I've heard of people using large amounts of glyconutrients before surgery to remove a tumor and they found the tumor completely encapsulated.

Other people had their tumor completely disappear, over time. I'm sure they were doing other things too - eating good foods, etc.

Might be something to look into.

Thanks, Sharon.

This is something that Gerry has mentioned as well, and it is something I am now doing. From Gerry: "Immunostimulation from glyconutrients from mushrooms, lactobacilli and yeast cell walls, as well as mannose from aloe vera inner gel and some vegetables, will, among other things, stimulate natural killer (NK) cells which search and destroy cancer cells."


Mike

Gerry,

Your thoughts about chondroitin are well-put. However, I plan to err on the side of caution on this one because of chondroitin sulfate's link to cell proliferation and cancer cell differentiation. From a study on leukemia cells:

"Different glycosaminoglycans were tested to evaluate their effects on proliferation and differentiation processes of a monoblastic leukemia cell line (U-937). Heparin and derivatives (from 0.1 to 100 micrograms/ml) inhibit cell proliferation; heparan sulfate does not produce modifications, while chondroitin sulfate and dermatan sulfate (from 0.01 to 100 micrograms/ml) significantly stimulate cell growth. . . . while chondroitin sulfate and, to a lesser extent, dermatan sulfate, induce a strong decrease of differentiative markers." (Exp Cell Res. 1994 Nov;215(1):119-30)

About using MSM: I have been using MSM along with chondroitin for over ten years--and glucosamine even longer. They have probably saved me from having my knee replaced. I am wondering, however, about continued use of MSM since I am now taking so many supplements and nutrients designed to attack the cancer cells.

On the one hand, MSM seems to increase cell permeability, but may also speed the rate at which substances leave the cell, if I am not mistaken. I am wondering if it is advisable to speed up this process?? On the other hand, MSM may deliver extra oxygen to the cancer cells and thereby make them more aerobic and hasten their destruction. Does this make sense to you?

Mike

Mike,

You�ve been bombarded with numerous suggestions of things to try. I�ll add another one that I just ran across. The February 2007 issue of Life Extension Magazine has an article on vitamin D. This issue is not yet available on line so I can�t give you the link yet�I will add it as soon as possible. Following is a paragraph copied from the article:

Life Extension Magazine�February 2007
Dr. Michael F. Holick has published numerous papers detailing the relationship between inadequate vitamin D levels and increased risk of diseases ranging from osteoporosis and arthritis to cardiovascular disease and cancers. Activated vitamin D is one of the most potent inhibitors of cell growth,� he notes, a fact that may explain its importance in cancer prevention. �I don�t see any downside to taking pharmaceutical levels of vitamin D to fight prostate cancer,� he adds.

One more thing to consider.

Mari

Mike,

Go to www.HealthSalon.org and read the posts in the cancer and alternative therapies sections regarding ozone therapy. There is a clinic in Mexico doing the most powerful form of ozone therapy available. Only place in North America. You could give them a call and see what they say regarding your condition.

I have provided many links at the above site to teach about what ozone can do.

I have also heard about an effective treatment in Canada using heat to the prostate. But don't know how to find that info now. Anyone?

Arrow

LEF now carries a higher-dosage Vitamin D product (5,000 IUs per capsule). The price is pretty reasonable.

https://tinyurl.com/3x5e8z

__________________
You're officially invited to come visit my new blog: www.healthyfellow.com

No problem being cautious. However, one's caution must have a sound basis.

I just read the abstract. And from what I could gather, it was done on cells in a test tube or Petri dish, not in a living body. And they tested only a group of substances. So my response is, what else would we expect but that one group would have more proliferative effects than another? But this does not mean that if such substance is taken in, it would cause or aggravate leukemia.

Like, what if they tested carbs against protein against fat? Will we then avoid whatever of the three would show the most proliferative effect? I think such would be a wrong conclusion. At the very least, they should do the test on a living organism, like a lab mouse or rat. Unless a study reaches that phase, it is absolutely wrong to draw conclusions on what we should avoid. (Similar such studies, even in lab animals, now identify virtually any substance to be carcinogenic. So it's impossible to have clinical cancer? )

Or what if the cell line used was not a cancer line but, say, white blood cells like macrophages or lymphocytes? Again, for sure one of the substances would have a more proliferative effect than the others.

We should be thorough in our interpretation of studies like these.

We may be confusing some things here. Being able to pass through cell membranes is a property of the substance, not its effect on the cell membrane. MSM is a variant of DMSO which is well known for its ability to penetrate. So for MSM and DMSO, there isn't really any change in cell permeability. It's simply the substance that can penetrate. (DMSO is also known to "carry along" substances with it. I suspect MSM would share the same property. MSM is simply DMSO with an additional oxygen atom.)

As for MSM's role in cancer (or DMSO for that matter), you'll be surprised what a "MSM cancer" search in google brings up. I think it's more for beneficial than harmful to cancer patients. (So far, I just browsed through the titles of the first page of search results.)

The reason I brought up MSM is that it's raw material for a lot of substances, including chondroitin. So if you're wary of taking chondroitin, then just take MSM and leave it up to the body to decide what to do with it. (As a source of sulfur, it can be used to build cysteine which is an important component of many proteins like enzymes, immunoglobulins, etc., as well as connective tissue matrix. It's also the raw material, as cysteine, from which our body makes alpha lipoic acid/ALA, as well as glutathione which is part of superoxide dismutase.)

Gerry

Gerry,

Some years ago I got my hands on some pharmaceutical-grade DMSO to use on my arthritic knee. Knowing that it carries other substances more easily through cell membranes, I experimented by adding some glucosmine and chondroitin to the DMSO, hoping they would be carried more directly to the joint. Unfortunately, they did not blend too well together, but I think some got through because I began to stink more than ever. My wife did not like getting close to me as a consequence, so I give up on that experiment.

With regard to MSM and cell permeability, however, I thought I had read that it makes the cells better able absorb nutrients and release toxins by virtue of its impact on the cell membrane. I had been using MSM BEFORE drinking any wine, thinking that the toxic by-productcs of alcohol would more readily pass out of the cells.

In re-checking, I found the following:

"One well-known nutritionist, Earl Mindell, Ph.D., has a different idea on this. In his book, The MSM Miracle, he notes that MSM may relieve pain by making cells more flexible and permeable. These qualities help equalize a pressure differential involved in pain. He notes that when pressure outside the cell drops, cells inflate and become inflamed. Nerves then register the inflammation and we feel pain. MSM has been shown to add flexibility to cell walls while allowing toxins to exit and nutrients to enter the cell. This softens the tissue and helps to equalize pressure buildup that results in inflammation and pain.

"Jacobs and Lawrence, although agreeing with Mindell on the benefits of MSM, are not yet ready to champion the role of MSM in increased cell permeability. They note that although cell permeability is a function of DMSO, and that MSM is a derivative of DSMO, there is no evidence that MSM has this function."

But it appears that Jacobs has changed his mind. He writes:

"MSM has definite anti-inflammatory and circulation-enhancing properties. It also appears to provide greater cell permeability that results in improved uptake of nutrients at the cellular level."

So perhaps it would be a good idea to use MSM as part of an anti-cancer protocol. Maybe it will help B17, arteminisn, etc. get into the cancer cells more efficiently.

Mike

I take 2,000 to 4,000 IU per day. I have purchased some 50,000 IU capsules for emergency use in the event of an infection. I've tested it once when I thought I was coming down with the flu. I took 200,000 IU per day for two days and stopped the infection. I bought the mega capsules from LifeSpanNutrition.
[quote:5a7e8a8054]Interactions Between Vitamins A and D

If there is one, single most important shortcoming in the research investigating the toxicity of vitamin D in humans, it is that despite decades of controlled animal experiments showing that each of the fat-soluble vitamins protect against the toxicity of the others, research in humans continues to address the toxicity of vitamin D as if its actions were independent of vitamins A, E, and K.

In 1937, Wayne Brehm presented before the Ohio State Medical Association the results of an experiment comparing the effects of the administration of cod liver oil with that of vitamin D2 to over 500 pregnant women. Vitamin D2, especially in conjunction with calcium, produced extensive abnormal calcification of the placenta, in one case extending into the uterine wall, and in three cases producing kidney stones within the developing fetus; cod liver oil, by contrast, produced no more tissue calcification than seen in controls.50 Brehm could not demonstrate, however, whether the results of his experiment were attributable to the difference between vitamins D2 and D3, to a protective effect of vitamin A, to a protective effect of other constituents of cod liver oil, or to some combination thereof.

The same year, Agnes Fay Morgan, Louise Kimmel and Nora Hawkins became the first American researchers to demonstrate that vitamin A protects against the toxicity of vitamin D.51 Citing German research that had been completed over the previous three years showing that the lethal doses of several fish liver oils fed to mice were identical to that of synthetic vitamin D2 when the liver oils were stripped of their vitamin A,52 and that large doses of vitamin A protected against vitamin D toxicity,53 the Morgan team fed rats various concentrations of vitamin A with toxic doses of vitamin D in various forms. The doses of vitamin D used were 4,000 IU per day or greater, which is the bodyweight-adjusted equivalent of a typical human consuming over 5,000,000 IU per day. The researchers used synthetic vitamin D2 and concentrates of the liver oils of tuna, cod, sea bass and halibut. Although vitamin D2 was most toxic, massive doses of all forms of vitamin D when combined with low doses of vitamin A decreased growth and bone mineralization and increased the calcification of the lungs, heart and kidneys, while vitamin A consistently protected against these effects in proportion to its dose.

In 1951, French researchers showed that intramuscular injections of a natural fish oil concentrate containing massive amounts of vitamin A (and potentially other protective factors) prevented growth retardation, kidney calcification and death induced in rats by intramuscular injections of massive doses of vitamin D2. This showed that the interactive effect is independent of intestinal absorption.54

Vitamin A has since been shown to substantially protect against skeletal defects, bone demineralization and soft tissue calcification induced in rats by large amounts of vitamin D2,55 nearly eliminate similar effects induced in rats by vitamin D3,56 and completely eliminate similar effects induced in turkeys by vitamin D3,57 even though each of these studies used doses of vitamin A that were only half the doses used of vitamin D.

More recently, a group of researchers from the University of Georgia's Department of Poultry Science showed that vitamin D3 increased the need for vitamin A in chickens even when the dose of vitamin D was insufficient to guarantee protection from rickets,58 and that even small to moderate doses of vitamin D decreased liver stores of vitamin A regardless of whether they were supplied in the diet or by exposing the chickens to ultraviolet light.59

Why would vitamin D have depleted the chickens of vitamin A? In 1935, the German researcher F. Thoenes put forward the hypothesis that vitamin D requires vitamin A in order to function, and that high doses of vitamin D cause toxicity by producing a state of relative vitamin A deficiency.60 Over 70 years later, molecular biologists have now proven at least the first part of his hypothesis correct. On August 25, 2006, a team of researchers from Spain and Germany published a report showing that 9-cis-retinoic acid, one of the hormonally active forms of vitamin A, is an essential factor for the full functioning of vitamin D.61 In the absence of 9-cis-retinoic acid, activated vitamin D and its receptor could only bind weakly to DNA and could therefore only exert a small effect on gene expression. When 9-cis-retinoic acid was available, however, it formed a large complex that included its own receptor, vitamin D, and the vitamin D receptor; this complex was able to bind to DNA very strongly and vitamin D was able to fulfill its full function. Most striking, the "defective" vitamin D receptor that is present in a genetic form of rickets that cannot ordinarily be cured by vitamin D became fully functional in the presence of 9-cis-retinoic acid.

Although the body can convert the all-trans-retinol form of vitamin A found in foods and supplements into 9-cis-retinol,62 it is tempting to speculate that this research may show an advantage to cod liver oil over other sources of vitamin A, which naturally contains a substantial amount of 9-cis-retinol.63

If high doses of vitamin D use up vitamin A, they might leave less vitamin A for other important processes�one of those processes is preventing the calcification of kidneys, whether that calcification is induced by vitamin D or by some other means. French researchers recently found that when they fed rats the equivalent of a daily human dose of 15,000 IU of vitamin A, the administration of oxalate was less effective at inducing the deposition of calcium oxalate crystals in the kidneys; on the other hand, if they administered oxalate first, the subsequent administration of vitamin A was not able to correct the condition.64 This might explain why researchers in the 1930s and 1940s were finding that over 90 percent of patients with kidney stones suffered from clinically verifiable vitamin A deficiency,65 yet in most cases administration of vitamin A was unable to correct the problem.66

Nevertheless, researchers at that time also observed that kidney stones in some cases continued to get worse in spite of vitamin A therapy,67 and when cod liver oil concentrate was administered to rats in amounts providing the equivalent to a daily human dose of over 136,000,000 IU of vitamin D, the vitamin A appeared to ameliorate the growth retardation, bone demineralization and kidney calcification to a much greater extent than it ameliorated the calcification of the lungs and heart.51 Thus, it appears that vitamin A is only one piece of the puzzle.
Should We Stay Away From Cod Liver Oil?

In the Vitamin D Council's May, 2006 newsletter, Dr. John Cannell wrote that vitamin D deficiency is the rule in most of the world except in the Scandinavian countries, yet, he wrote, "hip fractures in these same countries are the highest in Europe, probably from the excessive vitamin A in cod liver oil. Stay away from cod liver oil."68

To support his contention that cod liver oil contributes to hip fractures, Dr. Cannell supplied a single reference.69 This reference was a compilation of estimated fracture rates in different European countries. Norway, which is the Scandinavian country where cod liver oil is widely used,70 was not included. The incidence of hip fracture was strongly associated with life expectancy; the authors suggested that this was in part because the countries with the best medical care were the most likely to readmit patients for a fracture after they had already been discharged once, and therefore count the same fracture twice. Sweden, where 47 percent of fractures were counted more than once, had the highest fracture rate of any country. No information about the intakes of vitamin A, vitamin D, or cod liver oil was reported in the study.

Oslo, Norway has nevertheless reported the highest fracture rate in the world.71 Although 25 percent of the Oslo population uses cod liver oil daily,70 those who use cod liver oil daily during part or all of the year have a lower risk of fracture than those who do not.72 Of the several studies examining the relationship between blood levels of vitamin A and fracture risk, the only study to list cod liver oil as a source of vitamin A found that the people with the highest levels of vitamin A had the lowest risk of fracture.73

There is one, single clinical trial testing the effect of cod liver oil on fracture risk.74 In this study, the researchers compared the consumption of a daily teaspoon of standard cod liver oil containing 400 IU of vitamin D to that of a daily teaspoon of cod liver oil that had been stripped of its vitamin D. The cod liver oils were administered to residents in 51 nursing homes over a period of two years. Although there was no difference between the two groups, probably because 400 IU is only half the dose of vitamin D generally required to reduce fracture risk,33 the fracture rate of those taking both forms of cod liver oil was lower than the overall fracture rate for those living in the nursing homes in which the trial was conducted. Rather than support the admonition to "stay away from cod liver oil," these findings suggest that cod liver oil can protect us against bone fractures, especially in old age.
Interactions Between Vitamins K and D

Whereas vitamins A and D act as hormones, communicating to cells which proteins they should make, vitamin K activates a select group of vitamin K-dependent proteins after they have already been made. Since some of the proteins that vitamin K activates are the very same proteins that cells make in response to signals from vitamins A and D, it would be a serious error of omission to begin a discussion of either our requirements for or the toxicity of vitamin D without first examining its interactions with vitamin K.

Although vitamin K is most commonly known for its ability to activate blood clotting factors, it is also responsible for the activation of two other important proteins: osteocalcin, which is involved in the mineralization of bone matrix, and matrix Gla protein (MGP), which protects soft tissues from calcification.75 Since vitamin D is necessary for proper bone mineralization and its most common toxic effect is the calcification of soft tissues, the importance of the relationship between vitamins K and D should already be clear.

Molecular biology clarifies this relationship even further. Osteocalcin is produced exclusively by osteoblasts, which are the cells that form new bone matrix. While collagen forms the main framework of bone matrix, osteocalcin is responsible for its mineralization.76 Osteoblasts make osteocalcin when they are signaled to do so by the hormonal forms of vitamins A and D. When osteoblast cells are incubated with activated vitamin A or activated vitamin D alone, their expression of osteocalcin increases only minimally; by contrast, when the same cells are incubated with activated vitamins A and D together, osteocalcin expression increases dramatically.77

This osteocalcin, however, cannot function until it is activated by vitamin K.75 Therefore, no one of these three nutrients can contribute to bone health without the presence of the other two.

Epidemiological evidence and clinical trials confirm the importance of vitamin K to osteoporosis. Blood levels of inactivated osteocalcin are strongly associated with an increased risk of fracture, while vitamin K intake is strongly associated with a reduced risk of fracture. One study showed people with the highest levels of inactivated osteocalcin to have six times the risk of fracture than those with normal levels. As expected, clinical trials show that vitamin K supplementation increases the activation of osteocalcin, decreases bone loss, and increases bone mineral density.75

Epidemiological studies show an inverse correlation between bone mineral density and calcification of the arteries�a major contributor to heart disease�suggesting that osteoporosis and heart disease are linked by the common thread of vitamin K deficiency.75 Since vitamin K is necessary for the activation of MGP, which has been proven to be responsible for protecting soft tissues from calcification,78 researchers from the Netherlands set out to investigate whether vitamin K intake was associated with a reduced risk of heart disease and whether or not this might be mediated by its protection against arterial calcification.

Between 1990 and 1993, they collected data on the vitamin K intakes of more than 4,500 people over the age of 55 and used a procedure called radiography to measure the extent to which disease, who had died from it, and how this related to vitamin K intake and arterial calcification. Calcification of the arteries turned out to be the best predictor of heart disease. Those in the highest third of vitamin K intakes were 52 percent less likely to develop severe calcification of the arteries, 41 percent less likely to develop heart disease, and 57 percent less likely to die of it.79
Sources of Vitamin K

There are two forms of vitamin K: vitamin K1 is found in green vegetables and plant oils, especially olive oil; vitamin K2, which is produced by intestinal bacteria in small and probably inconsequential amounts, is found in animal foods and fermented plant foods.87

Although vitamin K1 is most abundant in the diet, it is very poorly absorbed. Even the addition of two tablespoons of butter88 or corn oil87 to spinach could only increase absorption of vitamin K1 to between 10 and 15 percent. By contrast, the absorption of vitamin K2 is close to 100 percent.87

The two forms of vitamin K are not physiologically equivalent: vitamin K1 is preferentially used by the liver to activate clotting factors, while vitamin K2 is preferentially used by bone to activate osteocalcin and by soft tissues to activate MGP.85 vitamin K1 offers no protection against Warfarin-induced soft tissue calcification, while vitamin K2 offers complete protection.85 Likewise, in over 4,500 men and women enrolled in the Rotterdam Study, intake of vitamin K2 was strongly associated with a reduced risk of arterial calcification and heart disease, while vitamin K1 had no relationship to either variable at all, even though it constituted a full 90 percent of the dietary vitamin K.79 It is therefore vitamin K2, and not vitamin K1, that we would expect to simultaneously enhance the effectiveness of and increase the safety of vitamin D.

Since vitamin K2 is produced by lactic acid bacteria,89 lacto-fermented foods are an excellent source of vitamin K2. Sauerkraut contains more than four times as much vitamin K2 as beef and more than twice as much as pork, although natto, a Japanese fermented soy food, contains the most vitamin K2 of any food measured. The K2 in lacto-fermented foods, however, is not the exact same form as the K2 in animal products. Whether or not the difference is important is unclear. Egg yolks, butterfat, and goose meat, especially goose liver, are excellent sources.87 Among organ meats, brain, pancreas, and salivary glands contain the highest amounts, while bone contains less but is substantially richer than muscle meat.90 Chicken and duck are decent sources, followed by beef and pork.87

By contrast, fat-free animal foods do not contain any vitamin K2 at all, and low-fat animal foods contain less vitamin K2 than their full-fat counterparts.91 Although sourdough bread is fermented partly by lactic acid bacteria, it does not contain vitamin K2.87 Surprisingly, vitamin K2 is nearly or completely absent from most seafood that has been measured, including wild Alaskan fish such as salmon and halibut87,91 although the eggs of fish have not been analyzed. By contrast, seafood is an excellent source of vitamin D. That these two vitamins are distributed in the food supply so differently underscores the need for a balanced and varied diet.

Although there are no studies investigating whether supplementation with high doses of vitamin K can reverse the toxic effects of massive doses of vitamin D, there are several lines of evidence, described in more detail in the sidebar below, that strongly suggest vitamin D produces toxicity by depleting the body of vitamin K: first, mice that by genetic defect are born completely lacking the vitamin K-dependent MGP protein bear a striking resemblance to animals that have been fed toxic doses of vitamin D; second, the anti-clotting drug Warfarin exerts toxic effects almost identical to those of vitamin D by depleting the body of vitamin K; third, vitamin K completely protects against the toxic effects of Warfarin, suggesting it would likewise protect against the toxic effects of vitamin D.
The Warfarin Connection

Although there are no studies investigating whether supplementation with high doses of vitamin K can reverse the toxic effects of massive doses of vitamin D, there are several lines of evidence that strongly suggest that vitamin D produces toxicity by depleting the body of vitamin K.

First, mice that by genetic defect are born completely lacking the vitamin K-dependent MGP protein bear a striking resemblance to animals that have been fed toxic doses of vitamin D. These mice suffer from extensive calcification of the aorta and its branches, the arteries, the trachea and the lungs. Just as those fed toxic doses of vitamin D, the MGP-null mice also suffer from bone demineralization and growth retardation. Although the mechanism by which vitamin D toxicity causes growth retardation has never been clarified, experiments with MGP-null mice show that the zones of cartilage responsible for elongation of the bones become extensively calcified, disrupting the process of bone growth. Finally, like animals fed massive doses of vitamin D, these animals lived for a short period of time before their defect caused them to die.78

The second line of evidence comes from the synergistic toxicity produced by vitamin D and the anti-clotting drug, Warfarin. Like other coumadin derivatives, Warfarin�originally introduced as a rat poison in 194880�inhibits blood clotting by interfering with the recycling of vitamin K. Like those fed toxic doses of vitamin D, animals fed Warfarin develop extensive calcification of the soft tissues,81 the same that has been reported to occur in people on long-term and moderate-term treatment with various coumadin derivatives.80,82 When researchers injected rats with 300,000 IU per kg bodyweight of vitamin D3 each day for three days and every 12 hours thereafter, the rats suffered the expected soft tissue calcification. As expected for this dose of vitamin D, the rats were all still alive on the tenth day. When vitamin D3 was combined with Warfarin, however, the soft tissue calcification was dramatically amplified and all rats died by the ninth day. The combination of vitamin D and Warfarin produced the same result that would have been achieved with a higher dose of vitamin D.81

The final line of evidence is drawn from two findings: first, the same drugs that counteract calcification induced by Warfarin also counteract calcification induced by vitamin D; second, vitamin K is capable of completely abolishing calcification induced by Warfarin, suggesting that it would also be capable of completely abolishing calcification induced by vitamin D.

University of California researcher Paul A. Price (no relation to Weston Price) showed that ibandronate, a drug currently used to treat osteoporosis, completely abolished the calcification induced in rats by subcutaneous injections of both Warfarin83 and massive doses of vitamin D3.84 Ibandronate protected not only against calcification of the aorta, arteries, trachea, lungs, and kidneys, but also against vitamin D-induced anorexia, weight loss, lethargy, and death. Although the mechanism by which ibandronate exerts its protective effect is not understood, these studies strengthen the concept that a common mechanism underlies the toxicities induced by both Warfarin and vitamin D.

Subsequently, researchers in the Netherlands showed that vitamin K itself is sufficient to completely abolish Warfarin-induced soft tissue calcification.85 This convincingly shows that Warfarin, which is an established inhibitor of vitamin K recycling, causes soft tissue calcification by inducing a vitamin K deficiency, and strongly suggests that vitamin D does something very similar.

Since vitamin D toxicity is remarkably mirrored by mice that lack a vitamin K-dependent protein, since Warfarin induces a remarkably similar type of toxicity by inducing vitamin K deficiency, since Warfarin and vitamin D toxicity respond to similar treatments, and since Warfarin's toxicity can be completely abolished by providing sufficient vitamin K, it follows that vitamin D toxicity is likely to be at least in part a form of vitamin K deficiency.

Recent research on how vitamins A and D affect the synthesis of MGP may connect the interaction between all three vitamins. When MGP is activated by vitamin K, it protects the soft tissues from calcification. Although it isn't known whether MGP is actively harmful in its inactive form, it is known that calcified arteries accumulate abnormally high amounts of the inactive protein,75 and that toxic amounts of vitamin D dramatically increase its synthesis.81 If vitamin D produces its toxic effects by stimulating the synthesis of more of this protein than vitamin K can keep up with, it would explain why vitamin A is so protective: in the cells that line the walls of blood vessels, vitamin D increases the synthesis of MGP, while vitamin A decreases its synthesis.86 It may be, then, that an extreme imbalance between vitamins A and D leads to the synthesis of abnormally high amounts of MGP. If there is enough vitamin K to activate all of the MGP, it will help protect the soft tissues from calcification. If, instead, the vitamin K cannot keep up with the level of MGP being produced and the pool of vitamin K becomes depleted, soft tissue calcification ensues.

Although this mechanism is not proven, it would provide, if it is correct, a revolutionary insight into why vitamins become toxic when administered by themselves but health-promoting when provided in the context of a balanced, nutrient-dense diet.
Viewing Vitamin D Through the Proper Paradigm

Vitamin D's interactions with other nutrients in the diet make it clear that we cannot consider the subject of either vitamin D requirements or vitamin D toxicity by looking at vitamin D alone. Vitamins D2 and D3 are in some respects very different from one another. The types of fat we eat, drugs we use and toxins to which we are exposed affect our ability to efficiently use vitamin D. Vitamin A is an essential factor in vitamin D's hormonal function, and vitamin K is necessary to activate the proteins made in response to vitamins A and D. Vitamin D toxicity appears to result from a depletion of vitamin K, and animal evidence suggests that even small amounts of vitamin D increase the need for vitamin A. Therefore, we must ask a most important question when we consider the various studies on vitamin D requirements and vitamin D toxicity: what was the dietary context in which the vitamin D was consumed? Otherwise, we are in danger of drawing the wrong conclusion.
Vitamin D in Adults: Requirements and Safety

Recommendations for what constitutes an adequate intake of vitamin D vary 20-fold. While the U. S. Institute of Medicine31 recommends a mere 200 IU per day for adults under the age of 50, some leading vitamin D researchers such as Dr. Reinhold Vieth and Dr. Robert Heaney recommend 3,000 to 4,000 IU per day as both necessary and safe.33,98

These differences result largely from the different paradigms through which these researchers interpret the uncertainties within the available data. The Institute of Medicine follows in the tradition of the National Research Council, which set the adult RDA for vitamin D at 0 IU in 1941 because it had not yet been proven that adults require vitamin D.99 Likewise, in 1997, the Institute of Medicine set the adequate intake at what it supposed would protect against severe vitamin D deficiencies like rickets and osteomalacia, which have been proven beyond a doubt to be a result of vitamin D deficiency. Other researchers take into account the fact that humans living in the tropics have always obtained between 4,000 and 10,000 IU per day from sunshine; extensive circumstantial evidence suggests that these higher amounts protect against cancer and autoimmune diseases, and support a general state of vibrant health.33

Recommendations for what constitutes a safe intake of vitamin D also vary widely. Dr. Vieth argues that 4,000 IU of vitamin D per day is safe even if one obtains an additional 4,000 IU per day from sunlight,33 while the Institute of Medicine has set the tolerable upper limit at 2,000 IU per day. Krispin Sullivan, on the other hand, takes a much stricter position. Sullivan, a well-researched author and clinical nutritionist, argues that any intake of vitamin D beyond 800 IU per day from food, supplements and sunshine combined is unsafe without testing and supervision.100

Two approaches are necessary in order to distinguish between the relative merits of each of these positions: first, to establish a general perspective through which we can view uncertainties in the scientific evidence, we must consider what quantity of vitamin D our ancestors typically obtained throughout our pre-modern history; second, we must apply our understanding of the interactive nature of the fat-soluble vitamins to the available evidence.
Does Vitamin D Interact with Vitamin E?

There are two international studies, of which only the abstracts are available in English, investigating the effect of large doses of vitamin E on the toxicity of vitamin D. A Russian study conducted in 1977 found that a combination of massive doses of vitamin E and selenium combined were able to reduce the soft tissue calcification induced by equally massive doses of vitamin D2 by between 54 and 96 percent, depending on the tissue.95 A more recent Ukrainian study showed vitamin E to substantially reduce the free radical damage induced in the arteries of rabbits by large doses of an unspecified form of vitamin D.96

Whereas there is evidence that vitamin D toxicity is the result of a relative deficiency of vitamins A and K, the Russian and Ukrainian studies could simply be explained by a model wherein vitamin E fills a generic antioxidant function that has nothing specifically to do with vitamin D.

Nevertheless, our understanding of vitamin E is rapidly changing. Researchers are now questioning whether vitamin E truly functions primarily as a free radical scavenger as has long been assumed, and research is accumulating showing that vitamin E's primary function may be to act as a hormone and regulate gene expression. Some of vitamin E's hormonal functions appear to involve the retinoid X receptor, which also interacts with vitamins A and D and their respective receptors, suggesting that the functions of vitamins E, A, and D may be more interrelated than we currently realize.97
Defining Toxicity

Before we approach these questions, however, we need to have an accurate understanding of what vitamin D toxicity is; otherwise we would not know what to look for. Because vitamin D toxicity is usually accompanied by an elevated level of calcium in the blood, called hypercalcemia, researchers have generally equated the two and assumed that the toxic effects of vitamin D are the result of elevated calcium levels.31 However, the available evidence does not support this concept of vitamin D toxicity.

First, both vitamin A56,103 and ibandronate84 (a drug that also inhibits Warfarin toxicity) reduce or eliminate the soft tissue calcification and other toxic effects of vitamin D without substantially reducing the vitamin D-induced hypercalcemia. Second, Warfarin, a vitamin K inhibitor, produces a toxicity profile almost identical to that of vitamin D, but does not increase serum calcium levels.81 Third, one group used vitamin D to produce calcium deposition in the kidneys of chickens at doses that did not lead to hypercalcemia.104 This finding is consistent with a case report of four post-menopausal women who were taking undetermined doses of vitamin D without their knowledge in the form of supplements that appeared to be contaminated with large amounts of vitamin D2: these patients had abnormally high vitamin D levels, three times the calcium in their urine as is normal, and appeared, albeit inconclusively, to have associated bone loss. Yet none of these subjects had hypercalcemia.105 Taken together, these data suggest on the one hand that blood levels of calcium can become elevated without leading to toxicity, and on the other, that toxicity can occur even in the absence of elevated calcium.

Dr. Vieth points out that elevated levels of calcium in the urine, called hypercalciuria, would be a more sensitive measure of vitamin D toxicity, though most studies unfortunately have not looked for this endpoint.33 Even this hypercalciuria, however, is difficult to interpret. Urinary calcium would naturally be expected to increase to some degree from the enhanced intestinal absorption provided by sufficient levels of vitamin D.

More importantly, vitamins A and D cooperate to maintain calcium and phosphorus levels in the blood, apparently by stimulating the absorption of these minerals in the intestine. In rats, when the two vitamins are combined, vitamin D increases calcium levels and decreases phosphorus levels, while vitamin A decreases calcium levels and increases phosphorus levels.106 The only researchers to study this interaction in humans have confirmed that vitamin A does indeed attenuate the rise in serum calcium induced by vitamin D, but they did not study the effect of either vitamin on serum phosphorus.107 Excretion of either mineral into the urine reflects the ratio between them in the blood: hypercalciuria will occur not only when calcium levels are too high, but also when phosphorus levels are too low.108 It therefore is not clear whether hypercalciuria resulting from vitamin D supplementation reflects a "toxic" dose of vitamin D, or simply reflects a relative deficiency of vitamin A.

The best measures of vitamin D toxicity would be long-term studies lasting several years that measure the formation of kidney stones, use radiography to determine the degree of arterial calcification and measure markers of bone resorption. These studies would only be of substantial value if they took into account, at a minimum, the intakes of vitamins A and K, as well as the use of Warfarin and other coumadin derivatives, which not only synergize with vitamin D to produce toxicity,81 but have themselves been shown to produce arterial calcification in humans over the course of several years.82 Such studies simply do not exist.
Is the "Adequate Intake" Really Adequate?

In 1997, the U. S. Institute of Medicine's Food and Nutrition Board set the "adequate intake" (AI) of vitamin D for adults under the age of 50 at 200 IU per day.31 The Institute estimated that 100 IU per day is adequate in the complete absence of sunlight, and doubled this figure to 200 IU so as to provide a margin of uncertainty. This figure is based on two studies: first, one study that did not account for sunlight showed a daily supplement of 100 IU per day given to women consuming less than this was able to correct osteomalacia; second, a study of Nebraskans consuming between 130 and 200 IU per day during the winter showed that they maintained vitamin D levels of 12 ng/mL, which is high enough to protect against osteomalacia but is associated with an increased risk of fracture.114

These Nebraskans suffered from hyperparathyroidism and malabsorption of calcium, which led the authors of the study to conclude that although "200 IU vitamin D [per day] may prevent vitamin D deficiency per se, it is not sufficient to normalize calcium absorption" and warned that this "would be expected to cause negative calcium balance and osteoporosis."101 However, the Institute concluded that an AI of 200 IU per day "may actually represent an overestimate of true biological need."31

For adults between the ages of 50 and 70, the Institute cited a study showing 800 IU per day of vitamin D protected against bone loss compared to 200 IU per day. Although the authors concluded that 200 IU per day "is inadequate to minimize bone loss,"102 the Institute strangely decided that, since there was no evidence in the study that a dose lower than 800 IU per day wouldn't have been just as effective, there was therefore no evidence that people at this age require more than 200 IU per day. This fuzzy math was achieved by ignoring the 100 IU per day that the low-dose group received from diet. By pretending that the low-dose group was only consuming the 100 IU per day that they were given as a supplement, the Institute was able to claim that it was "uncertain" that 200 IU wouldn't have been just as effective as 800 IU�despite the fact that 200 IU is exactly what the group with the greater bone loss was consuming. The Institute then doubled this dubiously derived figure to provide a margin for uncertainty and set the AI to 400 IU per day for this age level.31

For adults over 70, the Institute cited literature showing that 800 IU per day is necessary to reduce the risk of hip fracture. Despite citing numerous studies showing that 400 IU per day cannot reduce the risk of hip fracture, the Institute concluded that 300 IU is adequate because it protects 85 percent of the elderly from having a vitamin D level below 10 ng/mL. It doubled this figure to provide a margin of uncertainty, establishing the AI at 600 IU�25 percent lower than the minimum dose shown to lower fracture risk.31 This is a strange definition of "adequacy" indeed.
The Way It's Always Been

In order to establish a starting point from which to interpret the available data, it is instructive to consider what amounts of vitamin D our ancestors have obtained throughout our history, prior to the rapid modernization that we have experienced over the past several centuries, which has far displaced our foodways and lifestyles from those that constituted the context of our evolution and provided us with our birthright to radiant health.

The clearest way to estimate this amount is to study how much vitamin D is obtained from sunlight by people leading active outdoor lifestyles in environments that are saturated with UVB sunshine on a year-round basis. Vitamin D synthesis in the skin reaches an equilibrium with its degradation in a rather short period of time so that only a fixed amount of vitamin D synthesis is possible on a given area of skin during each exposure. Over time, the skin adjusts its melanin content in order to further fine-tune the amount of vitamin D synthesized. Since the body has such a well-designed process for regulating the amount of vitamin D obtained from sunlight, it seems unlikely that it would allow the synthesis of inherently toxic amounts of vitamin D or even amounts in great excess of those needed for optimal health.

In order to determine how much vitamin D a person receives from foods and sunshine combined, researchers measure the levels of 25-hydroxyvitamin D, or calcidiol, in the subjects' blood. This is the semi-activated form of the vitamin; because it is the primary storage form, it reflects the amount of vitamin D obtained from food, supplements and sunshine, and is therefore the best measure of a person's vitamin D nutritional status.31 (These values are usually reported in nanograms per milliliter, which is abbreviated ng/mL. For the purpose of simplicity, I will refer to serum calcidiol levels as "vitamin D levels.")

Farmers and lifeguards who live and work in sun-rich environments have vitamin D levels between 55 and 65 ng/mL.109 A recent, rigorously controlled study showed that in Omaha, Nebraska, healthy middle-aged males required a daily intake of 5,000 IU in order to maintain 60 ng/mL from October through February.110 In the more northern climate of Toronto, Canada, men and women of a similar age took 4,000 IU per day from January through June, a period of time during which their sunshine exposure would be increasing. The average vitamin D level at the end of the study was only 40 ng/mL, although one person's level reached as high as 48 ng/mL.111 One would expect that 4,000 IU would have been even less effective in environments farther to the north. These studies suggest that someone living in the tropics obtains an amount of vitamin D from food and sunshine that is substantially in excess of 5,000 IU per day.

Krispin Sullivan reports that in her practice she has found that a person's vitamin D level continues to increase while the person takes a constant dose of vitamin D over the course of two to three years.112 If this is true, then dose-response studies lasting five months would be insufficient to estimate the amount of vitamin D that people living in the tropics obtain from sunshine. In the aforementioned studies, however, doses between 4,000 and 10,000 IU all appeared to reach a plateau in four to five months, which is precisely what would be predicted by conventional models of pharmacology based on vitamin D's half-life.109

Nevertheless, researchers have not conducted studies with these doses that have lasted longer than five months. Studies examining the effect of these doses over two to three years, which would be able to test Sullivan's contention, are necessary if for no other reason than to convince physicians and authorities of the safety of obtaining doses of vitamin D argued by many leading researchers to be necessary for optimal health. Although the uncertainty should be acknowledged, our best estimation is that sun-rich environments provide 5,000 IU or more per day of vitamin D.
Hypersensitivity to Vitamin D

Certain conditions involving alterations in vitamin D metabolism make it unsafe for a small number of individuals to supplement with vitamin D or consume vitamin D-rich foods without the supervision of a knowledgeable and caring physician. These include:

* Primary hyperparathyroidism
* Sarcoidosis
* Tuberculosis
* Lymphoma
* Kidney failure
* Liver failure

If you have one of these conditions, consult with a physician before making a decision to increase the vitamin D content of your diet.
To Test or Not to Test?

Dr. Vieth has adequately criticized the study that formed the basis of the Institute of Medicine's upper limit of 2,000 IU per day: this small study, short of duration, did not chemically verify the dose of vitamin D used, nor did it quantify the study subjects' actual vitamin D levels and was thus unable to account for the input of vitamin D from all sources; although it found 3,800 IU (the Institute divided this amount by an "uncertainty factor" to derive the upper limit) to produce a substantial rise in serum calcium, more rigorously controlled studies have not been able to replicate the finding.111 Since hypercalcemia is not a productive model of vitamin D toxicity, however, we must instead look at real endpoints such as bone loss, calcification of the arteries, kidney stones, lethargy, anorexia, and other symptoms associated with vitamin D toxicity.

In her self-published book, Naked at Noon: Understanding Vitamin D and Sunlight, Krispin Sullivan has emphasized one study and several anecdotes that examine critical endpoints like heart disease and bone loss to support her argument that any amount of vitamin D exceeding 800 IU per day from all sources�including sunlight�is unsafe without testing and supervision.46
Testing Vitamin D Levels

All people must make a personal decision whether or not to test their vitamin D levels based on the amount of vitamin D they are consuming, their own perception of its risk, and any concern they may have that they are not consuming enough. If you choose to test your vitamin D level, there are several things to keep in mind:

* Order the calcidiol test, not the calcitriol test. The correct test is also called 25-hydroxyvitamin D or 25 (OH) D
* The laboratory's reference range is likely to use a very wide definition of "normal." Sufficient levels of vitamin D are at least 32 ng/mL, and ideal levels are probably between 40 and 50 ng/mL.
* Your vitamin D levels will rise over the spring and summer and decline over the fall and winter. Your vitamin D level during one season will therefore not necessarily reflect your vitamin D level for other seasons.
* The scientific data does not clearly and consistently define an ideal level of vitamin D, and we do not know to what degree intakes of other nutrients affect what constitutes the ideal level.

It is difficult to conceive of an argument against testing. After all, physicians routinely test cholesterol levels on the tenuous assumption that modifying them will impact their patients' risk of heart disease. There is no agreement within the scientific literature identifying an ideal level of cholesterol, no agreement on what should be done if a level is too high or too low, and no end in sight to the raging debate over whether statins should be added to the water supply or whether they are contributing to side effects ranging from congestive heart failure to amnesia in millions of people. By contrast, there is clear agreement on what level of vitamin D is deficient and moderate agreement on what level is ideal�and cod liver oil is cheaper than Lipitor, even boosting your memory rather than destroying it to boot.

To contend that amounts exceeding 800 IU per day are dangerous without testing, however, demands such an extreme degree of personal restriction that it requires a rigorous level of substantiation to be justified. In order to guarantee an intake within 800 IU per day, many fish, modest amounts of cod liver oil and exposure of more than the face and hands to summer sunshine would all be considered unsafe.

Recognizing that some people do not have medical insurance, that not all insurance companies will pay for a vitamin D test, that some people have very little money, and that most people have many competing priorities, the risk that such small amounts of vitamin D pose needs to be quantified. According to Dr. Robert Heaney, one of the experts who sat on the Institute of Medicine's upper limit panel, over whose objections (along with Dr. Michael Holick's) the policy-makers established the current limit, if everyone in the American population took 2,000 IU per day of vitamin D, the vitamin D levels of 0.6 percent of the population would rise above 60 ng/mL.98 This amount is 2.5 times that which Sullivan recommends as safe to consume without testing. Although there is clearly the possibility that the metabolism of some people will defy the statistical calculations, this is also true for the metabolism of virtually every other chemical in the body.

Sullivan argues that researchers who assume the safety of any amount of vitamin D that can be naturally provided by sunlight are making an assumption that could put some people in danger. To support this, she cites, in addition to several anecdotes, one human study. Researchers studying the vitamin D levels of males residing in South India found that those with levels exceeding 89 ng/mL had over three times the risk of heart disease as those with levels under 89 ng/mL.113 This study is difficult to interpret because it is retrospective: since the patients' vitamin D levels were measured after they were have other explanations. For example, subjects who were diagnosed with heart disease may have increased their vitamin D levels afterward by following advice to increase their outdoor physical activity or increase their consumption of fish. Nevertheless, since heart disease is associated with vitamin K deficiency and can result from soft tissue calcification,79 which is one of the primary results of vitamin D toxicity, the study is worth a closer look.

According to Sullivan, the study showed that toxic doses of vitamin D can be obtained from sunlight alone because the researchers used a test that was specific for vitamin D3, which is not available as a supplement in India. On the contrary, the researchers noted that the South Indian diet is rich in fish, which provides vitamin D3, and various tubers such as cassava. Cassava is an unusually high source of vitamin D2, which may be more toxic than vitamin D3. Because of the subjects' dietary intake of vitamin D2, which the researchers did not attempt to quantify, the use of a test specific for vitamin D3 made the researchers unable to quantify the total amount of vitamin D circulating in the subjects' blood.

The only rigorous dose-response study available110 shows that it would take someone living in an environment similar to Omaha, Nebraska substantially more than 10,000 IU per day over an extended period of time to reach the level of vitamin D associated with heart disease in this study. More importantly, we don't know what the subjects' intakes of vitamins A and K were, nor whether any of them were taking pharmaceutical coumadin derivatives, all of which are mediating factors in the toxicity of vitamin D. If the diet of these subjects was rich in vitamin D2-containing tubers and the meat of fatty fish but was not rich in the organs of fish and other animals, butter, egg yolks, or lacto-fermented foods, the combination of extensive sunshine and diet may have provided a high amount of vitamin D without the synergistic and protective context of the other fat-soluble vitamins.
Dangers of Vitamin D?

In Naked at Noon,46 clinical nutritionist Krispin Sullivan offers several anecdotes in support of the potential toxicity of moderate doses of vitamin D.

The first is a report of four cases of apparent vitamin D toxicity published in a 1997 issue of The Annals of Internal Medicine.105 Four post-menopausal women were found to have elevated vitamin D levels, up to 88 ng/mL, and urinary calcium three times the normal level. Although the authors were criticized for not providing rigorous measurements demonstrating bone loss, the patients were originally referred to them for osteoporosis, and when their vitamin D supplements were discontinued, their bone mineral density improved, suggesting that the toxic level of vitamin D was contributing to bone loss. An analysis of the supplements these women were taking showed that they contained at least ten times the vitamin D advertised on the label. Two products advertised as "animal extracts" were found to be contaminated with massive amounts of vitamin D2, the vegetarian form of vitamin D.

The second anecdote offered is an unpublished report of a psoriasis patient who was receiving narrow band UVB treatment. Sullivan suggests that since artificial, narrow band UVB treatment contains only that portion of the spectrum that is responsible for the synthesis of vitamin D and not other portions of the spectrum that degrade it, toxic amounts of vitamin D can be synthesized. The patient's vitamin D level rose to 127 ng/mL, which is theoretically toxic. Physicians are clearly obliged to measure their patients' vitamin D levels when administering a treatment that affects those levels.

The third anecdote is an unpublished report of a woman taking a 2,000 IU per day from a vitamin D3 supplement. After 14 months, she began suffering from bone ache, fatigue, and depression. Six months later, her vitamin D level was 95 ng/mL. Tests revealed she had elevated urinary calcium and 6 percent bone loss. Within weeks after dropping the supplement, her symptoms disappeared. Despite the resolution of her symptoms, her vitamin D level continued to rise in response to the summer sun, reaching 110 ng/mL three months later. Given the inconsistencies in the timeline of her recovery, the supplement should have been analyzed to confirm that its labeled dose was accurate, that it did indeed contain vitamin D3 as labeled and not vitamin D2, and an attempt should have been made to determine whether she was sensitive to some unlabeled component of the supplement. No such attempts, however, were made.

There continues to be no published report of toxicity resulting from an intentional dose of vitamin D3.
Revising Our Understanding of Vitamin D

The need to revise our understanding of vitamin D and its toxicity is clear: the conventional understanding that vitamin D's toxicity results from its excessive elevation of calcium levels cannot account for the observations that toxicity can result without elevated calcium and that elevated calcium can result without toxicity. The ability of the fat-soluble vitamins to protect against the toxicity of each other clearly demonstrates a model of toxicity that makes the study of any one vitamin on its own inherently inconclusive.

Many questions about how long-term intakes of vitamin D affect blood levels, whether an ideal level of vitamin D can be truly defined, and whether there is any such thing as an inherently safe or inherently toxic dose remain to be scientifically resolved. What is clear is that the protective and synergistic context of a nutrient-rich diet is not only underappreciated, but is essential to consuming vitamin D in a way that provides optimal benefit and maximum safety. Dr. Vieth has written that the purpose of supplementing with vitamin D is to "compensate for the biological consequences of modern life."33 Lack of exposure of bare skin to sunshine is not the only biological consequence of modern life for which we must compensate; we must also return to the nutrient-rich foods on which our ancestors thrived and of which modernity has disposed: the fats and organs of animals raised on the pasture of mineral-rich soil, foods preserved by traditional fermentation rather than modern refrigeration, and the mineral-rich gifts of the oceans in which life originated.

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18. Engelsen, et al., "Symposium-in-Print: UV Radiation, Vitamin D and Human Health: An Unfolding Controversy: Daily Duration of Vitamin D Synthesis in Human Skin with Relation to Latitude Total Ozone, Altitude, Ground Cover, Aerosols and Cloud Thickness," Photochemistry and Photobiology, 81 (2005) 1287-1290.
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24. Determined by a search of https://www.pubmed.com for "statin vitamin D" on August 27, 2006. One study was excluded from this analysis that reported calcitriol and all hydroxylated vitamin D metabolites combined but did not report calcidiol or any reasonable marker of vitamin D nutritional status.
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27. Ismail, F. Corder, C. N. Epstein, S. Barbi, G. Thomas, S. "Effects of pravastatin and cholestyramine on circulating levels of parathyroid hormone and vitamin D metabolites," Clin Ther., 1990; 12(5): 427-30.
28. Wilczek, H. Sobra, J. Justova, V. Ceska, R. Juzova, Z. Prochazkova, R. Kvasilova, M. Pacovsky, V. "[Iatropathogenic effect of Mevacor on vitamin D metabolism]," Cas Lek Cesk, 1989; 128(40): 1254-6.
29. Folkers, K. Langsjoen, P. Willis, R. Richardson, P. Xia, L. J. Ye, C. Q. Tamagawa, H. "Lovastatin decreases coenzyme Q levels in humans," Proc Natl Acad Sci USA, 1990; 87(22): 8931-4.
30. Price, W. A. "Why Dental Caries With Modern Civilizations? XI. New Light On Loss of Immunity to Some Degenerative Processes Including Dental Caries," Dental Digest, 1934 July; 240-245.
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32. Assuming 60 ng/mL of calcidiol, for which 5 ng = 1 IU, and 100 ng/ml of vitamin D, for which 25 ng = 1 IU. The reasonableness of this calculation was confirmed by Dr. Bruce Hollis (personal communication).
33. Vieth, R. "The Pharmacology of Vitamin D, Including Fortification Strategies." In Feldman, D. Pike, J. W. Glorieux, F. H., eds., Vitamin D: Second Edition, Burlington: Elsevier Academic Press (2005) 995-1015. (Review)
34. Green Pastures, "High Vitamin Cod Liver Oil � High Vitamin Butter Oil, Cod Liver Oil � Green Pastures," https://www.greenpasture.org/products/cod_liver_oil. Published January 1, 2006. Accessed August 28, 2006.
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44. Trang, H. M. Cole, D. E. C. Rubin, L. A. Pierratos, A. Siu, S. Vieth, R. "Evidence that vitamin D3 increases serum 25-hydroxyvitamin D more efficiently than does vitamin D2" Am J Clin Nutr, 1998; 68: 854-8.
45. Armas, L. A. Hollis, B. W. Heaney, R. P. "Vitamin D2 Is Much Less Effective than Vitamin D3 in Humans," The Journal of Clinical Endocrinology & Metabolism, 2004; 89(11): 5387-5391.
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48. Laing, C. J. "Comparative Biology of Plasma Vitamin D Binding Protein." PhD thesis. Department of Animal Science, University of Sydney, Sydney, Australia, 2000.
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51. Morgan, A. F. Kimmel, L. Hawkins, N. C. "A comparison of the hypervitaminoses induced by irradiated ergosterol and fish liver oil concentrates," The Journal of Biological Chemistry, 1937; 120(1): 85-102.
52. Dalmer, O. Von Werder, F. Moll, T. Z. physiol. Chem. 1934; 224: 86. As cited in Morgan, et al., 1937; op cit.
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54. Teulon, H. Paulais, R. Gounelle, H. "Action freinatrice des huiles de poisson a haute teneur en vitamine A sur l'intoxication calciferolee du rat (voie parenterale)," Societe de Biologie

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Does anyone know how to translate micrograms of Vit D into International Units? I bought some for husband, but not sure about amounts to take in this way of labelling. EU regulations, and so on - - -

https://www.nafwa.org/downloads/vitD.htm

snip

Sometimes labels will have vitamin D in micrograms (ug) instead of IU�s. To convert, 1 ug = 40 IU�s. Example: 5 ug = 200 IU of vitamin D.

Thank you Joyce. That is helpful.

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• Quote:

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