The Truth About Vitamin D: Fourteen Reasons Why Misunderstanding Endures
Author: Amy Proal15 Sep 2007
During the 1960s, a large number of studies began to point to the idea that estrogen therapy might ease the pangs of menopause. In a best selling book called Feminine Forever, a Brooklyn gynecologist named Robert Wilson argued that menopause was an illness rather than a natural state associated with aging. Soon, an increasing number of older women began to take supplemental estrogen in an effort to replace the hormones that their own bodies had stopped secreting. The treatment, known as hormone replacement therapy or HRT, became one of the most popular medical treatments in America.
The American Heart Association, the American College of Physicians, and the American College of Obstetricians and Gynecologists all agreed that a sufficient number of studies had been done to prove that HRT was unequivocally helpful in helping older women ward off heart disease and osteoporosis. By 2001, 15 million women were taking HRT, including 5 million elderly women.
Then, in 1998, a clinical trial concluded that estrogen therapy actually increases the likelihood that women with heart disease will suffer a second heart attack. It was followed by a trial in 2002 which concluded that HRT puts postmenopausal women at a greater risk for heart disease, stroke, blood clots, breast cancer and even dementia. Suddenly, It became painfully clear that HRT may offer a benefit to women who begin to use it early in life, but for those who start the treatment in their later years, it can be very dangerous.[1]
Gary Taubes writes in The New York Times Magazine, “The question of how many women may have died prematurely or suffered strokes or breast cancer because they were taking a pill that their physicians had prescribed to protect them against heart disease lingers unanswered. A reasonable estimate would be tens of thousands.”[1]
This HRT story, which Harvard epidemiologist Jeffrey Avorn calls the “estrogen debacle” and a “case study waiting to be written” is a glaring example of how even the most widely held medical beliefs can turn out to be wrong. The story is fraught with biased studies, overconfident clinicians, and researchers who failed to think critically.
Most alarming, however, is the fact that the medical community is currently oblivious to yet another public health disaster of epic proportions - one that is affecting the entire population. In an effort to curb chronic disease, well-intentioned researchers are promoting vitamin D, a substance that, according to recent molecular modeling research, can act as an immunosuppressive steroid. Studies which incorrectly interpret the reason for low vitamin D in patients with chronic disease have been seized upon by the media, and form the basis of massive advertising campaigns – which, along with ill-informed recommendations by doctors and researchers, have created a perfect storm of misunderstanding and bad advice.
What follows are fourteen pieces of a puzzle that, when complete, reveal a massive misunderstanding of the actions of vitamin D.
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]
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]
Patients 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.”[7]
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.
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.[24] 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. [25]
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.[26]
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.”[27][28]
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 no follow-up study was done on the group. 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.[29]
“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.
During the rare instances where researchers have tracked study subjects for decades, ingestion of vitamin D is rarely associated with improved health. Take, for example, a study recently performed by researchers from several institutions, including the University of Oulu in Finland and the Imperial College in London. The team found a clear association between high-dose vitamin D supplementation in infancy and an increased risk of atopy, allergic rhinitis, and asthma later in life. Those subjects given higher levels of vitamin D during infancy were found to suffer from higher levels of atopy, rhinitis and asthma, but not until the research team checked back with them at 31 years of age.
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.[30]
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.[31]
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,”[32] 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.[33]
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.[34] 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.
Similarly, researchers at the University of Tokyo found that VDR knock-out mice (mice grown without Vitamin D Receptors) showed a marked increase (10 times) in serum 1,25-D and a clear reduction - to almost undetectable levels- in serum 25-D. Such levels persisted at seven weeks until the mice eventually died.[35]
While there are clear biological differences between humans and rodents, having a Vitamin D Receptor with no activity - because it is blocked by bacterial substances and 25-D - is analogous to having no VDR at all. So the Tokyo team’s data on VDR null mice also strongly supports the fact that a blocked VDR naturally leads to high levels of 1,25-D and very low levels of 25-D.
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.”
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][31] 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]
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?
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.
Osteoporosis 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.
If 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 third study, this one published in 2006, conducted by the Women’s Health Initiative, came to the identical conclusion.[77]
In the case of the above studies, it’s quite possible that calcium did have a positive effect on the bone mass of the study subjects. It’s just that the positive effects of calcium were probably offset by the negative effects of VDR blockage and elevated 1,25-D caused by consumption of the vitamin D supplements.
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 secosteroid 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 in order to estimate an 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 remains 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.
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. But when too much 25-D and bacterial proteins bind and inactivate the Vitamin D Receptor these anti-cancer genes are not transcribed correctly.
Because 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 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.[