin D2.

It seems you are not entirely correct.

http://www.livestron...-of-vitamin-d2/

Animal Sources

Very few natural foods contain vitamin D, making it difficult to attain recommended levels without sunlight exposure. According to the National Institutes of Health, the flesh of fish, especially salmon, mackerel, sardines, cod and tuna are the best food sources of vitamin D in general, although the D3 form is more prevalent in these foods. Fish oils, such as cod liver oil, are also very rich in both vitamins D2 and D3. Smaller amounts of vitamin D2 are found in beef liver, shrimp, Swiss cheese and egg yolks.

Sponsored Links

http://www.livestron.../#ixzz2BjLc0KPL

No. Livestrong is incorrect. I note that they don't provide a reference to their erroneous statement and a search of the National Institutes of Health site does not show what they said.

Vitamin D2 is not found in animal or fish oils. The vitamin D in animal products is based on the cholesterol molecule - cholecalciferol.

Ergocalciferol is derived from the ergot fungus, which grows on plants and mushrooms. Thus, vitamin D2 is found in a limited number of plant foods such as mushrooms, alfalfa, sunflower seeds, and avocado.

[stephen_b]

Regardless, it's interesting that D2 might have a role separate from D3. We've kinda treated D2 as D3's less successful sibling.

[mikey]

D2 has been described in many articles as basically being undesirable for supplemental use.

But more to the point, the study has little value compared to what actually is important when Alzheimer's Disease is manifesting.

Alzheimer's can be cured with both coconut oil and, if a UCLA human study finds what a mouse study found, high dose niacinamide.

See: http://www.michaelmo...mendations.html

[JamesNV]

...
Vitamin D2 is not found in animal or fish oils. ...

FYI Green Pastures found significant amounts of D2 in their cod liver oil.

[Hebbeh]

...
Vitamin D2 is not found in animal or fish oils. ...

FYI Green Pastures found significant amounts of D2 in their cod liver oil.

http://www.westonapr...zoxNjoiZCdpbnZl

Fish, unlike mammals, birds and reptiles, do not respond to sunlight and rely on vitamin D found in phytoplankton and other fish. Salmon must feed on phytoplankton and fish in order to obtain and store significant vitamin D in their fat, flesh, skin, and organs.

[Hebbeh]

As usual, no one size fits all...it depends on our individual genetic variations...

http://www.scienceda...21113161506.htm
Genetic Variation May Modify Associations Between Low Vitamin D Levels and Adverse Health Outcomes

ScienceDaily (Nov. 13, 2012) — Findings from a study suggest that certain variations in vitamin D metabolism genes may modify the association of low serum 25-hydroxyvitamin D concentrations with health outcomes such as hip fracture, heart attack, cancer, and death, according to a study appearing in the November 14 issue of JAMA.

Vitamin D status is defined by the circulating concentration of 25-hydroxyvitamin D. Lower serum 25-hydroxyvitamin D concentrations are associated with greater risks of many chronic diseases, prompting ongoing clinical trials to test whether vitamin D supplementation can reduce the risk of disease development. Certain complex metabolic pathways suggest that interindividual variability in vitamin D metabolism may alter the clinical consequences of measured serum 25-hydroxyvitamin D, according to background information in the article.

Gregory P. Levin, Ph.D., of the University of Washington, Seattle, and colleagues conducted a study to investigate whether known relationships between serum 25-hydroxyvitamin D and certain diseases would differ according to common variation in 25-hydroxyvitamin D metabolism genes. The study consisted of an examination of 141 single-nucleotide polymorphisms (SNPs) in a group of 1,514 white participants from the community-based Cardiovascular Health Study. Participants had serum 25-hydroxyvitamin D measurements in 1992-1993 and were followed up for a median (midpoint) of 11 years (through 2006). Replication meta-analyses were conducted across the independent, community-based U.S. Health, Aging, and Body Composition (n = 922; follow-up: 1998-1999 through 2005), Italian Invecchiare in Chianti (n = 835; follow-up: 1998-2000 through 2006), and Swedish Uppsala Longitudinal Study of Adult Men (n = 970; follow-up: 1991-1995 through 2008) cohort studies.

The researchers found a SNP within the vitamin D receptor (VDR) gene that significantly modified associations of low serum 25-hydroxyvitamin D concentration with major health outcomes of hip fracture, heart attack, cancer, and death over long-term follow-up. "Findings were observed within a large community-based study of older adults in the United States and were consistent in magnitude and direction across individual disease outcomes, and replicated in a meta-analysis of 3 large independent cohorts. An additional vitamin D receptor SNP significantly modified the low 25-hydroxyvitamin D-disease association in a meta-analysis that included results from the discovery and replication cohorts. The discovered SNPs, which are common in European populations, identified subsets of individuals for whom associations between low 25-hydroxyvitamin D concentration and disease outcomes were either strongly positive vs. null. These results suggest that individuals with specific 25-hydroxyvitamin D metabolism genotypes maybe particularly susceptible to, or protected from, the potential adverse health effects of low vitamin D."

The authors add that "these findings represent a first step toward identifying what may be clinically relevant effects of 25-hydroxyvitamin D metabolism genes and may contribute to a better understanding of the biological impact of genetic variation within the vitamin D receptor. Further studies are needed to confirm these observed associations and to enhance knowledge of how variation in vitamin D metabolism genes may stratify individuals as to their susceptibility to vitamin D deficiency. Evaluating the identified interactions in randomized clinical trials of vitamin D supplementation, when available, would help to assess the validity of our results and pave the way toward identifying individual patients who may benefit most from vitamin D interventions."

Story Source:
The above story is reprinted from materials provided by JAMA and Archives Journals.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
Gregory P. Levin et al. Genetic Variants and Associations of 25-Hydroxyvitamin D Concentrations With Major Clinical OutcomesVitamin D Concentrations and Clinical Outcomes. JAMA: The Journal of the American Medical Association, 2012; 308 (18): 1898 DOI: 10.1001/jama.2012.17304

Edited by Hebbeh, 14 November 2012 - 04:35 AM.

[mikey]

...
Vitamin D2 is not found in animal or fish oils. ...

FYI Green Pastures found significant amounts of D2 in their cod liver oil.

In speaking with the customer services rep at Green Pastures, she acknowledged that D2 found in their cod liver oil was from vegetables eaten by the cod. It is not produced by the cod or, as is said in many studies, from animals of any kind.

[Hebbeh]

...
Vitamin D2 is not found in animal or fish oils. ...

FYI Green Pastures found significant amounts of D2 in their cod liver oil.

In speaking with the customer services rep at Green Pastures, she acknowledged that D2 found in their cod liver oil was from vegetables eaten by the cod. It is not produced by the cod or, as is said in many studies, from animals of any kind.

No kidding. FYI...cod don't make any D on their own....perhaps you missed this part...

http://www.westonapr...Y1O3M6MTA6ImQna

Fish, unlike mammals, birds and reptiles, do not respond to sunlight and rely on vitamin D found in phytoplankton and other fish. Salmon must feed on phytoplankton and fish in order to obtain and store significant vitamin D in their fat, flesh, skin, and organs.

Which means that fish get D via D2 from phytoplankton as they can't make their own.

Edited by Hebbeh, 22 November 2012 - 08:09 AM.

[Kevnzworld]

Regardless, it's interesting that D2 might have a role separate from D3. We've kinda treated D2 as D3's less successful sibling.

This Study found ( quote )

Conclusion:D3 is approximately 87% more potent in raising and maintaining serum 25(OH)D concentrations and produces 2- to 3-fold greater storage of vitamin D than does equimolar D2. For neither was there evidence of sequestration in fat, as had been postulated for doses in this range. Given its greater potency and lower cost, D3 should be the preferred treatment option when correcting vitamin D deficiency.
http://jcem.endojour...96/3/E447.short

[Hebbeh]

Regardless, it's interesting that D2 might have a role separate from D3. We've kinda treated D2 as D3's less successful sibling.

This Study found ( quote )

Conclusion:D3 is approximately 87% more potent in raising and maintaining serum 25(OH)D concentrations and produces 2- to 3-fold greater storage of vitamin D than does equimolar D2. For neither was there evidence of sequestration in fat, as had been postulated for doses in this range. Given its greater potency and lower cost, D3 should be the preferred treatment option when correcting vitamin D deficiency.
http://jcem.endojour...96/3/E447.short

Yes but the study in question wan't concerning D3 levels....it was the question of D2 levels (or lack of) playing a role in alzheimer's. You need to read the study posted and the relevance of.

Edited by Hebbeh, 22 November 2012 - 08:17 AM.

[Kevnzworld]

Regardless, it's interesting that D2 might have a role separate from D3. We've kinda treated D2 as D3's less successful sibling.

This Study found ( quote )






Conclusion:D3 is approximately 87% more potent in raising and maintaining serum 25(OH)D concentrations and produces 2- to 3-fold greater storage of vitamin D than does equimolar D2. For neither was there evidence of sequestration in fat, as had been postulated for doses in this
range. Given its greater potency and lower cost, D3 should be the preferred treatment option when correcting vitamin D deficiency.
http://jcem.endojour...96/3/E447.short

Yes but the study in question wan't concerning D3 levels....it was the question of D2 levels (or lack of) playing a role in alzheimer's. You need to read the study posted and the relevance of.

I saw that. There are so many studies posted in this thread, that it gets confusing. When I read that study, my first thought was...of course higher consumption of oily fish could contribute to lower rates of Alzheimer's . ( EPA/DHA ). The vitamin d2 is correlated, but not necessarily the cause.


" The idea that a lack of the storage form originating from foods such as oily fish and egg yolks might be implicated in the development and progression of Alzheimer's definitely merits further research," Professor Naughton said."

Edited by Kevnzworld, 22 November 2012 - 08:57 AM.

[Hebbeh]

http://www.scienceda...30430131623.htm


Researchers Pinpoint Upper Safe Limit of Vitamin D Blood Levels, Study Suggests


Apr. 30, 2013 — Researchers claim to have calculated for the first time, the upper safe limit of vitamin D levels, above which the associated risk for cardiovascular events or death raises significantly, according to a recent study accepted for publication in The Endocrine Society's Journal of Clinical Endocrinology & Metabolism (JCEM).

There is increasing evidence that vitamin D plays a pivotal role in human physiology. Vitamin D deficiency has been linked to cardiovascular events and mortality, but previous studies have found supplementation fails to decrease mortality or cardiovascular events, while other studies found only minor positive effects.
"The unpredictable results from previous studies may be due to the misconception that 'the higher the better,'" said Yosef Dror, PhD, of Hebrew University in Rehovot, Israel, and lead author of the study. "Although our study did not directly test the impact of vitamin D supplementation, we believe our results suggest it may be possible that only moderate supplementation within a narrow range of serum calcidiol (the main vitamin D fraction in the blood) will be associated with the most positive results."
Researchers conducted a study of 422,000 people aged 45 years or older, who underwent vitamin D blood assays. They found for the first time that the safe range of vitamin D levels with respect to coronary morbidity lies between 20 to 36 ng/mL. Vitamin D levels below and above this range adjusted rates of increased mortality and morbidity significantly.
More than 60 percent of the tested population had insufficient blood levels of vitamin D. Half of these subjects had severely low vitamin D levels which was associated with a 1.5 times increased risk of acute coronary morbidity or mortality. Three percent of those tested had elevated vitamin D levels above 36 ng/mL, which was associated with a 1.13 times elevated risk of coronary morbidity or death.
"Supplementing the entire population may jeopardize those found within the upper-normal range, shifting them to levels that are beyond the range associated with the lowest morbidity rates," said Dror. "Although we could not assess the impact of Vitamin D supplementation, our results may suggest that such supplementation to increase vitamin D blood levels, with strict monitoring to avoid overload, may have a significant influence on public health. This hypothesis still needs to be assessed in intervention trials"
Other researchers working on the study include: Shmuel Meir Giveon of Tel-Aviv University in Israel; and Moshe Hoshen, Ilan Feldhamer, Ran Balicer and Becca Feldman of the Clalit Research Institute, Clalit Health Services in Israel.

Story Source:

The above story is reprinted from materials provided by The Endocrine Society.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

• Y. Dror, S. Giveon, M. Hoshen, I. Feldhamer, R. Balicer, B. Feldman. Vitamin D Levels for Preventing Acute Coronary Syndrome and Mortality: Evidence of a Non-Linear Association. Journal of Clinical Endocrinology & Metabolism, 2013; DOI: 10.1210/jc.2013-1185