Vitamin D Myths Exposed

[Old Herb Lady]

Ever wonder why the government started caring about your health and fortifying your food with Vitamin D ?
They add it to the milk, cereals, juices, yogurt, margarine?? Hmmm.

14 Misunderstandings -------




1. Vitamin D is not a vitamin; it is an immunosuppressive steroid.

Let’s start with this fact: the vast majority of doctors touting the benefits of vitamin D are not aware of discoveries made by researchers in the field of molecular biology, which have clearly shown that the “vitamin” D derived from diet and supplements is not a vitamin, but a steroid with immunosuppressive properties when elevated.[2]

There are several forms of vitamin D. The form of vitamin D we get from food, diet, supplements and sun exposure is called D3. D3 is converted by the liver into 25-D, which functions as a steroid. 1,25-D, the activated form of vitamin D, functions as both a steroid and a hormone. It is produced inside various types of cells, including those of the immune system and the kidneys, as well as in response to sunlight.[3] In healthy individuals, the kidneys continually convert 25-D into its active form, 1,25-D.[4][3]

According to a paper published by the Institute of Biomedical Research in Birmingham, England, “The active form of vitamin D, [1,25-D] is a potent immunomodulatory seco-steroid” meaning that it is a steroid-like molecule which is able to control the activity of the immune system.”[5]

Molecular modeling has shown that the hormonal 1,25-D form binds and activates the Vitamin D Receptor. The Vitamin D Receptor plays a fundamental role in the body. It transcribes 913 genes, and researchers at McGill University in Canada just released a paper saying it may actually transcribe 27,091.[6] But, the Vitamin D Receptor also performs another critical function – it serves as a switch that regulates the activity of the innate immune system.[7][8][9]

A molecular model comparing the structure of 25-D and of 1,25-D[10]According to recent 10]According to recent molecular models, the steroid 25-D binds the Vitamin D Receptor and affects the activity of the immune system as well, but in a manner opposite to 1,25-D. When the steroid 25-D binds the Vitamin D Receptor, it decreases the activity of the receptor, causing the innate immune system to slow down and shut off. This effect begins around 20 ng/ml and gradually increases with higher levels of 25-D, until the VDR becomes completely blocked.[11]

At the moment, most researchers understand that 1,25-D activates the Vitamin D Receptor. However, they are unaware of the models which demonstrate that 25-D has the opposite effect. Consequently, they do not understand that when people start to supplement with extra vitamin D (which is converted into 25-D) the Vitamin D Receptor begins to turn off, not on.

Most of these researchers are also unaware of a new understanding about the cause of many chronic diseases. As a person falls ill with a chronic disease, L-form bacteria begin to live inside the cells of the immune system and in various tissues.[12][13] These bacteria create proteins that, just like elevated 25-D, are able to bind and block the Vitamin D Receptor.[14] Together, elevated 25-D and bacterial proteins block the ability of the Vitamin D Receptor to turn on the immune system more than either substance alone.

Molecular modeling has also shown that the medication Olmesartan (called Benicar in the United States) is able to bind and activate the Vitamin D Receptor (VDR). Not only does Olmesartan activate the receptor, but, because its concentration can be controlled, it can reactivate the VDR even when it would normally be blocked by bacterial proteins or by excessive levels of 25-D. Olmesartan also binds a number of other receptors involved in the inflammatory response.[15]

Long thin L-forms emerging from a cell as shown in a photo taken by Andy WrightPatients on a medical treatment known as the Marshall Protocol are able to use Olmesartan, along with pulsed, low-dose antibiotics to slowly eliminate L-form bacteria over the course of several years. These patients also eliminate vitamin D from their diets and block sunlight in an effort to lower the amount of 25-D blocking the Vitamin D Receptor. Hundreds of patients on the Marshall Protocol, who are sick with a wide array of previously incurable chronic diseases, are reporting symptomatic improvement or complete resolution of symptoms. Their case studies, many of which are documented on the Marshall Protocol study site, confirm in a clinical setting the molecular models which show that elevated 25-D is immunosuppressive.[16][10]

The Vitamin D Receptor also directly controls the expression of many of the antimicrobial peptides (AMPs).[8][9][17][14] The AMPs are proteins that kill bacteria, viruses, and fungae by a variety of mechanisms including disrupting membranes, interfering with metabolism, and targeting components of the machinery inside the cell. When 25-D reaches the level at which it inactivates the receptor, the AMPs are no longer produced, and bacteria can spread more easily throughout the body.

People infected with L-form bacteria are particularly prone to the effects of 25-D on the Vitamin D Receptor. That is because their L-form bacteria have created proteins which have already bound and deactivated the Vitamin D Receptor to varying degrees. Extra amounts of the steroid 25-D only bind and shut down the receptor even more, further inhibiting the innate immune system, the transcription of thousands of genes, and the production of the AMPs.

“It is when L-form bacteria die that they begin to cause a major increase in symptoms for the host, since as they die they release a large amount of toxins and cytokines, proteins that generate pain and fatigue. ”The above scenario is all too familiar, since L-form bacteria are found everywhere in our environment, from soil, to water, to sperm, to inside the womb.[18] Consequently, it seems that few people will remain free of them for long and most will acquire substantial levels of them as they age.[19]

L-form bacteria have evolved mechanisms that allow them to live for long periods of time within the cells, and when alive, generally persist without generating too many symptoms.[20]

It is when L-form bacteria die that they begin to cause a major increase in symptoms for the host, since as they die they release a large amount of toxins and cytokines, proteins that generate pain and fatigue. Furthermore, as L-form bacteria die, the cell that they have parasitized dies as well, and cellular debris is released into the bloodstream. These substances cause the tissues to become inflamed, resulting in what is known as “Th1 inflammation.”[21]

As previously discussed, the innate immune system is responsible for killing L-form bacteria and is controlled by the Vitamin D Receptor (VDR). Elevated levels of the steroid 25-D and bacterial proteins bind and inactivate the VDR, causing the immune system to work less effectively.

As the immune system becomes increasingly inhibited, fewer L-form bacteria are killed. Furthermore, the Vitamin D Receptor is no longer able to transcribe the antimicrobial peptides, and fewer bacteria are killed by DNA fragmentation. As fewer bacteria die, fewer inflammatory cytokines are released, and fewer toxins and cellular debris enter the bloodstream. As the level of inflammation temporarily decreases, a patient will start to feel better.

This seeming wellness is illusory. Without the innate immune system and the antimicrobial peptides to keep L-form bacteria in check, the pathogens easily spread to new cells, new tissues, and new organs.

Many people who begin to supplement with vitamin D or spend extended periods of time in the sun only have a small or moderate amount of L-form bacteria in their bodies. Since these people’s immune systems are not yet severely compromised (their VDRs are not yet partially blocked by bacterial proteins), their bodies kill a fair share of the bacteria, resulting in minor aches and pains. But if 25-D rises to the level at which it inhibits their immune systems, less bacteria die, Th1 inflammation decreases, and their minor symptoms may be temporarily relieved.

Naturally, such patients feel that the extra vitamin D is helpful. It may take decades before their L-form bacterial load rises to the threshold at which they are diagnosed with an “autoimmune” illness, or have a stroke or heart attack. At this point later in life, they seldom make the connection between their current illness and the extra vitamin D they have been taking with no apparent ill effect for such a long period of time.

“If you think about it, it seems little wonder that vitamin D has become so popular. It’s basically an over-the-counter steroid.” It’s easy to see how people infected with even minor amounts of L-form bacteria tell their doctors that supplementation with vitamin D and increased exposure to the sun make them feel better. As Joyce Waterhouse, PhD, a researcher affiliated with Autoimmunity Research Foundation stated in a discussion of vitamin D in diseases caused by L-form bacteria, “If you think about it, it seems little wonder that vitamin D has become so popular. It’s basically an over-the-counter steroid.”[22] Even the Vitamin D Council, a California non-profit agency who promote the use of vitamin D, say on their website that “vitamin” D is a steroid. Yet this group fails to question the full implications of their own statement.

Other steroids are commonly known to be immunosuppressive. Take the corticosteroid medication prednisone, a particularly effective immunosuppressant that affects virtually all of the immune system.[23]

Prednisone is given to patients with diseases such as multiple sclerosis, rheumatoid arthritis, sarcoidosis, and lupus. Most doctors continue to think that these diseases are “autoimmune” in nature, and result when the body somehow mounts an immune response against its own cells and tissues. Hence, the desire to slow the immune system.

But when one understands that the diseases listed above are caused by L-form bacteria, the entire scenario becomes reversed. Prednisone, just like elevated 25-D, prevents the immune system from killing bacteria. Patients experience short-term relief and resolution of symptoms as the die-off slows down. But nobody would ever claim that prednisone actually cures “autoimmune” diseases. Instead, in the long run, patients taking prednisone generally become much more ill and require increasing amounts of palliative medication.

“At the moment there is a significant gap in communication between the molecular biologists who have realized that “vitamin D” is a steroid, and doctors who continue to think of it as a nutrient. ”At the moment there is a significant gap in communication between the molecular biologists who have realized that “vitamin D” is a steroid, and doctors who continue to think of it as a nutrient. But now that the actions of 25-D and 1,25-D have been confirmed by molecular modeling, it seems unlikely that doctors will be able to cling to the “vitamin” label for much longer.

As John Arbuthnot, author of Of the Laws of Chance states, “There are very few things we know which are not capable of being reduced to mathematical reasoning……and where a mathematical reasoning can be had, it’s as great a folly to make use of any other, as to grope for a thing in the dark when you have a candle standing by you.”[24]

Of course, it’s only been over the past five years that biomedical researcher Trevor Marshall has revealed how L-form bacteria affect the Vitamin D Receptor, and exactly how 25-D affects the immune system. So clearly, before these very recent discoveries, researchers were forced to study vitamin D while missing vital pieces of the puzzle. However, it seems that in their enthusiasm to identify vitamin D’s benefits, many experts have not sufficiently absorbed the medical literature, literature that well before Marshall’s work revealed the complexities associated with the Vitamin D Receptor, the lynchpin of the innate immune system.





Vitamin D metabolism[24] is much more complicated than some clinicians and researchers realize. Click to enlarge.If researchers made themselves aware of work done by colleagues such as Dr. Tian Tian Wang at McGill University, they would know that when 25-D and 1,25-D bind the vitamin D receptor, they adjust the transcription of at least 913 genes. A search on the website Pubmed reveals that an average of 24] is much more complicated than some clinicians and researchers realize. Click to enlarge.If researchers made themselves aware of work done by colleagues such as Dr. Tian Tian Wang at McGill University, they would know that when 25-D and 1,25-D bind the vitamin D receptor, they adjust the transcription of at least 913 genes. A search on the website Pubmed reveals that an average of one paper a day is published on the actions of the Vitamin D Receptor.[25] Perhaps, armed with an understanding of this research, they would hesitate before recommending that the public take such high doses of the “vitamin.” It is only prudent that such a powerful seco-steroid and its transcriptional activity be understood to a far greater extent lest we all further subject ourselves to what is nothing short of an unofficial clinical trial of historic proportions.

Not surprisingly, the few researchers who understand the complexities of vitamin D seem concerned about supplementation. Recently, Professor Ronald M. Evans, a Fellow of the Salk Institute, delivered a seminar to the FDA about the public health policy on vitamin D. Given that vitamin D is seco-steroid rather than a vitamin, he indicated that he would advise his family against adding vitamin D to their diets. [26]

Based on the above, it’s not surprising that researchers at Duke University found that elderly men and women who consumed higher levels of calcium and, in particular, vitamin D are significantly more likely to have greater volumes of brain lesions, indicating regions of damage that can increase risk of cognitive impairment, dementia, depression and death. The team found that vitamin D intake, (mean 341 IU and maximum intake 1014 IU), was the only variable that retained a significant correlation with the brain lesions when analyzed by a multivariate analysis.[27]

Unaware of the latest research on the immunosuppressive properties of high levels of vitamin D, the researchers hypothesized that the calcium rather than the vitamin D was the main culprit in causing the lesions. They speculated that in patients given extra calcium, the calcium might be deposited inside the blood vessels of the brain rather than the bone. According to their theory, vitamin D would accelerate the process because it is involved in regulating calcium absorption and metabolism.

A much more likely explanation is that the lesions result when L-form bacteria in the brain cause the release of cytokines that damage the tissues. Sometimes the resulting inflammation damages blood vessels and promotes calcification, but it is the L-form bacteria, not the calcium that is the true culprit.

The connection between bacteria and calcification in heart disease has already been noted. Researchers at the Hospital Das Clinicas in Brazil found significantly higher concentrations of Chlamydia pneumoniae and Mycoplasma pneumoniae in calcified nodes of blood vessels throughout the body, including the heart and the aorta - causing them to suggest that “these bacteria may be associated with the development of calcification and inflammation.”[28][29]







2. The vast majority of studies fail to account for the long-term effects of vitamin D.

The decrease in bacterial die-off among patients consuming a lot of vitamin D does mean that, at least in the short-term, less cytokines and toxins are released into the tissues and inflammation decreases. Since these substances damage the tissues, we frequently hear about studies stating that vitamin D can correct problems with the kidneys, parathyroid function, or resolve other maladies.

Although the decrease in toxins, cytokines, and overall inflammation may be helpful in the short-term, over longer periods of time, the negative consequences of L-form bacteria spreading throughout the body inevitably surpass any temporary beneficial effect created by a decreased level of toxins and cytokines, particularly since L-form bacteria have been implicated in such a vast array of diseases.[18]

In April of 2000 a study published in the Archives of Internal Medicine by doctors at the State University of New York at Buffalo found that five patients confined to wheelchairs with severe weakness and fatigue were able to walk after supplementing with 300,000 IU’s of vitamin D (a huge amount!) over a period of six weeks. Sadly, the patients were not “cured”, and almost certainly relapsed in the months following the study. They were simply feeling the effect of a temporary decrease in cytokine and toxin release that resulted after the high levels of vitamin D completely shut down their innate immune systems. In fact, one of the patients actually died in the weeks during which vitamin D was administered.[30]

“Instead, as in the Archives study, they track subjects over the course of weeks, months, or one or two years, during the period of time when study participants are usually feeling the palliative effects of the steroid.”One of the abiding weaknesses of studies on vitamin D is that researchers do not follow subjects consuming the steroid for a sufficient period of time. Instead, as in the Archives study, they track subjects over the course of weeks, months, or one or two years, during the period of time when study participants are usually feeling the palliative effects of the steroid.

Researchers will rarely, if ever, track subjects over the course of decades, the length of time needed to begin to note the negative changes that L-form bacteria cause later in life. In fact, L-form bacteria grow so slowly that researchers in the future will surely have to check back with their subjects at least 20-30 years after they begin supplementing with vitamin D in order to determine whether or not the steroid has contributed to the development of a chronic disease.

[Old Herb Lady]

3. Chronically ill people are not deficient in vitamin D.

We are continually bombarded with studies claiming that patients with chronic disease are deficient in vitamin D. But this is not the case, and the misunderstanding comes from a misplaced focus on 25-D.

Numerous studies have demonstrated that the level of the hormone 1,25-D rises in patients with many chronic diseases.[22] Chronically ill patients starting the Marshall Protocol sometimes have a level of 1,25-D exceeding five or six standard deviations above the “standard” value.[31]





1,25-D affects a range of hormonal pathways. Click to enlarge.Sometimes called the body’s “master hormone”, 1,25-D directly controls the pathways that regulate the body’s other hormones including the thyroid, sex, and stress hormones. Consequently, elevated 1,25-D greatly contributes to the pathogenesis of chronic disease, since as a person’s level of 1,25-D rises to an unnaturally high level, the master hormone can no longer correctly regulate the above pathways.[32]

A wide array of studies also point to the fact that 25-D is low in people with numerous chronic inflammatory diseases.

What explains these altered levels of 1,25-D and 25-D? (Note: If you find that the next few paragraphs seem complicated, hang in there! You will still be able to follow the rest of the article.)

As previously mentioned, in patients with chronic disease, L-form bacteria create proteins that affect the Vitamin D Receptor (VDR) in a manner similar to 25-D. They bind and inactivate the VDR, preventing it from transcribing a wide array of genes and enzymes.

In a paper recently published in BioEssays, “Vitamin D discovery outpaces FDA decision making,”[33] Marshall describes how in healthy individuals, the VDR transcribes an enzyme called CYP24. CYP24 breaks down excess 1,25-D, ensuring that the level of 1,25-D in the body stays in the normal range. But in chronically ill individuals, the VDR (which is blocked by bacterial proteins) can no longer transcribe CYP24. The level of 1,25-D in the body becomes significantly elevated since there is no CYP24 to keep it in check.

1,25-D binds to the PXR receptor, a receptor that is involved in making another enzyme called CYP27A1. CYP27A1 is responsible for converting D3 into 25-D in the liver. Elevated 1,25-D affects the activity of the PXR receptor in a way that causes less D3 to be converted into 25-D, meaning that the level of 25-D in chronically ill individuals drops.

Yet another factor contributes to the low level of 25-D seen in patients with chronic disease. An enzyme called CYP27B1 normally regulates the amount of 25-D converted into 1,25-D. When more CYP27B1 is produced, conversion occurs at a greater rate.

L-form bacteria release cytokines, proteins that cause pain and fatigue. These cytokines activate a protein called Protein Kinase A (PKA). PKA in turn activates CYP27B1, causing more 25-D to be converted to 1,25-D. The level of 25-D in the body decreases, and the level of 1,25-D increases.[34]

A study conducted by researchers at the University of South Carolina supports this scenario. The team gave healthy subjects high levels of 1,25-D and verified that it can indeed inhibit the conversion of vitamin D into 25-D. They found that this phenomenon also occurs in certain diseases in which patients naturally develop a high level of 1,25-D.[35] Consequently, the low 25-D observed in patients with chronic disease is not a sign of vitamin D deficiency, but is an indicator of the disease process.

What happens when doctors and researchers take note of the low level of 25-D in patients with chronic disease? They all too often conclude that the low level of 25-D is contributing to or causing the disease. With such a mindset, doctors are all too eager to give patients oral supplements of 25-D in an effort to “remedy” the situation.

“Unfortunately the exact opposite is true. The level of 25-D in the body is not causing the illness, it is a result of the disease process.” Unfortunately the exact opposite is true. The level of 25-D in the body is not causing the illness, it is a result of the disease process, and as clear an indication as any that the patient is suffering from a significant degree of L-form bacterial infection. It’s similar to the connection between folic acid and heart disease - low levels of folic acid often lead to an increase in the amino acid homocysteine – a compound that at high levels has been linked to increased incidence of cardiovascular disease (CVD). Yet, extensive studies have revealed that giving patients with CVD folic acid supplements does not lower levels of homocysteine, and that high levels of the compound in patients with CVD is simply a result of the disease process.[36]

Key to this misunderstanding are the doctors and researchers who fail to test the level of 1,25-D in patients with chronic disease. If they did, they might pick up on the fact that 25-D is low precisely because 1,25-D is elevated.

This certainly explains why a research team at the University of Wisconsin Osteoporosis Clinic, who did not test subjects’ levels of 1,25-D, seemed puzzled by the results of a study which revealed that some participants getting abundant sun exposure still displayed low levels of 25-D.[37]

Or take for example, scientists at Musgrave Park Hospital in Belfast, Ireland, who published in 2006 the results of a study that tested the level of 25-D in 75 patients with fibromyalgia, but failed to test the subjects’ levels of 1,25-D.[38] Surely the research team must have been perplexed by the fact that, although all of the subjects seemed to be consuming perfectly adequate levels of vitamin D, 69.3% were suffering from vitamin D “deficiency” because their serum levels of 25-D were considered to be too low.

As with most chronic diseases, fibromyalgia is an illness in which L-form bacteria create proteins that prevent the VDR from transcribing the enzymes needed to keep 1,25-D in the correct range.[39] But since the researchers who conducted the study failed to test the level of 1,25-D in their subjects, they focused solely on the diminished level of 25-D and were, it seems, completely oblivious to the actual disease process. This led them to incorrectly conclude “Vitamin D deficiency is common in fibromyalgia and occurs more frequently in patients with anxiety and depression.”

In a similar study, published in 2003 in the Mayo Clinic Proceedings, researchers in Minneapolis tested vitamin D levels in patients suffering from chronic, non-specific, musculoskeletal pain: 93% of them turned out to be vitamin D “deficient.”[40] If these studies’ authors can’t understand the process, it’s easy to understand how other researchers who look over their results would interpret the data to mean that patients with fibromyalgia need to consume even more 25-D, in order to correct the so called “deficiency.”



Incomplete Research: Eight Examples of Studies that Neglected to Test for the 1,25-D Metabolite



Association of subclinical vitamin D deficiency with severe acute lower respiratory infection in Indian children under 5 y.



Vitamin D deficiency in systemic lupus erythematosus



Serum 25-hydroxyvitamin D and colon cancer: eight-year prospective study



Is vitamin D important for preserving cognition? A positive correlation of serum 25‑hydroxyvitamin D concentration with cognitive function



Low vitamin D status: a contributing factor in the pathogenesis of congestive heart failure?



The vitamin D epidemic and its health consequences



Vitamin D status predicts physical performance and its decline in older persons



Bone mass and vitamin D deficiency in adults with advanced cystic fibrosis lung disease


The failure to test for 1,25-D in subjects with chronic disease is as pervasive as it is troubling. The FDA continues to accept results from studies that do not bother to measure 1,25-D.

Naturally, when representatives of the FDA and other health agencies interpret the results of these studies they correlate chronic disease with vitamin D deficiency, and inevitably suggest that people should supplement with increased amounts of the “vitamin” in order to reverse or prevent chronic disease.

Of course, the media picks up on the conclusions of experts incorrectly attributing the low levels of 25-D in their patients to vitamin D deficiency. A recent article in US News and World Report states, “Research on vitamin D has flooded out over the past few months, linking a growing array of health ills to low levels of the nutrient.”[41]

On the tanning website, tantoday.com, Jeffrey Dach, MD, laments in his article “Vitamin D Deficiency, the Ignored Epidemic” that the majority of people living in “sunny Florida” showed vitamin D deficiency (less than 20 ng/ml), or insufficiency (less than 40 ng/ml).[42] This seems odd, considering the fact that if a person spends only 8-10 minutes in the sun they will obtain the entire RDA requirement for vitamin D even if they are not consuming foods with vitamin D or fortified products.

Citing published medical research, Dach goes on to report that vitamin D deficiency has been reported in 57% of 290 medical inpatients in Massachusetts, 93% of 150 patients with overt musculoskeletal pain in Minnesota, 48% of patients with multiple sclerosis, 50% of patients with lupus and fibromyalgia, 62% of the morbidly obese African American Women, 83% of 360 patients with low back pain in Saudi Arabia, 73% of Austrian patients with Ankylosing Spondylitis, 58% of Japanese girls with Graves’ Disease, and 40-70% of all Finnish medical patients.

What Dach doesn’t realize is that the opposite is true. The low 25-D measured in the above studies is a consequence, rather than a cause, of the disease process. In reality, the numbers cited are an indication that the diseases mentioned are caused by L-form bacteria.

An increasing body of research points to the fact that obesity is linked to certain species of bacteria in the gut. Sure enough, a study published in the Journal of Clinical Endocrinology and Metabolism by researchers at Tufts University found that subjects with the highest percentage of body fat had 20% lower blood levels of 25-D than those with the least body fat.[43]

Michael F. Holick, one of the foremost vitamin D “experts” in the country, told the National Institutes of Health symposium “Vitamin D and Health in the 21st Century” that the nation faces “severe vitamin D deficiency” which, if not properly addressed, will have profound far-reaching health consequences. According to Holick and other “experts,” we are in the midst of a “silent epidemic of vitamin D deficiency.”[44]

There’s no disputing the extent to which broad segments of the population have “low” levels of 25-D or that there is an epidemic of chronic disease and obesity. According to the CDC, seven of every ten Americans who die each year, or more than 1.7 million people, die of a chronic disease,[45] and according to researchers at John Hopkins University, 75% of U.S. adults and 24% of U.S. children will be overweight or obese by 2015.[46]

“Or, is this epidemic actually due to excess vitamin D consumption, and the immunosuppressive effects of 25-D on people infected with L-form bacteria?”Could it really be true that Professor Holick’s “silent epidemic” is one of vitamin D deficiency? Or is this epidemic actually due to excess vitamin D consumption and the immunosuppressive effects of 25-D on people infected with L-form bacteria?

To be fair, most researchers and “experts” who study vitamin D are well-intentioned. They are deeply concerned about the health of the public, and are trying their best to battle chronic disease.

But the failure of most doctors and experts to question the level of not just 25-D but 1,25-D in the subjects they examine shows a lack of understanding of the fundamental aspects of vitamin D metabolism. Given that this pair of metabolites is so closely tied to each other, wouldn’t any kind of understanding of the true nature of the vitamins D warrant measuring both?

Some claim that 1,25-D levels are not really important because they sometimes appear to fluctuate, and so do not measure them. Or, when they do measure 1,25-D, they automatically attribute a high 1,25-D combined with a low 25D to secondary hyperparathyroidism, a condition in which the kidneys produce more 1,25-D to compensate for inadequate calcium intake. Rather than recommend more calcium, such clinicians mistakenly recommend more vitamin D.

But secondary hyperparathyroidism can be ruled out by measuring parathyroid hormones, which researchers usually fail to do.[47][32] More thorough studies on several inflammatory diseases[48][49][50] specifically ruled out secondary hyperparathyroidism as a cause for the high level of 1,25D relative to 25D.

Furthermore, some researchers and physicians who test 1,25-D do not realize that the sample must remain frozen before analysis in order for the resulting reading to be accurate. With the limited data most researchers are habitually collecting, it’s easy to understand how they have made the mistake of interpreting the low levels of 25-D in their subjects as an indicator of “deficiency.”








4. Healthy people are not deficient in vitamin D and do not need to consume extra amounts of this steroid.

Based on the misunderstanding discussed above, researchers working with vitamin D and doctors administering the steroid seem fixated on the idea that more is always better. When a study about vitamin D presents inconclusive data, researchers inevitably suggest that the reason they didn’t generate a significant result was that their subjects should have taken more of the substance, which the public invariably understands as an endorsement of the idea that there is no limit to the amount of the vitamin D one should consume.

The prospect of identifying and distributing a substance of near universal benefit to the public’s health has always had an undeniable appeal to researchers, a fact which may have made them less careful about vitamin D. Janet Foutin, a board member of Autoimmunity Research Foundation writes, “There was a flurry of activity to discover vital substances early on, and in that rush, the various forms of vitamin D were confused with one another and have been since– causing regulatory agencies to base their recommendations on faulty assumptions.”

Researchers picked up on the feel-good, seemingly salutary, effects of vitamin D decades ago. It was on this basis that the FDA now encourages food producers to fortify their products with vitamin D, to the point where it is extremely difficult to find non-fortified milk in the United States.

In the United States, the FDA has determined that vitamin D can be added to breakfast cereals, grain and pasta products, milk, milk products such as cheese and butters, and soy milk.[51] Canada goes so far as to require milk, evaporated milk, powdered milk, goat milk, and margarine to be fortified with vitamin D.[52] The drive to supplement dairy products is as aggressive as ever. Even many developing countries currently fortify their milk with vitamin D.

Furthermore, vitamin D is a fat-soluble substance that is stored for weeks or even months inside cells of fatty tissues and the liver.[53] Unlike water-soluble vitamins that need regular replacement in the body, fat-soluble vitamins are eliminated much more slowly than water-soluble vitamins, meaning that it’s relatively easy to maintain an adequate level of vitamin D in the body.

“ Consequently, over the past few years, the “healthy” range for 25-D obtained from bloodwork has been adjusted upward”Countries in Europe do not require that products be fortified with vitamin D, and although many food producers fortify their products anyway, a fair amount of people obtain fresh food from local markets and supermarkets. Many people are puzzled by “the French Paradox” or the fact that some Europeans are able to eat a diet high in fat and still maintain a normal weight, whereas Americans eating a diet high in fat tend to become obese. A recent study by Thorpe et al found that nearly twice as many Americans are obese compared to their European counterparts. Perhaps this difference can be attributed to the amount of vitamin D in the food supply.

But since the vast majority of the public still consume large amounts of fortified products, it is difficult to find people who have a truly natural level of vitamin D in their bodies. Consequently, over the past few years, the “healthy” range for 25-D obtained from bloodwork has been adjusted upward to reflect the fact that people consume fortified dairy products. The FDA now suggests that people maintain a level of 25-D between 30-32 ng/ml, which is in the range at which it becomes immunosuppressive.[54] This means that the levels of 25-D in people eating a diet without fortified foods is inevitably considered to be too low, out of range, and ultimately a menace to their health.

With all the extra vitamin D we have added to the food chain, we no longer know what amount of 25-D the body would maintain under natural circumstances. Could it be that the people we call “Vitamin D deficient” actually have a normal level of 25-D? Studies which have tested the level of 25-D in people who live in countries where vitamin D is not added to the food chain prove this scenario to be true. A study which tested the level of 25-D in 90 “healthy, ambulatory Chilean women” showed that 27% of the premenopausal and 60% of the postmenopausal women had 25-D levels under 20 ng/ml.[55] A study on healthy Bangladeshi women found that approximately 80% of the women had a level of 25-D under 16 ng/ml.[56]

A molecular model showing capnine, a type of protein created by L-form bacteria bound into the Vitamin D Receptor.Add to this mess the fact that the vast majority of people considered to be “healthy” already harbor L-form bacteria. These people can tolerate even less 25-D because their Vitamin D Receptors have already been deactivated by bacterial proteins.

Nevertheless, Dr. Holick has advised the FDA: “The 1997 daily recommended allowances for Vitamin D are totally inadequate to protect public health. New science supports a significant revision of the recommendation. Adults should be getting 1000 International Units (IU) of vitamin D a day, not the 200-600 (IU) that was recommended in 1997. Rewriting the recommended daily requirements as soon as possible should be a top priority.”[44]

Similarly, Dr. Rainhold Vieth, another outspoken advocate for extra vitamin D, is adamant that the daily requirement of vitamin D should be in the range of 4,000 IU, or ten times the Recommended Daily Allowance.[57] The FDA seem to be listening, considering that they are close to accepting a rule change that will amend one of the first health claims authorized in 1993 through the Nutrition Labeling and Education Act on the relationship between calcium and osteoporosis.

“The addition of even more vitamin D to the food supply will, without a doubt, continue to raise the average person’s level of 25-D well past the point at which it becomes immunosuppressive. ” They have proposed to change the claim by adding high levels of vitamin D into the equation, with calcium, for a reduced risk of osteoporosis. The addition of even more vitamin D to the food supply will, without a doubt, continue to raise the average person’s level of 25-D well past the point at which it becomes immunosuppressive.[58]

According to Clarisse Douaud at NutraIngredients-USA.com, a news source for the food and supplement industry, “The proposal is likely to be welcomed by the vitamin industry - at both supply and finished product levels - since it communicates the importance of vitamin D. Moreover, it does not restrict the advice to just some demographics, which could help marketers target new sectors of the market more effectively.”[59]

Should the FDA really get into the business of systematic immunosuppression any more than it already has?

[Old Herb Lady]

5. The public does not require extra sun exposure in order to prevent vitamin D “deficiency.”

One of the complaints of vitamin D promoters is that people have been trained to cover up with sunscreen and heavy clothing due to concerns that they will get wrinkles or skin cancer.[60] Many such promoters of vitamin D including Holick, who is the author of the book The UV Advantage, advise people not to wear sunscreen despite the elevated risk of skin cancer that might result. This is a major problem, considering the fact that exposure to sunlight greatly elevates the level of vitamin D in the body, which directly fuels the ability of L-form bacteria to dysregulate the immune system.

Holick told the New York Times, “I recommend that whatever your ethnicity or skin tone, you get outdoors without a sunscreen somewhere around 20 percent of the amount of time it would take to cause a sunburn, however long that might be.”[61]

Holick stands by this advice despite the fact that in February he was rebuked and forced to resign from the dermatology department at Boston University’s medical school.[62] Part of the reason given was that his work is partly funded, and actively promoted, by the Indoor Tanning Association, an industry group with obvious financial interests.

On the official website of the Vitamin D Council, a group that heavily promotes consumption of vitamin D, executive director John Jacob Cannell states, “We are saying that brief full body sun exposure may slightly increase your risk of skin cancer but it is a much smarter thing to do than dying of vitamin D deficiency. The only way to be sure you have adequate levels of vitamin D in your blood is to regularly go into the sun, or use a sun bed (avoiding sunburn).”[63]

According to the Council, if you totally avoid the sun, “You need about 4,000 units of vitamin D a day, which means you can’t get enough vitamin D from milk (unless you drink 40 glasses a day) or from a multivitamin (unless you take about 10 tablets a day), neither of which is recommended.”[64]

However, it’s been questioned whether sunscreen even blocks the majority of vitamin D production in the body. Scientists at the University of Melbourne took note of the level of 25-D and 1,25-D generated in two separate groups of study participants. One group wore SPF 17 sunsceen during the study period while the other group used a placebo.

They concluded that, “No person, including those aged 70 years and over, developed any vitamin D levels outside the normal reference range during the period of the study. The data suggest that over an Australian summer sufficient sunlight is received, probably through both the sunscreen itself and the lack of total skin cover at all times, to allow adequate vitamin D production in people who are recommended to use sunscreens regularly.”[65]

“In my two decades of practice, I’ve never seen vitamin D deficiency caused by lack of sun exposure due to sunscreen use, yet the evidence that UV rays from the sun cause skin cancer is overwhelming.”The fact that people wearing sunscreen can still produce vitamin D has been confirmed by data collected from patients on the Marshall Protocol study site. Many patients on the Marshall Protocol are forced to avoid the sun in order to keep 1,25-D in the correct range, and experience an increase in symptoms when the metabolite is increased. Even when wearing heavy loads of sunscreen, patients still report symptom increase in response to light, suggesting that vitamin D can be created from the UVA rays which most standard sunscreens do not block adequately[66].

The American Academy of Dermatology says it is “deeply concerned” about the current claims about vitamin D and sun exposure put forth by Holick. “I am not aware of any scientific studies that support this claim,” said Dr. David J. Leffell of the Yale School of Medicine Department of Dermatology. “In my two decades of practice, I’ve never seen vitamin D deficiency caused by lack of sun exposure due to sunscreen use, yet the evidence that UV rays from the sun cause skin cancer is overwhelming.”[67]

“I read better things in ladies’ magazines,” said Dr. Barbara Gilchrest, chair of the dermatology department at Boston University, and an authority on melanoma, the deadliest form of skin cancer. Holick’s book “is an embarrassment for this institution and an embarrassment for him.”[62]







6. Vitamin D does not reverse osteoporosis.

Doesn’t vitamin D help reverse bone less? No. An increasing number of large, recent studies are demonstrating that this is not the case.

Instead, current research has demonstrated that osteoporosis and osteopenia are often the direct result of infection with L-form bacteria which produce inflammatory cytokines and inactivate the Vitamin D Receptor. The only way to achieve long-term reversal of bone loss is to kill the L-form bacteria driving the disease process.

An osteoclastOsteoporosis and osteopenia result when the level of the hormone 1,25-D in the body rises above a certain range (above 43 pg/ml). Elevated levels of 1,25-D actually stimulate bone osteoclasts, cells that remove minerals from the bone.[68]

Stimulated osteoclasts dissolve bone material, causing it to be reabsorbed into the bloodstream. Not only does this lead to osteoporosis, but it can also lead to calcium being deposited in the soft tissues of the body, including those in the lungs, breasts and the kidneys (where it forms kidney stones).[69]

The elevated 1,25-D seen in people with osteoporosis is generally the result of L-form bacterial infection.[69] As previously discussed, L-form bacteria create proteins that bind and block the Vitamin D Receptor, preventing it from transcribing the enzyme CYP24. Since CYP24 is needed to keep levels of 1,25-D in check, the level of 1,25-D becomes greatly elevated in individuals without the active enzyme.

Furthermore, in chronically ill individuals, the cytokine release stimulated by L-form bacteria activates the pathway which causes increased production of CYP27B1, the enzyme that converts 25-D into 1,25-D. As more conversion occurs, the level of 1,25-D in the body rises.

L-form bacteria inside a white blood cell, picture by Emil WirotskoIf osteoporosis results in part from an increase in cytokines generated by L-form bacteria, then it would make sense that treatment to decrease cytokine release would, in the short term, reverse bone loss. Several studies have shown this to be true.

One of the inflammatory cytokines released as a result of infection by L-form bacteria is called TNF-alpha. A research team at the Rheumatoid Arthritis Center in Lyon, France found that a drug which blocks the production of TNF-Alpha led to an increase in the subjects’ spine and femoral bone mineral density (3.9% and 2.5% respectively). Another study, this one by researchers at the Kerckhoff Clinic and Foundation in Germany, on a different group of subjects, confirmed the results, this time finding a 2.7% and 13% increase in bone density of the spine and femur.[70]

It should be noted that these TNF-alpha blocking drugs do not provide a permanent solution to osteoporosis, since L-form bacteria will continue to spread as the drug is administered. Also, TNF-alpha blocking medications are known to have serious side effects. However, the research is of interest since it confirms the importance of Th1 inflammation in osteoporosis.

So how can osteoporosis and osteopenia be reversed? Some clinicians have patients supplement with vitamin D and calcium in an attempt to reverse bone loss. To begin with, patients with chronic disease may obtain less of a benefit from calcium supplements since the calcium metabolism of patients suffering from chronic disease is different from that of healthy individuals.[71][51]

Supplementation with vitamin D only exacerbates the disease process. Supplements are taken orally in the form of vitamin D which is converted to 25-D in the liver. 25-D further blocks the ability of the VDR to transcribe the enzymes which keep 1,25-D in the correct range. This results in greater bone loss as even more 1,25D is produced.

A problem with many studies on bone mass is that participants are given both calcium and vitamin D supplements at the same time. If participants demonstrate a small increase in bone density, which of the two supplements should be given credit for their improvement? Based on what we know about the actions of elevated 1,25-D, certainly the calcium, not the vitamin D, accounts for any positive changes in bone mass noted among study participants.

The largest meta-analysis of calcium and vitamin D trials in people over 50 was recently published in the Lancet. It combined the results of 29 randomized trials in which researchers had given participants supplements of calcium and vitamin D. The researchers state on page 663 of their paper that the “addition of vitamin D supplementation was not shown to offer additional risk reduction over and above the use of calcium alone.” They did find a small reduction in fracture risk (12%) correlated with calcium supplementation.[72]

Similarly, a study by researchers at the Indiana University School of Medicine found that calcium supplementation (750 mg) improved bone density over a four-year period, whereas vitamin D supplementation (600 IU) had no effect. In fact, the effect of calcium on bone loss was blunted in subjects with the highest levels of vitamin D, causing the team to point out the danger of over-supplementation of the elderly with vitamin D if they are on an adequate calcium intake.[73]

Another study, published in the Archives of Internal Medicine, also found that simply taking vitamin D as a supplement did nothing to improve bone health in black women. In the study, researchers randomly assigned 208 healthy black women, aged 50 to 75 years, to receive either 20 micrograms a day of vitamin D3 or a placebo. In addition, all the women received calcium supplements. After two years, the researchers increased the dose of vitamin D3 to 50 micrograms per day. All of the women underwent bone mineral density scans every six months during the three years of the study, to check for changes in bone health.

“There was really no difference in bone loss with vitamin D supplementation: our conclusion is that it does not need to be increased. ”According to the study’s lead author, “There was really no difference in bone loss with vitamin D supplementation: our conclusion is that it does not need to be increased. Raising vitamin D levels did not show an advantage in terms of bone health.” However, calcium supplementation did cause an increase in bone mineral density in both groups.[74]

On the other hand, some large studies have demonstrated that both calcium and vitamin D supplements do nothing to help strengthen the bones. In 2005, researchers at the University of York in the UK published in the British Medical Journal a study on 3314 people aged 70 years and older who were at risk for hip fractures because of decreased bone mass. The women supplemented with 1000 mg of calcium and 800 IU of vitamin D over a period of 24- 62 months.

By the study’s end, there was no measurable change in the bone quality of any of the women. The researchers found “no evidence that calcium and vitamin D supplementation reduce the risk of clinical fractures in women with one or more risk factors for hip fracture.”[75]

Another study published in 2005 in the The Lancet by researchers at the University of Aberdeen in the UK generated the same results.[76] Yet a 76] Yet a third study, this one published in 2006, conducted by the Women’s Health Initiative, came to the identical conclusion.[77]

And then there are studies showing that vitamin D actually decreases bone mineral density. In 1999, researchers at Cedars-Sinai Medical Center in Los Angeles conducted a small study on patients with osteoporosis and hypercalciuria, a disease in which excessive calcium is excreted in the urine. The participants were taking supplements containing high levels of vitamin D. They were asked to stop taking the supplements for three years, and their bone mass was monitored during that period of time. After stopping the supplements, the level of 25-D in their blood returned to the normal range, the hypercalciuria resolved, and there were annual increases in bone density of all subjects involved.

The study’s authors concluded: “Occult vitamin D intoxication was detected in patients who were using dietary supplements that contained an unadvertised high level of vitamin D. Resolution of vitamin D intoxication was associated with a rebound in bone mineral density.” Their study is particularly valuable because their 3-year follow-up phase showed that the increase in bone mineral density persisted after initial recovery.[78]

Similarly, researchers at the University of Science and Technology in Norway just released the results of a study that measured the forearm bone mineral density of 3,042 Norwegian women, aged 50 - 70 years old. They found that those women who had not taken cod liver oil (a substance that contains high levels of vitamin D) during childhood had higher bone mineral density compared to those who had ingested cod liver oil.[79] Since the study compared childhood intake of vitamin D to bone density at least 4-5 decades after ingestion, it is a good example of how only those studies which track vitamin D intake over long periods of time are likely to pick up on the harm the secosteroid causes in the longterm.

“Resolution of vitamin D intoxication was associated with a rebound in bone mineral density.” In the long run, the best way to reverse the condition is to bring the level of 1,25D in the body back into a range where minerals will no longer be leached from the bones and the level of inflammatory cytokines can return to normal. In the meantime, getting the RDA of calcium from foods and supplements without vitamin D can be helpful.[69]

Another misconception among some clinicians is the idea that vitamin D enhances the absorption of calcium. This is not the case. 25-D is a simple steroid which does not affect the genes responsible for calcium absorption. In contrast, the Vitamin D Receptor is a receptor that transcribes thousands of genes,[6] some of which do affect the metabolism of calcium.

As biomedical researcher Trevor Marshall says, “In chronic disease the two things (vitamin D itself and the VDR) are NOT synonymous.”[80] In patients with chronic disease, the VDR is unable to function properly. As previously discussed, this is due in large part to L-form bacteria that create proteins which inactivate the VDR, to a point where it can no longer correctly transcribe a wide array of genes, including some involved in calcium metabolism.

Once again then, it is only by killing the bacteria responsible for causing the disease process in the first place that the VDR can function properly, allowing the genes that affect the absorption of calcium to be turned on in the correct fashion. The mistaken notion that more vitamin D automatically means more activation of the Vitamin D Receptor, and hence greater calcium absorption, is probably the single greatest reason why vitamin D has been incorrectly identified as the solution to bone loss in people with chronic inflammatory disease.

In the same vein, low calcium in the bloodstream can lead to a condition called secondary hyperparathyroidism. The condition alters the level of Parathyroid Hormone in the body, which can result in bone loss. In patients with the disease, the kidneys try to compensate for the low level of calcium by increasing the conversion of 25-D to 1,25-D. Because the illness involves the vitamins D, many doctors mistakenly think that supplementation with the steroid might help the problem. However, the truth is that this condition is best corrected by bringing the level of calcium intake back into range.

Joyce Waterhouse, Ph.D. has recently described in detail a number of flaws in studies that use the relationship between low 25D and secondary hyperparathyroidism to estimate the optimal level of 25D. One problem is that they usually fail to ensure that subjects are consuming adequate calcium before assessing the relationship between 25-D and PTH. Thus, when researchers at Winthrop University Hospital in New York made sure that subjects consumed adequate calcium, they found that only a small percentage of patients with low 25-D actually had elevated levels of PTH, and that just 16 ng/ml of 25-D is usually enough to keep PTH in the correct range.[81] This was confirmed by a recent study which found that PTH levels frequently remain normal even in patients with very low 25-D. The bone density of the elderly subjects in the study also remained the same as subjects taking higher levels of 25-D as long as their PTH remained normal.[82]

When it comes down to it, 25-D accounts for only a very small percentage of variation in PTH levels, especially when subjects are taking adequate calcium. Several studies have shown that low magnesium, increasing age, or elevated serum phosphate and creatinine due to kidney disease also greatly contribute to the level of PTH, causing researchers at the University Hospital of New Norway to conclude that elevated PTH “is therefore probably a result of a combination of factors.”[83] It’s not surprising then, that several studies have noted that giving vitamin D to patients with low levels of 25-D often does nothing to bring PTH back to normal levels.[84]

In the end, it is perfectly possible that when calcium intake is adequate, most of what remain of the association between low 25-D and elevated PTH is simply part of the pathogenesis of chronic disease and osteoporosis. Just as the low 25-D seen in patients with chronic disease is the RESULT rather than the CAUSE of the disease process, elevated PTH in patients with low 25-D may simply be an indicator of inflammation caused by L-form bacteria.

[Old Herb Lady]

7. Extra vitamin D does not reduce the risk of cancer.

The language of some studies, especially in the sections where researchers are asked to interpret their results, has suggested that supplementing with vitamin D might help people ward off cancer. Other research provides evidence that this is untrue.

In fact, the latest study by the National Cancer Institute - the first study to actually look at the relationship between measured vitamin D in the blood and subsequent total cancer deaths - failed to show an association between baseline vitamin D status and overall cancer risk in men, women, non-Hispanic whites, non-Hispanic blacks, Mexican Americans, and in persons younger than 70 or 70 years or older.[85]

The findings, which appear in the Journal of the National Cancer Institute, are based on an analysis of data for 16,818 subjects who participated in the Third National Health and Nutrition Examination Survey. The subjects were at least 17 years of age when the survey was undertaken between 1988 and 1994 and they were followed through 2000. The researchers did find an association between vitamin D and colorectal cancer risk, most likely for reasons that will be addressed later in this section.

When asked by a correspondent from CBS News if vitamin D can reduce the risk of cancer, David Fishman, head of the National Ovarian Cancer Early Detection Program at New York University said, “I don’t believe vitamin D is the answer. I wish it was as simple as saying ‘If you take vitamin D, cancer will be cured. I don’t think it’s that simple.”[86]

The Mayo Clinic’s website states, “It remains unclear if vitamin D deficiency raises cancer risk, or if an increased intake of vitamin D is protective against some cancers. Until additional trials are conducted, it is premature to advise the use of regular vitamin D supplementation to prevent cancer.”[87]

L-form bacteria may be responsible for at least part of the pathogenesis of cancer. For one thing, L-form bacteria have been found in the tissues of patients with cancer. Some studies have found that people with certain types of cancer, such as prostate cancer, display the same dysregulated vitamin D metabolism observed in people with other chronic diseases now known to be bacterial in origin.[22]

L-forms of various shapes and sizes inside the cells of a patient with breast cancer, photo taken by Alan CantwellSeveral forms of bacteria have already been linked to cancer. Researcher Alan Cantwell used acid-fast staining to identify L-form bacteria in patients with Hodgkin’s Disease, lymphoma, prostate cancer and other immunological diseases.[88] Both gastric cancer and gastric MALT lymphoma (lymphoma of the mucosa-associated lymphoid tissue) have been associated with H. pylori bacteria, and the bacterium has been categorized as a group I carcinogen by the International Agency for Research on Cancer (IARC).[89]

Other research has shown a link between a cancer of the eye, ocular adnexal lymphoma (OAL) and Chlamydia bacteria. In October, researchers at the San Raffaele H. Scientific Institute in Milan published, in Journal of the National Cancer Institute, the results of a study which demonstrated that the antibiotic doxycycline is proving to be an effective treatment for this form of cancer. “Our prospective trial revealed that doxycycline is a fast, safe, and active treatment for OAL, both at initial diagnosis and at relapse,” the study’s authors wrote.[90]

In 2006, D.L. Mager and team published a review article in the Journal of Translational Medicine called, “Bacteria and Cancer: Cause, or Cure?” According to Mager, “An overwhelming body of evidence has determined that relationships among certain bacteria and cancers exist.” In the paper, Mager details how research teams around the world have implicated Salmonella typhi in gallbladder cancer, Streptococcus bovis and E.coli in colon cancer, and Chlamydia pneumoniae in lung cancer. According to Mager, the mechanisms by which bacterial agents may induce carcinogenesis include “chronic infection, immune evasion, and immune suppression.”[91]

“Everybody knows inflammation induces cancer.” This suggests that, just as in other chronic diseases, long-term supplementation with vitamin D slows the immune system and facilitates the proliferation of L-form bacteria, ultimately driving the progression of cancer. Over time, L-form bacteria release more cytokines into the tissues, resulting in elevated levels of inflammation.

“Everybody knows inflammation induces cancer”, stated Francesco Marincola, MD, Senior NIH Investigator, at a recent conference. But how? According to biomedical researcher Trevor Marshall, “Th1 inflammation feeds the initial proliferative stage of cancer. Without Th1 inflammation the cancer cells can’t get adhesion to the ‘healthy’ cells and tissues, and can’t become proliferative. Then, as the cancer starts to metastasize, the inflamed stem cells are critical in enabling the spread of the inflammation, and the metastasis of the cancer.”[92]

Furthermore, the Vitamin D Receptor is known to transcribe genes that work to prevent the spread of cancer. These include Metastasis Suppressor Protein, a protein that slows the creation of cancer cells, and Mitochondrial Tumor Suppressor 1 gene.

A molecule of 25-DBecause inflammation induces cancer, it’s no surprise that research teams who follow their subjects for only a few years find that vitamin D seems to be “preventing” cancer. What they actually pick up on is the temporary decrease in cytokine production that results when 25-D slows the immune system and less L-form bacteria are killed. In the short term, as less bacteria die, less cytokines are released into the tissues, resulting in a temporary decrease in inflammation.

But in the long run, L-form bacteria will take full advantage of the subjects’ weakened immune systems. The bacteria will increase in number and spread to new tissues and organs. Decades later, the subjects will display higher levels of inflammation and higher rates of cancer and/or other chronic diseases, because even consistent immunosupression with vitamin D will no longer sufficiently prevent so many L-form bacteria, both alive and dead, from releasing cytokines into the tissues. Consequently, researchers who follow their study participants for the longest periods of time are often the ones to claim that supplementation with vitamin D offers no benefit when it comes to fighting the cancer.

Several months ago, researchers at Creighton University published the results of a study which found that vitamin D might lower the incidence of colorectal cancer.[93] But Jacques Rossouw at the National Institutes of Health criticized the study. His group conducted a 93] But Jacques Rossouw at the National Institutes of Health criticized the study. His group conducted a similar study that tracked the effects of vitamin D on 46,282 postmenopausal women with colorectal cancer and monitored the women over a longer period of time. “In our study we found absolutely no indication of an effect of calcium or vitamin D [on cancer] — zero,” he said. “And that’s over a seven-year period. It was a much larger study and a much longer study,” Rossouw told the press.[94]

Dr. John Milner, chief of the Nutrition Science Research Group at the National Cancer Institute, agrees that skepticism is necessary. “We need to put this in the context of the entire diet and lifestyle and understand why we’re getting some effect,” Milner said. “I don’t want to minimize it, but let’s see a little bit more before we start jumping into public health policies.”[95]

“In our study we found absolutely no indication of an effect of calcium or vitamin D [on cancer] — zero. And that’s over a seven-year period. It was a much larger study and a much longer study”Researchers at the Moores Cancer Center in California have published several disastrously misleading studies in which they incorrectly interpret the role of vitamin D in the pathogenesis of cancer. One study, published recently in Nutrition Reviews, combines data from researchers who tested the level of 25-D in subjects around the globe during the winter months. Not surprisingly, the researchers, who failed to question the subjects’ levels of 1,25-D, picked up on the fact that patients at a higher risk for colorectal and breast cancer had lower levels of 25-D. In reality, the low 25-D observed in the subjects resulted from the downregulation of 25-D under the influence of elevated levels of 1,25-D

The researchers incorrectly state that higher levels of vitamin D offer a “protective effect” against cancer. Their conclusion: supplementing with up to 2,000 IU’s of vitamin D daily could prevent an estimated 600,000 cases of cancer. Unfortunately, virtually the opposite is true.[96] In reality, the “protective effect” they are picking up on is simply the point at which 25-D becomes immunosuppressive and a temporary decrease in cytokine release begins.

These studies are the equivalent of giving subjects prednisone and concluding that prednisone offers a “protective effect” against cancer because it slows the immune system, leading to a temporary decrease in bacterial die-off. In addition, no study to date has tested whether study participants given high doses of vitamin D later develop a wide array of other chronic illnesses such as diabetes, arthritis, and heart disease. Surely if they looked, they would pick up on a higher incidence of inflammatory disease in the groups of subjects taking vitamin D.

A particularly telling study on vitamin D and prostate cancer by researchers at the University of Tampere in Finland revealed that the highest rate of prostate cancer occurred when subjects’ levels of 25-D were either particularly low (under 8 ng/ml) or particularly high (over 33 ng/ml), giving a U-shaped curve.[97]

It is very likely that the subjects with low 25-D were displaying the dysregulated vitamin D ratio (low 25-D, high 1,25-D) seen in patients with chronic disease, and that the patients with high 25-D were consuming very large amounts of vitamin D, amounts so large that the liver had no choice but to convert much of it into 25-D. These patients were sick indeed, since the high levels of 25-D suppressed their immune systems, disabling their ability to fight the progression of the cancer. Consequently, the researchers concluded that high levels of vitamin D might be associated with a higher risk of prostate cancer.

Similarly, a team of researchers at the National Cancer Institute in Rockville, Maryland conducted a study on men to determine the relationship between their levels of 25-D and pancreatic cancer risk. The researchers tracked the men for over 16 years. They found that in the long term, high 25-D levels greater than 26 ng/ml were associated with a three-fold increased risk for pancreatic cancer, suggesting that individuals consuming high levels of vitamin D were more likely to fall ill with the disease. Again, according to molecular modeling research, 26 ng/ml is near the range when 25-D significantly shuts off the Vitamin D Receptor, particularly when it is already partially blocked by bacterial proteins.

“Contrary to expectations, subjects with higher prediagnostic vitamin D status had an increased pancreatic cancer risk compared with those with lower status”They stated, “Contrary to expectations, subjects with higher prediagnostic vitamin D status had an increased pancreatic cancer risk compared with those with lower status…. Our results are intriguing and may provide clues that further the understanding of the etiology of this highly fatal cancer.”[98]

Researchers at the Chinese Academy of Medical Sciences in China found a similar association between excessive vitamin D intake and esophageal and gastric cancers in men. Male subjects with levels of 25-D in the range of 48.7 ng/ml were much more likely to develop one of the two forms of cancer.[99]

This same association between very high levels of 25-D (suggesting subjects are consuming large amounts of vitamin D) and higher rates of illness has also been observed in heart disease. A group of researchers at the Sree Chitra Tirunal Institute for Medical Sciences and Technology in India explored the relationship between elevated vitamin D (due to excessive sun exposure) and heart disease. The researchers tested the level of 25-D in 143 men with heart disease and 70 healthy control subjects. They found that the subjects with heart disease had much higher levels of 25-D in their blood, levels over 89 ng/ml, which is well beyond the level that causes the VDR to completely shut down.[100]

Many people who hear about studies on cancer and vitamin D also don’t realize how easy it is for researchers to manipulate statistics in order to demonstrate positive associations.

Take, for example, a recent study published in the American Journal of Clinical Nutrition by Lappe et al, who gave study participants 1,100 IU’s of vitamin D over the course of four years (during the time when the short-term immunosuppressive effects of the steroid would be at its strongest). The researchers divided the participants into three groups. One group took no vitamin D, a second took calcium, and a third group took calcium and vitamin D. The team concluded that vitamin D significantly reduces the risk of cancer.[93]

The study’s biggest flaw is that the researchers discarded the data of subjects who developed cancer during the first year of the study. Their excuse: cancers during the first year would have been present but undiagnosed at entry. Of the 50 people who developed cancer during the four-year study, 13 were removed based on this premise, and only 37 cases of cancer were actually analyzed. But the 13 people who developed cancer during the first year were likely to be the study participants with the highest loads of L-form bacteria. They would have been the people to suffer the most from the negative impact of elevated 25-D on the immune system. If data from the 13 participants would have been included in the study, the results would have reflected much less of a “benefit” from vitamin D. Even the researchers admit that “their conclusion was strengthened by both the observational, substantial improvement in risk reduction when cancers occurring early in the trial were excluded.”

Recall for a moment the study on breast cancer by the Women’s Health Initiative discussed earlier in this paper. The researchers concluded that vitamin D might offer a small benefit in preventing breast cancer. The story was picked up by the media and advertised ad nauseam. The authors’ inboxes were no doubt brimming with media requests.

“Neither use of supplemental calcium nor vitamin D intake was associated with [breast cancer] risk.” However, the media does not seem interested in broadcasting the results of other studies which have determined that vitamin D offers no benefit whatsoever in preventing breast cancer. A second study by the Women’s Health Initiative found no reduction in risk of breast cancer among postmenopausal women supplementing with 1000 mg calcium and 440 IUs of vitamin D.[101] Researchers at the American Cancer Society conducted 101] Researchers at the American Cancer Society conducted a study on 68,567 postmenopausal women and found that “neither use of supplemental calcium nor vitamin D intake was associated with [breast cancer] risk.”[102] And researchers at the Northern California Cancer Center 102] And researchers at the Northern California Cancer Center found no association between dietary vitamin D intake during adolescence and subsequent breast cancer risk.[103]

Of course, since we know our picture of cancer remains relatively incomplete, we shouldn’t reject the possibility that vitamin D might offer some small benefit in preventing the disease. If L-form bacteria didn’t exist, then it might make sense to supplement with vitamin D in the hope that this might be true. But is it worth the risk when 25-D also slows the immune system, facilitating the spread of L-form bacteria into new tissues and organs, and also prevents the Vitamin D Receptor from transcribing the antimicrobial peptides and several anti-cancer genes? To say nothing of evidence which points to the probability that L-form bacteria and their subsequent dysregulation of the immune system are the ultimate cause of cancer in the first place.

Take, for example, 1,25-D. Several laboratory studies have shown that elevated 1,25-D may have a small anti-tumor effect.[104] But elevated 1,25-D is also key in allowing L-form bacteria to spread unchecked from cell to cell. Elevated levels of 1-25-D leach calcium from the bones. High levels of 1,25-D affect muscle function, particularly the cardiac muscle.[105][106] Studies which have detailed the intricate feedback pathways between the two forms of vitamin D have shown that elevated levels of 1,25-D are also immunosuppressive.

Consequently, any effect that 1,25-D might have in reducing tumors comes with a price - a price so large that it puts patients at much greater risk for Alzheimers, arthritis, diabetes, heart disease, strokes, and a vast array of other chronic diseases. And it may even have long term cancer promotion effects that cancel out any purported short-term benefit.

So, although elevated 1,25-D might possibly turn out to have a short-term beneficial effect on one small part of the complex disease process that is cancer, the effects on the L-form bacteria that also contribute to the illness mean that, in the end, it generates a plethora of negative consequences, consequences which contribute to more insidious, far-reaching and long-lasting aspects of the disease.








8. Vitamin D deficiency does not cause rickets.

Rickets is a softening of the bones that leads to fractures and deformity. The majority of cases occur among children in developing countries who suffer from severe malnutrition.

This child’s bowed legs are a symptom of rickets.This past March a team of biologists at Harvard Medical School published the results of a study on rickets. The researchers engineered mice without vitamin D receptors (VDRs). Since vitamin D can have no effect on the body unless it can bind to the VDR, the mice could use no vitamin D whatsoever in their bodies. The researchers found that if the mice were given a diet high in calcium and phosphorous they did not develop rickets and their bones were just as strong as normal mice with active Vitamin D Receptors.[107]

A second study, by the same research team, corrected rickets by replacing calcium and phosphate ions in the bloodstream of mice without Vitamin D Receptors, thereby confirming the results. The team concluded that rickets is not caused by a deficiency of vitamin D but instead results from hypophosphatemia, a condition where the level of phosphorous in the blood is too low.[108]

Clearly, low calcium was part of the problem as well. Diminished levels of calcium cause an increase in Parathyroid Hormone, which subsequently causes the body to excrete too much phosphorous. This causes the level of phosphate in the body to drop, leading to the altered bone formation seen in rickets. Joyce Waterhouse, PhD, a researcher associated with Autoimmunity Research Foundation writes, “Low phosphorus is the proximate cause — but low calcium intake is generally the ultimate cause.”

In 2004, a study published in the American Journal of Clinical Nutrition by researchers from the Mayo Clinic, Oregon University School of Medicine, and other institutions confirmed that a low level of calcium can lead to rickets. The team assessed the absorption of calcium in 15 Nigerian children with active rickets. They found that all 15 children had resolution or improvement of rickets after six months of treatment with calcium supplements.[109]

“Rickets in toddlers is a large problem in parts of Africa, especially Nigeria. It is not due to vitamin D deficiency but is caused by not having enough calcium in the diet.”Consequently, the US Department of Agriculture website clearly states “Rickets in toddlers is a large problem in parts of Africa, especially Nigeria. It is not due to vitamin D deficiency but is caused by not having enough calcium in the diet.”[110] It’s certainly no surprise that children in Africa, who get copious amounts of sunlight, are not suffering from a disease caused by vitamin D deficiency.

In North America, too, the role of calcium is being reexamined. DeLucia et al emphasize that “Nutritional calcium deficiency may occur in North American infants and is not limited to the setting of developing countries.”[111] Some attribute a recent small increase in rickets in North America to an increase in breast feeding, claiming that this is due to breast milk being low in vitamin D. However, breast feeding is also often accompanied by a diet low in calcium, particularly after weaning (e.g., juices rather than milk). Also, in recent years, more people have begun to avoid milk due to a greater awareness of lactose intolerance.

Marshall suggests that rickets may be related to Th1 inflammation, as a number of patients on the Marshall Protocol with Th1 illnesses and their close relatives report having had rickets as children.[112] Vitamin D proponents claim that vitamin D added to the food supply was responsible for a historical decrease in rickets. But the history of rickets shows that a typical rickets case often had a history of smallpox, measles, or whooping cough.[113] Plus, a 112] Vitamin D proponents claim that vitamin D added to the food supply was responsible for a historical decrease in rickets. But the history of rickets shows that a typical rickets case often had a history of smallpox, measles, or whooping cough.[113] Plus, a 1997 study in Ethiopia found a high association between pneumonia and rickets.[114] This provides more suggestive evidence that infection, either obvious and acute, or subtle and chronic, may play a role in the development of rickets and may exacerbate the effects of a low-calcium diet.

Does vitamin D come into the picture at all?

If a child with rickets is severely deficient in vitamin D, as well as in calcium and phosphorous, administering a small amount of vitamin D (which will be immediately converted into 1,25-D) can help by allowing the Vitamin D Receptor to turn on genes that affect the absorption of calcium. This probably explains why in the early 19th century, some children given high does of vitamin D were said to be cured from rickets.

However, if supplementation is continued, the level of the precursor form of vitamin D (25-D) in the body will soon reach the point at which it becomes immunosuppressive. With the negative effects of this situation in mind, it makes much more sense that patients low in calcium should simply be given extra calcium, which can remedy the situation without the need for vitamin D.

Thus, it goes without saying that the involvement of vitamin D in the above process does not justify the high levels of vitamin D currently added to the food chain in the name of “preventing rickets”, and that the health of the public would be much better served by regulations ensuring that they obtain adequate calcium and phosphorous rather than vitamin D.

[Old Herb Lady]

9. Most researchers fail to consider the alternate hypothesis about vitamin D.

When it comes to studies about vitamin D, researchers simply do not consider the alternate hypothesis, the idea that additional supplemental vitamin D might be harmful or unnecessary, and that that low 25-D in many chronic diseases is a consequence of the disease process rather than a cause. At a recent conference on vitamin D organized by the American Cancer Society, Dr. Len Lichtenfeld, Deputy Chief Medical Officer of the organization, stated unequivocally, “There is no dispute among medical professionals that vitamin D is beneficial for our health.”[115]

“This study is “not as ringing an endorsement of calcium and vitamin D as one might like.” If the results of a study show that vitamin D didn’t help the subjects involved, the study’s authors seem all too eager to explain away the results or discard the findings. Take the recent $18 million dollar study on vitamin D and calcium conducted by the Women’s Health Initiative. The study of more than 36,000 middle-aged and older women – the largest ever to test the health benefits of vitamin D – found that calcium and vitamin D had essentially no benefit on the bone density of the women involved.

After seven years of taking the supplements the group given supplements showed a 1% increase in hip-bone density but ranked no better statistically in avoiding fractures of all kinds.[77] This study is “not as ringing an endorsement of calcium and vitamin D as one might like,” said one of the study’s authors, Dr. Norman Lasser at New Jersey Medical School. For one, the researchers might have considered whether the 1% increase in hip-bone density was due to the calcium, and not the vitamin D.

Nevertheless, the researchers who conducted the Women’s Health Initiative study tried to explain away the findings. An article about the study from the Associated Press stated, “Many experts downplayed the meaning of the negative finding. Dr. Bess Dawson-Hughes, a Tufts University vitamin expert who helped shape the dietary guidelines, said they should remain unchanged for now.” The article went on to state that, “Some researchers said the effect would have been clearer with higher doses of vitamin D, perhaps up to 1,000 units daily.” Furthermore, nearly every researcher, including the team who conducted the study, denied the implications of the findings, urging people to continue taking vitamin D despite the fact that the study showed it had no beneficial effect. About this, the article wrote, “Even so, experts are urging women to stick with government advice to keep taking the supplements anyway.”[116]

In fact, the leader of the study, Rebecca Jackson at Ohio State University stated, “Based on our findings, women, particularly those over 60, should consider taking calcium with vitamin D for bone health and to guard against fracture.”[117] Jackson’s advice is at odds with her own findings. It’s as if she is referring to data that doesn’t exist. It seems that researchers like Jackson are so prepared to say that vitamin D is beneficial that even when studies prove it isn’t, they say it’s helpful anyway.

Meanwhile, a second analysis of the same study group found that the supplements did not lower the women’s risk of colorectal cancer. Naturally, the researchers once again questioned the data. The San Diego Union Tribune wrote, “While the results were also disappointing, researchers speculated that a benefit might show up with more time.”[118] No one bothered to comment on the finding that the women taking vitamin D had a 17% increased risk of developing kidney stones.

Perhaps the most recent example of researchers’ blindness to the implications of even their own results is on display in the August 25, 2007 issue of the Lancet. The largest such meta-analysis to date, Dr. Tang and team statistically analyzed a total of 29 studies involving 63,897 study participants with an eye towards definitively measuring the connection between fractures and bone loss, and vitamin D and calcium supplementation. Their abstract states clearly enough in the interpretation section, “We recommend minimum doses of 1200 mg of calcium, and 800 IU of vitamin D.”

“The addition of vitamin D to calcium did not change treatment effect significantly…. It was not significant.”This language is interesting in that it is just not supported by the substance of the findings. On page 661: “The addition of vitamin D to calcium did not change treatment effect significantly…. It was not significant.” On page 663: “Although addition of vitamin D supplementation was not shown to offer additional risk reduction over and above the use of calcium alone, a significant difference was observed between the effects of different vitamin D doses. This discrepancy could be due to statistical artifact.”[76]

What is this “artifact”? “Our analysis was limited by the scarcity of vitamin D doses higher than 800 IU,” the researchers claim. “It is possible that vitamin D does have a beneficial effect when the dose is large enough (>800 IU).”

It’s also possible that these researchers are having it both ways, using ambiguous results to support two nearly opposite conclusions. In one breath (above), they blame the “scarcity” of vitamin D data at higher levels (>800 IU) for not being able to measure a significant effect. And then, in the abstract no less, they conclude that “treatment effect,” meaning fracture risk reduction, was better with “vitamin D doses of 800 IU or more than with doses less than 800 IU of vitamin D.”

A similar bias can be seen in a recent meta-analysis by researchers in Lyon, France, who concluded that subjects who began taking vitamin D were 7% less likely to die in the next few years than those who did not. In the paper, the team fails to mention that the benefit of vitamin D given alone, without calcium, was not statistically significant. Furthermore, four of the studies analyzed actually showed a greater rate of death among subjects taking vitamin D (though the death rate was only statistically significant in one of the studies). Two of these four studies were using a single injection with a very large amount (300,000 IU) of the steroid.[119]

How can these contradictions be allowed to persist?

It seems that many researchers are under pressure to demonstrate that their data is statistically significant. Researchers obtain the money to conduct a study by applying for a grant, and inconclusive or insignificant results are not likely to impress the institutions in charge of distributing resources. It may be that many of the scientists who bolster claims of statistical significance have already received large grants and are eager to show that the money was spent on an analysis worthy of note.
The lockstep perception of the healthiness of ingesting vitamin D has even led some experts to downplay the effects of its toxicity. According to the school of nutrition at Colorado State University, “Because fat-soluble vitamins are stored for long periods, they generally pose a greater risk for toxicity than water-soluble vitamins when consumed in excess.”[120] In excess, vitamin D is highly toxic. It causes calcification of soft tissues, and may cause calcified kidneys and kidney failure. Too much vitamin D may disrupt the level of calcium in the blood and produce fatigue and mental confusion.

In 1997, researcher Bernadette Marriott wrote an editorial in Annals of Internal Medicine entitled “Vitamin D Supplementation: A Word of Caution” in which she argues that vitamin D supplements be recommended with caution and care.[121]

In a section on their website called “The Truth About Vitamin D Toxicity” John Jacob Cannell, the Vitamin D Council’s executive director tries to invalidate Marriott’s concerns by repeating the advice of vitamin D “expert” Reinhold Vieth, who feels that fear of vitamin D toxicity is unwarranted, and such unwarranted fear, bordering on hysteria, is rampant in the medical profession.[63] Cannell himself states that “In fact, living in America today while worrying about vitamin D toxicity is like dying of thirst in the desert while worrying about drowning.”

And to whom is the NIH listening?

The National Institutes of Health held a recent conference that examined a range of scientific perspectives related to vitamin D and bone health across the life cycle. They invited Professor Reinhold Vieth, one of the most vocal advocates for very high vitamin D supplementation, to advise them on the issue of vitamin D toxicity. He was scheduled to give a speech about “Potential Adverse Outcomes of Vitamin D.”[122] Although the transcripts of 122] Although the transcripts of the conference are not yet publicly available, it would be reasonable to think he mentioned few, if any, causes for real concern.








10. When it comes to vitamin D, the current medical climate of consensus is hostile to new ideas.

Sir Isaac Newton once wrote, “If I have seen farther than others it is because I have stood on the shoulders of giants.” But even intellectual giants get it wrong from time to time. Many researchers today seem to regard the work of the most prestigious among them– at least in the field of vitamin D– as giants, and there is little room for questioning of basic assumptions.

“For many current scientific fields, claimed research findings may often be simply accurate measures of the prevailing bias.” The fact that researchers seem so hesitant to say anything negative about vitamin D reflects the blanket assumption that vitamin D simply cannot be harmful. Arguments to the contrary are assumed to be untenable and entirely without merit. This is due in no small part to the reality that researchers today are overly committed to the idea of replication, the requirement that new findings must be supported by and stem from earlier research. As John P. A. Ioannidis writes in the Journal of PLOS Medicine, “For many current scientific fields, claimed research findings may often be simply accurate measures of the prevailing bias.”[123]

New research draws on the inferences of other studies conducted in the field, and it is required that conclusions be reviewed and accepted by peers who must share the same set of assumptions. If and when someone puts forth findings that turn an established area of medicine on its head, those findings are unceremoniously questioned and dismissed.

Janet Foutin, a staff member of Autoimmunity Research Foundation writes, “Even the most credible researchers must start upon a research foundation of previous empirical studies or it won’t be taken seriously in the community from which it springs. This consensus contamination is widespread and makes it very difficult to introduce process-or-content foundation-level changes.” In other words, when new medical research is always derived from previous work, fundamental changes to researchers’ assumptions are slow in coming.

The case of Barry Marshall and Robin Warren, the team of researchers who discovered that ulcers are caused by H.pylori bacteria rather than stress is particularly instructive. When that duo first put forth their findings, published in 1982,[124] other doctors and researchers rejected their data and walked out of their lectures. It’s not as if published explanations of ulcers invoking stress and food intake weren’t internally consistent or validated in other peer-reviewed papers. Those papers just had one little problem: they were wrong. The medical community’s refusal to consider the alternative and, ultimately correct, explanation offered by Marshall and Warren lasted decades.

[Old Herb Lady]

11. Research touting vitamin D’s benefits is often biased, methodologically weak, and ultimately misleading.

Studies about vitamin D can often be biased, methodologically weak, or both. Publication bias is the tendency of scientists to report findings that report statistical significance, but to bury examples that are inconclusive. The tendency towards publication bias is well-suited to prolonging any number of false positive conclusions, including the proposition that consumption of vitamin D is healthy.

An article published last September in the Wall Street Journal discussed how scientific journals are much more likely to publish studies which reveal positive qualities of a medication or supplement rather than those which demonstrate a negative or null effect.[125]

For example, throughout the 1990s, publication bias gave the impression of a link between oral contraceptives and cervical cancer. But in reality, a 2000 analysis concluded that the studies finding no link between the two factors had seldom been published. In the end, the analysis found there was only “a spurious statistical connection” between oral contraceptives and cervical cancer.

In fact, another analysis, conducted in 1999, found that the percentage of positive studies in some fields routinely tops 90%. According to Lee Sigelman of George Washington University, “That is statistically implausible, suggesting that negative results are being deep-sixed.” As a result, “what we read in the journals may bear only the slightest resemblance” to reality.[126] “You hear stories about negative studies getting stuck in a file drawer, but rigorous analyses also support the suspicion that journals are biased in favor of positive studies,” says David Lehrer of the University of Helsinki.

Various forms of bias may also be perpetuated by drug and supplement companies looking to make a profit. Several reports have revealed that some companies will even pay their own staff to help researchers write up the results of studies. The final papers eventually end up in scientific journals.

For example, in 2001, the American Journal of Kidney Diseases published an article that touted the use of synthetic vitamin D. Its author was listed as Alex J. Brown, an associate professor at Washington University in St. Louis.But recently, that same article was featured as a work sample by a different person: Michael Anello, a freelance medical writer, who posted a summary of it on his web site. Mr. Anello says he was hired to write the article by a communications firm working for Abbott Laboratories, which makes a version of the vitamin D product.

“Promotion has a different goal than publishing a legitimate research study”According to Anna Wilde Mathews, a staff reporter at The Wall Street Journal, “It’s an example of an open secret in medicine: many of the articles that appear in scientific journals under the bylines of prominent academics are actually written by ghostwriters in the pay of drug companies. These seemingly objective articles, which doctors around the world use to guide their care of patients, are often part of a marketing campaign by companies to promote a product or play up the condition it treats.”[127]

Sabine Kleinert, an executive editor at The Lancet, says she makes a genuine effort to reject articles that have a marketing spin. “Promotion has a different goal than publishing a legitimate research study,” says Dr. Kleinert. She suspects companies sometimes influence medical writers “to write it up in a certain way to make a product sound more efficacious than it is.”[128]

As opposed to research bias, methodological flaws are easier to identify– if one cares to look. So conditioned are we to hearing that vitamin D is helpful, when a study reveals the substance’s “benefits” few people take the time to analyze how the data was collected or ultimately interpreted. Because of this, the methods that researchers use to collect data on patients taking vitamin D rarely come under scrutiny.

Results from recent research attempting to demonstrate a protective effect of ingested vitamin D have been alternately inconclusive and lacking in sound methodology. Yet, all too often, researchers (and their colleagues and the media) conclude that such an effect exists. One such study, published in Annals of Internal Medicine in May of this year, claims as a part of its conclusion: “Findings from this study suggest that higher intakes of calcium and vitamin D may be associated with a lower risk of developing premenopausal breast cancer.”[129] Before you run out and begin gulping down vitamin D pills as the local news anchor might have you do, what is the basis for this claim? Let’s take a look.

The study was conducted on 10,579 premenopausal women and 20,909 postmenopausal women by the Women’s Health Study Group. The women were asked to fill out baseline questionnaires about lifestyle, medical history, and were required to specify how often they ate certain foods. Participants self-reported whether they were taking vitamin D supplements, calcium supplements, and multivitamins. Then, the researchers followed up with the women over a ten-year time period to determine if they developed breast cancer.

The media took the results of the study and generalized the conclusion to all women despite the fact that in the results section of their paper, the researchers had clearly stated that among the postmenopausal women subjects, vitamin D intake was not inversely associated with breast cancer risk. There was also no association between calcium and vitamin D intakes and more aggressive breast cancer in postmenopausal women.

Furthermore, although the difference between those who ingested the highest and lowest levels of vitamin D did result in differing rates of breast cancer, those groups differed in other very substantial ways. Women in the group who consumed higher levels of vitamin D were 67% less likely to be a smoker, burned over 39% more calories doing physical activity, and drank about a fifth less alcohol. The researchers here assure us that they statistically controlled for these factors. But, if you have a purported effect of just a few percentage points, how strong can your conclusion be when you are studying two such substantially different groups?

This phenomenon is known as the “healthy-user bias.” Until the power of this effect is sufficiently and widely appreciated, researchers will continue to publish the results of studies that fail to account for a wide variety of lifestyle differences, many of which may be impossible to quantify.

Jerry Avron, a Harvard epidemiologist argues that when it comes to large epidemiological studies the healthy-user bias has the potential for “big mischief.” For example, in one large population studied by Elizabeth Barrett-Cinner, an epidemiologist at the University of California, San Diego, having gone to college was associated with a 50% lower risk of heart disease. Other studies have established a connection between a person’s income and a lower risk of heart disease. Considering all these factors, is it possible to isolate one single factor, such as vitamin D, as the reason for a small decrease in disease noted in a particular study?[1]

“Women in the group who consumed higher levels of vitamin D were 67% less likely to be a smoker, burned over 39% more calories doing physical activity, and drank about a fifth less alcohol.” It wouldn’t so far-fetched to assume that women who take vitamin D are more likely to get better health care and be aware of prevailing health advice. After all, they’ve probably heard about studies like this one! Why else would they be consuming extra vitamin D? For a substance that ultimately is said to have a negative or absent net effect on the development of cancer, these circumstances represent an infinite loop of self-fulfilling prophecy.

In fact, even with a marginally significant correlation between vitamin D intake and a lesser risk of cancer in premenopausal women coupled with a study population, the enormity of which can only be described as a statistician’s dream, the 95% confidence interval was gaping: 0.42 - 1.00. You can think of confidence intervals as an indication of how reliable an estimate is. In this case, the answer would be not very reliable.

Compounding matters was the method used to gather food frequency data from study participants. No researcher’s first choice of gathering data is a survey. But, in this particular case, the data was gathered in an especially problematic way. Study participants were asked to remember back to what they consumed over the previous year, a method at which people appear to be notoriously poor.

A different group of researchers performed two simultaneous tests on the same participants. For one test, subjects were asked to recall the amount of vitamin D they had consumed in the previous year and for the second they were to fill out four one-week dietary records at regular intervals over the course of a year. The researchers found only a 0.35 correlation between the amount of vitamin D the subjects reported taking with the first method as compared to the second, meaning that the subjects had a very low tendency to correctly recollect the amount of vitamin D their food diaries suggested they were taking.[130]

This methodological flaw is a problem and shows up from time to time in studies done in this manner, precisely because it magnifies the potential for systematic error. Once more, the problem with this particular survey is that the study participants who are more likely to engage in a wide range of known and unknown cancer-protective behavior by limiting alcohol intake, being more physically active, etc. are also more likely to know that researchers think they should be having more vitamin D and remember it that way. Therefore, it is probable that they over-reported their vitamin D intake. With the results of the study mentioned above showing that there was a very weak correlation between the amount of vitamin D participants reported taking over the course of a year and the amounts of vitamin D they reported consuming when given a weekly survey, it would be hard to argue otherwise.

Why would researchers use this kind of methodologically weak survey? The short answer is that their in-house statistician told them they needed the numbers– tens of thousands of participants. The one-year recollection survey is a crude instrument, but it is relatively easy to administer to a study cohort the size of a small city, and that is a minimum number you’ll need to demonstrate any statistical connection between vitamin D intake and cancer. Even with these numbers, this study, for the record, comes up just short on statistical significance in spite of its methodological flaws. Returning once more to the original concluding language of the Annals paper, it would seem like a stretch to conclude that if you’re a premenopausal woman, taking vitamin D has any demonstrable effect on cancer.

Even when researchers give their subjects vitamin D, they may fail to account for differences in lifestyle between women who carefully follow instructions and take supplements as directed and those who do not correctly follow the guidelines. This phenomenon is known as compliance effect. Avorn argues, “Girl Scouts in the group, the compliant ongoing users, are probably doing a lot of other preventative things as well.”[1]

David Freedman, a statistician at the University of California, Berkeley, has written books on clinical trial design and analysis. Freedman says in The New York Times, “Women who take their pills as directed year in and year out are known to be different from ordinary women, so it is a mistake to generalize from them to the entire population.”[131]

“Women who take their pills as directed year in and year out are known to be different from ordinary women, so it is a mistake to generalize from them to the entire population.”In fact, in an article in The New York Times Magazine, Gary Taubes puts forth Freedman’s findings, explaining that “whenever epidemiological studies compare people who faithfully engage in some activity with those who don’t - whether taking prescription pills, or vitamins, or exercising regularly or eating what they consider a healthy diet - the researchers need to account for the compliance effect or they will most likely infer the wrong answer. They’ll conclude that this behavior, whatever it is, prevents disease and saves lives, when all they are really doing is comparing two different groups of people who are, in effect, incomparable.”

Taubes explains, “No matter how well designed and how many tens of thousands of subjects they might include, they [observational studies] have a fundamental limitation. They can distinguish associations between two events. But they cannot inherently determine causation - the conclusion that one event causes the other. As a result, observational studies provide what researchers call hypothesis generated evidence - what a defense attorney would call circumstantial evidence.”[1]

While no research methodology can be completely free of bias or methodological weakness, one potential bright spot, in certain cases, is that of molecular modeling. Increasing numbers of researchers are using molecular modeling to accompany or replace experiments using human volunteers. Molecular models display exactly how molecules in the body fit together. For example, software can take a virtual molecule of 25-D or 1,25-D and demonstrate exactly how they fit into the Vitamin D Receptor.

It was molecular modeling software that allowed a research team at McGill University to identify over 900 different genes transcribed by the Vitamin D Receptor.[6] And it was molecular modeling that allowed biochemical researcher Trevor Marshall to discover exactly how 25-D binds and inactivates the Vitamin D Receptor, proving with inarguable precision that the molecule is immunosuppressive as it reaches higher levels. As Marshall says, “The primary difference between mathematical science and evidence-based medicine is that one is definitive and one is interpretive. As we enter the 21st century, the tools to reduce some important medical dilemma to mathematical precision are now available in Molecular Genomics.”[11] And when molecular modeling evidence is combined with clinical data showing the reversal of many chronic diseases, the evidence is even stronger.








12. The dairy and supplement industries are intent on heavily promoting vitamin D.

In order to understand why we hear such unreservedly positive things about vitamin D, one must appreciate the extent to which supplement and food interest groups such as the one representing the dairy industry promote its use. Thanks in no small part to media campaigns sponsored by the dairy and supplement industries, vitamin D has become widely known as the “sunshine vitamin” and is touted to health-conscious individuals in an effort to make them feel that vitamin D is part of a responsible lifestyle.

Let’s start with the supplement industry, a syndicate which is certainly cashing in on vitamin D’s health “benefits.”

On the same online supplement retailer which lists how vitamin D can be used in connection with 21 different health conditions, we are offered oils and spreads, protein powders, breakfast bars, any number of other nutraceuticals, and some 40 different multi-vitamins, all of which contain the secosteroid.[132] NEEDS, another online retailer, sells 37 different supplements with vitamin D and approximately 130 fish oils containing vitamin D, some priced over $30.00 a bottle.[133]

If you think that vitamin D isn’t heavily promoted by the food and dairy industries, think again. Consider the recent marketing battles that have emerged after the FDA proposed a rule change in its guidelines about vitamin D. Within the next few months, the FDA is expected to smooth the way for manufacturers intent on adding “high” levels of vitamin D to a variety of food products.

According to an article in Packaging World Magazine by Stephen Barlas, ”It is predicted that this will set off a scramble by both milk, milk product, and juice marketers to redo their product labels and packaging in order to take advantage of the new guidelines.”[134]

A petition from the Beverage Institute for Health and Wellness, which is funded by the Coca-Cola Co.— one brand of which is Minute Maid fruit juices and drinks— is petitioning the FDA to allow a broader claim about vitamin D to be made. At present, few product retailers choose to make the osteoporosis/vitamin D health claim because of the qualifications required to accompany it, such as noting that calcium only benefits “young adult white and Asian women who engage in regular physical activity.”

Minute Maid’s new line of Vitamin D-fortified productsUnder the request advocated by the Beverage Institute, a food would have to be considered “high” in both calcium and Vitamin D before it could make an osteoporosis health claim. That would mean a product would have to contain at least 20% of the Daily Value (DV) of Vitamin D and/or calcium per reference amount customarily consumed. Minute Maid’s orange juice and some of its offshoots contain more calcium than the milk products now eligible to use the calcium/osteoporosis claim, and contain about the same level of Vitamin D. On April 25 Minute Maid introduced its Enhanced Juice line. It includes new Minute Maid Multi-Vitamin and Minute Maid Active variety, and a calcium-fortified orange juice offering: Home Squeezed Style + Calcium + Vitamin D.

But according to Barlas, “producers of reduced-fat, low-fat and fat-free milk and yogurts will also benefit from a more streamlined and expanded claim. Once the FDA decision is finalized, milk and fruit juice marketers will begin battling one another for new market share.”

Cary Frye, vice president of regulatory affairs for the Intl. Dairy Foods Assn. (IDFA), says, “It is certainly clear that the intent of the petition is to be able to make stronger claims for fortified orange juice in preventing osteoporosis, to compete with milk in that regard. But the new simpler claim will be available to all foods, and it will be up to the dairy industry to leverage its nutrient-dense foods so as to market milk as the superior beverage choice.”

Of course, companies such as Colombo, Dannon and Yoplait, all of which sell vitamin D-fortified yogurts, are unlikely to take the challenge sitting down. Tom Nagle, senior vice president of marketing for IDFA, stated, “Fortified juices have made progress in consumer perception, but it is our intention to protect our number-one position with consumers.” In order to remain competitive, these companies are predicted to add the vitamin D/osteoporosis claims to their products as well.

But don’t leave out the fishing industry. Vital Choices seafood company sends out an “official newsletter” with articles such as “Wild Salmon Affirmed as Top Vitamin D Source”[135] and “Vitamin D May Lower Risk of Ovarian, Breast, Kidney, and Colon Cancers”, accompanied by a chart showing exactly which of their products are highest in vitamin D.[136]

With vitamin D appearing in so many foods, and people eating them, often regardless of the total amount of the substance they are consuming, along with the additional amount produced by sun exposure, the danger of this trend becomes obvious.

The dairy industry generates millions off the claim that vitamin D increases the absorption of calcium, a claim to which more and more studies are taking exception. It’s no small secret that industry marketing campaigns have nothing to do with science and are all about generating a profit.

Not long ago, the National Dairy Council partially funded a small study to measure the effects of consuming dairy on weight loss. That study consisted of about 30 participants, only 11 of which were in the high dairy group. The subjects were instructed to follow a reduced-calorie diet, which many have argued was actually the key to their weight loss success.

An advertisement by the dairy industry touting milk’s supposed weight-loss benefitsOn the basis of that suspiciously humble study, the Council mounted the “3-A-Day” campaign, a multi-million dollar marketing offensive spent on advertisements connecting milk to weight loss. In 2006 the milk producers even enlisted high-profile celebrities for their “Great American Weight Loss Challenge” and “Body by Milk” promotions.[137]

The Dairy Council has persisted with their campaigns despite a number of research studies showing a contrary association, linking milk and dairy consumption to weight gain, and regardless of the fact that the Physicians for Responsible Medicine have filed a petition stating that the weight loss claims are misleading.

Now that an increasing number of studies are showing no association between vitamin D and osteoporosis, will the dairy and supplement industries persist with their campaigns involving vitamin D? If left unchecked, the answer is probably yes. And the public will continue to get information about vitamin D off the side of a beverage carton rather than from the molecular biologists who truly understand the actions of the steroid.

[Old Herb Lady]

13. The media is neither well-informed nor objective about vitamin D.

There is no doubt about it— the media love vitamin D. Here’s a sample of articles that turn up on the web.
Sunshine Vitamin D - Sunshine Vitamin Brightens Smiles
The Sunshine Vitamin, The Crucial Need For Vitamin D
Critics Now Accept the Sun as Your Healthiest Source of Vitamin D
Vitamin D Deficiency, the Ignored Epidemic of the Developed World
How The Sunshine Vitamin Zaps Disease
Let the Sunshine Vitamin Brighten Your Day
The Wonderful Healing Properties Of The Sunshine Vitamin D
Sunshine: Don’t Leave Home Without It
Vitamin D - The Sunshine Vitamin!
Almost Everyone Needs More of the Sunshine Vitamin
Shining a Light on the Health Benefits of Vitamin D
Vitamin D Deficiency: the Silent Epidemic
The Miracle of Vitamin D

It’s not as if the media is purposefully intending to deceive. The supposedly and unequivocally positive benefits of vitamin D make for good copy. The vitamin D story is one of the media’s rare opportunities to convey a positive message, and they seize it whenever possible. Consumers of media are weary of hearing about skyrocketing obesity, about the failure of once promising drugs like Vioxx. They are also scared of cancer. Nothing attracts viewer interest more than the promise that the information presented will offer some way to get an edge on chronic disease. Vitamin D as the freely available anti-cancer wonder drug fits the bill very nicely. What members of the media do not realize, just like researchers who don’t dig deep enough to seek out the alternative hypothesis, is that high-level vitamin D’s feel-good effects are due entirely to its immunosuppressive nature.

“The vitamin D story is one of the media’s rare opportunities to convey a positive message to their viewers, and they seize it whenever possible.”Just like the supplement industry, the media will often unknowingly take a small study about vitamin D and blow it completely out of proportion. Newspapers, magazines, TV shows, talk shows, radio programs - all pick up the same story and repeat it over and over again, until it seems as if twenty different studies have been published on the subject rather than one. And the language is often overly dramatic. In an article about vitamin D published in US News and World Report called “The ABCs of D, Almost Everyone Needs More of the Sunshine Vitamin”, the author states, “A single nutrient keeps bones strong, wards off diabetes, and protects against tuberculosis, cancer, colds, and the flu. Sound too good to be true? There’s more: It’s free. But you’re almost certainly not getting enough.”[41]

So many articles about vitamin D end with copious amounts of advice about how to get more of the “vitamin.” We see tables, which are attempts to help the reader maximize D intake. The authors often chime in with advice, basing their statements on data that is already misleading and on biases already unchecked. The vitamin D publicity sequence: from data to interpretation to scientific publication to media generalization is not unlike the children’s game telephone, in which each subsequent interpretation is less accurate than the one that preceded it.

Not surprisingly, the media invites vitamin D “experts” to weigh in, communicating their mistaken views on vitamin D to a vast number of viewers. The following was taken from an interview with vitamin D expert Michael Holick that was published in The New York Times, “A visit to the office of Dr. Michael F. Holick in the Boston University Medical Center quickly conveys his enthusiasm for his favorite hormone, vitamin D. On the office walls are letters from sixth graders responding to a talk he gave.[61]

”The important fact I learned from you yesterday is that most living things or persons need vitamin D,” one child wrote. Added another, ”Even frogs need vitamin D.” To advance his point he handed a reporter a copy of a paper he had recently written, ”Vitamin D: The Underappreciated D-lightful Hormone That Is Important for Skeletal and Cellular Health.”

Oh dear.








14. We must take immediate action to remedy the health crisis that has resulted from faulty conclusions about vitamin D in chronic disease.

When it comes to public health, a few false assumptions can have disastrous and far-reaching consequences. The failure of researchers to understand that the low levels of 25-D observed in their subjects is not the cause, but the result of chronic disease, has put the public at greater risk for developing diseases that range from Alzheimers, to diabetes, to cancer, and is directly feeding an epidemic of chronic disease. The chronic diseases caused by L-form bacteria are far more common than currently realized, and are often only noticed as subtle signs of aging, such as osteoporosis, obesity, fatigue and arthritis.[19]

As I write, well-intentioned researchers striving to improve public health, are unknowingly touting a steroid that allows L-form bacteria to proliferate and spread. People taking extra vitamin D are not getting better. Instead, they are feeling a short-term palliative effect from a steroid that slows the immune system, preventing L-form bacteria from releasing the cytokines that result in Th1 inflammation.

It is critical that everyone from clinicians to medical researchers to policymakers understand that recent research has shown the immunosuppressive effects of 25-D and the transcriptional effects of 1,25-D. New research that has also revealed how to correctly activate the Vitamin D Receptor once it has already been turned off by proteins created by L-form bacteria. Given this research, it’s no less important that the various industries touting the benefits of vitamin D immediately stop those marketing campaigns.

“It is incumbent upon the FDA and every other food regulatory agency around the world to scale back and reverse plans to add even more vitamin D to the food supply.” Most importantly though, it is incumbent upon the FDA and every other food regulatory agency around the world to scale back and reverse plans to add even more vitamin D to the food supply. Given the FDA’s explicit mission “to protect the public health” and the balance of research which is rapidly accumulating against vitamin D, the agency will simply have no alternative.

Vitamin D is far more often a cause, and not a cure for disease. And that discrepancy makes a world of difference. It is the difference between advising the public to supplement with vitamin D and telling people to avoid supplementation at all costs. It is the difference between preventing a disease and speeding its progression, the difference between fighting an epidemic of chronic disease, and watching more and more people fall ill every day. And it’s a change that needs to happen right now.

In The Structure of Scientific Revolutions, Kuhn argues that, at first, a scientific revolution takes place slowly, and that changes in mentality happen gradually as serious thinkers reconsider ideas. He states that “If the paradigm is one destined to win its fight, the number and strength of the persuasive arguments in its favor will increase. More scientists will then be converted, and the exploration of the new paradigm will go on. Gradually the number of experiments, instruments, articles, and books based upon the new paradigm will multiply.”

But when it comes to vitamin D, there is no time for Kuhn’s incremental revolution.

It’s no secret that the scientific community is particularly resistant to the long-term harmful effects of vitamin D. Understanding its role in chronic illness will require a vast number of people to admit they have been wrong. Uttering a collective “oops” will not come easily to the medical profession. One can hope that the urgency of this health crisis will inspire doctors, researchers, experts, and everyone with a stake in vitamin D to swallow their pride and strive to make things right for the common good.

Along with the revolution in attitude towards vitamin D is the equally important acceptance of the role of L-form bacteria that block the Vitamin D Receptor, and the treatment that can eliminate them. Instead of using short term palliatives, like vitamin D supplements, there is evidence that these bacteria can be now be killed, meaning that many debilitating chronic diseases can now be cured.

It’s hard to say how this scientific revolution will pan out. One likely scenario is that those with the greatest stake in it, those most sickened by chronic disease, will simply demand that everyone - from the industry to the media to their doctors to medical researchers and regulatory agencies - take good note of the future of conventional wisdom about vitamin D.



http://web.archive.org/web/20080405150223/http://bacteriality.com/2007/09/15/vitamind/

[BrewTech]

I used to get sick all the time.

Now that I take Vitamin D3 supplements, my body functions better, and I don't get sick.

That's all I need to know. Fuck their research.

This post is crap. And that's sad because OHL was is a favorite poster of mine. By posting this BS, she just jumped the shark as far as I am concerned.

[osoab]

Thanks OHL, I will have to read this another day.

[Old Herb Lady]

I used to get sick all the time.

Now that I take Vitamin D3 supplements, my body functions better, and I don't get sick.

That's all I need to know. Fuck their research.

This post is crap. And that's sad because OHL was is a favorite poster of mine. By posting this BS, she just jumped the shark as far as I am concerned.


It does increase your immune system. It's saying there is a top off, tho, where it starts to decrease your immunity. Wow. Thanks alot Brew. Whatever then.

That was a very painful thing to read from you, you don't have to agree with it, it's just information to read if ever so inclined to do so.

I DON'T even agree with ALL of it.

[BrewTech]

It does increase your immune system. It's saying there is a top off, tho, where it starts to decrease your immunity. Wow. Thanks alot Brew. Whatever then.

That was a very painful thing to read from you, you don't have to agree with it, it's just information to read if ever so inclined to do so.

I DON'T even agree with ALL of it.

OK, maybe my reply was a little harsh. I apologize.

Vitamin D is your friend. You can have my Vitamin D when you pry it from my cold, dead fingers!

[beefsteak]

OHL, thanks for the time you spent formating then posting this info.


beefsteak

[lapis]

I DON'T even agree with ALL of it.

I don't either. Although I do think we should exercise caution with supplementing, some of the information is downright questionable. I've read about The Marshall Protocol, and while I think perhaps it is helpful in treating a few diseases, it doesn't apply to most people. I'll post some things I've found.

As for rickets, it certainly HAS made a resurgence in the last 12 or so years, and it's probably due to a lot of factors. More to follow as time allows.

[lapis]

Professor Marshall's recent "discovery"




Mary from Minneapolis writes:

Dr. Cannell:
I understand Dr. Marshall conducted a study and found vitamin D is bad for you. What kind of study did he do?

Dr. Cannell replies:

I have been inundated with letters asking about Professor Marshall's recent "discovery." Some have written that to say they have stopped their vitamin D and are going to avoid the sun in order to begin the "Marshall protocol." The immediate cause of this angst is two publications, a press article in Science Daily about Professor Marshall's "study" (which is no study but simply an opinion) in BioEssays.

Dr. Trevor Marshall has two degrees, both in electrical engineering. Before I begin, I want to again remind you that I am a psychiatrist who works at a state mental hospital. In my duty to full disclosure, I must say that I have known a lot of psychiatrists in my life and a few electrical engineers. If I knew nothing else of a disagreement between two people but their professions, I would believe the electrical engineer, not the psychiatrist.

In reading his two articles, Dr. Marshall's main hypotheses are simple:



Vitamin D from sunlight is different than vitamin D from supplements.
Vitamin D is immunosuppressive (http://www.vitamindcouncil.org/news-archive/2008/professor-marshalls-recent-discovery/#immunosuppressive) and the low blood levels of vitamin D found in many chronic diseases are the result of the disease and not the cause.
Taking vitamin D will harm you, that is, vitamin D will make many diseases worse, not better.

If you read his blog, you discover that the essence of the Marshall protocol is: "An angiotensin II receptor blocker medication, Benicar, is taken, and sunlight, bright lights and foods and supplements with vitamin D are diligently avoided. This enables the body's immune system (http://www.vitamindcouncil.org/news-archive/2008/professor-marshalls-recent-discovery/#immune%20system), with the help of small doses of antibiotics, to destroy the intracellular bacteria. It can take approximately one to three years to destroy all the bacteria." That is, Dr. Marshall has his "patients" become very vitamin D deficient.

Again, Dr. Marshall conducted no experiment and published no study. He wrote an essay. He presented no evidence for his first hypothesis (sunlight's vitamin D is different than supplements). From all that we know, cholecalciferol (http://www.vitamindcouncil.org/news-archive/2008/professor-marshalls-recent-discovery/#cholecalciferol) is cholecalciferol (http://www.vitamindcouncil.org/news-archive/2008/professor-marshalls-recent-discovery/#cholecalciferol), regardless if it is made in the skin or put in the mouth. His second hypothesis is certainly possible and that is why all scientists who do association studies warn readers that they don't know what is causing what.

Certainly, when low levels of vitamin D are found in certain disease states, it is possible that the low levels are the result, and not the cause, of the disease.

Take patients with severe dementia bedridden in a nursing home. At least some of their low 25(OH)D levels are likely the result of confinement and lack of outdoor activity. However, did dementia cause the low vitamin D levels or did low 25 (OH)D contribute to the dementia?

One way to look at that question is to look at early dementia, before the patient is placed in a nursing home. On the first day an older patient walks into a neurology clinic, before being confined to a nursing home, what is the relationship between vitamin D levels and dementia? The answer is clear, the lower your 25(OH)D levels the worse your cognition.

These studies suggest that the low 25(OH)D levels are contributing to the dementia but do not prove it. Only a randomized controlled trial (http://www.vitamindcouncil.org/news-archive/2008/professor-marshalls-recent-discovery/#randomized%20controlled%20trial) will definitively answer the question, a trial that has not been done. So you will have to decide if vitamin D is good for your brain or not. Dr. Marshall seems to be saying demented patients should lower their 25(OH)D levels. Keep in mind, an entire chapter in Feldman's textbook is devoted to the ill effects low vitamin D levels have on brain function.

It is true that in some diseases, high doses of vitamin D may be harmful. For example, in the early part of last century, the AMA specifically excluded pulmonary TB from the list of TB infections that ultraviolet light helps. They did so because many of the early pioneers of solariums reported that acutely high doses of sunlight caused some patients with severe pulmonary TB to bleed to death. Thus, these pioneers developed very conservative sun exposure regimes for pulmonary TB patients in which small areas of the skin were progressively exposed to longer and longer periods of sunlight. Using this method, sunlight helped pulmonary TB, often to the point of a cure.

Furthermore, it is well known that sunlight can cause high blood calcium (http://www.vitamindcouncil.org/news-archive/2008/professor-marshalls-recent-discovery/#calcium) in patients with sarcoidosis. In fact, sarcoidosis is one of several granulomatous diseases with vitamin D hypersensitivity (http://www.vitamindcouncil.org/news-archive/2008/professor-marshalls-recent-discovery/#vitamin%20D%20hypersensitivity) where the body loses its ability to regulate activated vitamin D production, causing hypercalcemia (http://www.vitamindcouncil.org/news-archive/2008/professor-marshalls-recent-discovery/#hypercalcemia).

Furthermore, although medical science is not yet convinced, some common autoimmune diseases may have an infectious etiology (http://www.vitamindcouncil.org/news-archive/2008/professor-marshalls-recent-discovery/#etiology). I recently spoke at length with a rheumatologist who suffers from swollen and painful joints whenever he sunbathes or takes high doses of vitamin D. As long as he limits his vitamin D input his joints are better. To the extent vitamin D upregulates naturally occurring antibiotics of innate immunity, sunlight or vitamin D supplements may cause the battlefield (the joints) to become hot spots. I know of no evidence this is the case but it is certainly possible.

However, if Dr. Marshall's principal hypothesis is correct, that low vitamin D levels are the result of disease, then he is saying that cancer causes low vitamin D levels, not the other way around. The problem is that Professor Joanne Lappe directly disproved that theory in a randomized controlled trial (http://www.vitamindcouncil.org/news-archive/2008/professor-marshalls-recent-discovery/#randomized%20controlled%20trial) when she found that baseline vitamin D levels were strong and independent predictors of who would get cancer in the future. The lower your levels, the higher the risk. Furthermore, increasing baseline levels from 31 to 38 ng/ml (77.5 to 95 nmol/L) reduced incident cancers by more than 60% over a four year period. Therefore, advising patients to become vitamin D deficient, as the Marshall protocol clearly does, will cause some patients to die from cancer.

I will not write again about Dr. Marshall's theories. No one in the vitamin D field takes him seriously. Personally, I admire anyone willing to swim against the tide and raise alternative theories. I have done the same with influenza and autism. However, I agree with the New York Times and Jane Brody's conclusion: "In the end, you will have to decide for yourself how much of this vital nutrient to consume each and every day and how to obtain it."

Jane Brody. An Oldie Vies for Nutrient of the Decade. New York Times. 2008 Feb 19.

I agree. You will have to decide for yourself.

Page last edited: 04 October 2011

[lapis]

Here's a couple of questions people have asked the Weston Price Foundation about The Marshall Protocol and vitamin D that you may find interesting.



************************************************** ****

The Marshall Protocol (http://www.westonaprice.org/letters/letters-spring-2010)

It was stated in the Caustic Commentary, “More News about Vitamin D,” (Spring, 2008 ) (http://www.westonaprice.org/caustic-commentary/caustic-commentary-spring-2008), that the work of the Autoimmunity Research Foundation (ARF), a California non-profit, was part of the pharmaceutical industry’s strategy to counter evidence on the benefits of vitamin D. On the contrary, the ARF receives no support from drug companies and is run entirely by volunteers, with no paid staff at all. People who volunteer for the ARF are motivated by their own improved health using the approach developed by the ARF, or the potential they see in the Foundation’s work for helping themselves, family members and the wider community. I am one of these volunteers, not the Executive Director, as the Commentary mistakenly mentions.

The work of the ARF arises from the discoveries of its founder and director, Professor Trevor Marshall, PhD, building on decades of research on the role of bacteria in chronic inflammatory diseases. Dr. Marshall has developed an approach that restores functioning of the vitamin D receptor, which he has found to be compromised by intracellular and biofilm bacteria that block the receptor (www.medicalnewstoday.com/ (http://www.medicalnewstoday.com/) articles/94642.php) in order to evade the immune system. Blockage of the receptor by the bacteria leads to dysregulation of vitamin D levels, which can be mistakenly interpreted as a vitamin D deficiency and lead to the many studies showing a correlation between disease states and low vitamin D levels.

In what may seem paradoxical at first, Dr. Marshall has found that reversing the disease process and eventually regaining health typically requires an avoidance of supplemental vitamin D as part of the overall anti-bacterial approach. This is because supplementation can often contribute to the blockage of the vitamin D receptor by raising levels of the precursor form, 25-D, into a range that can add to receptor blockage. Receptor blockage leads to poor innate immune system function and overgrowth of bacteria and other pathogens. High vitamin D levels can also act like a steroidal immunosuppressant and cause short-term symptom reduction at the cost of long-term bacterial increase.

I would also like to respond to points made in the commentary related to the interpretation of a study by Payne and others, showing a correlation between higher vitamin D intake in older adults and higher brain lesion volume (www. fasebj.org/cgi/content/meeting_abstract/ 21/6/A1072). It was assumed in the commentary that any correlation with brain lesions must be due to the use of vitamin D2 instead of vitamin D3. The brain lesion study used data from patient questionnaires on intake of vitamin D from all sources, both supplemental and dietary and did not administer pharmaceutical vitamin D (which is usually in the D2 form). Since this was a recent study and the vitamin D used in most commonly used OTC supplements, and the vitamin D added to milk is D3, it seems unlikely that any negative effect was due to the supplemental component of the vitamin D intake being from the D2 form. Also, I should note that the highest vitamin D intake in the study was below 1100 IU and many of the people getting the higher levels of vitamin D would have been getting them from multi-vitamin supplements, dairy products with added vitamin D and A, fish and fish oil and thus would have been getting some vitamin A from those sources. We have not found any difference between patients consuming vitamin D3 versus those consuming vitamin D2 prior to beginning the ARF’s approach (also called the Marshall Protocol). In any case, the brain lesion study is only a small part of the case to be made supporting the validity of the Marshall Protocol (www. AutoimmunityResearch.org http://members. aol.com/SynergyHN/shpt and http://bacteriality.com/category/brainlesions/, http://members.aol.com/SynergyHN/ MPIntro).

I am not by any means a supporter of pharmaceutical use unless truly necessary and see our goal as to eliminate the pathogens and consume a healthful diet, so as to not need pharmaceutical intervention. I think the Marshall Protocol has more in common with the Weston A. Price Foundation’s mission than might first appear. Dietary changes, including an increase in sugar and refined grains is, in our view, just one of the changes in cultural practices that have led to an increase in chronic disease. A number of the recent changes that have occurred have also led to an increase in intracellular bacteria that block the vitamin D receptor and thus there is a need for an approach that reverses the current trend. Recent findings indicate that we may not only be able to accomplish recovery from diseases such as autoimmune diseases and fibromyalgia, but even potentially eliminate inflammatory diseases of aging, such as heart disease, osteoarthritis and even cancer.

Joyce Waterhouse, PhD
members.aol.com/SynergyHN



Editor's Response: Thank you for your letter of correction. Regarding the study on brain lesions, this study was cross-sectional and not longitudinal, and cross-sectional studies are less capable of discerning cause and effect than prospective longitudinal studies because there is no evidence that the vitamin D supplementation preceded the development of the brain lesions. Furthermore, the study did not measure vitamin A. Vitamin A intakes were probably low for the simple fact that physicians now warn seniors against excessive vitamin A intake. For example, a recent review states that physicians should explicitly warn their patients against exceeding the RDA for vitamin A even though the tolerable upper intake limit set by other bodies is four times greater than the RDA. (Jackson HA, Sheehan AH. Effect of vitamin A on fracture risk. Ann Pharmacother. 2005;39(12):2086-90). There is no evidence from the abstract that the patients who were supplementing with vitamin D were getting any more vitamin A than those who weren’t. It would be interesting to see whether there is any correlation of brain lesions with naturally occurring vitamin D in foods like cod liver oil, shrimp, liverwurst, egg yolks, etc., which also supply vitamin A. Weston Price did not find problems in populations consuming far more than 1100 IU vitamin D per day from natural food sources.


VITAMIN D PROBLEMS? (http://www.westonaprice.org/letters/letters-spring-2010)

I have been following the WAPF diet since 2000 with excellent results. In the winter months I have been supplementing my fermented cod liver oil with one each of Carlson’s 1,000 IU D3 and 1,000 IU D3 and 25,000 IU A. After taking them for a week or so I get significant pain (inflammation) in a joint (elbow, wrist or knee) that I can only describe as if I cracked the joint into a painful position that is worse at either extreme in the range of motion. When I discontinue the Carlson’s supplementation I return to normal in a few days.

Today I came across the Marshall Protocol website (http://mpkb.org/ doku.php/home (http://mpkb.org/%20doku.php/home)), which says for many inflammatory, autoimmune diseases all vitamin D should be stopped along with other protocols for several years. I would love to hear your comments on this. It may well warrant an article in Wise Traditions.

Glenn Mingo,
Churchville, Virginia


Editor's Response: The position of the Weston A. Price Foundation is that we should obtain our vitamins A and D from foods like cod liver oil rather than from isolates supplements. Your experience with the supplements proves our point. It is more likely that the problems you experienced were caused by taking the large doses of A and D as isolated supplements, leading to an imbalance or deficiency of another vitamin—such as vitamin K2—rather than an intolerance for vitamin D because of autoimmune disease, especially as vitamin D is known to support immune function.

[lapis]

One last thing (I think) about The Marshall Protocol. It is extremely long and technical, so I'll provide just part of it:

Is the MP Treatment for Sarcoidosis Helpful for Other Chronic Diseases? (http://stuff.mit.edu/people/london/universe.htm)

MP’s Vitamin D Theories Are Not Supported by Lab Studies. (http://stuff.mit.edu/people/london/universe.htm)

Updated Dec 19, 2009

The MP treatment plan was originally designed to treat an inflammatory condition known as sarcoidosis. The treatment consists of using the drug Benicar, combined with the avoidance of all sources of vitamin D, and eventually adding various antibiotics, especially minocycline. After being used by sarcoidosis patients for some years, it was then theorized and claimed that the treatment could treat other inflammatory conditions. Eventually it was also claimed that it could treat fibromyalgia and CFS, conditions which are not recognized by the medical literature as being inflammatory in nature.

Sarcoidosis is an inflammatory disease, which is characterized by the presence of granulomas. Granulomas often occur as an immune response to certain types of infections and foreign bodies. However, no specific cause for sarcoidosis has yet been found. Many suspect an infectious cause, and studies are ongoing to find the infection (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Nadaf%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus). Others believe that while an infection may trigger the disease, that genetic and immune factors can significantly affect the course of the disease. Several articles state that over 50% of sarcoidosis patients eventually undergo remission without any treatment (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=11816825&dopt=Abstract). The other patients develop a chronic form, which requires treatment to resolve. Steroids (glucocorticoids) that suppress the immune system are the main drugs that are used to treat sarcoidosis. Other immune suppressant drugs and antibiotics are also being used. However, many cases are hard to treat, and symptoms can last for years. Given the scarcity of traditional treatment options, it’s not surprising that someone has found an alternative way to treat it.

One of the main beliefs of the MP is that an infection is the cause of all the conditions that the MP claims it can treat, and that an excess of vitamin D prevents the body from properly fighting the infection. In the early years of the MP, one of the main beliefs was that an excess of the active form of vitamin D, 1,25(OH)2D, was the problem. However, the medical literature only mentions a few specific diseases where this production contributes noticeable amounts of 1,25(OH)2D to the circulating levels. Sarcoidosis is one of those diseases.

In conditions such as sarcoidosis, activation of immune cells, i.e. macrophages and T cells, results in the production of 1,25(OH)2D. The MP claimed that this was also occurring in unrelated conditions, such as CFS, fibromyalgia, and chronic Lyme.

However, many people with those other conditions were not found to have elevated 1,25(OH)2D. This was eventually explained by the belief that the inactive form of vitamin D, 25(OH)D, is capable of reducing inflammation and blocking the production of 1,25(OH)2D. The MP claims that if people lower their 25(OH)D levels, by avoiding vitamin D intake, that this would result in elevated levels of 1,25(OH)2D, and this would prove that inflammatory, or “TH1 production” of 1,25(OH)2D was occurring. Furthermore, the MP also believes that 25(OH)D actually blocks 1,25(OH)2D from attaching to the vitamin D receptor, preventing 1,25(OH)2D from properly stimulating the immune system. The MP claims that this blocking prevents the body from fighting the infection. Thus, they now believe that 25(OH)D is also harmful, and they recommend avoiding vitamin D, in order to reduce 25(OH)D to below normal levels. The MP has continued to include new theories, such as the possibility that a substance from bacteria is also blocking the vitamin D receptor. None of this these theories have yet to be tested in any lab studies.



Positive Results from the MP Do Not Prove the MP’s Vitamin D Theories.



Does vitamin D really hinder these diseases? The medical literature does not support this claim, nor does it support the belief that 25(OH)D blocks the effects of 1,25(OH)2D. Indeed, a 2009 study has shown just the opposite, that 25(OH)D has agonistic activities similar to that of 1,25(OH)2D (http://www.ncbi.nlm.nih.gov/pubmed/19944755): And in fact, the avoidance of vitamin D in the MP treatment, has really never been properly studied, to see what, if anything, it contributes to the effects of the treatment. The treatment was designed for sarcoidosis, and was then applied to other conditions, without testing to see whether avoidance of vitamin D is actually of any benefit for those other conditions. Perhaps any benefits from the MP for other conditions, are due to the other aspects of the treatment. For example, other treatment plans that simply use only antibiotics, have been successful at treating inflammatory conditions (http://www.rheumatic.org/). Indeed, there are even cases of sarcoidosis being successfully treated simply by antibiotics (http://www.ncbi.nlm.nih.gov/pubmed/18344642). Additionally, minocycline, which is the primary antibiotic use by the MP, may be especially potent in inhibiting granulomas (http://www.ncbi.nlm.nih.gov/pubmed/8002645?dopt=Abstract).

And what about Benicar? Is Benicar helping sarcoidosis in the way that the protocol theorizes? ARBs such as Benicar have many useful effects on the body. Benicar not only has positive effects on the vascular system, but also has both anti-inflammatory and antioxidant effects. It may also be capable of increasing insulin sensitivity and affecting calcium metabolism. Studies about new effects of ARBs are constantly being published. Benicar could be helping sarcoidosis in one way, while helping other conditions in totally different ways. Indeed, it has been shown that the the angiotensin II "AT1 receptor activity is essential for the unrestricted development of full-scale innate immune response (http://www.ncbi.nlm.nih.gov/pubmed/19259805).” Thus, blocking the AT1 receptor, which ARBs such as Benicar do, will reduce the immune system’s innate response to infections. This is ironic, given that the MP claims tthat it’s treatment restores the innate immue system’s response.

The MP claims that Benicar acts as a vitamin D agonist, but there is no lab study that supports this claim. If Benicar was a VDR agonist, it would of great use, as many companies are trying to produce such an agonist. Yet, there has been no sign that the company that makes Benicar, believes that it has any affect on the VDR. Additionally, Benicar has not been studied at the high doses used by the MP, for the conditions that the MP treats. The more complete blocking of angiotensin II receptors at such high doses, might have even more positive effects than are presently known. And it might just be, that Benicar’s many positive effects, are capable of offsetting the negative effects of the vitamin D deficiency that results from the MP treatment.

Thus, there is no clear evidence that a reduction of vitamin D has any significant positive effects in the MP. Both Benicar and antibiotics are known to have many positive effects, for many different conditions. However, there is no proof in the medical literature, that reducing 25(OH)D to below normal levels, has any positive effects.

And what about the negative reactions to the MP treatment, that the MP claims is the body’s response to the killing of the infectious bacteria by the treatment. Are these reactions actually that, or are they simply side effects from the treatment?

The MP has yet to conduct any lab tests to support their theories. They have run computer simulations to support their beliefs about interactions of vitamin D metabolites, Benicar, and other substances, with the vitamin D receptor (VDR), but there is no guarantee that such simulations can accurately predict what actually happens in the body. For example, the author of the MP predicted that some of the statin drugs could interact with VDRs (http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T1B-4M23HDG-K&_user=501045&_coverDate=10%2F13%2F2006&_rdoc=1&_fmt=high&_orig=browse&_cdi=4886&_sort=d&_docanchor=&view=c&_ct=1&_refLink=Y&_acct=C000022659&_version=1&_urlVersion=0&_userid=501045&md5=8723673b88488d4b2b1981ff25005453). But actual lab tests showed no such interaction. (http://www.ncbi.nlm.nih.gov/pubmed/17105579?ordinalpos=9&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum) Indeed, the idea that statins have vitamin D type properties, was originally proposed by a non-MP researcher, and he has written that the MP author “is perhaps over-optimistic in suggesting that modern molecular biology can give precise answers to questions about actions of drugs because knowledge is inevitably incomplete.” (http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T1B-4M23HDG-M&_user=501045&_coverDate=10%2F13%2F2006&_rdoc=1&_fmt=high&_orig=browse&_cdi=4886&_sort=d&_docanchor=&view=c&_ct=1&_refLink=Y&_acct=C000022659&_version=1&_urlVersion=0&_userid=501045&md5=f542fece5d99be463878a021f99bc28c) Perhaps the lack of proof that Benicar affects the VDR, is the reason why, in some published articles by people involved with the MP, that they mention that their treatment uses a “VDR agonist”, without specifically mentioning that it is Benicar (http://www.ncbi.nlm.nih.gov/pubmed/19758177).

Since learning about the MP, I have tried to read as many medical studies as I could, that discuss sarcoidosis, ARBs, and vitamin D, and have learned many facts that I’ve not seen discussed elsewhere. Therefore, I’m presenting that information here, for anyone who is interested in the MP.

The intent of this web page is not to dissuade people from using the MP treatment. Instead, the intent is to question the validity of the theories connected with the treatment. These theories are often presented as being facts on MP web pages. Perhaps this is due to cognitive dissonance. Whatever the reason, many people who read those web pages end up believing that these theories are facts, when they are not. I have therefore decided to write this web page, in order to separate fact from theory, and to also point out when the MP theories are not supported by known facts. Given that the MP itself has changed some of its own views, such as recognizing that not everyone needs to avoid sunlight, we believe that it’s reasonable to question some of the other beliefs also.



The MP believes that excess 1,25(OH)2D production is occurring in many diseases, but the MP defines the upper
limit for normal 1,25(OH)2D to be 45 pg/ml, while lab tests and studies define it to be 60-65 pg/ml.

Flaws in MP 2009 Study “Vitamin D Metabolites as Clinical Markers in Autoimmune and Chronic Disease”



The MP believes that vitamin D metabolites play a role in sarcoidosis and many other diseases.

Vitamin D is a substance which the skin creates due to sunshine exposure. It is also found in supplements and certain foods. Vitamin D can either be stored in the body, or metabolized by the liver into 25(OH)D, which then circulates in the bloodstream and tissues. Only later is it then converted to the metabolite 1,25(OH)2D, which is the form that has hormonal active properties.

1,25(OH)2D both stimulates and inhibits the immune system. 1,25(OH)2D enhances the activity of immature immune cells (cell-lines, bone marrow cells), while it inhibits the activity of more mature cells (peripheral blood monocytes and peritoneal macrophages).

Some researchers believe that this dual effect allows 1,25(OH)2D to stimulate the immune system, while providing a mechanism for preventing overstimulation.

One of the ways that this comes into play, is when immune cells produce 1,25(OH)2D themselves. For example, when macrophage immune cells are activated by the TH1 (inflammatory) cytokine IFN-gamma, they are able to produce 1,25(OH)2D. This type of production is far different from the more common renal production of 1,25(OH)2D, which is controlled by the presence of calcium. Renal 1,25(OH)2D production controls calcium levels in the body. Thus, if you increase calcium intake, it will decrease the need for 1,25(OH)2D, and renal 1,25(OH)2D production will be reduced.

However, TH1 production of 1,25(OH)2D does not respond to calcium. And in certain conditions, where excess inflammation occurs, excessive amounts of 1,25(OH)2D can be generated, which is then reflected by increasing serum levels. However, this requires immune cells to be activated, and this has not been shown to be occurring in conditions such as CFS and fibromyalgia. Furthermore, IFN-gamma is a necessary requirement for unregulated immune 1,25(OH)2D production to occur (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=9215298&ordinalpos=15&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum). IFN-gamma levels are increased in inflammatory conditions such as sarcoidosis, which helps to explain the excess 1,25(OH)2D that occurs in those conditions. However, IFN-gamma is not increased in CFS and fibromyalgia.

In fact, in CFS, IFN-gamma may actually be decreased (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&dopt=AbstractPlus&list_uids=9466535). Thus, there is a lack of evidence that 1,25(OH)2D TH1 production occurs in those other conditions.
The MP believes that an excess of 1,25(OH)2D impairs the immune system in sarcoidosis, preventing it from properly fighting pathogens called Cell Wall Deficient bacteria, or CWD. (Note: CWD are not mycoplasmas (http://books.google.com/books?vid=ISBN0849387671&id=mincr2Hi81UC&pg=RA7-PA13&lpg=RA7-PA13&ots=HiulUrn9kX&dq=mycoplasma+cell+wall+deficient&sig=i8Lu2mF-hJ6rmAPt7Ri2uZ4eWW4).) Some researchers have theorized that CWDs play a role in a number of diseases. For example, lab studies have shown the possibility that CWD may alter the way the immune system responds to an infection (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17168999&query_hl=12&itool=pubmed_docsum), However, there still is much controversy regarding whether CWD have any significant effects in human disease (http://www.jimronline.net/content/html/fullhtm.asp?ArticleID=545), and studies have yet to confirm that CWDs play a role in sarcoidosis (http://www.ncbi.nlm.nih.gov/pubmed/12576359). For a more detailed critique of the MP’s theories on bacteria, click here to another person's web page (http://www.sciencebasedmedicine.org/?p=681).

In any event, if 1,25(OH)2D is somehow a factor in preventing a proper immune response against a pathogen, it would be important to know if significant TH1 1,25(OH)2D production was occurring. One way would be to simply test serum 1,25(OH)2D. The MP believes that if the serum level of 1,25(OH)2D is above 45 pg/ml, then it is abnormally high. They obtained this figure from the Merck manual. However, the Merck’s normal range of 1,25(OH)2D was defined decades ago, and is most likely based on older laboratory testing assays, which were known to have problems. (http://www.ncbi.nlm.nih.gov/pubmed/6607788?dopt=Abstract) The MP recommends using Quest laboratories to test 1,25(OH)2D levels (http://www.marshallprotocol.com/forum2/366.html). However, Quest themselves defines the normal range to be 15-60 for adults (27-71 for younger than 17 years). (http://www.questdiagnostics.com/brand/business/files/ped_sjc.pdf) These values have been confirmed by studies. For example, in a study which showed that 1,25(OH)2D levels decrease with obesity (http://www.ncbi.nlm.nih.gov/pubmed/18320256), the average 1,25(OH)2D level for the study population was 108.2 pmol/L (41.6 pg/ml), with a standard deviation upper limit of 56.4 pg/ml.. However, for subjects with the lowest BMI (body mass index), the average 1,25(OH)2D was 45.8 pg/ml, with a standard deviation upper limit of 62.1 pg/ml. A previous similar study showed even higher levels, i.e. an average 1,25(OH)2D level of 44 pg/ml for obese subjects, versus 52 pg/ml for nonobese subjects (http://www.ncbi.nlm.nih.gov/pubmed/15001609?dopt=Abstract) The MP gives no clear reason why they believe that the upper limit should be according to Merck. Thus, many people are being told by the MP that they have elevated 1,25(OH)2D, when it might not necessarily be so.

In a 2009 study on 1,25(OH)2D by people involved with the MP, entitled "Vitamin D metabolites as clinical markers in autoimmune and chronic disease" (http://www.ncbi.nlm.nih.gov/pubmed/19758177), it was stated that “the threshold for elevated 1,25-D was selected as 110 pmol/L based on the observation that all healthy patients in a clinical care setting showed levels under this range”. This conflicts with the studies mentioned above, where 110 was shown to be at or even below the average level. Other studies also support a higher average level. For example, one recent study in the USA showed that 3 different groups of 500 or more people, had average1,25(OH)2D levels of 113 , 112, and 126 pmol/L (http://www.ncbi.nlm.nih.gov/pubmed/18593774). In another study in Denmark, on healthy postmenopausal women, the average level of serum 1,25(OH)2D was 118 pmol/L, with the range being (97-147).

Furthermore, the MP study tested 1,25(OH)2D levels in patients with various diseases, and they declared that anyone with levels above 110 pmol/L had “elevated levels”. Besides the fact that this threshold is much lower than many other studies show, the characteristics of the healthy and patient populations were not stated in the study. There is no indication that they were similarly matched.

This is necessary, because besides the fact that obesity can affect 1,25(OH)2D serum levels, there are many other factors that affect 1,25(OH)2D serum levels, such as age, as 1,25(OH)2D levels decrease with age. Hormone replacement therapy, diuretics, or pharmacological doses of calcium, can also affect 1,25(OH)2D levels. And for postmenopausal women, 1,25(OH)2D levels are dependent on 25(OH)D levels, as shown by the previous Denmark study. The Denmark study made sure that the participants were not taking any vitamin D supplements. The MP study did not control for any of these factors. Even given the Denmark women were not using vitamin D supplementation, the average 25(OH)D levels for the Denmark study was 57 nmol/L. This is of note, because the MP believes that such levels of 25(OH)D are only achieved due to vitamin D supplementation. As stated in the MP study, “25-D levels remained above range [50 nmol/L] in the majority of our cohort suggests that subjects were supplementing with vitamin D or simply eating a plethora of foods that are now artificially fortified with the secosteroid/hormone.” The Denmark and many other studies, in contrast, show that such levels, and even much higher levels can be naturally achieved without vitamin D supplementation. This topic will be discussed at length later in the article.

The MP article also made reference to studies that show “deleterious or no beneficial effect of vitamin D supplementation on certain diseases”. Interestingly, the first referenced study, regarding prostate cancer vitamin D, did not actually involve vitamin D supplementation (http://www.ncbi.nlm.nih.gov/pubmed/18505967), but simply tested 25(OH)D levels. This and some other studies, have shown a possible increased risk of certain types of cancer at high 25(OH)D levels. One possible reason for this, has been proposed by the long time vitamin D researcher Professor Vieth. He believes that any possible deleterious effects from high levels of 25(OH)D, may be caused by varying 25(OH)D levels that occurs due to the seasons (http://www.ncbi.nlm.nih.gov/pubmed/19667164). The change of sunlight during the different seasons, changes serum 25(OH)D levels. However, the regulation of tissue production 1,25(OH)2D may not immediately respond to the change in serum 25(OH)D levels. There may be a delay before the tissues adjust enzyme levels. Thus, when 25(OH)D level decrease, 1,25(OH)2D production at the tissue levels may be inadequate, until enzyme levels adjusted. Most studies on cancer so far, have not actually used high levels of vitamin D supplementation. Such supplementation would sustain high levels of 25(OH)D throughout the year, and this might provide year round positive effects to prevent cancer.



Testing Methods used by the MP for Dysregulated 1,25(OH)2D Production are flawed,
due to the fact that serum 1,25(OH)2D is affected by Calcium, Phosphate, PTH, and other factors.



For many years, the MP also believed that excess production of 1,25(OH)2D could be proven by computing the ratio of serum 1,25(OH)2D to 25(OH)D. A high ratio was believed to indicate the presence of TH1 1,25(OH)2D production, and this meant that your condition could be treated by the MP. The MP now states that this test is often unreliable. Instead, they now use absolute levels of 1,25(OH)2D and 25(OH)D. But 1,25(OH)2D can be significantly influenced by many factors that have nothing to do with TH1 production of 1,25(OH)2D, so that neither the D-ratio nor the absolute test are reliable ways to prove TH1 production of 1,25(OH)2D. And it is because of the fact that 1,25(OH)2D levels can be influenced by many factors, that 25(OH)D is the main test used by the medical community to determine a vitamin D deficiency, and not 1,25(OH)2D.

The conversion rate of 25(OH)D to 1,25(OH)2D can vary due to a number of factors. For example, 1,25(OH)2D levels can vary significantly during the menstrual cycle (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6897337&query_hl=20&itool=pubmed_docsum). Also, a study has shown that women with PMS have high serum levels of 1,25(OH)2D, and low levels of 25(OH)D (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7608284&query_hl=16&itool=pubmed_docsum). This is partially due to a direct influence of estrogen on renal 1,25(OH)2D production. Estrogen supplementation has been shown to increase 1,25(OH)2D levels (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9405729&query_hl=37&itool=pubmed_Docsum). Using the MP criteria, some of these women with PMS would be deemed by the MP to have TH1 1,25(OH)2D production, when they did not.

Although the D ratio test is used less, the MP web page still states that “a D-ratio that is higher then 2 is a sign of inflammation. A normal ratio in a healthy person is between 0.75 to 1.75.” (http://www.marshallprotocol.com/forum2/366.html) However, in practice, normal people do have a ratio of 2 or higher. For example, a recent study on postmenopausal women aged 45-58, showed that the average ratio was 1.98 (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15868280&dopt=Abstract). Additionally, this study compared women who had different forms of the vitamin D binding protein (DBP). DBP binds to vitamin D metabolites in the serum and tissues. Different genetic forms exist. The D ratio was found to be different for women who had different forms of the DBP.

This is theorized to be due to the fact that the different forms have different metabolic rates. For women with one specific form, the D ratio was found to be an amazing 2.49. Thus, the D ratio test is flawed, yet it was used for many years to diagnose people with a TH1 condition. Therefore, it’s unknown how many people who have tried the MP during those years, really had a TH1 condition.

The most obvious flaw in measuring 1,25(OH)2D, is the fact that serum 1,25(OH)2D is significantly affected by dietary calcium (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=468987&ordinalpos=42&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum). Taking more calcium will decrease 1,25(OH)2D levels. Thus, one possible way to see if elevated 1,25(OH)2D is due to insufficient calcium, rather than due to TH1 production, is simply to significantly increase one’s calcium intake. If a decrease of 1,25(OH)2D occurs, then the elevated 1,25(OH)2D would likely be due to a calcium deficiency. A lack of calcium could simply be caused by a low calcium diet. Calcium insufficiency is very common in many countries (http://www.ncbi.nlm.nih.gov/pubmed/19724293), including the US (http://www.ncbi.nlm.nih.gov/pubmed/17490974). A lack of calcium could also be due to an undiagnosed gastrointestinal disease. For example, in celiac disease, one study showed serum 1,25(OH)2D levels as high as 80 pg/ml (http://www.ncbi.nlm.nih.gov/pubmed/9207263). Indeed, it is possible that some people on the MP who initially had high levels of 1,25(OH)2D, may simply have not been taking or absorbing enough calcium. And in fact, some people on the MP have eventually added calcium supplementation, which has then lowered both their PTH and 1,25(OH)2D levels (http://www.marshallprotocol.com/forum11/8193.html). One wonders how many people who started the MP due to high 1,25(OH)2D levels, had high levels simply due to not taking enough calcium. Note however, that it is possible to have calcium insufficiency (http://www.ncbi.nlm.nih.gov/pubmed/19488668), yet still have normal PTH levels, so that testing for PTH is not necessarily a good indicator of calcium status.

1,25(OH)2D production is also dependent on dietary phosphate (http://www.ncbi.nlm.nih.gov/pubmed/3753709) Thus, in addition to calcium, phosphate also affects 1,25(OH)2D levels. Any changes in dietary phosphate, intestinal phosphate absorption, or renal phosphate reabsorption, can affect serum levels of 1,25(OH)2D. In fact, some people with CFS and fibromyalgia may actually have phosphate diabetes, a condition that depletes phosphate (http://www.ncbi.nlm.nih.gov/pubmed/9683977).

Another problem with the ratio test is the following requirement listed on an MP web page: “The D ratio is not a sufficient indicator of vitamin D dysregulation, especially when 25-D levels rise above 15 ng/ml. (http://www.marshallprotocol.com/forum2/366.html)” The reason for this is the belief that 25(OH)D reduces inflammation and therefore blocks the TH1 production of 1,25(OH)2D. The problem with that statement, is that even in healthy people, at the levels of 25(OH)D that the MP recommends, a significant rise in PTH levels occurs, which results in increased levels of 1,25(OH)2D (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=10837301&dopt=AbstractPlus). Therefore, a high ratio of 1,25(OH)2D to 25(OH)D at those levels of 25(OH)D, can have nothing to do with increased inflammation, and thus cannot be used as an indicator of inflammation.

Interestingly, there is no proof that higher levels of 25(OH)D, can significantly reduce TH1 1,25(OH)2D production. For example, there is a study on sarcoidosis patients whose levels of 25(OH) D were on average 25 ng/ml, and giving them oral vitamin D still resulted in a significant increase of 1,25(OH)2D production (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7419722&query_hl=70&itool=pubmed_docsum). In that study, oral Vitamin D.(100,000 IU) was given to people with and without sarcoidosis. People without sarcoidosis had no change in their 1,25(OH)D levels due to this dose. However, in sarcoidosis patients, this dose caused the 1,25(OH)2D levels to significantly rise, during which 25(OH)D levels rose to almost 50 ng/ml, well past the point at which the MP claims that 25(OH)D starts to block 1,25(OH)2D. But there was no sign of reduced 1,25(OH)2D production from 25(OH)D. Instead, in all patients, an approximate doubling of 25(OH)D levels, resulted in a doubling of 1,25(OH)2D levels, no matter what their initial 25(OH)D levels were.

[lapis]

In the interest of disclosure, I got a lot of the links from a thread called "The Marshall Protocol, STAY AWAY FROM THIS ONE (http://www.natmedtalk.com/showthread.php?t=1643)" on a health forum. It's a long thread with lots of posts by Ted Hutchinson, who is a good writer on several health forums.

[lapis]

"Resurgence in Childhood Rickets Noted (http://articles.latimes.com/2001/apr/15/news/mn-51264)"

Medicine: The bone-softening disease is caused by lack of sunlight and vitamin D. Milk substitutes and sunscreen may be contributing to the problem.

April 15, 2001 (http://articles.latimes.com/2001/apr/15)|ERIN McCLAM | ASSOCIATED PRESS


ATLANTA — Childhood rickets--a bone-softening disease that had become so rare the government stopped keeping statistics on it--is making a comeback, in part because some youngsters are not getting enough sunlight, health officials say.

Rickets, a vitamin D deficiency that causes bones to soften and bend and often results in bowlegs, was once a major health problem. The addition of vitamin D to milk in the 1930s virtually eliminated the disease.
http://articles.latimes.com/images/pixel.gif

But health officials say that health departments across the country are seeing a resurgence.

The government attributes the comeback to the popularity of milk substitutes like soy that lack certain nutrients; the failure to supplement breast milk with vitamin D; and a lack of childhood exposure to sunlight. Sunlight stimulates the body to produce vitamin D. [NOTE that non-dairy milks contain the vegetarian vitamin D2 ergocalciferol rather than the D3 from animal products which seems to be more effective in raising people's vitamin D levels.]

The resurgence has been seen particularly among children breast-fed by black mothers. Dark-skinned people absorb less sunlight.

"It's something people have become lax about," said Dr. Norman Carvalho of Children's Healthcare of Atlanta, a children's hospital. "We've been living under the assumption that rickets doesn't occur anymore. But there's a definite increase in the number of cases we're seeing. It seems to be a trend."

Carvalho led a Georgia study of malnutrition in children that appears in the April issue of the journal Pediatrics.

The 1997-99 study concluded that about one in 200,000 children in Georgia is hospitalized with rickets. But Carvalho cautioned that the rate is probably higher because the study was conducted in the South, where children may get more sun, and because there is no national reporting system.

The study offered no overall national numbers, and there are no earlier figures with which they can be compared.

Among the study's conclusions: Children are not getting enough vitamin D because their parents are keeping them indoors more, leaving them at day-care centers or trying to protect them from skin cancer.

"Parents are working long hours," Carvalho said. "Parents are coming home after dark, and their children are only getting out in the sunlight over the weekends."

The renewed concern over rickets poses a dilemma for health officials, who have long urged parents to put sunscreen on their children to protect them from ultraviolet rays--which cause skin cancer but also produce vitamin D.

"We really can't promote increased sun exposure for children," said Kay Tomashek, an epidemiologist at the Centers for Disease Control and Prevention in Atlanta. "So it's so important for parents to discuss with physicians the child's nutrition needs."

That includes being more careful about milk substitutes, which are growing more popular among health-conscious Americans, vegetarians and people with allergies.

Some soy milk products do not have sufficient vitamin D for toddlers, and some rice-based milks do not have enough protein.

The CDC also urged doctors to be more vigilant about telling pregnant women to make sure their children get enough vitamin D.

http://articles.latimes.com/images/pixel.gif
http://articles.latimes.com/images/pixel.gif
Health officials also said they are studying ways to improve tracking of rickets nationwide.

"It's a lack of awareness," Carvalho said. "A lot of physicians have never seen a case of rickets. They may not even recognize it. People are just not familiar with these conditions anymore."

[lapis]

Global Health Watch: Rickets showing up in some British children (http://articles.latimes.com/2011/jan/19/news/la-heb-ricketts-britain-20110119)

BOOSTER SHOTS: Oddities, musings and news from the
health world

January 19, 2011 (http://articles.latimes.com/2011/jan/19)|By Janet Stobart, Los Angeles Times

Rickets, a bone disease caused by vitamin D deficiency and which used to stalk the poverty-stricken slums of 19th century England, has reappeared in modern Britain.

In the southern port city of Southampton, Tyler Atrill, 12, an active girl who always played outside in one of the sunniest areas of Britain, was diagnosed with rickets last November, the Telegraph (http://www.telegraph.co.uk/health/8268321/Schoolgirls-rickets-blamed-on-sunscreen.html) reported this week. Tyler's mother Lisa, who is a nurse, told the newspaper that her daughter had been suffering severe leg pains for three years and was finally diagnosed with a disease thought to have disappeared from Britain in the 1920s.

http://articles.latimes.com/images/pixel.gif
Tyler is one of more than 40 children treated for rickets in the last year by Southampton General Hospital. Dr. Nicholas Clarke, an orthopedic surgeon from the hospital, said the phenomenon was "quite astonishing. We are seeing cases across the board, from areas of deprivation to the middle classes. ... This is almost certainly a combination of the modern lifestyle, which involves a lack of exposure to sunlight and covering up in sunshine."

Lisa Atrill said she covered her children in sunscreen whenever they went out in bright sunshine.

There are no official figures, but doctors around the country say a number of cases have sprung up in recent years. Last year the British Medical Journal (http://www.bmj.com/content/340/bmj.b5664.extract) published findings of the spread of the disease in the United Kingdom, quoting a survey showing "more than 50% of the adult population have insufficient levels of vitamin D and that 16% have severe deficiency during winter and spring.”

Particularly at risk are people in northern England and Scotland, where statistics of other bone-related diseases, multiple sclerosis and rheumatoid arthritis are higher than in England.

In September, the Scottish government launched a campaign advising people to take vitamin D supplements to make up for the lack of sunshine.
http://articles.latimes.com/images/pixel.gif

[lapis]

I used to get sick all the time.

Now that I take Vitamin D3 supplements, my body functions better, and I don't get sick.

That's all I need to know. Fuck their research.

I have had the same results as you, especially now that I'm concentrating more on taking it with a lot of magnesium and some vitamin k2, and sunbathing when possible. However, I do wonder what the long-term consequences are, and I thank OHL for posting this information so that I don't get comfortable and set in my thinking and closed off to other ideas.

[Old Herb Lady]

OK, maybe my reply was a little harsh. I apologize.

Vitamin D is your friend. You can have my Vitamin D when you pry it from my cold, dead fingers!


Thank You BrewTech for this and for your beautiful apologetic PM. It was rude of me not to acknowledge your PM/apology.
You are completely forgiven & I appreciated the kind words. Did you write that all by yourself or who did ? It seems so very sincere !

[Silver Rocket Bitches!]

I take 5000 iu daily. I never realized that it acts as a OTC steroid. Thanks for the info.

[Shami-Amourae]

tl;dr

[LastResort]

The way the MSM pumps vitamin D like its the best thing ever really makes me skeptical...

[Celtic Rogue]

I take D3 10,000IU daily. Results... I am off of 3 blood pressure meds... 123/82 was my last measurement... boy is that worth it alone. Also I have not had the flu or other normal seasonal colds I used to get. This is all anecdotal evidence... but this alone I will take D3. Just my experience... not to be construed with medical advice... do you own due diligence!

[Awoke]

OLH, the link is not loading for me. Thanks for posting this info. I am going to read it over in detail before forwarding it on, but I wanted to copy it into a word file for portability.

[lapis]

That's weird, it loads fine for me on Firefox. But you can also find similar information if you search for vitamin D + Marshall Protocol.

[lapis]

The way the MSM pumps vitamin D like its the best thing ever really makes me skeptical...

The headlines sure make it seem like it but when you read through their stories, the doctors are still recommending the old 400 or 600 i.u. amount (http://www.vitamind3-cholecalciferol.com/vitamin-d-rda.htm).


I take D3 10,000IU daily. Results... I am off of 3 blood pressure meds... 123/82 was my last measurement...

Oh boy I hope it doesn't do that to me. I have the opposite problem; my blood pressure is very low.

[Neuro]

Thank you OHL for posting this, I think it is important to realise that vit D works like a hormone, but is not secreted as one, iow you get it through sun light and diet (or supplements), as with any hormone you can get too much or too little of it. If you get it through a normal diet or sun light there are several feedback mechanisms that would limit the dose you get, but those pathways would be over ruled if you take it as a supplement, and you may get too much. It is also important to realise that different people have different needs, someone who is immunosuppressed would react very differently towards it compared to someone who has an hyperactive immune system with inflammatory disorder. Further a dark skinned person don't make as much vit D as a white, and may need supplements if they live at latitudes that are unnatural for their skin type. I do think though there is a lot suggesting that lack of vit D (or at least sunshine) in the winter months is responsible for the winter epidemics... However if the flu doesn't kill you it is bound to make you stronger... Getting a flu or a cold once in a while may not necessarily be a bad idea...

[Bigjon]

Clearing Up Confusion on Vitamin D (http://articles.mercola.com/sites/articles/archive/2009/03/14/Clearing-Up-Confusion-on-Vitamin-D--Why-I-Dont-Recommend-the-Marshall-Protocol.aspx)-- Why I Don’t Recommend the Marshall Protocol
Posted By Dr. Mercola | March 14 2009 | 81,281 views
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by Dr. Mercola

Ever since I started promoting the benefits of vitamin D there has been a small but vocal minority of advocates of what is referred to as the “Marshall Protocol”.

As much as I would like to ignore it due to its lack of validity, I can no longer do so, because so many people are using this information and at the very least, they are placing their health at great risk and in many cases they are damaging their health.

Therefore, to remain silent would be irresponsible, so I am going to address this issue once and then put it to rest.

I felt it was important to share my views on what I perceive is a dangerous view of vitamin D physiology. It has been my common strategy for as long as I have been in medicine to be open to new ideas and concepts and I have carefully evaluated Dr. Marshall’s protocol and even attended one of his lectures in Chicago nearly ten years ago.

It was somewhat comical to attend his seminar as most of the people attending were wearing very large, wrap around UVB blocking glasses typically worn after cataract surgery. I knew at that point that the operating premise was seriously flawed. The belief that ANY exposure to the sun was dangerous and needed to be avoided gravely concerned me.

“Dr.” Marshall is Not a Physician and Doesn’t Even Have a Biology Degree

For those of you who are not familiar with the protocol recommended by Trevor Marshall, I will briefly summarize its basic tenets, as I understand them, before going on.

First it is important to note that Dr. Marshall is not a medical doctor but freely uses the doctor salutation to add credibility to his questionable theories.

Marshall is an Australian electrical engineer who developed an interest in biomedical engineering out of a desire to cure his own sarcoidosis, which he developed in the 1970s[i]. He has no medical degree. His theories come from mathematical molecular models, not clinical studies.

Sarcoidosis is Only Disease Where Vitamin D Levels Are an Engima

Sarcoidosis is an inflammatory condition that produces tiny lumps of cells called granulomas in various organs of the body. These granulomas clump together into large or small groups, resulting in organ damage. They most commonly occur in the lungs, lymph nodes, skin and eyes, and symptoms can wax and wane over many years.

Symptoms can vary from very minimal to life threatening. Some medical experts believe sarcoidosis is an autoimmune process, and others believe some substance or pathogen has triggered the inflammation. There is no agreement yet about the cause of this illness.

Marshall states the treatment he developed has cured his disease and claims that his protocol, the Marshall Protocol (aka MP) will cure a long list of chronic inflammatory and autoimmune diseases. According to one of his most vocal advocates, Amy Proal[ii], the MP cures sarcoidosis, Chronic Fatigue Syndrome (CFS), fibromyalgia, Crohn’s disease, and rheumatoid arthritis (RA), and many others.

Marshall proposes the following:

All chronic diseases are the result of infection by certain bacteria that hide out and proliferate inside the cytoplasm of the cells they infect. These cells include macrophages, the very cells of the immune system the body uses to kill invading pathogens. Once inside these cells, they generate the release of inflammatory cytokines, which cause the person pain and/or fatigue.

The infected cells sustain themselves by congregating into communities called biofilms, which produce a protective matrix that allows them to more effectively evade the immune system and resist antibiotics.

The reason these bacteria are able to proliferate in this way is directly related to vitamin D. Marshall argues that vitamin D is immunosuppressive—it effectively shuts down your body’s immune system. Therefore, he states, the lower your vitamin D is, the better, because vitamin D from any source (food, supplements, or sunlight) in any amount drives the disease process.

The low vitamin D levels [meaning serum 25(OH)D] found in many people with chronic diseases are a result of the disease, rather than the cause. Marshall explains this by saying that the disease process causes 1,25-D to rise to an unnaturally high level. This in turn causes a cascade of reactions leading to a drop in 25(OH)D, leading to the low blood levels we observe in blood tests.

Given these premises, his treatment plan consists of the following:

Avoid sunlight and vitamin D as if they were the plague. He restricts people from eating foods high in vitamin D, as well as having them hole-up inside for months on end. If they go outside, they cover up completely, including wearing special sunglasses.

Patients take a medication called Benicar (olmesartan), which is an angiotensin II receptor blocker (ARB). This is supposed to reactivate the immune system by opening up the VDRs (vitamin D receptors), allowing the body to once again manage the infections.

Patients concurrently take pulsed, low-dose antibiotics to further combat the infection.

The protocol is continued for 3-5 years. Before patients begin to feel better, they can expect to feel much worse due to the “Herx” reaction (Jarisch-Herxheimer reaction). Herx is the effect of bacterial dye-off, releasing toxins into the bloodstream, stimulating the production of inflammatory cytokines, which make the patient feel bad.

So, Marshall believes, if you don’t feel bad, it’s not working.

Why One Size Doesn’t Fit All

Probably because Marshall is an engineer and not a physician, his approach reveals a lack of appreciation of the complexity and variation of the human system. Your body is not a piece of electronics that can be predicted to act a certain way every time. A radio is a radio is a radio, but not so with the human body. It is more than a sum of its parts, making medical science as much an art as it is a science.

This is precisely why clinical trials are necessary before conclusions about causation can be drawn. There are simply too many variables.

What Marshall has done is take conclusions from his research for a cure for his own condition (sarcoidosis), and then applying it to everything from soapsuds to unicorns. The error in logic would not be so disturbing were it not for the fact that he is doing a lot of harm to people who desperately seek help for their pain.

Our Ancient Ancestors Had Constant Sun Exposure

First, let me address the most basic premise here—that vitamin D and sunshine promote disease. Besides being contrary to current research, this goes against our evolutionary history.

Our ancient ancestors had regular and consistent sun exposure as they were from sub tropical environments and did not spend nearly all day indoors like most of us do when we work. We’ve spent thousands of years hunting and gathering outdoors, particularly in equatorial regions, and most of that time we certainly wore far less clothing than we wear today. It makes no sense that we would have developed the need to avoid sunlight altogether.

Nature has designed a system in which humans go into the sun, make thousands of units of cholecalciferol, which the liver then converts to 25(OH)D. Our organs then make a steroid hormone, 1,25-D, which helps to regulate genes in every organ of the body[iii].

As Dr. John Cannell, Executive Director of the Vitamin D Council, says, “We assume nature created this for a good reason.”

Inflammation Requires Holistic Approach

I can agree with Marshall on the idea that inflammation is a major underlying factor in many chronic diseases. However, ,inflammation must be addressed with a holistic approach that includes diet and nutritional type, exercise, sleep, stress, psychological factors, environmental toxins, and many other things. None of these is mentioned, that I can find, in the Marshall Protocol.

And it is my firm belief that medication should rarely if ever be the first avenue of treatment for anything. Most healing can be achieved by supporting your body’s own ability to heal itself by strengthening your immune system.

The Antibiotic Issue

Taking antibiotics for years, as directed by the MP, is just ludicrous and is an invitation for disaster.

There are certainly times when antibiotics are necessary, but they are widely overused. For every time they are used appropriately in traditional medicine, there are at least 10 to 20 times when they are inappropriately used, and this is what has resulted in antibiotic-resistant bacteria.

Marshall claims that, by “pulsing” several different antibiotics, antibiotic resistance is avoided. However, there is evidence to the contrary in the literature.

Mark London, of MIT, has written a very detailed, comprehensive analysis of the MP[iv]. He states that overuse of macrolides (Zithromax, clindomycin, and others) is known to result in resistant bacteria, and the risk is even higher when macrolides are combined. There is also cross-resistance between macrolides. Therefore, Marshall’s claim that his protocol prevents antibiotic resistance is false.

In the past I have used antibiotics for rheumatoid arthritis when I was applying Dr. Thomas Brown’s protocol. Even though Dr. Brown clearly helped many thousands of patients with this, after using it for many years I realized that even better results could be achieved without the use of antibiotics.

If infectious agents do underlie disease, which is certainly possible but remains to be proven, antibiotics are not the answer. There are many natural choices for anti-infectives that are much safer and have fewer side effects than antibiotics.

For example, for thousands of years, Chinese medicine has been curing infections with herbs, mushrooms, bark, and other natural agents.

If you have an infection, your best strategy is to get your immune system into shape by addressing the things I mentioned above, none of which are addressed by the Marshall Protocol.

“Herx” Reactions, or Something More Ominous?

Jarisch-Herxheimer reactions are a major part of what patients are told to expect once they begin the MP.

The MP teaches that, in order to know that you have one of these infections, you go onto the MP, and if you have a Herx reaction (which they basically define as feeling bad in any number of ways), you can conclude you’re on the right path. By the same token, they say, if you don’t “Herx,” then you don’t have an infection.

However, Herx reactions are known to occur only with certain types of infections such as Lyme and syphilis. They normally occur only early in treatment and typically last a few days or weeks, not months or years, and only in some people—not in all people3[v][vi].

Therefore, any test that is based on whether or not a Herx reaction occurs is meaningless, since the lack of a reaction doesn’t rule out the presence of an infection. Similarly, an increase in your symptoms doesn’t necessarily mean you’re having a Herx reaction.

So-called Herx reactions can be explained by well-documented medication side effects. For example, Minocycline has been known to cause dizziness and nausea in some people. Benicar has many documented side effects at much smaller doses than what the MP calls for, including headaches, chest pain, muscle pain, and coughing.

How do you know that your “Herxing” isn’t just a reaction to the Benicar?

Also, the MP can cause an elevated PTH level (Parathyroid Hormone), which in itself can cause symptoms of fatigue, poor concentration, irritability, depression, insomnia, headaches, and palpitations[vii].

To say that everyone who has any increase in symptoms while on the MP is just having a “Herx reaction” is simply ignorant and foolhardy, as well as negligent as it causes the patient to ignore potentially dangerous signals that something else could be wrong!

This is just what happened to a man by the name of Steve Carroll. Mr. Carroll is someone who tried the MP and nearly died of Addison’s disease, as a direct result of the Marshall Protocol. His symptoms were of a growing adrenal crisis. However, the MP advisors told him that he was simply “herxing.”

When he consulted his own physician, who took him off the protocol and saved his life, Mr. Carroll contacted the MP “forum” advisors[viii]. He was met with nothing but resistance and denial, and told that his own physician was wrong. The Marshall forum advisors refused to even consider the possibility they might be wrong, and that using Benicar with people who have weak adrenal function (namely low cortisol and aldosterone production) is very dangerous and can lead to an adrenal crisis.

A documentation of the dialog between Mr. Carroll and the MP folks is quite telling and has been posted verbatim online[ix].

As Mr. London writes:

“Giving a medicine to see if a person will get better from it, and then continuing that medicine due to the fact that a positive benefit occurred, is of course extremely common. However, giving a medicine specifically to see if a person will get worse from it, and then continuing that medicine because this occurred, is quite rare.

While it’s true that many medicines will first cause side effects before the positive benefits occur from it, these side effects are almost never considered to be a sign that the medicine is the proper medicine to use to treat a person.”

Measuring 1,25-D is Like Herding Cats

Marshall states that 1,25-D levels are elevated in people with chronic infectious diseases. [Remember, 1,25-D is the active form of vitamin D, once it’s been converted from 25(OH)D.]

He relies on 1,25-D levels as indicators of the disease process. However, 1,25-D values can fluctuate tremendously up and down for many reasons, other than disease processes. 1,25-D is influenced by calcium, phosphate, and PTH, just to name a few, which makes it meaningless to use it as a marker for dysfunctional vitamin D production or regulation.

In fact, some studies show little to no correlation between 1,25-D and 25(OH)D levels[x][xi]. Many body tissues have the ability to generate 1,25-D themselves, as a way to self-regulate, rather than solely relying on serum 25(OH)D.

This is why the standard used by the medical community for assessing health is serum 25(OH)D, which is not subject to these variables and fluctuations. This test has been standardized, recognized and used by every vitamin D expert in the world. I have talked to many of the leading vitamin D researchers and not one of them had anything favorable to say about the misinformation Marshall is promoting.

What about the Cancer Studies Cited by MP Advocates?

On her website called Bacteriality, Amy Proal mentions a number of cancer studies that reportedly demonstrate that vitamin D does not decrease cancer risk. Upon close inspection, however, several of those studies involve people supplementing with very low doses of vitamin D, lower than what is considered effective by most vitamin D experts. The supplementation levels are 600-800 IU per day, which is too little to prevent much of anything.

Dr. John Cannell, one of the foremost experts on vitamin D today, scripted a response to the MP, which he sent out in his newsletter[xii]. He makes the point:

If Marshall’s hypothesis is correct, that low vitamin D levels are the result of disease, then he is saying that cancer causes low vitamin D levels, not the other way around. The problem is that Professor Joanne Lappe directly disproved that theory in a randomized controlled trial[xiii] when she found that baseline vitamin D levels were strong and independent predictors of who would get cancer in the future.

The lower your levels, the higher your risk. Furthermore, increasing baseline levels from 31 to 38 ng/ml reduced incident cancers by more than 60% over a four-year period. Therefore, advising patients to become vitamin D deficient as the MP clearly does, could cause some patients to die from cancer.

It is worth noting that the amount of vitamin D subjects in the Lappe study received was 1,100 IU per day, higher than any of studies cited as negative toward vitamin D, and this study was of longer duration.

Can Any Value Be Found in Marshall’s Work?

Marshall arrived at most of his theories from his personal battle with sarcoidosis, and he certainly can’t be faulted for taking an aggressive approach to finding a solution for what is traditionally viewed as an incurable disease. After all, many serendipitous discoveries in history came about in unusual ways.

I strongly believe his efforts have gone astray, however, in assuming all those other chronic diseases fit the same model.

Sarcoidosis is a condition marked by abnormal immune responses, one of the many unique features of that condition. For example, according to Dr. Cannell, in sarcoidosis, the body can’t regulate activated vitamin D production, resulting in hypercalcemia12. But these immune responses are not found in all of the other inflammatory conditions, so any treatment effective against sarcoidosis is thus treating a rather unique condition and may not necessarily be as effective for other conditions.

If the MP does indeed help some people with sarcoidosis and various other conditions as it seems to, based on some people’s reported experiences on the web, there is no guarantee it is working in the way Marshall assumes it is.

For example, Benicar and the various antibiotics all have various effects, both positive and negative, on various conditions, which could be one explanation for why some folks feel better. Benicar has been shown to have some anti-inflammatory properties, among others. Some antibiotics have anti-inflammatory and analgesic effects themselves (minocycline, for example).

It could be this effect that makes patients feel as if they are getting better. If so, patients might experience a recurrence of symptoms once the meds are discontinued.

What About Melatonin?

Since light suppresses melatonin, it would be expected that melatonin levels would rise when you avoid light. Melatonin has significant effects on your immune system. In fact, in 2006, a study showed that melatonin was a safe and effective treatment for sarcoidosis![xiv] Melatonin has also been shown to help other conditions, including CFS, fibromyalgia and colitis.

How does anyone know it isn’t the melatonin that is causing some people to feel better? If so, there are much better ways to increase your melatonin level than by sacrificing sunlight and valuable vitamin D!

The point is, there are many other factors that could explain why the MP could seem to help sufferers of sarcoidosis, besides the one he claims. To really determine what is causing what, a series of controlled studies would have to be done. He has drawn a lot of conclusions without the clinical studies to separate out the variables.

I believe that Marshall is placing people’s health at risk by having them participate in a clinical trial via the Internet--and a badly designed one at that—with inadequate details and precautions about what the health consequences might be.

My Recommendation

Stick to what you know works, and if there is merit to any of Marshall’s theories, studies will bear that out in time. It would seem that the only indication for MP would be sarcoidosis. I believe it would be unwise to use it for other conditions, but even for sarcoidosis there are a number of effective non-drug approaches to address it.

I would have to agree with Dr. Cannell that you would be hard-pressed to find any reputable person in the vitamin D field who takes Marshall’s theories seriously. They are poorly substantiated and lack corroborating evidence.

Go with what you know. Health comes from getting back to the basics…nutrition, exercise, restorative sleep--and yes, appropriate exposure to sufficient sunshine to normalize your vitamin D levels.


[i] Wikipedia, http://en.wikipedia.org/wiki/Trevor_Marshall

[ii] Amy Proal’s website, Bacteriality: Exploring Chronic Disease http://bacteriality.com/about-the-mp/ (accessed February 11, 2009)

[iii] Cannell JJ, “Vitamin D and mental illness,” the Vitamin D Council website, http://www.vitamindcouncil.org/mentalIllness.shtml (Accessed February 12, 2009)

[iv] London M, Is the treatment for sarcoidosis helpful for other chronic diseases? MP’s theories are not supported by lab studies. July 2, 2008 http://stuff.mit.edu/people/london/universe.htm (accessed February 11, 2009)

[v] Herrell D, “What is a Herxheimer reaction?” http://www.angelfire.com/biz/romarkaraoke/Herx.html (Accessed February 12, 2009)

[vi] Silver Colloids, “The Herxheimer reaction—feeling worse before feeling better” http://www.silver-colloids.com/Pubs/herxheimer.html (Accessed February 12, 2009)

[vii] http://www.parathyroid.com/parathyroid-symptoms.htm

[viii] Marshall Protocol Study Site, http://www.marshallprotocol.com/

[ix] http://www.lassesen.com/cfids/advised_reading.htm

[x] Breslau NA, Preminger GM, Adams BV, Otey J, Pak CY. “Use of ketoconazole to probe the pathogenetic importance of 1,25-dihydroxyvitamin D in absorptive hypercalciuria,” J Clin Endocrinol Metab. 1992 Dec;75(6):1446-52 PubMed http://www.ncbi.nlm.nih.gov/pubmed/1464646?dopt=Abstract (Accessed February 11, 2009)

[xi] Abreu MT, Kantorovich V, Vasiliauskas EA, Gruntmanis U, Matuk R, Daigle K, Chen S, Zehnder D, Lin YC, Yang H, Hewison M, Adams JS. “Measurement of vitamin D levels in inflammatory bowel disease patients reveals a subset of Crohn’s patients with elevated 1,25-D and low bone mineral density,” Gut.2004 Aug;53(8):1129-36 PubMed http://www.ncbi.nlm.nih.gov/pubmed/15247180 (Accessed February 11, 2009)

[xii] Cannell J, April 2008 newsletter. “Cholecalciferol is cholecalciferol” http://www.vitamindcouncil.org/newsletter/2008-april.shtml

[xiii] Lappe JM, Travers-Gustafson D, Davies KM, Recker RR, Heaney RP. “Vitamin and calcium supplementation reduces cancer risk: results of a randomized trial.” Am J Clin Nutr 2007 Jun;85(6):1586-91. PubMed http://www.ncbi.nlm.nih.gov/pubmed/17556697?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum (Accessed February 11, 2009)

[xiv] Pignone AM, Rosso AD,, Fiori G, Matucci-Cerinic M, Becucci A, Tempestini A, Livi R, Generini S, Gramigna L, Benvenuti C, Carossino AM, Conforti ML, Perfetto F. “Melatonin is a safe and effective treatment for chronic pulmonary and extrapulmonary sarcoidosis,” J Pineal Res. 2006 Sep;41(2):95-100 PubMed http://www.ncbi.nlm.nih.gov/pubmed/16879313?dopt=AbstractPlus (Accessed February 11, 2009)

Vitamin D Dose Recommendations
Age Dosage
Below 5 35 units per pound per day
Age 5 - 10 2500 units
Age 18 - 30 5000 units
Pregnant Women 5000 units
WARNING:
There is no way to know if the above recommendations are correct. The ONLY way to know is to test your blood. You might need 4-5 times the amount recommended above. Ideally your blood level of 25 OH D should be 60ng/ml.

[Son-of-Liberty]

The article posted in the OP's is retarded.

First off even a half hour in the sun a white person can produce at least 10,000 IU a day.

Our ancestors spent much more time in the sun then we do. So they were getting at least 10,000 IU a day. Why God or nature would design us to make so much of something that was harmful makes no sense at all.

The assertion that it suppresses the immune system is also flawed. My understanding is that it modulates the immune system making it work more efficiently. It isn't overreacting and causing massive inflammation from every little bug going around.

We always think that a strong immune system is good but too strong and it can make you quite ill. Think cytokine storm from the bird flu. Vitamin D could potentially protect you from yourself.

Lately I have been taking large doses of A and D anytime I feel like I might be getting sick and so far I wake up the next day feeling fine. I also take about 5,000 IU of D a day normally. So far I feel great and have not noticed any side effects or negative reactions. It is all positive.

[letter_factory]

Thanks for posting the article. My daughter had some kind of sinus infection for the past few weeks. During the day, she was fine, but at night, her nose would get completely stopped up. She would wake up and unable to go to sleep. Normally, we have her on different kinds of almond milk, rice milk, etc, but mom was worried and put her on organic cow milk....Then I read this article and switched her back to rice milk, almond milk, etc. I think they put some different kind of vitamin d in it. anyway, now she's fine....Mom thinks it's a coincidence, I'm just glad my daugher can breathe through her nose and sleep better.

[lapis]

I read this article and switched her back to rice milk, almond milk, etc. I think they put some different kind of vitamin d in it.

Yes, the non-dairy milks are fortified with vitamin D2, a.k.a. ergocalciferol.

[Old Herb Lady]

http://www.youtube.com/watch?v=2wYuHA5P-OQ




THE VITAMIN D SCAM



By Shane Ellison M. Sc.
The People's Chemist
May 18, 2010
NewsWithViews.com

Vitamin D hype has everyone swallowing the “sunshine vitamin” like Oprah swallows fat loss scams. Scared of cancer? Eat vitamin D. Can’t get into your skinny jeans? Eat vitamin D. Got diabetes? Eat vitamin D. Tired of your wife yelling at you for watching too much Celebrity Apprentice? Eat vitamin D.

Nobody is immune from “D” hype. Famed nutrition gurus from around the world have been pushing vitamin D on the masses. Thankfully, I’m not a nutrition guy. The thought of spreading wishy-washy advice with a cute trendy smile makes me nauseous. I enjoy solitude, research and more solitude. So much that I don’t even carry my cell phone, just a bad attitude. And that’s why I’m a chemist, because I enjoy sleuthing for real answers behind the hype, especially when it comes to “pills.”

The Wonders of Sunshine

In the early 1930’s, some dude (a pharmaceutical shill) learned that as sun rays beamed down to earth at light speed – 670,616,629 miles per hour – our skin produced a family of hormones known as secosteroids in response. I call these “sunshine hormones.”

Using state of the art chemistry methods, dozens of these sunshine hormones have been identified and more are being characterized every day. Nobody is sure how many there are, or how they interact. But one thing is for certain; they work in orchestra-like unison to activate a host of positive actions in the body. There is no one single player as we have been led to believe.

Sunshine hormones make you happy by giving rise to feel-good compounds in the brain, which partly explains why so many retired folks flock to Florida. They also activate the expression of over 900 genes, which help control things like bone density, blood sugar, inflammation and much, much more.

Truth be said, nobody knows the entire scope of benefits associated with sunshine hormones. Nor do we fully understand how they interact. But we do know that our skin understands that too much of them can be toxic. Fortunately, the body has a clever way of preventing the overdose.

After about 20 minutes in the sun, the friction created by the bombardment of sunshine blasting the skin creates heat, which in turn, shatters the creation of excess sunshine hormones in the skin, thereby making it impossible for us to produce too much of a good thing.


Profiting from Sunshine

In the 1930’s, seeing great profit potential in sunshine hormones, Big Pharma went to work manufacturing a copy cat. In that pursuit, they narrowed the scope of our sunshine hormones and postulated that it was a single isolate that was responsible for the vast, biological benefits of sunshine. At the same time, they disregarded the unique balance and protection mechanism built by the body to guard against toxicity. Once successful in designing their “Franken-chemical,” they launched a campaign to systematically contaminate our vitamin and food supply with it and make billions.

Turning Sunshine into a Drug

Today, Big Pharma cartels BASF and Hoffman La Roche are the largest manufacturers of the synthetic hormone isolate. To get the masses to swallow it, they erroneously named it “The Sunshine Vitamin,” AKA vitamin D. Consumers, stimulated by ads, couldn’t wait to start choking it down, so much that old ladies bragged about taking the “drug disguised as a vitamin” to their hairdressers. In reality though, it’s as close to being a sunshine hormone as a tootsie roll is to being chocolate, or a porno is to having sex. I’m not the only one pointing out this fact.

“Vitamin D is not really a vitamin,” wrote scientists for the New England Journal of Medicine. For something to be a vitamin, it should provide the body with an essential nutrient that it cannot make on its own, but requires for survival.

Since synthetic vitamin D is a drug, foreign to the body, and not required for survival, it’s technically a fraud – an impostor posing as a vitamin. It has “vitamin like” activity, which initially tricks the body into thinking the host of associated co-hormones is present. But this biological ruse proves to be devastating to the body over time.

Before the vitamin D scam was fed to consumers, the deadly “D” was fed to rodents as a means of eradicating the pesky creatures. In their report, “The Endocrine System,” the University of Colorado, reminds us, "Ingestion of milligram quantities of vitamin D over periods of weeks or months can be severely toxic to humans and animals. In fact, baits laced with vitamin D are used very effectively as rodenticides [rat poison]." This is in stark contrast to naturally produced sunshine vitamins, and it isn’t hard to understand.

Once swallowed, the copycat hormone bypasses our innate protective mechanisms and throws hormonal balance out of whack. This “plugs” the body with calcium and induces calcification, which leads to heart failure, kidney damage, and more. Since it’s a “cumulative poison,” people who take the recommended dose every day as vitamin D are saturating their fatty tissues, and at the same time, offsetting their God-given hormonal intelligence. Anyone eating and drinking foods “fortified” with vitamin D are at serious risk. Nutrition guru Dr. Gary Null learned this the hard way.

After sucking down his “Power Meal” loaded with the vitamin D supplement, New York Daily News reported that Dr. Null was hit with "excruciating fatigue" that left him urinating blood and unable to walk. Upon checking into the hospital, Null was told that he could have died from his synthetic vitamin D (rodenticide) “overdose” - like suicide in slow motion. Null is suing his manufacturer for putting too much vitamin D in his products. He misses the point though: There is no safe dose.



Synthetic vitamin D is poisonous in any amount due to its ability to get crammed into fat cells and accumulate over periods of months (compared to 20 minutes when naturally produced), thereby disrupting hormone balance.

Nobody has ever been poisoned by naturally produced sunshine hormones.

Scientific Trickery

Promotion for the drug disguised as a vitamin is “business as usual” for the drug, food, and vitamin industries: They work together to instill fear and confusion designed to blur the lines between synthetic and natural. And they’ve done it with a “deficiency hypothesis” that has everyone regurgitating their “25-hydroxy vitamin D” levels in an attempt to avoid rickets, infection, cancer and even a bad haircut, so it seems. But it’s as weak as my PC laptop battery (I’m buying a Mac soon). Ever wonder who defines our “ideal levels?” (See Big Pharma cartels above.)

To date, only statistical associations are used to support the deficiency hypothesis, not causal ones. This is akin to saying that since everyone who died of a heart attack today had a coffeemaker in their home, the likely culprit is Mr. Coffee. It’s simplistic at best and outright stupid at worst, especially when this rationale is used to give it to babies as “vitamin D supplement drops.” But there are others…

The “rickets rationale” for supporting the use of synthetic vitamin D is the most frustrating. It purports that “vitamin D” cured the paralyzing disease, which is prima facie evidence of its healing qualities. Not true. The plethora of “sunshine hormones” produced by the skin, and those found naturally in cod liver oil, cured rickets, not vitamin D pills made in the stinky labs of Big Pharma. Purveyors of this myth have the Big Pharma marketing noose firmly around their neck, and probably don’t even know it.

If the rickets rationale didn’t win you over, the “cancer cure con” probably did. You’ve seen it plastered on the headlines of every paper in the U.S and even on well known, natural health websites: Vitamin D fights cancer. The redundancy itself should be your first clue that “something fishy” is going on. The anti-cancer statements come direct from short term trials performed by “advisors” to Big Pharma and published in the top nutrition journals! Worse, the trials only show a small statistical association of low cancer rates among vitamin D users over about a 5 year period. This is plain silly.

Cancer takes more than 5 years to develop. Even heavy smokers can survive 5 years without a cancer diagnosis, but we know cigarettes are a real threat. Thus, any study on cancer lasting five years has very little value. This same scheme was used by the cigarette industry to erroneously thwart off the cancer claims in the early 1970’s. Now it’s being used to pretend vitamin D staves off cancer. It’s a con, and long term vitamin D studies (which are being ignored) show just the opposite (just like they did with cigarettes, of course).

Those who eat vitamin D show significantly increased cancer rates at ten years. It’s not surprising because inflammation (via our immune system) fights cancer, and the Franken-chemical inadvertently lowers this “good” inflammation, thereby putting users at risk.

A massive campaign designed to make people fear the sun has been unleashed, driving people to hide indoors and consume the dangerous “D” in record numbers.

Ironically, the sun was previously known as Apollo, the God of Medicine. And yet, consumers go to great lengths to avoid it thanks to the propaganda. It’s their loss. As written about in my book, Over-The Counter Natural Cures, responsible sun exposure (minus the sun block) and the subsequent release of sunshine hormones has proven to directly ward off cancer, as well as a number of other serial killers like obesity and type II diabetes.

Vitamin D pills have never been proven to offer such vast benefits…

And if you can’t get adequate sunlight for whatever reason, Mother Nature produces “sunshine hormones” that won’t accidentally put you on a hospital gurney. Salmon, mackerel, sardines, beef/chicken liver, eggs, and select non-fortified cod liver oils are all smart choices for the “solar challenged.”

Combined, statistical associations and short term trial results used to promote dangerous D are nothing more than scientific trickery mastered by the same industry that pushed deadly HRT (hormone replacement therapy) drugs, Vioxx, and mercury laden vaccines on unsuspecting victims. The same tricks are now being used to make a dirty buck off the natural health trend sweeping America.



In conclusion, I’m sounding the alarm that a slow vitamin D poisoning is happening worldwide. Vitamin D supplements and fortified foods are attacking the body from numerous sources, where it’s behaving like the rat poison it is. You choose, sunshine or vitamin D pills (D2, D3 or otherwise)?




Highlighting the Vitamin D pill controversy, The New York Times recently wrote that “The excitement about their health potential is still far ahead of the science.” Amen. As long as excitement remains ahead of common sense and science, I’ll take chocolate over a Tootsie Roll, and sit under the sun – probably drinking tequila – over swallowing dangerous D. Nothing like the real thing.

© 2010 Shane Ellison - All Rights Reserve







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Ellison’s entire career has been dedicated to the study of molecules; how they give life and how they take from it. He was a two-time recipient of the prestigious Howard Hughes Medical Institute Research Grant for his research in biochemistry and physiology. He is a bestselling author of Over-The-Counter Natural Cures, which helps you live healthier and pay less with $10 lifesaving supplements for under $10! Learn more here.

E-Mail: shane@health-fx.net


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http://www.newswithviews.com/Ellison/shane158.htm

[Old Herb Lady]

The article posted in the OP's is retarded.

First off even a half hour in the sun a white person can produce at least 10,000 IU a day.

Our ancestors spent much more time in the sun then we do. So they were getting at least 10,000 IU a day. Why God or nature would design us to make so much of something that was harmful makes no sense at all.

The assertion that it suppresses the immune system is also flawed. My understanding is that it modulates the immune system making it work more efficiently. It isn't overreacting and causing massive inflammation from every little bug going around.

We always think that a strong immune system is good but too strong and it can make you quite ill. Think cytokine storm from the bird flu. Vitamin D could potentially protect you from yourself.

Lately I have been taking large doses of A and D anytime I feel like I might be getting sick and so far I wake up the next day feeling fine. I also take about 5,000 IU of D a day normally. So far I feel great and have not noticed any side effects or negative reactions. It is all positive.


First off- there are thousands of healing benefits /gifts from God & nature via the sun BESIDES vitamin D.
Just because we all are brainwashed into thinking sun-vitamin d, sun-vitamin d, repeat repeat blah blah blah
The sun is VERY healing and I am a sun addict. Think outside the box. Go bigger, go better, go higher besides vitamin D !!!!!
Just the sunlight alone helps to massively increase your immune system by enhancing your mood.
It kills bacteria, it calms your nerves, it helps heal skin diseases etc, I could go on all day about the healing benefits of the sun so chill out.

-- and the first drug/medicine given for a cytokine storm is none other than a STEROID.

Also God & nature do not "dose" healing & wellness and put them into I.U's & milligrams
and God & nature doesn't make you take this supplement with that supplement so that the ratio
of whatever supplement doesn't get depleted.
Only FAKE-MAN-MADE "VITAMIN" PILLS do that.
Anything copied from nature & made in a laboratory is not a vitamin.
Vitamin D is NOT a sunshine vitamin.



I can't wait until this vitamin d scam gets more people thinking about what they're doing.

[lapis]

Nutrition guru Dr. Gary Null learned this the hard way.

After sucking down his “Power Meal” loaded with the vitamin D supplement, New York Daily News reported that Dr. Null was hit with "excruciating fatigue" that left him urinating blood and unable to walk. Upon checking into the hospital, Null was told that he could have died from his synthetic vitamin D (rodenticide) “overdose” - like suicide in slow motion. Null is suing his manufacturer for putting too much vitamin D in his products.

To be fair, this was due to a manufacturing error; instead of the 2,000 i.u. of vitamin D the Power Meal was supposed to contain, it had 1 MILLION, and Null took it every day for a month. Try that with a Big Pharma drug and see if you live to tell the tale!

'Death' is now Null and void (http://www.nypost.com/p/news/local/death_is_now_null_and_void_vyaG1Y990RjL2dew3nPDvM)

But yeah, the best way to get vitamin D is sunshine, cod liver oil and other foods.

[lapis]

First off- there are thousands of healing benefits /gifts from God & nature via the sun BESIDES vitamin D.
Just because we all are brainwashed into thinking sun-vitamin d, sun-vitamin d, repeat repeat blah blah blah
The sun is VERY healing and I am a sun addict. Think outside the box. Go bigger, go better, go higher besides vitamin D !!!!!
Just the sunlight alone helps to massively increase your immune system by enhancing your mood.
It kills bacteria, it calms your nerves, it helps heal skin diseases etc, I could go on all day about the healing benefits of the sun so chill out.

-- and the first drug/medicine given for a cytokine storm is none other than a STEROID.

Also God & nature do not "dose" healing & wellness and put them into I.U's & milligrams
and God & nature doesn't make you take this supplement with that supplement so that the ratio
of whatever supplement doesn't get depleted.
Only FAKE-MAN-MADE "VITAMIN" PILLS do that.
Anything copied from nature & made in a laboratory is not a vitamin.
Vitamin D is NOT a sunshine vitamin.

Those are good points.

I don't think taking D3 is as good as going out in the sun or eating the foods that contain it, but taking reasonable amounts with other co-nutrients like magnesium and vitamin K2 is not unhelpful. But it's a supplement, not a replacement.

[Twisted Titan]

taggging