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.[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 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 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 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 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.
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.”[119]
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.[120]
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.”[121] 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.[122]
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.”[123] 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.”[124]
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,[125] 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.
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.[126]
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.[127] “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.”[128]
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.”[129]
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.”[130] 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.[131]
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.”[132]
“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.[133] NEEDS, another online retailer, sells 37 different supplements with vitamin D and approximately 100 fish oils containing vitamin D, some priced over $30.00 a bottle.[134]
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.”[135]
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.”
Under 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”[136] 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.[137]
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.
On 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.[138]
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.
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.
This paper would not have been possible without the help of Joyce Waterhouse PhD and Paul Albert who spent extensive amounts of time informing me about research and editing my work.
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- Banerjee A Call for More Vitamin D Research. (2006). American Cancer Society. [↩]
- Ashizawa, N., Arakawa, S., Koide, Y., Toda, G., Seto, S., Yano, K., et al. (2003). Hypercalcemia due to vitamin D intoxication with clinical features mimicking acute myocardial infarction. Internal medicine (Tokyo, Japan), 42(4), 340-4. [↩]
- Capiati, D., Benassati, S., & Boland, R. L. (2002). 1,25(OH)2-vitamin D3 induces translocation of the vitamin D receptor (VDR) to the plasma membrane in skeletal muscle cells. Journal of cellular biochemistry, 86(1), 128-35. [↩]
- Demay, M. B., Sabbagh, Y., & Carpenter, T. O. (2007). Calcium and vitamin D: what is known about the effects on growing bone. Pediatrics, 119 Suppl 2, S141-4. [↩]
- Demay, M. B. (2006). Mechanism of vitamin D receptor action. Annals of the New York Academy of Sciences, 1068, 204-13. [↩]
- Graff, M., Thacher, T. D., Fischer, P. R., Stadler, D., Pam, S. D., Pettifor, J. M., et al. (2004). Calcium absorption in Nigerian children with rickets. Am J Clin Nutr, 80(5), 1415-1421. [↩]
- Graff, M., Thacher, T. D., Fischer, P. R., Stadler, D., Sunday, P., Pettifor, J. M., et al. (2007). Calcium Absorption in Nigerian Children with Rickets. Agricultural Research Service. [↩]
- DeLucia, M. C., Mitnick, M. E., & Carpenter, T. O. (2003). Nutritional Rickets with Normal Circulating 25-Hydroxyvitamin D: A Call for Reexamining the Role of Dietary Calcium Intake in North American Infants. J Clin Endocrinol Metab, 88(8), 3539-3545. [↩]
- Vitamin D Doesn’t Cause or Cure Rickets. (2007). Marshall Protocol Study Site. [↩]
- Weick, M. T. (1967). A history of rickets in the United States. The American journal of clinical nutrition, 20(11), 1234-41. [↩]
- Muhe, L., Lulseged, S., Mason, K. E., & Simoes, E. A. (1997). Case-control study of the role of nutritional rickets in the risk of developing pneumonia in Ethiopian children. Lancet, 349(9068), 1801-4. [↩]
- Banerjee A Call for More Vitamin D Research. (2006). American Cancer Society. [↩]
- Donn, J. (2006). Study shows benefits of vitamin D, calcium limited for older women. azcentral.com. [↩]
- Calcium, Vitamin D Supplements Have Little Effect on Women’s Bone Density, Risk of Colorectal Cancer, Study Says. (2006). Our Bodies Ourselves. [↩]
- Stein, R. (2006). Study shows limited benefits from calcium, vitamin D pills. San Diego Union-Tribune. [↩]
- Grant, A. M., Avenell, A., Campbell, M. K., McDonald, A. M., MacLennan, G. S., McPherson, G. C., et al. Oral vitamin D3 and calcium for secondary prevention of low-trauma fractures in elderly people (Randomised Evaluation of Calcium Or vitamin D, RECORD): a randomised placebo-controlled trial. Lancet, 365(9471), 1621-8. [↩]
- Autier, P., & Gandini, S. (2007). Vitamin D Supplementation and Total Mortality: A Meta-analysis of Randomized Controlled Trials. Archives of internal medicine, 167(16), 1730-7. [↩]
- Anderson, J., & Young, L. (2007). Fat-Soluble Vitamins. Colorado State University – Nutrition Resources. [↩]
- Marriott, B. M. (1997). Vitamin D Supplementation: A Word of Caution. Ann Intern Med, 127(3), 231-233. [↩]
- ODS 2007 Vitamin D Conference. (2007). [↩]
- Ioannidis, J. (2005). Why Most Published Research Findings Are False. PLoS Medicine, 2(8). [↩]
- Marshall, B. (2002). Helicobacter pylori: 20 years on. Journal of the Royal College of Physicians, 2(2), 147-152. [↩]
- Begley, S. (2006a). New Journals Bet ‘Negative Results’ Save Time, Money. Wall Street Journal. [↩]
- Begley, S. (2006b). Negative Research Results–Mostly Concealed in Journals. Alliance for Human Research Protection. [↩]
- Matthews, A. W. (2005). At Medical Journals, Writers Paid by Industry Play Big Role. Wall Street Journal. [↩]
- Bensman, S. J. (2005). Scientific Journal Shenanigans. SIGMETRICS archives. [↩]
- Lin, J., Manson, J. E., Lee, I., Cook, N. R., Buring, J. E., Zhang, S. M., et al. (2007). Intakes of Calcium and Vitamin D and Breast Cancer Risk in Women. Arch Intern Med, 167(10), 1050-1059. [↩]
- Jacques, P. F., Sulsky, S. I., Sadowski, J. A., Phillips, J. C., Rush, D., Willett, W. C., et al. (1993). Comparison of micronutrient intake measured by a dietary questionnaire and biochemical indicators of micronutrient status. The American journal of clinical nutrition, 57(2), 182-9. [↩]
- Kolata, G. (2006). Big Study Finds No Clear Benefit of Calcium Pills. The New York Times. [↩]
- Vitamin D. (2007). Netrition.com. [↩]
- NEEDS, Inc. Nutritional Information and Shopping Site. (2007). [↩]
- Barlas, S. (2007). Making no bones about calcium. Packaging World. [↩]
- Weatherby, C. (2007a). Vitamin D May Lower Risk of Ovarian, Breast, Kidney, and Colon Cancers. Vital Choices Newsletter. [↩]
- Weatherby, C. (2007b). Wild Salmon Affirmed as Top Vitamin D Source. Vital Choices Newsletter. [↩]
- U.S. government calls for end to dairy weight loss ads. (2007). Reuters. [↩]
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About Amy Proal
Amy Proal graduated from Georgetown University in 2005 with a degree in biology. While at Georgetown, she wrote her senior thesis on Chronic Fatigue Syndrome and the Marshall Protocol.
Amy has spoken at several international conferences and authored several peer-reviewed papers on the intersection of bacteria and chronic disease.
If you have questions about the MP, please visit CureMyTh1.org where volunteer patient advocates will answer your questions. Another good resource is the MP Knowledge Base, which is scheduled to be completed within the next year.
130 Responses for "The Truth About Vitamin D: Fourteen Reasons Why Misunderstanding Endures"
Well done Amy. Incredibly comprehensive study. You have done a lot of research. Thank you for providing this in an easy to follow format. Inge.
First off, I must say that this was very well written and thank you for putting together such a complete synopsis of the world of Vitamin D and the vast illusions portrayed both commercially and by confused reseaercher/physicians.
I do have a question. With low 25-D being the result of the disease prcoess and the Cytokine release from the disease, when will MP people with low 25-D know that they have reached the zenith of treatment? For instance, I was not avoiding sun or D foods/supplements before commencing the protocol, yet my 25-D level was only 11 ng/ml prior to starting. Obviously, this depicts the disease process you have clearly stated, but how will we know when the disease process is under control? Will our 25-D levels go up naturally from sun exposure instead of directly converting to 1-25D?
Also, what is a “healthy” 1-25D range? Mine was 45 pg/ml just before the MP, which does show quick conversion, yet is not terribly high above the 43 pg/ml limit that can cause osteoclasts.
This report adds to the understanding of vitamin D. However, while well referenced, and certainly enlightening in some areas (hypophospatemia in rickets and osteoporosis), it mixes low dose with high dose data, overlooks a great deal of epidemiological research (cancer rates are lowest where vitamin D levels are highest- the Equator), and it doesn’t explain that vitamin D has a dual role as both immune suppressor and immune activator. L-form bacteria are not the only agents that govern the vitamin D receptor. If true that L-form bacteria block the vitamin D receptor, then antibiotics should be shown to effectively remedy osteoporosis. This appears to be the case in menopausal subjects, but this implicates estrogen, another steroidal hormone, in the mix. [1: Bone. 1996 Dec;19(6):637-44;Pol J Pharmacol. 2003 May-Jun;55(3):433-41] The loss of estrogen is the controlling agent in age-related bone loss, regardless of infection. Dr. Cantwell’s work stimulates discussion and further investigation and his work is well regarded. However, your vitamin D pills, even though a steroid, are not ready for the waste basket.
Hi Joe,
So sorry about the delay in response. Thanks for your comments about the article.
The state of the immune system begins to change as patients spend increasing lengths of time on the MP. When patients start the treatment, the VDR is blocked by bacterial proteins and often 25-D. These substances have high affinities for the receptor and prevent 1,25-D from binding the VDR and activating the immune system as it would in a healthy individual. But as patients kill bacteria and eliminate vitamin D from the diet, the VDR gradually becomes more active. After a certain period of time (and it varies from person to person depending on the severity of infection), there are substantially less bacterial proteins and 25-D in the VDR and 1,25-D can once again bind the receptor and activate it as needed. This process happens very gradually and accelerates as patients reach the final stages of the MP. So the key is just to kill all of your L-form bacteria. You will reach a state of complete normalcy when all your bacteria are dead, allowing the VDR to function correctly. Then, I suppose, you could go in the sun and consume vitamin D to the extent that your level of 25-D never reaches around 20 ng/ml where it becomes immunosuppressive. If you don’t eat fortified foods and don’t seek out the sun, it seems feasible that you can keep your level of 25-D under 20 ng/ml while still living a completely normal lifestyle.
I don’t know an exact healthy range for 1,25-D. But I do know that it should be under 43 ng/ml because at levels higher than that, calcium starts to be leached from the bones. Consequently, when you started the MP your level of 1,25-D (which was 45 ng/ml) was in this range, clearly indicating Th1 inflammation. I think the moderators on the MP site could answer these questions in further detail as they have much more experience advising people about the D metabolites than I do.
It’s also important to keep in mind that many people who consider starting the MP are taking other drugs at the time of the D metabolite tests. Many of these drugs alter the level of 1,25-D in the body. For example, when I started the MP my 1,25-D was low. However I later found out that the antifungal medication I was taking at the time of my first D test caused levels of 1,25-D to decrease by 60 -70%.
Hope this helps,
Amy
Hi Mr. Sardi,
Thanks for your interest.
The piece does not confuse high and low levels of vitamin D. I state clearly that 25-D becomes immunosuppressive at around 20 ng/ml. That’s all there is to it. You say that other substances bind the VDR. Yes, many substances bind the VDR. But 25-D and L-form bacterial proteins have extremely high affinities for the receptor. When these two substances are docked into the VDR, other VDR binding molecules can no longer correctly bind the receptor. Including 1,25-D. Even healthy people are affected because thanks to fortified foods, the “healthy” range for 25-D is over 20 ng/ml, meaning that 1,25-D cannot correctly bind the VDR in these individuals as well.
Cancer rates are lower near the equator? Consider this. Generally, people living around the equator are members of third world countries. If they fall ill with cancer what are they going to do? Call the nearest radiologist and oncologist? Unfortunately, they have little access to healthcare and most of their cases go undocumented. The opposite is true for people in the northern hemisphere, where most first world countries are located. These people have the money and education to pay a multitude of doctors for cancer therapy, meaning that their cases are documented and accounted for. The same type of bias impacted CFS. For a long time, CFS was called the “yuppie flu.” Supposedly it was a disease that affected wealthy, white people. Then, it turned out that wealthy white people were the only ones who could afford enough doctor visits to get diagnosed with CFS. It is now accepted that the disease affects all members of the population equally.
Not to mention the fact that people living near the equator have dark skin. Dark skin produces vitamin D at a much slower rate than white skin. Plus, there is much evidence pointing to the fact that cancer is a bacterial disease. It’s common knowledge that pathogens are able to infect the host with greater ease in cold weather. Clearly more people catch the flu during the winter rather than the summer.
As for osteoporosis and estrogen. Did you see the diagram of the actions of 1,25-D at the beginning of section 3? 1,25-D, which is often called the master hormone, controls the feedback pathways for the sex, thyroid, stress hormones. So when 1,25-D goes out of range so does estrogen. The solution – kill the bacteria causing the 1,25-D elevation, bring 1,25-D back into range, and estrogen will also fall back into place. Patients are using the MP to treat osteoporosis, including myself. Many are reporting significant increases in bone density. Estrogen is a steroid, but is not capable of binding the VDR, and thus has no impact on the actions of the immune system.
Best,
Amy
As someone who has spent a lot of time trying to persuade others of the benefits of having optimal vitamin D status I found your article very thought-provoking as it challenged my entire understanding of Vitamin D3.
However, I feel you are being somewhat unfair in the way you present your arguments.
I find your opening analogy, before you discuss the 14 points, particularly unfair.
The HRT saga was trying to create a hormonal state in women of a certain age that was not normally present in women of that age.
As far as I understand it, the main Vitamin D3 researchers and those who are enthused by their work, are trying to re-establish the natural levels of Vitamin D people would have enjoyed had they not followed the advice of dermatologists to stay out of the sun and to cover their skin with sunblock/screen/or spf cosmetics before direct contact with sunlight.
We evolved in equatorial East Africa and would have received very generous solar radiation and had correspondingly high cutaneous synthesis of vitamin D3 year-round.
When I think of my childhood and the amount of time I spent outdoors in the late 1940’s early 1950’s without sun protection and the way my grandchildren are prevented from ever having direct sun exposure, I am concerned that current sun avoidance practice simply isn’t natural.
So the first point I would like you to consider is that your opening gambit is fundamentally unfair, as it compares the movement to encourage the general public to sustain NATURAL levels of Vitamin D3 status, with the UNNATURAL practice of artificially sustaining abnormal levels of Oestrogen And Progesterone for that age group.
Dear Mr. Hutchinson,
I think my comparison between vitamin D and HRT is right on. We have artificially added vitamin D to milk, yogurts, butters, pastas, and now even orange juice and other products.
You say, “The HRT saga was trying to create a hormonal state in women of a certain age that was not normally present in women of that age.”
I would respond that the policy of vitamin D supplementation endeavors to create a level of vitamin D that is not normally present in people who…well don’t eat fortified food.”
But you say we should be out in the sun all day. There are many faults with that argument. The first being that our ancient ancestors in Africa surely had dark skin, meaning they created much less vitamin D from the sun. It’s unfair to take a modern day North American white-skinned human and artificially put them into some ancient African atmosphere. We have now evolved to live under very different conditions. And who really knows how much sun these ancient ancestors got. Surely they knew how to seek shelter? Furthermore, quite a few human cultures developed in Northern continents with much less sunlight and survived just fine.
But I don’t know why I’m even wasting time trying to theorize about some distant African ancestor. Molecular modeling has proved that 25-D becomes immunosuppressive at levels around 20 ng/ml. That’s all there is to it. If you chose to seek out the sun and your level of D rises above this threshold, there’s no question that your immune function will decrease. Now that we have the knowledge to understand the vitamin D metabolites at such a precise level, why are you hanging onto a theory about sun exposure that is based on so much speculation?
Do you believe that sun exposure increases the risk for skin cancer? If so, is man intended to get skin cancer because our ancient ancestors supposedly were in the sun?
Last, but not least, the evidence that regular sunscreens even block the production of vitamin D is very weak. Patients on the Marshall Protocol continue to produce vitamin D despite wearing sunscreen. The zinc oxide in some sunscreens will block vitamin D production to a certain extent, but not even completely.
Our ancient ancestors did not have the technological tools of modern medicine at their fingertips. Now that we do, there is no more reason to act like an imagined ancestor in Africa.
Dear Ms. Proal,
Your article hit me like a brick – I just wish I had the time and knowledge to digest it all, plus all the links. I’m looking forward to all the comments and your replies. After clicking Reference #134,I wonder what I’ll do with the 200 7oz. cans of Vital Choice Canadian Pacific Sockeye Salmon left from the 300 cans I bought last year?
Cheers,
Oscar Falconi
Hi Oscar,
Thanks for writing. Yes, these massive misunderstandings surrounding vitamin D make for a very sobering subject. It’s so difficult to continue to watch articles come out telling people to consume more vitamin D. Ahhh!
The idea that vitamin D is major factor in the current epidemic of chronic disease is not an easy idea for mainstream medicine to swallow, but I think in the coming year we will see some changes. In February, Dr. Marshall will release a paper on this same subject, and in 2008 he will be chairing a session at the 6th Annual Conference on Autoimmunity which will focus on the role of vitamin D and the VDR in disease. Quite a few scientists will become informed at that point.
Meanwhile, I’m sad to learn that you have so much salmon! I must admit that salmon is delicious – probably the food I most miss while on the MP.
If you are symptomatic you may want to give those cans away to people who seem very healthy (maybe one can to each person!) Healthy people can consume some vitamin D, they just want to keep their level of 25-D below the range at which it becomes immunosuppressive. So I would say moderation is the key.
It’s sad to give up vitamin D rich foods while on the MP but it’s a very small price to pay for getting my health back and the fact that I am starting to live more of a normal life again.
There are some cultures that eat a lot of fatty fish – for example the Eskimos. But I find it interesting that the Eskimos have evolved to have dark skin. People with dark skin produce vitamin D at a much slower rate than those with white skin. So it seems that over time, their skin may have evolved to be dark in order to compensate for the higher levels of vitamin D they get through diet.
All the best,
Amy
Thank you for this eye opening write-up. How does one reverse the overuse of vit.D if they are immunosuppressed?
Hi July,
Thanks for writing. The first step would be to stop eating any food products fortified with vitamin D – milk in particular, and also any cheese, yogurt, or grains fortified with the “vitamin.” Except for milk it is possible to find “D-less” versions these products, just check the labels of food carefully.
The are very few non-fortified milks in the US. There are some in other countries. You can order one powdered variety in the US, or water down half and half which does not contain D.
Patients on the Marhshall Protocol must avoid all forms of vitamin D in order to assure that the VDR works at maximum capacity. So they also avoid vitamin D that is present naturally in foods. A list of those foods is available here:
http://www.marshallprotocol.com/forum2/2434.html
Patients on the Marshall Protocol also avoid excess sunlight and bright lights in order to lower the amount of vitamin D the body produces from these sources. They wear sunglasses to block light when necessary and cover up in the sunlight.
If you are not chronically ill, you probably don’t need to go to all these measures to keep vitamin D in the healthy range. The difference between “healthy” and sick people is that sick people have many more bacterial ligands also blocking the VDR. So just a little bit of extra 25-D can put them over the edge and into the immunosuppressive range.
In contrast, healthy people can consume a little more vitamin D because their VDR’s arn’t as blocked. In these cases, IMO people should avoid all fortified foods and not seek the sun (in terms of sunbathing.) Also of course no vitamin D supplements or multivitamins that contain D!
For healthy people I’d say the key is to eat the amount of vitamin D nature intended us to consume before we falsely added it to the food chain.
Hope this helps,
Amy
For the skeptics of what Amy has written – my wife and I have totally eliminated Vitamin D from our food sources….we’re also a lot more careful about avoiding light….we are both recovering from our illnesses – we are seeing symptoms we’ve had for decades vanish while on the Marshall Protocol, and that’s with one of us having managed to lower their 25-D levels to just under 5 ng/ml (that’s not a typo – it’s 5). And quite frankly, there are hundreds, perhaps more, chronically ill patients experiencing the same results. See for yourselves at marshallprotocol.com. Chronic disease has been on the increase for decades and just about everyone knows it – Vitamin D supplementation has done nothing to halt that progression. It seems to have done just the opposite. Benefits of Vitamin D supplementation appears to be a myth based on poor science. Thank you Dr Marshall for making the huge discovery and giving people their lives back!
After reading your story about L-bacteria, it seems very strange to me, that I’ve had no MS relapses since I started keeping my 25(OH)D over 40 ng/ml in 2004.
Hi Mr. Jorma,
Thanks for writing. You say that you have kept your level fo 25-D over 40 ng/ml for the past three years. In terms of the time it takes to note the consequences of the immunosuppressive effects of 25-D, three years is not a long enough period of time. Re-read section number 2 of the above article, “The vast majority of studies fail to account for the long-term effects of vitamin D” where I describe how researchers will have to following patients taking vitamin D for at least a decade in order to finally note the damage done by the secosteroid’s immunosuppressive effects.
Right now, the vitamin D you are taking is acting very similar to a corticosteroid medication. It is slowing your rate of bacterial death and as of now you have not yet relapsed and you feel less disease symptoms.
I strongly feel that if you continue to ingest vitamin D at this rate you will relapse in time because your bacteria are spreading with much greater ease during this period of immunosuppression. It is hard to argue with the precise molecular data showing that 25-D is immunosuppressive at 40 ng/ml. Thus, I strongly encourage you to decrease your consumption of vitamin D. Of course I also encourage you to at least try the Marshall Protocol and actually target the bacteria causing your disease.
Best,
Amy
Thanks for commenting, Amy
I think, I have to reconcider my Vitamin D-taking.
Best
Jorma
I was started on high doses of D by a psychiatrist in 2007. I felt much better but noted that my digestive system wasnt working as well and my.( An endoscopy diagnosed gastritis.) stomach started hurting Vitamin K seemed to help this. I am now taking 1000 to 2000 iu of D daily. I am not feeling as well and in fact searched directly for the immuno suppressive effects of vitamin D I could never take prednisone as it made me sicker. I am 71 years old. Do you recommend an abrupt stop to the D or a gradual withdrawal as it seems when I cut back I dont have as much energy. Also my dentist tells me that my gums are remarkably improved. I have read on recent posting from some top schools, such as Harvard Medical of the benefits of big doses of D so who really knows for sure Yours is the first negative article Ive read though I will try to find more
Anyway I would really appreciate your advice on how to discontinue D after being on a large dose
Thank You Patsy
Hi Patsy,
I’m sorry that psychiatrist started you on such high levels of D as the “vitamin” (which is actually a secosteroid) is affecting you as a steroid would, considering that at such high levels it is definitely remaining as 25-D and slowing the activity of your innate immune system.
So vitamin D has been “covering up” some of your symptoms and temporarily lowering some of your inflammation (sounds like particularly in your gums), but at the same time it’s allowing the bacteria causing your symptoms in the first place to spread with greater ease which is probably why you feel worse in other ways at the same time.
It is a good idea to stop taking the D, although stopping the secosteroid could very likely be accompanied by a rise in symptoms since it would no longer be working as a palliiative immunosuppressant. But it would be a good feeling to know that you are no longer taking a “vitamin” that is speeding up the progression of your disease.
I am not a doctor, but personally if I were stopping vitamin D I would wean off it over the course of several weeks so that I would be able to deal with any hormonal changes and symptoms that might rear their heads as the body adjusts to a lower level of the substance.
Once off the D, I don’t know if you want to consider killing the bacteria causing your digestive and other inflammatory issues. If you want to do that, even at a later stage in life, you could look into starting the Marshall Protocol – a treatment that kills the L-form bacteria now known to cause chronic inflammatory diseases. More about the treatment and L-form bacteria here:
“About the Marshall Protocol”
http://bacteriality.com/about-the-mp/
“Understanding L-form bacteria:
http://bacteriality.com/2007/08/15/l-forms/
If you or your doctor need further evidence to back up your choice to stop taking vitamin D you may want to take a look at the following paper by Marshall – “Vitamin D discovery outpaces FDA decision making”, which was just published in the peer reviewed Journal BioEssays and shows many of the feedback pathways between th different forms of vitamin D.
http://TrevorMarshall.com/BioEssays-Feb08-Marshall-Preprint.pdf
The paper give a good idea of exactly how much solid science is behind Dr. Marshall’s findings about vitamin D.
Best,
Amy
Dear Amy
A very interesting and thought provoking article on vitamin D. Congratulations and thank you.
My interest is in Rheumatology and the question relates to the levels of vitamin D and response to the new biologicals ( TNF alpha blockers). Do you think there is a connection as to how effective these anti TNF’s are and the vitamin D levels? Will the anti TNF’s work better in these chronic patients who may or may not have vitamin D deficiencies?
Hi Bhadrish,
Thanks for you kind remarks about my article. I’m glad you are approaching this new research about vitamin D with an open mind.
Well, I am not a doctor, but since TNF-alpha is definitely one of the cytokines secreted by the immune system in response to L-form bacteria, a TNF-alpha blocker should decrease inflammation in a patient with Th1 disease, leading to some symptoms relief. But the intervention is purely palliative. The L-form bacteria causing TNF-alpha to be secreted in the first place would continue to spread, leading to further symptoms and greater inflammation down the road.
So obviously I would recommend that any patient with a rheumatological disease do the Marshall Protocol in order to kill the bacteria causing the release of TNF-alpha. This is a curative solution that would result in actual resolution of symptoms.
Another thing is that TNF-alpha blockers tend to generate a fairly high level of side effects. Thus, if I wasn’t going to put a patient on the MP but just wanted to find a drug to lower their inflammation, I would give them an ARB such as Benicar rather than a TNF-alpha blocker. ARBs lower inflammation just as effectively or possibly even more so then the TNF-alpha blockers (from the studies I have read), but with few, if any side effects. As a class of drugs, ARBs have a excellent safety profile.
That’s my two cents!
Amy
Wait a second, I just re-read your post and I don’t think I actually answered you question. Sorry about that…
As for the relationship between the effects of TNF-alpha blockers and a patient’s level of vitamin D. Hmmm…..well, patients taking high levels of vitamin D would have high levels of 25-D already blocking the VDR, thus generating an immunosuppressive effect that would cause them to experience a temporary drop in inflammation and probably a sense of palliation. In these cases, since the patient’s level of inflammation has already being lowered by the effects of excess 25-D TNF-alpha blockers might have less of an effect.
But if a person has a VDR not blocked by 25-D they probably are more aware of their inflammation and their inflammatory symptoms are not temporarily palliated. Thus I would expect that a person in this situation might “feel” the anti-inflammatory effect of a TNF-alpha blocker more profoundly.
All of the above is purely speculative. In either case though, the hope is that neither a TNF-alpha medication or vitamin D would be used on a patient, but instead they would aim to kill their bacteria with the MP.
Amy,
You write well, and this piece clearly shows that you put a lot of time and effort into writing it. But writing well doesn’t make you right. And by the way, you really should learn what straw men are, and remove them from your writing. A piece is much more convincing to simply omit a topic than to use a strawman.
I consider myself to be very open to alternative medicine. The following statement is not a comment about if the Marshall Protocol is right or wrong.
To me, as an objective outsider, the MP seems almost like a cult. It has a messianic “leader.” It claims to have special knowleged or insight that others don’t have. It tries to sway others to its belief system. It has a convienient explanation to explain away some facts that dispute it (oh, it takes 20 or 30 years for the harm to show up…) It is convinced of the rightness of its views and the wrongness of other views.
Ask yourself this question as a thought experiment. Come on, really ask yourself. If a major, well-designed, study showed that the Marshall Protocol was wrong, would you
1) Say something like, oh well, and it seemed to fit so well. Let me find another theory that works.
or would you say
2) Well clearly the study was biased, and the establishment, and big pharma (or whoever) didn’t really design the study well, etc.
Ask yourself if there is any study that could come along that would change your point of view. If so, what would it take? If there is no study that could change your point of view then you are dealing with faith, not science.
I assess the MP the way I assess any almost anything that I read in the medical field. I make an internal probability statement about how likely is it that this is correct. My assessment of the MP is that it has between a .1% and 1% of being correct. And again, I’m extremely open-minded about this type of stuff.
Hi Frank,
Your comment is the typical response of somebody who has made no real effort to actually understand the science behind the Marshall Protocol but feels that they should step in and cast an opinion. In reality, the Marshall Protocol probably makes you nervous. It’s not easy to hear that so much of what the medical community considers right is wrong – that we will have to embrace several paradigm shifts and change the minds of people who are comfortable with current consenses. Perhaps you take vitamin D and feel the need to defend your choice, perhaps you don’t want to admit that if you became chronically ill you would have to spend 3-5 years dealing with tough immunopathology to get better. But one thing is for sure – you are not open-minded and you are not educated about the MP.
I can tell you have never watched any of Marshall’s many presentations, actually read his papers, or even made an effort to go through his latest BioEssays paper on vitamin D in an effort to truly understand the argument he has put forth, because if you had, you would never refer to the MP as a cult. That a ridiculous statement, and could only be made by somebody completely unfamiliar with the Marshall Protocol and how the treatment is affecting lives.
Tell me, if you were desperately ill with a chronic disease, to the point where most doctors had given up on you and all you were left with was a cabinet full of palliative drugs that hardly worked, how would your feel if a curative treatment option that actually worked came along? Wouldn’t you become enthusiastic about the treatment? The thing is people on the Marshall Protocol don’t have to wonder if the treatment is working. The know they are killing bacteria because of their calculated and often very strong response to MP antibiotics. Immunopathology means only one thing – that bacteria are dying. And not surprisingly, those patients to experience immunopathology find that their symptoms disappear as well.
When patients on the MP get their lives back, they understandably become fervent believers in the treatment. They also look at the people around them – people suffering from diseases that are being cured by the MP. And then you try to tell me that it’s “cultish” that they spread word about the treatment? They spread word about the treatment because it works and because they don’t want to see other people suffer.
Furthermore, the MP doesn’t “explain away” anything. What you consider explanations are scientific realities. Not ones you are familiar with of course so I guess it’s easier for you to dismiss them then investigate them.
You have no idea what kind of person I am and you are deluded if you think that I would try to rationalize a study which showed the MP doesn’t work. If a study was well designed and patients failed to improve I would absolutely accept those results and change my view on the treatment accordingly. What do you take me for, a liar? I have a strong scientific background and base everything I write on cited literature.
Yet, no study has shown that the MP doesn’t work and the data collected from the phase II trials on the Marshall Protocol study site is a constant indication that the treatment works. Sure, it’s an open-based internet trial, but nearly everyone on the treatment is reporting immunopathology, improvement, and recovery. When this recovery is backed by Marshall’s molecular research as well as numerous other studies (many of which are cited in my articles) we have a pretty powerful reason to communicate information about the Marshall Protocol and the science that forms its backbone to the public, to the NIH, to every single researcher and doctor as quickly and effectively as possible.
Best,
Amy
Prior to modern times humans spent many hours in the sun almost every day without sunscreen. They made lots and lots of vitamin D3. Probably 15,000 – 20,000 IU / day or so which is where the human body shuts down additional production. If it is so bad for us why does the body produce so much? Living outside under the sun goes back hundreds of thousands of years and even millions to early hominoids. We evolved under the sun or are adapted to it if you don’t believe in evolution. So now the sun and vitamin D3 is the cause of our health problems? VERY ILLOGICAL THEORY.
If you want to know why people in industrialized countries suffer from so much inflammation it is from consuming huge amounts of omega-6 fatty acids from foods containing soy bean oil, safflower oil, corn oil, cottonseed oil, etc and also meat and dairy from grain feed cattle. Read the Anti-Inflammation Zone by Dr. Barry Sears if you want to know the facts. The solution is to consume more long chain omega-3 fatty acids from fish oil and cut down on products from grain feed cattle and containing vegetable oils.
i have already addressed your first statement in a previous post so I will repeat my answer here:
You say we should be out in the sun all day. There are many faults with that argument. The first being that our ancient ancestors in Africa surely had dark skin, meaning they created much less vitamin D from the sun. It’s unfair to take a modern day North American white-skinned human and artificially put them into some ancient African atmosphere. We have now evolved to live under very different conditions. And who really knows how much sun these ancient ancestors got. Surely they knew how to seek shelter? Furthermore, quite a few human cultures developed in Northern continents with much less sunlight and survived just fine.
But I don’t know why I’m even wasting time trying to theorize about some distant African ancestor. Molecular modeling has proved that 25-D becomes immunosuppressive at levels around 20 ng/ml. That’s all there is to it. If you chose to seek out the sun and your level of D rises above this threshold, there’s no question that your immune function will decrease. Now that we have the knowledge to understand the vitamin D metabolites at such a precise level, why are you hanging onto a theory about sun exposure that is based on so much speculation?
Do you believe that sun exposure increases the risk for skin cancer? If so, is man intended to get skin cancer because our ancient ancestors supposedly were in the sun?
Last, but not least, the evidence that regular sunscreens even block the production of vitamin D is very weak. Patients on the Marshall Protocol continue to produce vitamin D despite wearing sunscreen. The zinc oxide in some sunscreens will block vitamin D production to a certain extent, but not even completely.
Our ancient ancestors did not have the technological tools of modern medicine at their fingertips. Now that we do, there is no more reason to act like an imagined ancestor in Africa.
In response to your second comment, it’s important to understand that the entire global population is suffering from inflammatory disease, certainly not only people in industrialized countries. Perhaps third world countries do not report as many cases of inflammatory disease as first world countries, but that is almost certainly because people in third world countries have much more limited access to health care.
Whereas someone in a first world country can afford to see multiple doctors again and again, some people in third world countries can not even afford a doctor, let alone see the doctor enough to have their case officially documented.
But people in industrialized nations, particularly the United States, consume so many vitamin D fortified products that yes, they are suffering from more inflammatory disease then people in other countries. The United States ranks 45th in life expectancy, behind Bosnia and Jordan.
The thing is, by saying that omega 3 fatty acids and soy products are not helpful for people with inflammatory disease you are agreeing with my point of view. Omega 3 acids are extremely high in vitamin D, so by saying they are harmful, you are actually confirming what I have said in the above article.
Geniestein in soy interferes with the operation of the VDR, as well as with the operation of two other receptors (PPAR-gamma and PPAR-alpha), all of which are key to the immune system. So I believe you are correct in saying that soy exacerbate inflammatory disease to some extent.
But inflammatory diseases are devastating. They leave people bedridden, sometimes completely destroy their ability to function mentally. Some, like heart disease and sarcoidosis are deadly. To say that the only factors at play are soy products is a bit ridiculous. Clearly there is more to the pathogenesis of chronic inflammatory disease then the consumption of certain foods. The bottom line is that these are severe bacterial illnesses.
Inflammatory disease was present long before humans began to consume higher levels of soy products. The neolithic ice man, who died thousands of years ago was said to have died from heart disease and several other inflammatory disease. The diseases were common during the middle ages. Later people such as Shakespeare and Beethoven died from inflammatory disease. Were they consuming too much soybean oil?
Inflammatory disease is much more complex then meets the eye. While soy does play a role in exacerbating inflammatory disease, bacteria are the main causal factor. The pathogens that cause inflammatory disease have learned how to take advantage of the VDR and thus numerous feedback pathways that control nearly all our hormones and AMP production. The only way to cure inflammatory disease is to use antibiotics to kill the pathogens at the heart of the disease process. Meanwhile, it is the secosteroid vitamin D, present in all vitamin D supplements. that is slowing the innate immune system’s of millions of people. Because “vitamin” D has such a direct effect on the ability of the immune system to keep the pathogens that cause inflammatory disease in check, this secosteroid is definitely the greatest factor to blame for the rise in chronic disease seen in industrialized countries.
Best,
Amy
I’m still trying to “absorb” all the hoopla over vitamin D (to “D” or not to “D”?, that is the question), but I noticed at the beginning of your article you say that D3 is converted to 25-OH D3 in the kidney. My understanding is that most of this conversion takes place in the liver. 25-OH D3 is activated to 1,25-OH D3 predominately in the kidney. You also state that 1,25-OH D3 is produced in various cells and when exposed to light; I assume you mean in skin cells. I wanted to point out that the study you cite demonstrates that keratinocytes can be stimulated to produce 1,25 in a controlled setting where the breakdown of 7-dehydrocholesterol is artificially inhibited. It would seem that their result does not demonstrate what you seem to imply at the beginning of your article that 1,25-OH D3 is produced in human skin under normal circumstances .
Hi David,
I’m glad you are taking the time an effort to investigate some of the latest research on vitamin D.
As for your second concern, I think based on your comment that I will put cite #4 a little earlier. I meant it to serve as a citation for the following comment “It is produced inside various types of cells.” That’s where the citation is relevant, because as source 4 describes, 1,25-D can also be produced in intestinal cells and some types of macrophages. Marshall has hypothesized that in these cell lines there may be an enzyme that takes the place of UVB radiation, allowing for the conversion of pre-vitamin D into 7 dehydrocholesterol.
About your first comment you are right! D3 to 25-D conversion occurs in the liver. I’ve made the change. I very much appreciate you pointing that out.
Best,
Amy
That the adverse affect of Vitamin-D supplementation may well take 20-30 years to show is made many times in this article.
I wonder what exactly is the basis of this statement. Do you have any study or theory to support this?
Hi Bassal,
While there is no specific paper to support the statement, it is a part of the theory or more accurately the hypothesis that Marshall has put out concerning vitamin D. Since Marshall was the first person to flush out vitamin D metabolism at the molecular level, he was also the first to realize the immunosuppressive actions of 25-D, and thus the first to understand that “vitamin” D is a secosteroid that causes short-term palliation and long-term harm.
The reason that ingested vitamin D makes people feel better is because as a secosteroid, it slows the innate immune system and thus the rate of bacterial death. So L-form bacteria and other persistent pathogens such as those in the biofilms are able to survive and spread much more easily.
Any of the hundreds of researchers to work with the L-form over the past century would tell you that L-form bacteria grow extremely slowly. When I asked Gerald Domingue, one of the top current L-form researchers “how slow is slow?” he responded that it takes at least 20-30 years, certainly decades for them to really spread and clearly cause new symptoms and new illnesses.
So when vitamin D blocks the innate immune system, the spread of L-form bacteria happens extremely gradually. It takes, as we have stated, decades before doctors would really be able to pick up on the extra symptoms a greater number of bacteria start to cause.
In the short-term vitamin D does act as an anti-inflammatory agent and this does offer patients palliation and relief. Perhaps if someone was only planning to live for ten more years and had a chronic disease they would chose the palliation offered by vitamin D and not worry about its long-term consequences.
But as bacteria spread over the course of decades, people who take vitamin D for long periods of time will definitely deteriorate much more later in life. For those of us like myself who got sick at a young age vitamin D is a terrible option as it would allow my bacterial load to easily rise for a significant portion of my life.
Some studies are starting to show that long-term studies on vitamin D at least tend to pick up on less positive results then those done in the short term. Remember the studies on prostate cancer discussed in the cancer section? One found that vitamin D decreased the risk of prostate cancer while a longer study found no such decrease. It is these pattens that we will surely observe in the future.
With such slow growing pathogens, studies that last only 2-5 years are not going to pick up on their effects, I guess that’s the main point.
Sorry I cannot over you any definitive papers at the moment.
You may be interested in reading Dr. Marshall’s recent paper on Vitamin D that was published in BioEssays which will allow you to understand his perspective on vitamin D in greater detail. Here’s the link:
http://TrevorMarshall.com/BioEssays-Feb08-Marshall-Preprint.pdf
Best,
Amy
Amy,
Wow, thanks for writing a couple of what are in essence books and making them available for free on the Internet! I have a couple of questions for you:
1.Are these L-form bacteria the same or similar to nano-bacteria? Has chelation been used with the MP, or is this not effective? The book: http://www.amazon.com/Calcium-Bomb-Nanobacteria-Disease-Cancer/dp/1594111014 their website: http://www.calcify.com/
2.Iodine. Because of its immune system enhancement and chelation effects, are inorganic supplements of this mineral used in the MP? http://iodine4health.com/
Thanks again for helping spread this information.
Fred.
Hi Fred,
Thanks for writing! Nanobacteria have cell walls so they are not L-forms. However, like L-form bacteria, they are very small in size. But I don’t think that nanobacteria are affected by the beta-lactams or form part of the normal lifecycles of classical bacteria in the way that L-form bacteria do. Yet they could very well still make up part of the pathogenic “pea soup” that any one person with chronic disease builds up over the years.
The primary pathogens that cause chronic disease are the ideopathic L-forms which seem to have metagenomic capabilities such as the ability to survive in a biofilm-like environment. It is these pathogens that create VDR-blocking ligands and are responsible for slowing the innate immune response. Still, as with any other co-infectious agent or pathogen, once the innate immune response is dulled because of the presence of the L-form bacteria, nanobacteria can surely survive better in the immunocompromised host, possibly contributing to symptoms.
No, chelation is not part of the Marshall Protocol. From what I understand, chelation helps remove heavy metals from the body. But what we are dealing with when bacteria are killed via the MP antibiotics is cellular debri (created by host cell apoptosis) and bacterial toxins. To my knowledge chelation wouldn’t remove such agents.
Then, there is also the issue that the compounds used for chelation could have unintended consequences on the receptors that control the immune response. The MP has a no supplement policy, as most supplements tend to have actions on receptors that we have yet to understand. In the absence of such knowledge, we feel that it’s best to allow the body to regain homeostasis on its own.
Best,
Amy
Vitamin D hormnone (1,25D) activates the innate immune system through the VDR. If healthy individuals (as opposed to those with Th1 disease) avoid all foods with vitamin D and avoid sunlight, how would they obtain enough vitamin D hormone to keep their innate immune systems activated?
Hi Ken,
It’s important to differentiate healthy people from those who harbor the Th1 pathogens and need to avoid ingested vitamin D in order to allow for optimal VDR activation during treatment.
Patients on the MP avoid ingested vitamin D because their vitamin D metabolites have been dysregulated by the Th1 pathogens. But after the pathogens have been killed and the dysregulation they cause has been corrected, patients can become normal people once again.
The ultimate goal of the MP is to allow patients to return to a place where one can get moderate amounts of sunlight and eat foods that naturally contain vitamin D. For example, when I no longer experience immunopathology I will begin to eat foods with vitamin D again (in moderation), except that I will only eat those foods that nature intended to contain vitamin D. There are several studies showing that those populations who do not eat products fortified with D maintain a level of 25-D that does not block the VDR.
But to take your question a step further, the incorrect notion that “vitamin” D is a nutrient is rapidly being replaced by the understanding that it is a secosteroid/hormone. The body generally synthesizes other hormones on its own, since their function to the body’s homeostasis is so vital. Since the D metabolites control so many genes and are intricately connected to immune function, the body probably has a means of creating 1,25-D even when a person is not exposed to exogenous vitamin D. Dr. Marshall believes there is probably an enzyme that converts 7-dehydrocholesterol (a precursor form of D) into 25-D, which is subsequently converted into 1,25-D. If this proves to be the case, even humans not exposed to vitamin D can probably produce the hormone/secosteroid on their own if circumstances dictate that extra production is necessary.
Certainly many underwater fish and animals that live in caves where they ingest no vitamin D and get no sunlight have been shown to have active Vitamin D Receptors and 1,25-D production. So. like such animals, humans may also be able to synthesize 1,25-D on their own.
Rickets, long thought to be cause by vitamin D deficiency, is actually due to a lack of phosphorous and calcium. So if a person were to continue completely avoiding vitamin D they should not develop Rickets
Truly, when you consider that the vast majority of Rickets cases currently occur in Africa, in young natives constantly exposed to blazing sun, it only makes sense that Rickets has other proximate causes.
Hope this helps!
I am a 59-year old woman of Norwegian-Irish ancestry living in southwest Colorado where there is plenty of sunshine year-round. I am a competitive cyclist and spend 1-3 hours a day outdoors. Several years ago I started drinking more milk to help prevent osteoporosis. I soon developed headaches which I eventually traced to the vitamin D. I have since tried different forms of vitamin D (liquid, capsules, and tablets), all with the same effect. Even too much sun exposure will cause these headaches (I am able to distinguish the vitamin D headaches from other types of headaches because they always occur in the front of my head on the right side).
I’ve had my vitamin D level checked twice and it’s been about19 ng/ml. I assume that this was the 25-D level. As far as I know, I have not had my 1,25-D level checked. My parathyroid is normal. My total cholesterol has always been high, however my HDL is high enough to bring my ratio down to 2.9. My monocytes have been around 10% for several years which, I think, indicates some kind of inflammation. (I mention this because I recently came across an article stating that 25-D could be low, not because of too low an intake, but because it is being converted by active macrophages into excessive levels of 1,25-D).
During the last year or so I have started to tire more easily and need to take naps almost every day. Just recently I stopped taking any form of vitamin D and am trying to limit my sun exposure by wearing long-sleeved jerseys and SPF-50 sunscreen. If I’m carefull about doing this then I don’t get the headaches.
Because my 25-D level is so low, the doctors don’t believe that vitamin D is responsible for my headaches and are trying to get me to take massive doses. Do you have any suggestions for what I should do? Thank you for any help you can give me.
Hi Martha,
I’m very glad you have posted about your reactions to vitamin D.
My first bit of advice – don’t listen to anyone who tells you to take extra vitamin D!!!! You are doing exactly the right thing my blocking exposure to extra sunlight and eating low levels of the secosteroid in your diet.
I’m not a doctor, but based on your description, it seems like you have accumulated a mild load of what are increasingly referred to as the Th1 pathogens – chronic bacterial forms that persist in the L-form and in the biofilms. These chronic pathogens are now increasingly linked to many forms of chronic inflammatory disease.
One of the disease these pathogens cause is Chronic Fatigue Syndrome and your need to take naps and the fact that you have less energy makes it sound like you may be developing the disease.
But no need to worry! The phase II FDA monitored clinical trial described in greater detail on the site – called the Marshall Protocol – can effectively kill the bacteria that may be causing your extra fatigue. Since you have been alerted to their presence early on, before becoming severely ill, they will be much easier to kill and the Marshall Protocol should take you a shorter time to complete.
How does vitamin D fit into the picture? To those of us familiar with biomedical researcher Trevor Marshall’s research (which forms the backbone of the MP) your headaches in response to vitamin D intake make absolute sense.
As people accumulate the Th1 pathogens, 1,25-D levels often start to rise or at least fluctuate to higher levels at some points. 1,25-D is not just a hormone, but a cytokine that can cause painful inflammation. When 1,25-D levels are too high they also have effects on receptors that control hormone function and cognitive symptoms.
Since your 25-D is low (which is a GOOD thing!) when you consume extra vitamin D it is probably immediately converted into 1,25-D. Since your 1,25-D might already be high due to infection, the extra 1,25-D only exacerbates the inflammatory effects of the substance, probably causing your headaches.
It’s important to understand that a low 25-D level (I’m fairly sure your 19 ng/ml level is 25-D since few doctors test 1,25-D) is a RESULT and not a CAUSE of the disease process.
As the bacteria that cause chronic disease accumulate, they slow the activity of the Vitamin D Receptor which normally transcribes an enzyme that is meant to keep 1,25-D levels in check. But when the enzyme is no longer created 1,25-D levels go up and then naturally downregulate the body’s level of 25-D. So your low 25-D is not a sign of “deficiency” but a sign that you probably do harbor some of the Th1 pathogens that cause the above vitamin D dysregulation.
So I truly hope you will look into the MP in greater detail. After reading as much information about the treatment as you can on this site and the Marshall Protocol study site itself (www.marshallprotocol.com), post any questions you might have about the MP on the following website:
http://www.curemyth1.org (Th1 refers to diseases caused by bacteria). The patient advocates on the site will answer your questions free of charge and will help guide you through the process of starting the MP.
Good luck!
Amy
In the case that I read about rickets I keep trying to see your point until in you in your own words stated Vitamin D was needed to turn on the swithch that would alow Calcium to be absorbed so how dose that make vitamin D of no use HELLO!!!!!!!!!!!!!!!!
Hi Lynn,
Yes…I’m here Hello.
Calcium absorption requires an active Vitamin D Receptor. The receptor, when in an active state transcribes genes associated with calcium homeostasis etc.
What you don’t seem to have understood from my piece is that there are different forms of vitamin D and not all of them active that Vitamin D Receptor.
1,25-D, the active form of vitamin D that functions as a secosteroid/hormone DOES activate the VDR.
But 25-D, the form of vitamin D obtained from diet, supplements, and excess sunlight SHUTS OFF the Vitamin D Receptor.
So what I’m saying is that the vitamin D you ingest from food and the extra vitamin D you might take as a supplement and most of the vitamin D you derive from sunlight will turn into a form that turns the Vitamin D Receptor OFF.
When the receptor is off, the genes for calcium are not transcribed. So taking vitamin D supplements in the hopes of increasing bone mass is counterproductive.
Best,
Amy
I recently covered up all my skin, in an effort to reduce my skin damages from the hot sun in Australia (I am a pale caucasian, a likely victim of the sun, of course), and then I discovered that I got this line of severe acne on my face, stopping at the high collar line which I wore for 3 months.
I have been following various parts of the Marshall Protocol process, because I have been preparing a posting on Acne.org, saying that UV exposure (and other sun exposure related issues) is what is causing Acne.
Since Acne is a bacterial disease really, I ended up implicating the ineffectiveness of the immune system in it, (because people with HIV commonly develop skin problems / infections after they are infected), and that is where I ended up (using Dr. Marshall’s and others’ research, including yours Amy), linking Vitamin D (which is stimulated in massive quantities) to the immune system issues.
Could over-exposure to UV radiation and the sun’s other rays (including heat which can damage the oil glands within the skin – relevant to Acne) be causing acne because of the sensitivity that results too much of the conversion process of Vitamin D in the skin? Could the site of the conversion (since my severe acne line stopped at the collar) of Vitamin D in the skin (a reaction which I am now proposing is actually not designed to occur, but that it is actually breaking up 7-dehydrocholesterol, which would otherwise circulate unimpeded and may be useful in other things) be a problem in Acne?
Or is it just as I am suggesting, that skin damages from the sun, lead to a bacterial infection in young people with a large number of oil glands in the skin, and then Vitamin D is implicated in the process, due to things that your researchers are now exposing about Vitamin D and bacterial infections?
Your thoughts would be very much appreciated, I am very appreciative of your intelligent answers.
Hi Owen,
You performed an interesting experiment by covering up your skin, and the results can certainly be explained by the Marshall Pathogenesis.
This is how I would explain what happened to you. Acne is definitely caused by bacteria. The exact species of bacteria are not yet fully known but there is a great chance that some of the forms are able to live inside the cells of the immune system (intraphagocytic) and that others live in communities called biofilms where they group together in order to most effectively evade the immune response.
As you read in the above article, the Vitamin D Receptor controls most of the components of the innate immune response, particularly the transcription of antimicrobial peptides that probably are able to kill acne causing bacteria (to a certain extent).
Normally the vitamin D produced by sun exposure is converted in 1,25-D, the active form of vitamin D. But when a person gets an overabundant amount of sunlight, it starts to remain in the precursor form 25-D – a form that Marshall has shown blocks transcription by the VDR (or shuts the receptor down).
When the VDR can no longer function properly, the antimicrobial peptides that would otherwise kill acne causing bacteria are no longer expressed. This means that the immune system targets less of the bacteria and mounts less of an inflammatory response to their presence. And here’s the key: it is when bacteria die that they cause a rise in symptoms for the host. That because it is when they are killed that inflammation and toxin release causes a rise in symptoms in the area in which they are present.
So ironically, the presence of acne is a sign that the immune system is actually targeting the bacteria causing the problem. When acne seems to get better in the sun what’s really going on is that the immune response is temporarily blocked from killing the acne causing bacteria and inflammation drops. But this is not a good thing! Because the immune system is not working up to par, the bacteria that cause acne spread with greater ease and the person probably ends up with worse acne if they ever get out of the sun.
So in your case, when you started to avoid sunlight, your immune system was able to kick in again and begin killing the bacteria causing your acne. But getting so much sunlight has certainly caused the bacteria that cause you acne to spread.
The Marshall Protocol allows patients to effectively kill acne causing bacteria and many patients have reported that their acne is going away or has gone away completely thanks to the treatment. Obviously patients on the MP avoid sunlight and vitamin D supplementation so that the immune system can work as its best while bacteria are being killed. Still, the goal of every MP patient is to be able to return to a place where they can get normal levels of sun and, because they no longer have bacteria, they will no longer have symptom flares.
So vitamin D isn’t damaging anything in the skin – it is damaging your immune system response.
Of course if you do the MP you have to expect that your acne will probably flare a get worse before it goes away. I had mild acne at some points during my youth. When I started the MP the pimples would re-appear. They would inflame as the bacteria in the pore were being killed and then go away permanently. Now my skin in very smooth.
I really hope you give the full MP a try! If you do start the treatment make sure you follow the guidelines exactly as stated.
If you have more questions about the MP the best place to ask them is at the following website:
http://www.curmyth1.org (Th1 refers to diseases caused by bacteria). The patient advocates on the site will answer your questions free of charge.
Best,
Amy
I just read your article “The Truth About Vitamin D: Fourteen Reasons Why Misunderstanding Endures”. Thank you for the obvious time and effort you put into that.
I agree that publication bias, flawed methodology and “groupthink” in the scientific literature often contribute to massive misunderstandings. The notion that high cholesterol causes heart disease, or that depression is caused by a chemical imbalance are two of many examples. Perhaps vitamin D is a third, but I haven’t made up my mind yet.
I have a healthy respect for clinical and experimental research. We’ve gained tremendous knowledge about how processes occurring at a molecular level influence the physiology and function of the body.
However, I also believe that evolutionary biology and simple common sense should play a role in our understanding of vitamin D. And the one fundamental question your article (and none of the Marshall Protocal information I’ve seen) addressed is this: how is it possible that vitamin D is a significant contributor to illness when humans evolved in equatorial regions with abundant sunshine? If vitamin D was detrimental to human health, why did human life emerge and involve in such vitamin D-rich regions?
I’d really like to know how you and the Marshall Protocol folks would respond to this.
I’ve had a chance to read some of your answers to this questions elsewhere on your site. While it’s true that dark skin produces less D than caucasian skin, substantial amounts are still produced – especially if one is exposed to bright sun for a couple of hours at a time, which is not at all an unreasonable assumption for our ancestors.
Also, epidemiological and population studies have shown that peoples such as the traditional Inuit did not have the modern, Th1-mediated inflammatory diseases we see today in spite of extremely high intake of n-3 fatty acids (in the form of seafood and fish liver/oil, which of course are very high in vitamin D).
I have more questions but I’m out the door now, and I’ll just wait until after you post. Perhaps you’ll answer them.
Thanks a lot for all of the time and effort you put into this.
Thanks,
Chris
Hi Chris,
I commend you for thinking about the development of chronic inflammatory disease from an evolutionary perspective. I also try to look at most scientific issues through the lens of evolution as it often sheds new light on the possible reasons behind certain occurrences.
You are correct in stating that man evolved in sun-rich regions. The degree of sun that they actually got daily is debatable. As I’ve mentioned before, I don’t think they were scorched. After all, a person’s rate of developing skin cancer rises quite a bit if they get even two serious sunburns, so I’m not sure that man evolved to fry in the sun. I’m guessing these ancestors had caves, hunted during the night as well as the day, and probably avoided the hottest periods of sun.
That being said, there’s no doubt that our ancestors got sun and there is no doubt that man evolved so that getting a moderate about of sun would be a beneficial thing. After all, most of the vitamin D produced from sunlight is converted into 1,25-D – the form of vitamin D that activates the cathelecidin and betadefensin AMPs and the genes transcribed by the VDR. It’s not surprising that the vitamin D system – which is so integral to the body’s immune and hormonal pathways – would develop to be activated by a substance that is so readily available. Since maintaining an active VDR is so crucial to human health, the fact that moderate sun exposure drives activation, and that sunlight is easy to obtain is logical.
But at this point we have to factor the evolution of not just ancient man, but also ancient chronic pathogens into the above picture. It seems like the chronic pathogens that cause inflammatory disease have been with us for eons and were around during the times of prehistoric man. After all, the Neolithic ice man is said to have died of a heart attack and had osteoporosis and periodontal disease. Back when our ancestors were first living in Africa and other sun-rich regions, who knows how well the these pathogens had evolved to take advantage of human health? My guess is that at that point in time they had not yet developed the ability to create ligands that block the Vitamin D Receptor – a evolutionary advantage on their part that would forever change the ability of certain humans to benefit from sun exposure.
Marshall has shown that the Th1 pathogens (the name we give to the vast microbiota of disease causing bacteria capable of infecting the human body) dysregulate the VDR by creating ligands that block its activity. His work has been backed by other research, for example this Indian study which shows that several types of common bacteria have develop ways to block AMP production:
http://www.ncbi.nlm.nih.gov/sites/pubmed/18717821
So once the Th1 pathogens evolved the ability to block the VDR and AMP production the ability of people who acquired them to benefit from sun exposure was altered. When the Th1 pathogens block the VDR two main things happen. Transcription of CYP24 – the enzyme that breaks 1,25-D down into its inactive metabolites – is no longer transcribed. So 1,25-D levels rise without a feedback system to keep them in check. All of a sudden, people with the Th1 pathogens start to accumulate too much 1,25-D and unfortunately at high levels 1,25-D has a strong affinity for the body’s other nuclear receptors. If it reaches high enough levels it distorts the systems they control (essentially the body’s hormonal pathways) and thwarts the production of the AMPs that these receptors also express (over 22 other families).
At that point, if a person get sun exposure it only adds excessive level of 1,25-D and to the vitamin D dysregulation created by the presence of the Th1 pathogens. Also since the VDR is already blocked by bacterial ligands, if any 1,25-D is converted into 25-D, the 25-D likely exacerbates blockage of the receptor rather than staying at the lower healthy levels it would maintain if the person was not infected. Bottom line – the Th1 pathogens have perverted once was once intended to be a beneficial occurrence for man – exposure to moderate sunlight – into a situation that now allows them to gain the upper hand and flourish.
You might argue then that people who don’t harbor the Th1 pathogens should be able to get sun. That’s true. The problem is the Th1 pathogens have become so prolific over the last few decades that almost everybody harbors at least some of them. And by the time people reach mid-life, most have relatively high loads.
So it follows that our population must kill off their Th1 pathogenic loads, and that’s exactly what the MP allows them to do. It should be noted that the goal of every MP patient is to reach a place where they can once again get normal sunlight . Once their bacterial loads are reduced 1,25-D can activate the VDR normally and sunlight exposure is healthy once again. This article describes the MP patient’s return to the sun in greater detail:
http://bacteriality.com/2008/02/23/misconceptions/#8
So it’s important to stress that avoiding sunlight is something patients do only on or before the MP when they harbor the Th1 pathogens that have distorted healthy vitamin D metabolism.
So essentially we are dealing with a microbiota that evolved an incredibly logical way to take advantage of mankind. If you were a chronic pathogen wouldn’t you try to dysregulate the system that controls AMP expression? And when humans are constantly getting sun how well would it work to your advantage to twist that exposure into a situation that benefitted your own survival? Unfortunately, such evolution seems to have taken place. The fact that we continue to use immunosuppressant drugs, beta-lactam antibiotics etc is only allowing the Th1 pathogens to spread with greater ease than ever before in history.
So let’s eliminate the Th1 pathogens. Then we can return, as a population, to one that can one again benefit from moderate sun exposure.
Finally, when it comes to the Inuits, I should add that while they eat fatty fish they have dark skin. But the main reason I think they may show less occurrence of certain inflammatory diseases is because the chronic bacteria that cause the diseases have not spread to the northern polar regions. They are somewhat isolated from other populations which actually provides a benefit in the sense that they don’t trade as much disease causing bacteria with others.
Hope this helps,
Amy
Amy,
Your explanation makes a lot of sense and I really appreciate the obvious time and effort you put into it.
I’ve been reading non-stop the past several days about the science behind the MP. I’ve also been exploring the connection between L-form/CWD bacteria, the VDR and Crohn’s disease – since that is what I am dealing with.
I’ve come across several papers acknowledging a link between impaired VDR function and Crohn’s, but of they’re looking at it from the “conventional” perspective, i.e. that it is vitamin D deficiency that is causing the VDR malfunction, and, subsequently, the Crohn’s disease. Of course now as I read these papers I’m keenly aware of the MP perspective – that the low levels of 25,D seen in these patients are a result of the disease, not the cause. The more I read about the science under the MP, the more open I become to this possibility.
There are still some questions that I’m hoping you can help me with. In this paper (http://www.ebmonline.org/cgi/reprint/229/11/1136) the authors point to several associations between autoimmune disease and vitamin D that don’t make sense to me within the framework of the MP:
- MS & IBD are more prevalent in Canada, northern parts of the U.S., and Northern Europe than in southern/Equatorial regions (which of course are more vitamin D rich)
- The severity of MS has been shown to fluctuate seasonally, with exacerbations occurring more in the spring than in other months.
- Recently, a large population study determined that vitamin D intake was inversely correlated with MS incidence. (Studies which show that intake of D ameliorates symptoms of existing autoimmune disease don’t conflict with the Marshall pathogenesis, because the D could simply be reducing immunopathology and leading to a temporary improvement. However, the correlation of increased D intake with a lower incidence of MS doesn’t seem to fit with the MP.)
- Munger et al. (15) looked at the vitamin D intake in more than 187,000 women from two separate cohorts (one cohort was followed for 20 years, the other for 10 years). Overall, the risk of MS was 40% lower in women in the upper quintile of vitamin D intake. (Same comment as above)
- A second study showed that vitamin D intake (sunlight not accounted for) was inversely associated with the risk of developing RA in a population of 29,000 women (16).
- Vitamin D supplementation (2000 IU/day) during infancy (10,366 children) also significantly reduced the development of IDDM (rate ratio of 0.22) when evaluated 30 years later (17).
(These last few studies cited above are rather large and long-term, which makes them harder to dismiss.)
The article goes onto cite references such as this:
More recently, experimental IBD has been shown to be accelerated by vitamin D deficiency and suppressed by 1,25(OH)2D3 treatment (44).
but of course this could be explained differently (according to the MP); namely, that the 25,D deficiency is a result of more accelerated IBD, rather than the cause of it, and that 1,25-D supplementation provides a temporary reduction of symptoms by reducing immunopathology – rather similar to what a corticosteroid would do.
Amy, I hope you know that I am not out to “poke holes” in the MP. I am really trying to get my head around it in light of all of the research I’ve read so I can evaluate it as a possibility for myself. I try to be as thorough as I can in this process, and I appreciate your patience as I move through it. A week ago I didn’t know anything about the MP, so it’s been a bit of a crash course.
Best,
Chris
Amy,
Here is one more study I am trying to make sense of in light of the MP:
Professor Joanne Lappe 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 reduced incident cancers by more than 60% over a four year period.
Lappe JM, Travers-Gustafson D, Davies KM, Recker RR, Heaney RP. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. Am J Clin Nutr. 2007 Jun;85(6):1586-91.
I suppose we could argue that the low levels of vitamin D which led to higher rates of cancer were actually a consequence of more severe infections with L-form bacteria, and that it was the bacteria that led to the cancer not the low D.
However, the finding that increasing baseline levels of D reduced cancer by 60% would seem to contradict the Marshall Pathogenesis.
This raises another question I’ve been curious about. It seems there is a possibility that the success of the MP is due to the Benicar and antibiotics alone, and not restricting vitamin D. I doubt that anyone has ever tried the MP without restricting vitamin D (for obvious reasons – it conflicts with the Marshall pathogenesis), but it seems that this possibility cannot be ruled out conclusively.
Thanks again for all the work you do Amy!
Good luck on your test, by the way.
Chris,
Ah, the Lappe study. You wouldn’t by chance be referring to citation #93 in this article? If you want feedback on that study, read my comment above.
“Has anyone tried the MP without vitamin D restriction?”
Many patients start the MP with a high level of 25-D because they have been supplementing prior to the start of the treatment. Even though they stop D in order to do the MP, since vitamin D is stored in the fat cells for 3-4 months, their level is often high before they start the MP. These people do not experience the same level of immunopathology as patients whose D is under 20ng/ml. Furthermore, as their 25-D levels start to drop, immunopathology starts to pick up pace. So, the need to keep 25-D levels low is clearly reflected in our clinical data.
Amy
The studies Chris brings up showing a relationship between vitamin D intake and the incidence of specific diseases are interesting. However I think we have to be careful in making conclusions based on them. Assuming the data from these studies are correct and the results of Marshall’s molecular modelling are also correct, the conclusions we draw from these studies must meet the results of Marshall’s molecular modelling.
Is it possible that within certain ranges of vitamin D supplementation, enhanced immunity from more 1,25D being available (25D converted to 1,25D) for VDR activation in subjects with low rates of infection could reduce the incidence of disease as seen in these studies?
It gets a little more complicated when we assume infection leads to many chronic inflammatory diseases. Perhaps if these studies gathered information on all diseases in the study subjects, we would find supplementation simply resulted in one set of diseases being traded with another set. Could vitamin D supplementation simply change the sequence of bacterial infection by different species?
Upon closer examination we may find systematic bias in the data collection for some or possibly all of these studies. How can one be sure that the supplementation data collected was correct? Can we rely on what the study subjects reported for their supplementation? Also was the vitamin D in the foods they ate taken into account? Perhaps those who supplemented with vitamin D also took other supplements, ate a healthier diet and got more exercise than those that didn’t. There are so many factors to consider.
All of these studies reported on incidence. Many studies have shown a very different relationship between vitamin D intake and the progression of disease. In any particular case how would one know whether vitamin D supplementation will prevent the onset of a disease or merely push an existing but not yet symptomatic one to develop?
So based on these studies at this point, I don’t think can conclude that vitamin D supplementation will or even can reduce the incidence of chronic disease.
Ken
Hi Ken,
Yes, when I actually take the time to read the full text of many articles on vitamin D I’m surprised by the variability in the subject data – essentially it seems that by moving around a few data points it’s easy to sway the data in one direction or another.
In this piece Steven Strauss takes a good look at an article about vitamin D and diabetes and finds some of the same correlations:
http://www.cbc.ca/technology/story/2008/07/07/strauss-vitamind.html
You are absolutely right that every study on vitamin D now needs to be considered in the light of several new alternate hypotheses that were elucidated thanks to molecular modeling. When low levels of 25-D are associated with greater incidence of disease, scientists now need to consider that the low 25-D levels are a RESULT and not a cause of the disease process. I believe half the studies on vitamin D can be interpreted to support the Marshall Pathogenesis based on that assumption alone.
Then there’s the alternate hypothesis that the drop in inflammation seen among patients taking vitamin D is a “positive” thing in the short-term but destructive in the long term – because it’s suppression of the immune response that allows for the drop in inflammation.
I know that at the end of his talk in Portugal Dr. Marshall is going to say, “show me your studies!” I will help you interpret them in the light of our new molecular discoveries. It’s not that all the data in these studies are wrong, it’s just that the data is not being interpreted in the correct way.
Someone taking vitamin D might actually live a little longer than someone who does not supplement with the secosteorid, mainly because inflammation can wear on the body. But what we need to look at is quality not quantity of life. Even if a patient taking vitamin D lives a bit longer than someone who lets their disease run its course without supplementation equivalent to steroid use, what is the quality of their few extra years? Surely by slowing their immune systems with the high levels of vitamin D they are consuming any last years are full of agony and symptoms.
Patients doing the MP don’t have to take either route. They eliminate the pathogens causing the inflammation and thus don’t need to palliate them with a steroid like 25-D or leave their diseases alone. So killing the bacteria at the heart of these diseases is the most logical solution.
When and if the population were ever able to become free of the Th1 pathogens, sure we could get moderate amounts of vitamin D again. We could eat non-fortified foods and avoid the sun along the lines of someone who is aware of the risk of skin cancer.
Such times are possible but right now, since the Th1 pathogens are already blocking the VDR in most people, the majority the population can not afford to consume much vitamin D as it accumulates as 25-D and adds to the blockage.
In cases where vitamin D levels are very low and a person has an acute disease like TB we could say that temporary supplementation would allow for the creation of 1,25-D and drive the VDR to fight the infection. But this is not a long-term solution. Eventually, if the patient keeps taking the D it will remain as 25-D and start to block the VDR. And in the cases of TB infection why not just give the patient a VDR agonist like Benicar which will active the VDR yet not interfere with vitamin D metabolism? I believe the in the future many new VDR agonists will be created that will activate the VDR.
Could vitamin D supplementation simply change the sequence of bacterial infection by different species?
No. All bacteria benefit when the immune system is slowed. Vitamin D in not interacting with the bacteria that cause chronic inflammatory disease it is simply affecting the ability of the immune system to respond to such bacteria.
Hope this helps,
Amy
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.
Amy & Ken,
While I recognize the possibility that what you say above is true, it is somewhat of an ex juvantibus line of reasoning. The claim that participants who developed cancer during the first year of the study did so because of high forms of L-form bacteria is pure conjecture base on a theory (Marshall Pathogenesis) that has not been proven. There is simply no evidence to support your assertion, and therefore that particular criticism of Lappe’s study doesn’t convince me that the data don’t suggest that low levels of D were predictive of cancer in that study population.
However, there is no evidence to disprove your claim either. And the further studies you mention above do not indicate a link between low levels of D and cancer, or D supplementation and cancer prevention.
The more I review the data, the more equivocal it seems. I hope that a greater understanding of D will lead to more clarity in the future.
P.S. The equivocality I’m referring to is reflected in the various studies and observations I shared in comment #40.
I left a comment before, about my Acne, but I have been following the other comments, and thought I would like to say something.
What needs to be put forward is that “Vitamin D” is only stimulated in most (if not all) food sources, as UV irradiates it. For example, UV rays stimulate “Vitamin D” in plankton, and then the fish eat it, and they are now a “source” of “Vitamin D”.
However, let me say that I do not believe this to be a good thing. If you read about the Marshall Protocol, you can see that it is the amount of the energy that allows for conversion of (in humans) 7-dehydro-cholesterol to pre-vitaminD, therefore I think that UVB just happens to be powerful enough to make this thing happen (in the skin).
To support what I am saying, mushrooms grow in the DARK, without much “Vitamin D”, and no UV rays.
However, after 5 minutes of UV irradiation, all this “Vitamin D” is found in the mushroom.
That is not a good thing, I think people need to do some more thinking about “Vitamin D”, because UV rays are not a “source”, I think it messes with VDR regulation, and people’s hormones.
UV rays are just not good, full stop. I think. They just had enough energy to do this change in the skin (Dr. Trevor Marshall supposedly says there is an internal enzyme process in the intestines or some macrophages, in that 7-dehdryo-cholesterol can be acted on by energy internally in the body, in order for it to become 1,25-D). I think that it is a “weakness”, that circulating 7-dehdryo-cholesterol can be acted on by UVB energy.
Think about the mushroom, along with stimulating huge amounts of “Vitamin D” (only after harvesting and consequential UV irradiation), the mushroom also turns brown / black, like people do. Just on the visual basis alone, I can tell this is not good, it is like “bruising”.
Re-thinking “Vitamin D” is such a good thing, seriously, I think people should think about the mushroom, it grows in the DARK, without much (or any) Vitamin D.
Some people say UV rays are necessary, because without them, there would be no “Vitamin D”, but I (and I do seem to be one of the few) think that there is no problem with this. I also think that there must be other ways for the body to produce it, if it is so “necessary”. I think it is more “necessary” because of UV exposure (because Vitamin D protects against cancer, and 1,25D shows significant anti-tumour properties), and not the other way around. If cities were covered in UV energy shields (maybe this is a project for the 22nd century or something), I think you would find plants grow better, and our eco-system might recover a little, and there would be less human problems as well. I say this because my plants seem to be growing fine indoors without UV rays (I have window tinting whcih is supposed to block UV rays), the “Vitamin D” issue does not seem to concern them at the moment.
Owen,
I think you bring up some interesting points and although I don’t think the intention of these postings is to engage in speculation, I’d like to suggest an alternate hypothesis to the prevailing one about vitamin D and sunlight:
Since the immune system repairs the damage done to our tissues by UV radiation, perhaps the increase in the production of 1,25D and other forms of the steriod from UV exposure is just the body’s natural defence against the UV radiation. Sunlight isn’t good because it creates vitamin D; it’s a threat that the body responds to by producing more vitamin D to activate the VDRs so the immune system can be more effective in responding to the threat.
Ken
I see what you are saying, but you have to look at the physics to it; 7-dehydro-cholesterol is circulating prior to UVB changing it. (7-dehydro-cholesterol is chemically close to pre-VitaminD). 7-dehydro-cholesterol, is a cholesterol pre-cursor, I believe that is its’ main intended function.
It therefore can not be the body’s natural response, (to produce 1,25D in response to sunlight), merely the body has been created in a way as that it does indeed have defences, and that UVB “activates” these defences. However, one does need to think about the connection between various chronic diseases and low cholesterol levels, in the context of UVB zapping 10-15% of the circulating pool of 7-dehydro-cholesterol.
I agree with you, that it is the body’s defence, I just do not think it was designed to occur this way, UVB activating the body’s defences seems dangerous to me, I can find many dangerous elements to high 1,25D levels. I do not think it is a good thing.
Yes, the body has defences, but has there been much thought into what prolonged activation of these “defences”, does inside the body? Can there be too much 1,25-D activating the VDR’s?
(Think about auto-immune diseases, the immune system turns on itself, supposedly, is too much activation of the VDR behind this?)
This doesn’t make any sense to me at all.
Humans evolved in a sunlight and vitamin-D rich environment. Yes, they had dark skin and probably did not stay out in the sun the entire day, but it is safe to say that they likely had serum D levels that were significantly higher than the average city dweller in the Northern hemisphere today.
1,25-D activates the VDR and the VDR in turn activates innate immunity. The human body evolved in the presence of UVB light, and it it makes little sense in my opinion to suggest that moderate amounts of sunlight are unhealthy for the average person.
Other populations which evolved far from the equator, and were likely to have a lot less exposure to UVB light during the winter (e.g. the Inuits) also likely had very high vitamin D serum levels due to extremely high consumption of fish livers, fish oils, seal blubber, etc. Yet according to population studies of Inuits following their native diets, they did not have Th1 inflammatory disease.
It is possible that, as Amy suggested, L-form bacteria did not have the ability to block the VDR at that point in human evolution and have since developed such an ability. That is an interesting theory, but of course can’t be proved or disproved at this point.
I am willing to accept the possibility that the situation changes when someone is infected with significant levels of L-form bacteria. In these cases, if Marshall’s molecular models are correct, exogenous D from sun or food could inactivate the VDR and depress the immune system’s capacity to eliminate the pathogens.
But even if this is true, it doesn’t mean D is not healthy for people who are not ill, and it doesn’t mean it’s unhealthy for people who are ill due to reasons other than L-form bacteria. I have not yet seen any convincing evidence to support the suggestion that we are *all* infected with pathogenic levels of L-form bacteria, or that such bacteria are the cause of all diseases humans suffer from. Is it possible? Yes. But it’s far from certain.
I am really trying to get to the bottom of this, and there are still many questions in my mind. Foremost are the studies I mentioned above comment #40 in which low vitamin D status was predictive of higher incidence of certain autoimmune diseases.
One might argue that those people had infections with L-form bacteria that were causing low levels of D. But if the infections were already present to the degree that their levels of D were low, then why weren’t they already experiencing Th1 inflammatory disease? Why are IBD and MS more prevalent in northern latitudes where vitamin D levels are lower? Are we to assume that vitamin D levels are lower in northern latitudes because of higher levels of L-form bacteria? There’s no logical reason that I can see to make such an assumption, other than trying to fit the available data to a particular theory.
It doesn’t make sense…because humans did not evolve. Once you get that bit right, it may make more sense to you. Adam and Eve were naked…Eve is the “mother of the living”. See the geneology in the Bible. The law of Biogenesis: Life comes from life, therefore disputing evolution. Evolution seems to think life comes from “no life”, thereby contradicting the law of biogenesis.
This is not an appropriate forum for a discussion on theology. I do not wish to argue with you about whether humans evolved or whether they came from Adam and Eve. Let’s just say we can agree to disagree on that point and leave it at that.
Nevertheless, assuming humans did evolve as suggested by the weight of scientific evidence, my questions above persist.
Well, you will never get the right answer, if you assume the wrong thing.
If you work from the wrong “assumption”, you will never get the right answer. It is a very appropriate place to discuss this issue. It is the foundation for why things are, as they are.
Unless you work with the truth, how do you expect the truth to prevail in answers to questions that you ask? A wrong underlying “assumption” will lead you to the wrong answers, and confusion, and many other mental problems.
Owen,
With all due respect, you are the one who will never “get” the mechanisms that surround the emergence and persistence of chronic inflammatory disease if you are unable to view them through the lens of evolution. This is a site about science, not religion, and so religious explanations about the origin of man or anything else are irrelevant to any discussion on this site.
About the mushrooms – you are correct in stating that mushrooms naturally grow in the dark and are thus naturally meant to contain low amounts of vitamin D. There are certain companies including the “Mushroom Council” that are trying to expose mushrooms to UV radiation in order to make them into vitamin D “superfoods.” Such mushrooms would have something like twice the RDA of vitamin D, and you are right, only 5 minutes of UV radiation would elicit such an effect.
In my opinion, it’s very frightening to artificially alter food in this manner. We can certainly say that man did not evolve to acquire such a vast amount of vitamin D from UV-irradiated mushrooms, particularly when dairy products, cereals, nutrition bars, pasta and other products are already fortified with the secosteroid. I think the UV mushroom issue shows how, thanks to artificial fortification, it’s quite easy for a person to consume a huge amount of vitamin D without having to eat much food.
However mushrooms are the only organisms we eat that make their own vitamin D. They make vitamin D because they are fungi and have enzymes necessary for vitamin D production. Other foods do not have such enzymes and the vitamin D they contain is inherent. That’s not to say that we don’t also mess with the content of vitamin D in animal meat. Since most farms now generally feed their livestock foods containing vitamin D, the vitamin D is stored in the animal fat cells which we proceed to consume. It marks yet another way in which the average person is easily able to consume much more vitamin D than nature intended.
Chris –
It seems that your issue lies in believing it is possible that nearly all inflammatory diseases are caused by pathogens. It’s not quite the stretch you might think. Inflammation is the immune system’s response to an infectious agent. When it comes to acute diseases like TB and pneumonia, we have no problems accepting that a wide array of different acute bacteria can cause a wide array of different acute diseases – so why not chronic diseases?
Dr. Marshall is not alone in pushing forward this hypothesis. Dr. Paul Ewald of the University of Louisville and Dr. Dave Relman of Stanford advocate similar hypotheses and have been doing so for some time, a period of time well before the MP was created.
Have you read the article on this site about the Human Microbiome Project? Human Microbiome Researchers openly admit that bacterial cells in the body outnumber human cells by 10 to 1. And what’s more there are probably thousands of chronic bacteria in the human body yet to be characterized and named. When so many chronic inflammatory diseases of “unknown” cause exist, doesn’t it seem logical that they are tied to the presence of this mass of chronic pathogens? By the way we are not just talking about L-form bacteria. There’s biofilm bacteria and many other types of persistent species that have developed unique survival mechanisms.
You say that you want to “get to the bottom of this” but I think you have been presented will most of the information about the Marshall Pathogenesis to make a decision about if the MP is right for you. If you keep endlessly looking for literature you will end up trying to make sense of a lot of contradictions that are hard to address. For example when you say that there is less chronic disease at northern latitudes, I can give you an equal number of studies showing that chronic disease is high in sunny areas.
At some point you need to make the decision to simply try the MP medications and see if you experience immunopathology. Maybe it would help to speak with a patient on the MP who has/had Crohn’s disease and is doing well? If so I can try to put you in touch with someone. Let me know.
Best,
Amy
Amy,
I do recognize the possibility that most disease may be caused by pathogens – bacterial or otherwise. I’m aware of Dr. Relman’s work and I know that even the CDC has published statements suggesting that many diseases not currently thought to be caused by pathogens likely are. In fact, this makes a lot more sense to me than the concept of “autoimmune disease”, which I have never gone along with.
Yes, I am bothered by many of the contradictions in the scientific literature, and I agree that there is no way currently to conclusively resolve them.
I would love to speak with a patient on the MP who was diagnosed with Crohn’s. I’ve been unable to find reports from people with Crohn’s on the MP study site, and although it’s clearly established that Crohn’s is a Th1 inflammatory disease (and thus amenable to treatment with the MP), it would be inspiring to hear from people with Crohn’s who’ve actually had success with the MP.
(As a side note, I’ve done some research of my own and have found some studies correlating Crohn’s with L-form/CWD bacteria. I’ve been aware of the hypothesis that Crohn’s is caused by MAP [mycobacterium avium subspecies paratuberculosis] for a few years, but I came across a study suggesting that it may be a CWD variety of MAP causing the problem.)
Also, I posted a message on “curemyth1″ requesting a list of MP-familiar doctors in my area a few days back, but never heard back. I’d love to make contact with a doc in my area and see if he/she has treated anyone with Crohn’s on the MP.
Thanks Amy.
BTW, my reluctance to jump in and do a therapeutic probe is due to my intensely negative experience with antibiotics in the past. Each time I’ve taken them I’ve gotten worse afterwards, and the worsening has often been “permanent” (i.e. lasting until now). So I’m a little scared of going for it unless I feel reasonably certain I will benefit.
Well, strictly on the “scientific” basis, I was in a bad road accident, and I got a massive blow to the back of my head, causing localised alopecia. The hair has fallen out there, and the accident was in 2006, two years ago, and well…to be honest, not much has been happening until, now…that is.
I am not on the Marshall Protocol (so I do not get involved with Benicar or anti-biotics), but with the mere absence of sunlight, and the avoidance of most ingested “Vitamin D”, there is now some REAL REGROWTH of that previously bald patch on the back of my head. I feel it now, and it is getting fuzzy! It is very very exciting.
I mentioned about the physics of 7-dehydrocholesterol change, due to the fact that I do not think adding in a VDR agonist is beneficial, (to artificially “activate” the VDR’s) as I am seeing the same benefits without any drugs or anti-biotics.
Why would you assume that alopecia caused by trauma to the head has anything to do with the VDR and its activation or inactivation by vitamin D?
I will be honest, you are looking at much more than the VDR if you were to do as I do, or as people on the Marshall Protocol do.
As I said, I am a caucasian; When I avoid the sun, I will also deplete less of the 7-dehydro-cholesterol in the skin, and they will be stronger probably, since cholesterol plays a key role in muscle repair, and cholesterol is so important in many things. The brain houses 10% cholesterol. There are other things going on besides VDR issues when you get out of the sun.
Avoiding the ingestion of Vitamin D is important because of the issues that Amy writes, when she writes so well on this subject.
As for the alopecia, I do apologise if my comment did mislead or deceive you, as it was not my intention. I did further analysis this morning after I posted the comment, and my hair has just grown long around the site of the alopecia, and the fuzz that I was feeling was the overlapping parts, so I posted carelessly, and as such, please consider that statement retracted.
In the final analysis, your body will heal better when you get out of the sun. The dark skinned people, they do not get their 7-dehydro-cholesterol levels zapped as fast as caucasians, and no-one can sensibly argue that they are not physically superior, take Asafa Powell, Usain Bolt, and the USA Basketball team performances in the recent olympics. It seemed that the events were hardly dominated by caucasians.
A lot more happens out of the sunlight, than just VDR issues, although Amy Proal and Dr. Trevor Marshall and their associates are obviously focusing on this issue.
However, if you research the role of VDR’s in baldness, you may surprise yourself, I did read some research recently that suggested a role that VDR’s did play, in baldness.
Ken already said that it is the immune system that repairs damages, therefore it is not an assumption, that healing of trauma induced alopecia would stand a better chance of healing (still very little healing, if any at all, as at 2 years, as I have posted now, with me having deceived my own self yesterday, due to feeling fuzz, but not being thorough in my investigation of the issue), if the immune system were not blocked up.
As I said before, with the mushroom, it can be easily visually observed, the harm in UV rays, and to say that one “needs” UV exposure, is very bad thinking. The darker skinned people are physically superior, especially the African Americans, and they would be the ones most at risk of a “Vitamin D deficiency”.
I had to say something, the constant mention of evolution, it INSULTS MY INTELLIGENCE. People want to create “science” that defies already defined laws. It just shows, people that like evolution, have no respect for laws. You are INSULTING people, suggesting that they formed from apes and monkeys. It is very and highly INSULTING. I can not just sit by and continue to get fed up when basic laws of science are circumvented, merely to support the “anti-God” religion, called Evolution, or as I see it (Evil-ution). You can not just expect people to say nothing on this issue, when Amy was the one to start it, in her replies, stating that people “evolved” with darker skin et cetera…and once you start defying laws of science (like biogenesis, life comes from life, things reproduce after their kind, thus man has never come from a lower life form, STOP insulting people).
Alopecia and VDR’s: “Humans with selected mutations in the vitamin D receptor (VDR) and mouse models lacking VDR develop alopecia” (BIKLE, ELALIEH, CHANG, ZHONGJIAN & SUNDBERG, 2006). Again, “These studies demonstrate that absence of the VDR leads to the development of alopecia…Investigations in transgenic mice have demonstrated that restricted expression of the VDR to keratinocytes is capable of preventing alopecia in the VDR null mice, thus demonstrating that the epidermal component of the hair follicle requires VDR expression to maintain normal hair follicle homeostasis…Therefore, VDR but not vitamin D deficiency results in alopecia” (Hoffmann & Valencia, 2004).
References:
Bikle, D., Elalieh, H., Chang, S., Zhongjian, X. and Sundberg, J. 2006, Development and progression of alopecia in the vitamin D receptor null mouse, Accessed August 2008, http://cat.inist.fr/?aModele=afficheN&cpsidt=17680056.
Hoffmann, R. and Valencia, A. 2004, A gene network for navigating the literature. Nature Genetics 36, 664 (2004), Accessed August 2008, http://www.ihop-net.org/UniPub/iHOP/bng/144290.html.
Amy Proal said that the conversion itself (Vitamin D in the skin) was not a problem in Acne. However, I think that this should be investigated: “Interestingly, in the skin of rats who the experiments were performed on: “85% of the 7-dehydrocholesterol was isolated from slices of skin that contained surface keratin and sebaceous glands” (R&S PharmChem Co. Ltd. n.d.), and they also found that “[m]ore than 80% of the labeled cutaneous 7-dehydrocholesterol was isolated with the sebaceous tissue”. Therefore this links 7-dehydro-cholesterol with sebaceous tissue, which could obviously be an issue with Acne.”
Since Acne is a disorder of sebaceous orginality, (a disorder of the sebaceous glands), I could therefore link the depletion of 7-dehydro-cholesterol in the sebaceous tissues, with sebaceous area issues. Since my line of Acne seems due to exposure, I would therefore link 7-dehydro-cholesterol depletion in sebaceous tissues with sebaceous gland disorder.
This shows to me that I do not think I would be wrong in saying that the synthesis of “Vitamin D” from UV exposure is harmful, and not beneficial.
Reference:
R&S PharmChem Co. Ltd. n.d., 7-Dehydrocholesterol–R&S PharmChem Co.,Ltd., Accessed September 2008, http://www.rspharmchem.com/7-dehydrocholesterol.htm.
Hi Owen,
Just to be clear I did not mean to imply there is no connection between acne and vitamin D. Based on the literature I have read and Marshall’s work I am of the opinion that acne is caused by bacteria. There are likely many different strains of bacteria that contribute to acne and some may be in the biofilm state.
Vitamin D is involved in the severity of acne because if excess vitamin D supplementation causes 25-D to rise to the point where it blocks the VDR, then the innate immune response will slow and the bacteria that cause acne will spread with greater ease.
Of course, less of them will die if the immune response is not as aggressive. Ironically this means that less inflammation occurs and the actual presence of acne on the skin decreases. So many people mistakenly think that getting high levels of sunlight or ingesting large amounts of vitamin D can “help” their acne. In reality vitamin D is simply suppressing the immune response from dealing with the acne causing bacteria – meaning that in the long term the acne will persist and probably worsen.
Best,
Amy
Hi Amy,
Your website is interesting, I hope you do not find my comments annoying. I suppose you would be used to the backlash of having a “contraversial” point of view on “Vitamin” D, the same as I am used to having “contraversial” views about pretty well everything! I do however, at this stage agree with you about “Vitamin” D.
To be clear in return, I was not saying you were implying that Vitamin D is not involved in Acne. You seemed to be saying (if you take note of my original comment) that there was no problem with the conversion process in the skin. You were saying that the condition implicates Vitamin D, because it is purely or mostly bacterial, and I do “slightly” disagree.
For a little while, I have had to study the physiology of the condition, under which I have been subjected. The acne was noticably severe in the form of it mostly stopping where I had my skin covered up, for 3 or 4 months in a row. I formed a pre-conclusion that it must be the sun that is causing the Acne then. I slightly disagree that bacteria is fully at fault in causing Acne, since I have heard that the bacteria implicated on the skin with acne, is normally present on everybody’s skin. However if there become pore abnormalities, excessive clogging of things can occur in the skin, and then the bacteria can get trapped in the pore. This is not the way it is supposed to function, as once the bacteria gets trapped, the immune system fights it, causing as you say; inflammation. That seems to be an immune system reaction to the trapped bacteria.
Where our point of views seem to differ, is that you seem to be indicating that internal bacteria are perhaps responsible for somehow causing immune system issues with the VDR, and the sunlight further worsens the situation by providing more 25-D to block the VDR activity, in relation to the formation of Anti-microbial Peptides and the like. I am not saying that you are wrong, because I think you are right. What I am saying is that I think there is more to it than that, since the physiology of Acne is a complicated and multi-faceted process.
Since the new research seems to be indicated such issues with “Vitamin” D, I have just taken a further step back, to relate the issue to the presence of 7-dehydro-cholesterol (7-DEHC) in sebaceous tissues (in the skin), which are affected by UV rays. I have done a little research and found that increased 7-DEHC levels improve the “Vitamin D status of organisms”, with increased 7-DEHC levels being associated with elevated serum levels of 25-D. If one were taking the old approach to looking at “Vitamin D”, this would have been considered to be a good thing. Obviously you, Amy, would consider this to be not such a good thing. I would tend to agree more with you at this stage, but I would think that both 25-D and 1,25D are designed to be present in some amount in the body, and I am of the opinion that the designed way this is to occur, is through the internal actions of an enzyme on 7-DEHC.
I feel this is important because darker skinned people do not get Acne as commonly as caucasians do. I am an extreme caucasian, with skin that gets freckles very easily. Darker skinned people (who get acne less often) do not get as much of their 7-DEHC (in sebaceous tissues, and other parts of the skin) changed (into pre-vitaminD) as caucasians do. I think that UV rays convert a LOT of 7-DEHC to preVitamin-D. Would this deplete the body’s overall level of 7-DEHC in the skin? My question is really whether 7-DEHC is actually designed to be in the skin in large quantities (especially in sebaceous tissue), and that darker skinned people are less at risk from having these levels effected by the sun.
Also, I find it interesting that there is only one part of the sunlight spectrum that causes this to occur: UVB rays, or wavelengths of light that fit between certain parts of the light spectrum, which we have defined as the UVB part. It is only UVB (and other strong light energy sources, but it seems likely to be the UVB part of the other lights that has this reaction) that effects 7-DEHC in the skin. This also is interesting to me, because UVB the part of the spectrum that is partially blocked by atmospheric ozone (ozone blocks 90% UVB, ozone blocks 0% UVA). Seeing that the ozone has been being depleted as well recently, this could be why the sun is as bad for me as it is, especially in Australia. UVA is not blocked by ozone as much (if at all), and this is not the part of the spectrum that affects 7-DEHC supposedly, but UVB does, and it is ozone that blocks most of the UVB.
This might mean that there may be an increase in Acne which may correlate to increases in UVB making it through ozone.
I suppose I am really saying that I am not surprised that “Vitamin” D has the problems associated with it, that you: Amy Proal and others are finding that it may have. I am of the current opinion that 7-DEHC levels in the skin should be kept stable, and that the action of UVB energy on these levels (causing “Vitamin” D production), is causing problems. Therefore at the end of the chain (with 25-D and 1,25D) I am not surprised that your research is showing the results that it is having.
What are your thoughts on 7-DEHC in the skin?
Thank you for your replies,
Regards,
Owen
p.s. You might make better sense of this than I can: “UVB-induced phytoplankton mortality promoted bacterial activity and these bacteria, possibly together with the material from dead phytoplankton, fuelled growth of protozoa that were UV-tolerant. This study showed that exposure to UVB can caused a complex mosaic of changes in the microbial community” (Davidson, 2001). Since it contains “microbial” issues, I thought you may be able to help me understand it.
Reference: Davidson, A. 2001, Australian Antartic Division – Effect of ozone depletion on Antarctic marine microbes, Accessed September 2008, http://www.aad.gov.au/default.asp?casid=2031.
Now I am really confused! I have had an underactive thyroid for about three years now. My doctor’s office just called yesterday and said it looked fine BUT I needed to start taking 2,000 units of vit D daily until I see him in 6 months.
I don’t know what to do now.
Hi Owen,
I see your comment/question and I’m afraid I just don’t have the time to give it the attention it deserves. I would like to reserve the right to come back to it later if I can. Thanks for understanding.
Hi Teresa,
I’m sorry to hear about your predicament. You know, I would prefer not to recommend a course of action that deviates from the one your doctor suggests. But, with all due respect, I think (s)he is making a suggestion based on an antiquated understanding of vitamin D supplementation.
I just got back from the Congress on Autoimmunity. (I gave an oral presentation on thyroid disease in women.) Dr. Trevor Marshall chaired the session vitamin D and autoimmunity. Marshall went first. Later Dr. Maurizio Cutolo spoke. If you can find a transcript of his talk, it’s telling. He says, “Dr. Marshall is right” at least three times.
Now, I’m not saying that he can fully appreciate everything we’re putting forth (I can’t know exactly what he thinks), but he did talk to me for 20-30 minutes afterward. Cutolo and others see the validity of our theories and clinical data, so much so that he agreed to start testing for 1,25-D in future studies instead of just 25-D. (Values of 1,25-D are often much higher in patients with chronic disease, sometimes five to six standard deviations from the mean. These values will suggest anything but deficiency.)
Here’s the problem for the pro-supplementation crowd. Vitamin D is an immunosuppressive steroid. Everyone knows it and acknowledges it. I know this sounds odd, but if you take a good look, the studies which support its successful use for the long-term relief of disease are scant to none. I say the burden of proof should be on those who suggest we deviate from thousands of years of not supplementing the human body. The evidence is just not there.
Even if you don’t find my argument credible, a prudent person would wait it out until there was iron-clad evidence, and there just isn’t. It’s the only conservative position, and, in my opinion, during this time of increased rates of chronic disease, it is the right one.
Best,
Amy
Thank you so much for this website. I have learned so much here. I am trying to really understand the Vitamin D and I am concerned about my ability to lower Vitamin D to an acceptable level for my innate system to really work well. I am avoiding ALL Vitamin D in my diet. I have to spend some time out side to go to work and to take care of my donkeys, but I wrap up, use the NoIrs, wrap up, use the sun screen, etc.. and i try to limit my trips to my donkeys to the early a.m. or the eveningand I still wrap up.
i am on 75 mino and Benicar Q4-6 with IP that includes productive cough (new for me), leg and arm cramps, fatigue and some other, more minor IP. I hope this means that bacterial killing is going on.
I was supplementing D and it was 54 for the D25 and 53 for the D1.25. prior to the supplementation it was 24.
.
I have read that the protocol will not really kick in until the Vitamin D is below 25, preferably 12 or below. How quickly can the Benicar lower the Vitamin D?
Hi Deedee,
It sounds like you are indeed on the right track. You’re taking your mino and Benicar. You’ve stopped supplementing with vitamin D and now you’re waiting for your 25-D to come down.
Also, it seems to me like you are already generating the immunopathology associated with recovery, so maybe the MP has “kicked in for you” even though your 25-D has yet to come down into a more proper range.
It is like you say true that the innate immune system is more productive when the body’s level of 25-D is lower. Sometimes it takes a year or more for a 25-D to come down below 25. That was certainly true for me.
Just remember that if you notice a strong uptick in your symptoms you can always titrate down the doses of your antibiotics.
Best,
Amy
One more thing Amy: you said that “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”, but I think that it has been strongly noted that the response of 7-dehydrocholesterol –> is due to UVB energy. Maybe the keratinocytes are just light sensitive, in order for 1,25-D to be formed?
However, it was when you specifically said that “patients still report symptom increase in response to light”, that I thought I would add that this might be to Vitamin A depletion, which is light sensitive, especially to UVA radiation.
Vitamin A and “Vitamin” D seem to be related, as toxicity of Vitamin A is reduced when oral “Vitamin” D is administered alongside?
Your thoughts? I just thought I would add that light sensitivity can be due to Vitamin A, which is light sensitive, especially to Vitamin A, and that is in the eyes and skin, meaning your eyes can be sensitive to the light as well.
I think it has been shown that 7-dehydrocholesterol is mainly reactive to UVB.
Vitamin A deficiency, which seems to be more of a TRUE deficiency results in: “Insufficient capillary formation and an insufficient capillaries position can cause an accumulation of waste products that serve as food for penetrating bacteria” (Unknown Author, n.d.), which could be the cause of the increased bacterial symptoms that you observed in response to only UVA light.
Unknown Author, n.d., All about vitamins, Accessed October 2008, http://www.natuurlijkerwijs.com/english/vitaminen.htm.
Sorry to be really annoying Amy, but as you are probably aware, some people are a little ‘iffy’ about the Marshall Protocol, such as the person who wrote this web page:
http://stuff.mit.edu/people/london/universe.htm.
How do you answer some of the things that that person raises, such as:
“The MP claims that Benicar acts as a vitamin D agonist, but there is no lab study that supports this claim”?
That person was saying that there is a lack of supporting evidence to support what the proponents of the Marshall Protocol are saying, and what seems more important to me is that the person in that article was saying that avoiding the sun alone can be responsible for some symptomatic relief, and that it may not necessarily have anything to do with “Vitamin” D.
The things that make sense to me are things like this, take seasonal effective disorder (SAD) for example. Supposedly this can be treated with “Vitamin” D, right? Well, since this SAD thing supposedly occurs to people who do not get much sunlight and during the wintertime, I do myself wonder whether all the “Vitamin” D that was made over the summertime, has really wreaked havoc on health during the wintertime, so that by summer-time, everything is a bit better again, as part of it.
“Vitamin” D supplementation actually working to treat SAD I am very skeptical of, I think there is some kind of placebo effect going on, or else it is for the 25-D “temporary palliatibility” things that you and others speak of, Amy.
I am really confused about the whole thing anyway, because that person does raise some interesting issues on that web-page there.
Plants can grow well without UVB and “Vitamin” D, in greenhouses which block most UV energy, so I really can not see how it is essential to human functioning. So far, I can not see that it is so essential, for 2 reasons:
1) The immune system can supposedly synthesise its own 1,25-D
2) “Vitamin” D helps to protect people from sun damage, so why go into the sun to get this “Vitamin”. It does not make any sense…
Hi Amy,
That was a nice well written and referenced report. Although I am an exercise physiologist (Ph.D.), my undergraduate major was biological sciences/biochemistry and in recent years (after pretty much exhausting myself with “exercise” – researching it, teaching it, and especially doing it!) I have focused more on human nutrition and currently teach in addition to physiology courses, nutrition and metabolism as well. Indeed, I thought I was about as current as one can be in this field until I came across Dr. Marshall’s work then your essay and needless to say that for the most part (I am not a microbiologist so I don’t know much about L-form bacteria in particular) I have to agree with much of what you say. In particular that excessive intake of vitamin D from foods and in particular supplements can very well be detrimental, especially in the long term, there are many benefits derived from the active form of vitamin D – 1, 25 D3 which is directly converted from its precursors in the skin from UVB, as nature intended. Very few foods have any significant vitamin D besides animals high up in the food chain with lots of body fat, e.g. marine mammals, cold water marine fish. Now you can understand how frustrated I am with standard nutrition texts because there are many other examples of misinformation. I don’t have time to discuss more on the MP until I am more familiar with it and perhaps you are correct, vitamin D is not well- tolerated by people with certain medical conditions and that this low tolerance my be a result of the inflammatory component(s). I am in full belief that all chronic illness is ultimately caused by poor nutrition and psychological factors that modulate immune function. And I agree that contrary to conventional thinking, vitamin D taken exongenously is NOT a nutrient but a “drug’!
By the way are you familiar with another theory about why people from equatorial latitudes have dark skin? Actually it’s possible that dark skin prevents UVB destruction of folate, not 1,25 D3 production.
Keep an open mind!
Frank
Hi Frank,
Thanks for sharing your insights. Indeed vitamin D is not a nutrient. We’ve fortified the food chain with a powerful secosteroid whose actions are directly tied to immune function. Have you read Dr. Marshall’s paper on vitamin D metabolism that was recently published in BioEssays? Take a look at Figure 1. Vitamin D metabolism is incredibly complex and affects the endocrine response as well.
“Vitamin D discovery outpaces FDA decision making:
http://TrevorMarshall.com/BioEssays-Feb08-Marshall-Preprint.pdf
The scary part is that most doctors still view vitamin D supplementation as a simple “vitamin in, benefit out model” which couldn’t be farther from the truth.
I definitely plan to keep an open mind when it comes to all areas of science. I’m glad you are doing the same!
Best,
Amy
Hi Owen,
Sorry not to write you back sooner. I have already addressed Mark London’s comments about the MP in the following post:
http://bacteriality.com/2008/08/09/berniemac/#comment-12242
As for SAD, as you may realize, it believe it is a primary example of a condition that fits the MP model. During summer people get more sunlight. Patients with chronic disease already have elevated 1,25-D levels due to VDR blockage. When they get even more 1,25-D from sun exposure levels of the hormone/secosteroid surge and dysregulate the nuclear receptors. This causes a system-wide drop in the antimicrobial peptides expressed by these receptors causing the person’s innate immune response to work less effectively.
So during the time when they are getting light the immune system targets less bacteria and there is less inflammation and immunopathology. During winter, 1,25-D levels drop back to a lower level and the immune system picks up more speed. It begins to attack any chronic bacteria at a faster rate, causing an increase in die-off symptoms and inflammation. The patient feels worse.
If you are arguing that humans do not need to supplement with vitamin D but can make it naturally than you agree with Dr. Marshall. He believes that enzymes likely exist that allow humans to manufacture vitamin D even when they are in the dark.
Best,
Amy
Hi Amy,
I thought I must have offended you, and you no longer wished to reply to my comments. I am glad that you have given me your assurance that this may not be the case.
Yes, I was saying that I was supremely sure that neither humans, plants or any other living (or even non-living) organism benefits from UVB exposure, and I thought that a healthy ozone layer would block it all out, thus rendering exogenous requirements for Vitamin D synthesis a nil factor. In other words, yes I was agreeing that I thought it must be the case that the body can make its own.
I was also saying that (since I read Mr. London’s page) under the presence of high enough calcium levels / calcium intake, 1,25-D levels are apparently not naturally that high anyway – independently of UVB exposure.
I did not realise you had already responded to Mr. London’s comments / webpage, but I will see what you said about it further up the page. My apologies for double posting that webpage link that you already have addressed.
The only conundrum that I have encountered during my period “in the dark” as you have referred to it as, is that visible parts of the sun spectrum such as deep violet, red, blue et cetera…, do have health benefits it seems while you are exposed to them, it seems like the health problems are due to ultraviolet light. That is what I think anyway, and therefore one sacrifices health “benefits” of other spectrums of sunlight, in the process of avoiding the damaging ultra-violet parts, such as dangerous erythema-inducing UVB. That is the conundrum anyway.
Thank you for your time, it has been appreciated. I have referenced both you and Dr. Marshall when I did an internet posting, and I surely do hope that the molecular modeling data is accurate, and that the MP model is correct. It does make sense anyway.
Frank,
Dark Skin (certain types of natural melanin) competes with UVB photons for 7-dehydrocholesterol, reducing the amount of 7-dehydrocholesterol that can be acted on by UVB to form preVitamin D. These people can grow great skeletons (very tall ones quite frequently), and also do quite well in olympic games. I do not see Vitamin D as much of a nutrient really.
You say God intended for people to be exposed to UVB? Why then if the ozone layer was “healthy”, would no or very little UVB get through then? Why does it have damaging effects to plants and other micro-organisms, affecting the food chain, and even CO2 absorption capabilities in the ocean? Why can some species of plants not even grow properly when exposed to UVB?
Hi Owen,
No, you have definitely not offended me. I’ve just been very busy working on two papers and quite a few grad school applications. But I’m very glad that you are interested in better understanding the Marshall Pathogenesis.
Best,
Amy
Oh, well that is good news Amy. I thought you might have been offended because I am anti-evolution. Many people have reportedly been somewhat ostracised by the scientific community because of this disposition, and I thought that I was joining that list because of the nature of some of my comments.
Yes, you must be being kept very busy with all your work. I hope it goes well for you anyway. I am interested in understanding the Marshall Pathogenesis, you are right. I will be honest to say that I am not sure that I completely agree with it, but I do think that it has a more sound basis than the case for “…you must take supplement pills et cetera…” that does seem to hold over the majority of thinkers in this area.
It is a real can of worms anyway, and I do honestly wish you all the best Amy with your research, and I do hope that your research will prove invaluable, something I am sure it will be proved. Best wishes, I will stop leaving comments now, and leave people from having to endure my potentially “annoying” side.
Man this is complicating sometimes!… So what is your perspective on all this with AML(acute myleoid leukemia)? I just had a bone marrow transplant 4 months ago. Have been fighting this for 2 plus years now and am 24 years young.
Im very health conscious and they told me my levels of VIT D were like 13ng on a 25(d) blood serum test. They wanted to put me on D2 at a dose of 50,000 IU once a week. I told them D2 is not even Vit D. I said ” D3 is Vit. D. I’ll find it by other means.”
I don’t drink pastuerized dairy so I don’t get it there. Although I drink Raw dairy which hasn’t been fortified all the time. So I checked out Weston Price and others and started on the cod liver oil from Garden of life about 1- 3 tsps. a day. Also read Dr Mercola’s stuff and started taking 2,000-4,000 IU a day of D3. So wow, I’ve been packing it in. Also they have me on prednisone to suppress my donor’s cells to prevent graft versus host disease… And on Prograf to suppress also..
So got any ideas how all this pertains to me? ALso, I started taking the cod liver oil because of its high in EPA and DHA. How can Omega 3’s be bad for you?
Sometimes it’s better off being ignorant, but it’s too late for that as now I’m up to my knees in it if you catch my drift…..
Any thoughts on the matter would be the most appreciated…. and thank you for all this information that is well documented…..
With Love and Peace,
J.D.
Hi JD,
I’m sorry about your leukemia. I too was extremely sick (bedridden etc) at 24. But I took action and I was able to reverse my disease. I know that, as you say, it can be exhausting to keep trying to figure out what is best for your health. But when it comes to vitamin D please, please don’t be content with being ignorant!
I know it must be a shock to read about the way vitamin D actually works at the molecular level and that it must seem somewhat ridiculous that your doctors are still not actively reading this new research. But change in medicine is painfully slow and in the end you are in charge of your own health.
Vitamin D is a secosteroid that slows the innate immune response. Whether or not leukemia is caused by bacteria (there is much evidence that it is) you need your immune system to be working as best as possible as you fight the disease. Prednisone is slowing your immune response. Your doctors will probably make you stay on that drug.
But taking extra vitamin D is completely unnecessary and is only decreasing your immune function more. Both D2 and D3 are turned into a form of vitamin D that blocks the Vitamin D receptor that activates the innate immune system. I urge you to avoid them both.
Fish oil and the Omega 3 fatty acids derived from such oil is extremely high in vitamin D. Omega 3’s that are not derived from fish oil do not necessarily contain D. So you could get your Omega 3’s from a source not related to fish.
You may be interested in this interview with a man who had bladder cancer and seems to have beat the disease by avoiding vitamin D and adapting elements of the Marshall Protocol (the treatment discussed in further detail on this site) to treat his disease:
http://bacteriality.com/2008/07/18/interview24/
I’m not in a place to offer you more medical advice but I do feel very strongly about the D. Ironically, your original D level of 13 ng is exactly in the range that we consider most healthy. There are hundreds of patients recovering from myriad diseases on the MP and recovery simply doesn’t start if their 25-D level is over 20 ng/ml.
Anyway, good luck as you continue with treatment. And don’t forget that the ultimate decision of what to take is up to you.
Best,
Amy
Be
80% of cholesterol in our body was produced by our liver this does not include our brain production of cholesterol yet. When specific spectrum of the sun hits our skin chemical reaction takes place and one of this is the chemical reaction in which cholesterol is preconverted to Vitamin D, it won’t be a complete VitD if the liver and kidney is not optimally functioning.-summary from a journal…
We are afraid of skin cancer due to the sun’s harmful radiation. But can our body not sense if we have enough exposure specially to UVB to which converts cholesterol to VitD? Can chemical reaction takes place without moelcules, elements or chemicals to react due to heat at specific reaction? Just the same will you have skin cancer if there is no cancer causing chemicals beneath or above your skin?
Are we not focusing to much on science of food production, origins and minerals our body requires? But forgetting that our body can decide what we need as long as its not synthetic or standardized extract…As long as it is nature’s preparation…not altered nature’s preparation. Does our current generation have longer lifespan compared to those generations before the advent of industrialization or what we called now scientific food production and living?
Thanks,
Hi Neil,
Researchers predict that our next generation may be the first to have shorter lifespans than their parents. IMO, the trend indicates an epidemic of inflammatory diseases due to chronic infection that are not being correctly treated by mainstream medicine.
As for cholesterol, the body can synthesize it in several ways and there is usually enough around for needed body functions to take place. The problem with the vitamin D metabolites in chronic disease isn’t whether or not there is enough cholesterol to produce them. Rather, the problem lies in how they are able to be dysregulated by chronic bacteria.
I agree with you that humans should only be consuming the vitamin D that nature intended to be in our food supply. Extra fortification of foods provides the public with way to much 25-D. The secosteroid subsequently compromises their immune systems, leading to increased disease incidence.
Best,
Amy
Hi Amy,
I accidentally came upon this website a few weeks ago while reading through some comments on Dr. Mercola’s website concerning vitamin D. There was a post there disputing the benefits of D and a link to your site here.
I have esophageal cancer (diagnosed 4/08) with mets to the liver and I had started taking vitamin D after reading about the evidence that it helps with cancer prevention/treatment. However, once I came across your site I stopped taking it while I read through your material, trying to determine what to believe. There is SO much information out there that it’s hard to determine who to believe.
I recently revisited this site and while reading through the posts here came across the article/blog that Mark London had written pertaining to the MP and vitamin D. I found it compelling. He seems to punch holes in the MP’s opinion on vitamin D and backs it up with numerous references to validate.
It is not my intent to discredit the MP. I know nothing about it, and very little about sarcoidosis, which from what I gather from reading the posts here it seems to be effective in treating.
However, I am still torn as to whether I should supplement with D or not. I guess I’ll have to determine what I feel is right for me. But, I have a couple of concerns/questions:
1 – If I remember correctly, you’ve stated in past posts that there’s no really effective tests to determine if one is infected with L-form bacteria. With that said, how can one make a determination whether the MP is right for them? Forsaking all other options (including D supplementation) and following the MP for someone like me in the hopes that it would kill potentially non-existent bacteria that may or may not be causing my disease could be fatal for me if in fact those bacteria aren’t present.
2 – Mr. London states, among other things, the following – “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.” — of course the article goes into much greater detail, but my point is that this doesn’t sound to me like vitamin D supplementation is harmful, but could in fact be helpful.
I guess my point here is that there is overwhelming research concerning the benefits of D, and more specifically for me, it potential in helping to fight my cancer.
By the way, I am NOT a believer in traditional, mainstream medicine. If I were, I believe I would be dead today. I have embarked on a path whereby I am assisting in the treatment of my cancer through alternative/natural therapies while my oncologist utilizes traditional chemotherapy (pressure from my family led me to agree to chemo) to keep the cancer in check. He didn’t really believe that my condition would improve – that he could only try to prevent the cancer from spreading as long as possible, but that I would succumb to it in the end.
However, through diet changes and supplementation I provided him with a pleasant surprise earlier this month. My tumor burden has been reduced by 80% on my liver, which was covered with tumors. It’s almost gone!! Needless to say, he was astounded. I don’t credit the chemo with this dramatic improvement, but rather the supplements and diet changes, maybe ALONG WITH the chemo. Oh yeah – I have SAILED through the chemo treatments with rarely a side effect – again, probably because of the things I’m doing to build up my immune system while the chemo tears it down.
My point is, I don’t think the MP is for everyone. There are other, just as effective treatments when it comes to dealing with diseases. For me it’s been vitamins C, E, IP-6 and CoQ10. I think the CoQ10 has been the most potent weapon in my arsenal to fight this dreaded disease that I think I’m winning – much to my oncologist’s astonishment and bewilderment. Now, with all of the evidence out there about D, I am re-considering incorporating it back into my regimen.
I would love it if you would take another look at Mr. London’s article and address some of the specific points he makes in there concerning D. Here’s the link again:
http://stuff.mit.edu/people/london/universe.htm
As I’ve read through your articles and these posts I’ve come to value your opinion, but I’m conflicted because the evidence supporting D is so overwhelming. Making the right decision could be a matter of life and death for so many of us facing health challenges.
Hi Greg,
I’m sorry to hear about your cancer.
The reason why I haven’t gotten to your comment is because I am taking a much needed vacation. Between Bacteriality, all the conferences, and grad school, it’s the first real break I’ve had in more than a year.
I’ve talked about Mark London before, and I’ll say what I said then. I have personally spoken with Mr. London and I am confident he does not understand what is being put forth. He is certainly welcome to have his say, but his statements are erroneous and/or misleading.
Maybe it’s just semantics but you call the MP an “opinion.” It’s not. It’s a theory and it’s backed by the latest molecular science and an actual working metabolism of vitamin D. If you don’t know what I mean by that, look at Figure 1 in Trevor Marshall’s Bioessay, which was peer-reviewed.
Maybe we’re looking at different papers (I have looked at a lot) but I just don’t see the so-called compelling evidence for vitamin D. Could the vitamin D crowd be wrong? Absolutely. Time and again, we see certain methodological flaws in the studies of the secosteroid’s benefits:
1. The wrong (inactive) metabolite is being measured.
2. The studies are over the short-term. How many studies of anabolic steroids would pick up a negative effect if they were only 6 months or even a couple years? (As you may now, it usually takes decades for the ill effects to be felt. Note that it also takes decades for chronic pathogens to build up the point that they cause disease. Hmm, I wonder if that’s a coincidence….)
3. Just like folic acid, vitamin D seems to have a minimal effect in people who are relatively healthy and pronounced negative effect in those who are already sick.
By the way, it’s not good enough to read the abstract. As you can see in this article, abstracts often don’t square with the results of the paper.
The research supporting any kind of supplement including vitamins C, E, IP-6 and CoQ10 is weak to non-existent. Some of these substance actually increase rates of disease when supplemented. Feel free to look it up.
People talk about taking vitamin D as if it’s the only conservative option. I’m sorry but taking a powerful immunomodulatory secosteroid is the least conservative choice. Even the smallest measure of prudence would suggest waiting until all the science is in.
Best,
Amy
Hi Amy,
I came across you website after searching “high vitamin D”. I recently had labs taken and it seems my Vitamin D (1.25 Dihydroxy) level is high 79, as the reference range is 15-60 pg /mL. I take no supplements and was taking Solodyn at the time of the lab draw. My doctor didn’t mention it at my follow-up appointment however I always ask for copies of lab work. Should I be concerned???? What should I be requesting from my doctor?
Thank you,
Dianna
Hi Dianna,
A 1,25-D of 79 pg/mL indicates the presence of strong inflammation and is consistent with Th1 pathology, which I talk about on this site… a lot.
Should you be concerned? Do you have symptoms of chronic disease? Lab results are not without merit, but I personally like to put more stock in symptom presentation. If you went on the MP, it would be to address the root cause of that higher than normal lab value – not just to change the lab value itself.
Right now, I would say your job is to learn more about the Marshall Protocol and see if it’s right for you. You can begin by watching my video overview and then registering at CureMyTh1.org where patient advocates will answer your questions free of charge.
I highly recommend you seriously consider the MP as a treatment option. Do all you can to educate yourself and then see where your doctor stands.
Best,
Amy
Amy:
I came across your website via comments under one of Dr. Mercola’s articles a month or two ago.
Was just wondering what you think of his current rccomendations regarding D levels and intake…
Hi Alex,
Dr. Mercola and I disagree. I believe low levels of 25-D are the result rather than the cause of disease. I believe that supplementation with D causes short-term palliation and long-term harm.
I’m afraid that the medical community just has not fully appreciated what it means for vitamin D to be an immunosuppressive secosteroid. Take a look at anabolic steroids, the kind used by bodybuilders. Anabolic steroids can make a person feel wonderful. I don’t have any studies, but I’m sure there are some out there, which say that taking AS makes symptoms of disease go away. Why don’t physicians prescribe those to everyone? Because use of anabolic steroids is harmful and disease-causing over the long term. Vitamin D doesn’t make you huge and hulking, but it does have the same molecular structure and the same ultimate effect as anabolic steroids.
I think we’ll find that these statements will be borne out by research in the years to come.
Amy
Hi Amy,
I appreciate your well-written article and comprehensive presentation of this theory on vitamin D and its interrelationship with infectious disease.
I am on the fence about the two opposing viewpoints about vitamin d–yours, and the one more favorable to vitamin d. I have read quite a lot on both sides, and I feel like I am fairly open to information either way.
I guess one of the reasons I am skeptical about vitamin d’s being harmful at moderately higher levels is that, we evolved in the sun. Yet, our disease rates (at least, the chronic diseases we face today at such alarming rates) are a much worse problem today than in centuries past, now that we are avoiding sunlight and slathering ourselves with sunscreen and other chemicals (talk about upsetting hormonal pathways!). Evolutionarily speaking, we were built for sun exposure.
Also, flu rates skyrocket in the winter when our vitamin d levels drop. If vitamin d was really being immunosuppressive, wouldn’t people be falling victim to these illnesses more in the summer, when their vitamin d levels were UP and they were “immunosuppressed”? Does Marshall have an explanation for this? I’m just curious…it’s one question that comes to mind.
Thanks for all the work you’ve done, and I’m so glad you’re feeling better.
Hi Val,
Good questions!
I’ve been asked the first one several times. At some point I hope to write an article on the topic that addresses in depth. In the meantime, when considering Homo Sapiens and sun exposure I believe one must look towards the evolutionary forces that have shaped both our development and that of the microbiota of bacteria we have come to harbor.
Early man may have evolved in a sunny environment, although I recently read a book that talked about our African ancestors. Apparently when they were in Africa, the glaciers were actually down as low as what is now New York City. Conditions in Africa were that of a current rainforest with heavy tree growth. Furthermore, it emphasized that humans lived in societies in large caves and that they often hunted at dusk. This book, by the way, was “The History of Sex” which I know is a somewhat unusual source!
But even with that in mind (and I would need to verify such conditions in greater depth) I’m sure our ancestors got plenty of sun. At this point one needs to think of the evolution of the vitamin D system in man. Over time, the Vitamin D Nuclear Receptor (VDR) acquired the ability to express the bulk of the body’s antimicrobial peptides. It also evolved to control a great number of genes (probably well over 1000) related to the progression of inflammatory disease.
It’s logical that the VDR, which is activated by 1,25-D derived from the sun would become one of the body’s most vital receptors. The sun is readily available, making sure that the receptor remains active in a healthy individual.
The question is, “When did man start to accumulate microbes that were able to take advantage of its receptors and pathways in order to persist in the body?” Early man surely dealt with less pathogens then are present today. Also, the pathogens had likely not yet developed many of the survival strategies they possess today.
A huge change in human health occurred when bacteria developed that ability to create ligands that slow the activity of the VDR. At this point they reversed, for their own benefit, man’s exposure to sunlight. When their ligands were bound into the VDR 1,25-D had much more trouble activating the receptor. Instead, it was left to accumulate in the cell cytoplasm where it reached unnaturally high levels that interfere with numerous hormonal pathways. This is what we see in our study subjects today. A pathogen-blocked VDR that is unable to function as it was once intended to.
So it appears that at some point in our evolution, the constant struggle between man and pathogen for dominance ended up favoring the pathogens. This made sun exposure affect those with a bacterial load differently than those with fewer microbes.
The MP works to kill VDR-dysregulating bacteria. At the treatment’s end, patient can once again get normal levels of sunlight (anything that would not cause skin cancer). Recovered patients can once again benefit from the sun in the way their ancestors did.
In terms of why chronic disease has risen greatly during this century, I would not blame lack of sun exposure. For one thing, sunscreen does not block the production of vitamin D in the skin. So while people avoid damage from UV light by putting on sunscreen, it does not hinder their vitamin D production. This is clear among our study subjects who cannot use sunscreen to limit vitamin D creation.
Secondly, the amount of light which we get compared to people in other centuries is debatable. Tan skin first became trendy over the past few decades. Before then, beauty was seen in pale skin. Hats and greater clothing coverage was the norm.
I believe that the rate of chronic disease has escalated during this century largely because of the flagrant use of myriad immunosuppressive drugs. These drugs temporarily palliate the inflammation generated by chronic bacteria but allow them to spread more easily because the immune system is compromised. These drugs are prescribed left and right, giving our pathogens a literal field day.
The ability of cold to compromise the immune response is a major reason why the pathogens that cause the flu are able to take hold more easily during winter. First, off not everyone gets so tan in the summer that it they would become immunosuppressed enough to acquire microbes more easily. Those patients at greater risk for immunosuppression from sun are those who already harbor higher bacterial loads, many of whom are not able to frolick in the sun. Other factors are surely at play but those are ones that come to mind.
Hope this helps.
Amy
Amy, I just want to let you know that I refer many people to this site, almost on a daily basis. Thanks for the great articles.
Amy
I read your site with a degree of scepticism, but convinced my wife to eliminate Vit D supplementation one month ago. Miraculously, the stomach pains she has experienced for almost a year have disappeared.
We will now proceed to having her normal D levels checked. I was wondering what tests might indicate
an overgrowth of L form bacteria.
Paul
Hi Deedee,
Thanks for letting me know that! I have been busy with grad school plans and writing papers but I hope to start writing for Bacteriality in full force again soon!
Take care,
Amy
Hi Paul,
While we feel confident that vitamin D use has a negative effect over the long term, it seems that consumption of vitamin D can elicit different responses. Some people feel better after taking additional vitamin D, noting a reduction in signs and symptoms of disease, and others such as your wife have intolerance reactions.
There are actually two vitamin D tests worth getting measure: 25-D and 1,25-D, and they are described here here. However, the ultimate test for chronic pathogens, as far as we’re concerned anyway, remains the therapeutic probe. Note that these URLs may change.
Hope this helps.
Best,
Amy
How is it that the minocycline is able to ‘reach’ and affect the bacteria, as aren’t the L-form bacteria intracelluar, and sequestered within our own body’s cells?
Why does it take (so many) years (3 or more, in many cases) for the effects of elevated 25-D levels (from supplementation/ sunbathing), and resultant inactivation of VDR, to result in symptomatology?
Has any research been conducted utilizing the Benicar, without the minocycline, and along with other immune supportive actions (e.g, establishing more restorative sleep; better managing stress; appropriate exercise; better nutrition/nutrient dense foods; etc.)?
Has any research been conducted utilizing the Benicar (and vit D avoidance/sunlight), but without the minocycline, and instead utilizing bacteriocidal substances, e.g., certain herbs, colloidal silver, etc.?
Hi Richard,
It’s not just L-forms – we’re talking about a metagenomic microbiota.
Can Benicar alone yield positive benefits? To some extent, yes. As a Vitamin D Receptor, the receptor which controls the innate immune response, Benicar is definitely a powerful antibacterial.
You mention certain other lifestyle modifications like improved sleep hygiene, stress reduction, exercise, and better nutrition. I know a lot of sick people who can’t sleep and it’s not because they’re not doing practicing sleep hygiene. People suffering from chronic disease can spend a lifetime devoted to good sleep, stress reduction, etc. and they’re still sick. To make progress and to generate immunopathology, you need the Benicar and you need those pulsed low dose antibiotics.
Why does it take so many years for vitamin D supplementation to result in negative symptomatology? Less bacteria die in the near term, which contributes to a decline in the signs and symptoms of disease. Over the long term, however, the bacteria proliferate. That is the nature of a steroid: short-term benefit, long-term harm. Take a look at this pre-print which just came out.
As for the other bactericidal substances you mention, I don’t see any science supporting them. We have a lot of work to do, but there is no way that a substance like colloidal silver is in the same ballpark as the MP medications.
Best,
Amy
Amy,
I have noticed that several patients suffering from Hashimoto have elevated PTH values due to the Hyperthyroidism.
High values of PTH induces also higher 1,25D values due to 1-alpha hydroxylase in the kidneys.
As therapy, high amounts of Vitamin D are prescribed in order to lower the PTH values (some times with succes)
Questions to you:
1) How can we distinguish between the additional 1,25D induced by PTH and such induced by the macrophages as in the Marshall Model
2) Why does high vitamin D dosis lead to lower PTH ? I suspect due to the blockage of VDR as Marshall describes.
Thanks a lot,
Alex
Hi Alex,
Sorry for the late reply. I’m not an expert when it comes to PTH. However I believe the answers to your questions are likely in this article written by a member of the MP staff:
http://synergyhn.com/lesions/
Best,
Amy
Fascinating and informative article. We need Oprah Winfrey to bring this to the forefront; and get Dr’s. Michael F. Roizen & Mehmet C. Oz to get on board.
The information in their books concerning vitamin D is wrong. As you know, Oprah has a huge audience that needs to be tapped into.
I’m finishing up Phase 2. The first five months were tough but there’s no doubt I’m improving and the lab results prove it.
Hi Brenda,
Thanks for writing and I’m so glad you are already improving on the MP!
Yes, I definitely agree. If we could get Oprah or another high profile celebrity to truly understand the MP science I doubt they would hesitate to present it to the public. The problem is that getting past the PR people that “guard” celebrities is nearly impossible. Especially when it comes to medical treatments – I’m sure hundreds of people try to contact Oprah about their medical ideas and it would be hard to distinguish ourselves as unique, solid, treatment in the few sentences a PR person may read.
However one day someone Oprah knows might be on the MP or she might read an article about it in the news. At some point, as the MP continues to spread she will hear about it…hopefully!
In the meantime she is unfortunately advocating vitamin D supplementation. She brought Dr. Oz on the show who tested her level of 25-D and found it to be low. Of course we know that a low level of 25-D is a CAUSE and not a RESULT of the chronic disease process, but Dr. Oz misinterpreted the test results as a sign of “deficiency.” So he told her to take vitamin D and unfortunately her audience is almost certainly doing the same – a great shame.
Best,
Amy
Your article correctly states low levels of Phosphorus (in blood) cause rickets, not lack of Vitamin D. Which is exactly the case in “Vitamin D Resistant Rickets” (aka X-linked hypophosphatemia, genetic rickets, phosphate diabetes, etc.) EXCEPT for the fact — that XLH/VDRR has:
NORMAL TO HIGH LEVELS OF CALCIUM in Blood Along with:
Low Blood Levels of Phosphorus
High Urine Levels of Phosphorus
High (blood) Parathryroid Hormone
Normal Levels (blood) of Vitamin D
What is your “take” or opinion on XLH/VDRR in relation to your above article/research? (i.e. about Rickets not being caused by lack of Vitamin D, BUT by low phosphorus and low calcium?)
I have my own personal theory, XLH/VDRR is evolutionary carry over, from ancient man, that enabled mankind to live thru the ice ages and in extreme cold temperatures — whereas XLH/VDRR was beneficial for survival. (Similiar to “Survival-of-the-Sickest” theory whereas diabetes enabled man to survive ice ages/extreme cold by pumping sugar in the blood, to prevent freezing, etc.) I believe a lot of these ancient peoples, that had rickets — the cause was not lack of Vitamin D in diet, but because they genetically responded, to survive harsh cold environments. (i.e. XLH/VDRR)
I enjoyed reading your site, and am going to re-read your articles more in-depth. I just was curious to your take on XLH/VDRR and how it fits into the scheme of things?
Hi Mary,
I don’t know too much about XLH/VDRR rickets and unfortunately don’t have time to do a literature search at the moment. Thanks for sharing your theory although I can’t comment on its accuracy.
I’m glad you plan to read more articles on the site and thanks for making it clear once again that Rickets is not due to a simple lack of vitamin D.
Best,
Amy
Hi Amy.
My level of vit D , test came back at 21. Does that mean that I could start the MP right away?
Love
Hilli
Hi Hilli,
Good to hear from you. We have created a Vitamin D Calculator, which will answer that question in greater detail.
Let me know if you have problems.
Best,
Paul
Wow, there is alot of “theorizing” going on here and alot of very unobjective statements being thrown around. All I will say is that it is very naive to break down ANY disease into a single cause- vitamin D, sunlight, bacteria, whatever. To do so, especially with autoimmune diseases, severely underestimates the complexity and variation of the human immune system. To claim or imply that a particular treatment for a disease will work for everyone is fraudulent and I certainly hope you are not doing so here. While I applaud outside the box thinking and the scientific process, I am disturbed by the fury with which you defend this largely unproven hypothesis. Just because something works for one person does not mean it works for anyone else. A model is not proof. Autoimmune disease treatment effectiveness is always complicated by the fact that most autoimmune diseases fluctuate through periods of activity and remission, making differentiation between treatment effectiveness and natural disease fluctuation difficult. I encourage you to continue your research and understanding of disease, vitmin D, etc. but DO NOT speak as if you know the truth and that all the research that contradicts your ideas are wrong, fraudulent, biased, or some multibillion dollar conspiracy. That is not a scientific argument and will only prevent acceptance of the concept, whether it is a valid hypothesis or not.
Hi “Phil”:
Well… the model is much stronger than you would give it credit. It has been supported by in silico and clinical evidence. You may disagree with the conclusions of posts like these, but this body of work has been accepted for publication in multiple peer-reviewed journals:
http://www.ncbi.nlm.nih.gov/pubmed/19393200
http://www.ncbi.nlm.nih.gov/pubmed/18200565
Here’s a pre-print of the first publication.
http://autoimmunityresearch.org/transcripts/AR-Albert-VitD.pdf
Best,
Paul
Hi Phil,
You say that I am definitive in my conclusions. Well, so are you. You state that I shouldn’t state or even imply that autoimmune diseases could all have the same underlying pathogenesis. How do you know that’s the case when our data clearly shows otherwise?
It seems like you are speculating on the MP’s validity based on preconceived notions of what disease can and cannot be – notions that have been driven by consensus for decades. On this site I’m trying to break free from such consensus and approach chronic disease from a new lens. This requires me to make new statements of chronic illness.
Instead of fighting my statements right off the bat, perhaps you would actually like to check out or research. So I hope you take a look at the links Paul provided.
Best,
Amy
Oh Phil!
You sure know how to throw a wet blanket over a good hypothesis!
I’m not aware of anyone including Amy who is willing to guarantee that the Marshall Protocol will cure every chronic disease, even if the Marshall Pathogensis implies that this MAY be possible. There is no fraud here. No one is trying to deceive anyone. As you may already know, outside the box research is often attacked without mercy. It requires vigorous defense and promotion to survive.
Many diseases have cycles of remission and activity. That’s why we need controlled trials and statistics to determine whether a treatment is effective or not. There is a controlled trial of the Marshall Protocol for patients with Ankylosing Spondylitis scheduled to take place in Western China Hospital and I’m confident there will be more trials over time as the success of the treatment becomes more evident.
The success of the treatment is evident for me since I personally know a few patients on the protocol who are now almost symptom-free after decades of suffering.
You must think this hypotheses has merit otherwise you wouldn’t waste your time writing here, would you?
Ken
I have seizures that are not controlled by medications. I decided to try Magnesium 1g/day to control them as well as other dietary changes. Somewhere along the way, I read that if I took Magnesium, I needed to be taking D3 as well; that the body wouldn’t properly use the Magnesium without the D3 supplementation. I started using 1000mg/3X a day. At the same time, I started taking fish oil for Omega 3’s, 1000mg/3X a day. I have followed this regimen for a year.
Last week, I had horrible headaches; this in spite of the Magnesium which is reputed to be good for migraine headaches. I also started having diahrea again. What had changed? For the last 6 months, I had been taking flaxseed oil instead of the fish oil. The combination of the fish oil/magnesium kept me in a constant state of diahrea. The flaxseed oil did not cause diahrea. Last week, I ran out of flaxseed oil and went back to fish oil. Not good.
Several weeks ago, I became concerned about the amount of D3 I was taking and cut back on it. Between the fish oil and the D3, I am convinced that I was overdosing myself on D3. I am familiar with Dr Mercola’s claims about D3 supplementation and I am skeptical about it. Then I started reading this site, and with the problems I was having between the D3 and the fish oil, I became convinced that I needed neither. My headaches have gone away. The intense muscular/joint pain has subsided. One of the primary problems with taking large amounts of magnesium is diahrea, but without the aggravation of the D3 and fish oil, my GI tract has settled down.
I am convinced that a varied diet will provide all that my body requires. I want to thank you for all the information provided on this website.
Molly
AP: “Molecular modeling has proved that 25-D becomes immunosuppressive at levels around 20 ng/ml. That’s all there is to it.”
I beg to differ that modeling proves anything.
Modeling might help men better understand complex systems given the underlying assumptions are correct and also given that a sufficient number of variable factors have been identified.
But to say that modeling proves anything is incorrect.
Hi Tony,
For that turn of phrase, Amy will concede that her tone could have been a bit more moderate. On the other hand, there is a boatload of in vivo and in vitro evidence that vitamin D is immunosuppressive. Even researchers who advocate widespread supplementation of vitamin D say this. Take another look at our peer-reviewed paper and the work we cite:
http://autoimmunityresearch.org/transcripts/AR-Albert-VitD.pdf
Best,
Paul
Hi Molly,
Sorry not to write you back more quickly! I find it so frustrating that such high levels of vitamin D are actually recommended to the public! As you know our data clearly shows that such supplementation would definitely have a negative effect……as it did in your case.
I certainly believe that all the vitamin D humans need can be obtained from a healthy well-rounded diet. And in cases where people are ill with a chronic disease, lowering vitamin D intake temporarily helps restore VDR homeostasis.
I’m so glad your headaches and GI symptoms are better!
Best,
Amy
In silico, indeed… you Marshall Zealots are HILARIOUS.
Hi Reiser,
Thank you for your outstanding comment. You are now on my Christmas list!
Amy
so……. The sun is bad? hmm… that mean all the kids are at risk of developing sickness because they’re in the sun?
Amy, with this new found knowledge, do you do your best to avoid Vitamin D?
Hi,
I’m not saying that little kids are getting sick by playing in the sun. This article focused on vitamin D levels and intake in patients with chronic disease. There is a great difference between the state of the Vitamin D Receptor in a patient who is sick with chronic disease and healthy children. In patients with chronic disease, the VDR becomes dysregulated by bacterial ligands.
Since the time I wrote this article, which provided evidence that gliding biofilm bacteria dysregulate the VDR, independent research groups have published studies showing that Mycobacterium tuberculosis, Borrelia, Epstein-Barr, and HIV also dysregulate the VDR. Other pathogens that have not been studied in such depth will also likely be shown to possess the same property as VDR dysregulation is such a logical survival mechanism for pathogens. If 25-D does slow VDR activity when it reaches a certain level, it will much more easily slow VDR activity in a person whose VDR is already blocked and dysregulated by pathogens.
In the case of healthy people whose VDRs are more functional, they can ingest more vitamin D and not reach a point of immunosuppression. We believe that in healthy people, eating a well-rounded diet with only those foods that naturally contain vitamin D (not fortified products) and getting sun exposure consistent with avoidance of increased skin cancer, should be fine. That is what I do.
But when patients are on the Marshall Protocol, they avoid vitamin D in order to maximize activity of the VDR. There are no MP guidelines saying that patients or healthy people must avoid sun. The reason why some people on the MP avoid sun is because they become photosensitive. Read more about that here:
http://bacteriality.com/2008/02/23/misconceptions/#8
Best,
Amy
1 year back I started taking 4200 IU (105 ug) D3 vitamin supplement each day because my level was 20 ng/L. Guess what. My chronic pain in my neck has gone, some eczema in my right ear has gone, my energy has increased and the most important is that I have not had any Cluster Headache attack for over 10 mounts. The first for me in 18 years. My D-level is now 60ng/L, witch is the same level found in the primates living in the free sunny nature.
Regards
NHS
Hi NHS,
Your reactions fit exactly according to our model with someone who is supplementing. We’re saying that vitamin D is a powerful palliative and immunosuppressant, and that people *will* feel better over the short-term.
Do “primates” really naturally have 60ng/ml (not per liter)? Where did you hear that from? We’re actually really curious.
Best,
Paul
Hi Paul
Yes, primates living in the nature and outdoor workers have levels between 60-90ng/ml. That’s what I heard from Dr. Holick and I’m convinced that a level about 60ng/ml is the right level to maintain a healthy body and to fell better in the short and the long-term.
Best
Niels
Yes, apparently some people who work outside near the equator have levels of 25-D approaching 60ng/ml. So, I guess that means everyone on the planet needs to supplement with D until their 25-D approaches 60…. The only problem with that statement is that it is based on a series of unproven assumptions, some of which our recent post addresses:
http://bacteriality.com/2009/08/10/iom/
Paul
Hi Amy
I have read a recent study that restricting Vitamin D can affect fertility? Can you comment on the impact of this for sarcoidosis patients?
Hannah
I work in health care and I have seen that most people are vitamin D defficient.
I suppose this article can be oh all its false here its the truth, but not the case.
Vitamin D defficiency is a global concern. The opposite its like saying Omega 3 are bad and Omega 6 are good. And some scientists believe it! Incredible
Dr Cannell and Dr Holick studies are impressive. I have seen great improvements simply giving vitamin D.
With all due respect… the depth of your analysis is not so different than that offered by the people you revere. I’m not surprised that you agree with them.
Paul
Hi Hannah,
It helps to see a study before you comment on it, but I assume this study showed a correlation between low levels of 25-D and reduced fertility. If this is the case, in our opinion, that only shows that the body has downregulated the metabolite so as to upregulate immune function. You should be aware that in a forthcoming paper Blaney et al. found elevated levels of 1,25-D, the active form of vitamin D among autoimmune patients. Did the research to which you refer mention anything about that tendency?
Amy’s forthcoming paper, Dysregulation of the Vitamin D Nuclear Receptor may contribute to the higher prevalence of some autoimmune diseases in women discusses how high 1,25-D may interfere with the body’s nuclear receptors including those responsible for producing the body’s sex hormones.
Doctors tend to diminish the significance of sarcoidosis, saying that it’s not contagious and that it can’t be inherited. But, there is a lot of evidence to the contrary. Women who give birth while sick with chronic inflammatory diseases may transmit that disease or some related disease to their fetus. Have a look at this Knowledge Base article:
http://mpkb.org/doku.php/home:pathogenesis:familial_aggregation
Given the fact that you have sarcoidosis, you may want to consider the Marshall Protocol:
http://mpkb.org/doku.php/home:patients
Best,
Paul
There seems to be a pattern of implying that immuno-suppression is always a bad thing. Isn’t this a poor assumption?
Surely an over-active immune system needs to be somewhat suppressed. If this is the case it would account for the benefits that some people seem to get surprisingly quickly when they supplement with vitamin D.
Naturally, over-suppressing (which could happen in time with over-supplementation) would swing the pendulum the other way so stopping the supplement would then produce a benefit.
Occam’s razor perhaps?
PK
I agree with you. An over-active immune system needs to be somewhat suppressed. However, I am not aware of any disease where the immune system is over-active — dis-regulated perhaps, but not over-active. I am aware of the following situations:
1) the immune system is impaired
2) impairment of the innate immune system causes the adaptive immune system to over-compensate
3) the immune system reacts to a transplanted organ
4) the immune system attacks the body’s own tissues (i.e. autoimmune).
The last situation could be the immune system reacting to an unidentified organism rather than the body’s own tissue. There may be other situations as well. The immune system is very complex.
Are you aware of any particular disease where the immune system is over-active?
Ken
Like Ken was saying, the whole point is the presence of disease-causing microbes. If there are no microbes causing disease, then vitamin D would probably be a good thing.
Paul
Hi Amy. I’ve been taking Vitamin D3 (5,000 IU) since September, and just last night I think I came down with the flu. The symptoms are not bad at all… no scratchy throat, no head aches, etc. However I realize that these are the result of an immune response. Because I believe I have a viral infection (as opposed to a bacterial one), do you think that if I stopped taking D3 today I would get a massive inflammatory response?
Hi concerned user,
I’m sorry you have the flu. I’m not surprised that you are less symptomatic than expected as our research indicates that since your are taking such high amounts of vitamin D you are probably quite immunocompromised. I very much hope you stop taking the vitamin D. If you do I don’t think you will get a massive immune reaction. “Vitamin” D is stored in adipose tissue and usually takes between 3-6 months to leave the body. The D you are taking has certainly accumulated in this fashion so that even if you stop taking it, I would think the activity of your immune response should return gradually as it gets out of your system.
If you stop the vitamin D and get the flu in the future I would expect that you would become more symptomatic. But remember that even though they are a huge pain, such symptoms are a sign of an active immune reaction to the pathogen present. If the pathogen is killed, it should not become part of your collective pathogenic microbiota that could contribute to autoimmune or inflammatory disease.
Best,
Amy
Hello Amy.
I wish you would look at other immune compromising agents such as mercury and other pollutants. Antibiotics as Marshal uses is not without side effects. Have you considered using natural methods of killing the L-form bacteria as MMS? I agree that the bacteria must be killed, but not in this health compromising way.
Cleansing is very very important in raysing the body ph, so that the bacteria dont like it. A zapper is also very good in killing it. And will do so with ore without low vit D-levels.
I know Vit D is immunosupressive, but that does not mean that I can not kill the bacteria while while calming my immunesystem.
That is my experience anyway.
Good luck to all, but think twice about allopathic medication, as there is nothing your body needs less than more poison
I have RA, and am almost there. I take vit D for my health, and have killed bacteria AND buildt health at the same time
Love Hilli
Hi Hilli,
I’m sure you’re doing what you feel is right, but the evidence for “the zapper,” for example, is nonexistent. Some of your other statements are no less problematic.
Best,
Paul
Thanks Paul
Yeah I know,, evidence is not easy to come by,, but getting better is good evidence also.
I am just saying that there is more ways to go about this.
Bless all that find their way,, and I wish all good health
I found it without harsh medications, and feel blessed for that.
Love Hilli
Amy- First, let me say I am just after the truth for myself and my scalp eczema and for my sister and her chronic Lyme. I don’t mean to be antagonistic, and in fact I am questioning the researchers on the other side of the D debate just as rigorously.
Below is a post I made on your work at CureMyTh1.org site and elsewhere on this site. I shall preface it first though. At the time I wrote it, and due to information elsewhere on your site, I referred to the level at which 25D becomes immunosuppressive as 32ng/ml. Perhaps your post here is newer, as you state this level at which 25D becomes immunosuppressive is 20ng/ml “and that’s just it.” What basis do you have for this conclusion? Were the studies in vivo or in vitro? Do you actually have a study demonstrating patients with baseline 25D below 20ng/ml prior to supplementation, and then showing as their levels increase during and after the supplementation period that their level of antimicrobial peptide production goes down and other real life immune system function indicators?
Here is my post with more questions:
Hello, here is a post I made on Amy Proal’s bacteriality site. I am genuinely looking for the truth here. anyone who can respond to any or all of my points/questions would be greatly appreciated:
Amy- Thank you for your site and your work. My interest in your information is two-fold. First, I have a sister who has post treatment chronic Lyme. Second, I stumbled upon Heaney, Vieth, VitaminDcouncil.org and grassrootshealth.net in my search to resolve my own scalp eczema.
I personally have only been taking higher vitamin D for about 3 weeks, but there has been a marked improvement in my scalp eczema.
I read one of the other posts here on the 14 misconceptions about Vitamin D and that 25D is actually immunosuppressive. Your information seems well referenced and very plausible, so you can understand my confusion now after having read through the information from Heaney, Vieth and others on the benefits of D3 supplementation.
It seems both sides have credible arguments and data. Yours especially seems very convincing, but I have some questions:
1. In reading your information, I saw that you have identified the bllod level at which 25D becomes immunosupressive ~32ng/ml. What basis do you have for this conclusion? I would very much like to read the actual paper this is drawn from to see the methods used in the study.
2. While your arguments seem very credible, in fact maybe more credible to me now than that from Heaney, Vieth and other D supplementation proponents, there is one logical barrier I cannot seem to get past with your arguments. We’ve evolved as humans through the millennia with this innate system for Vitamin D production from the sun. Prior to industrialization, or even civilized society, presumably hominids and early humans spent quite a lot of time out in the sun, and no doubt produced a lot of their own vitamin D. Even today, in tropical climates, studies I have seen on blood levels show them to be around 40ng/ml or higher for people who live in these areas while people from northen climes tend to have much lower levels, especially during winter. If 25D is indeed immunosuppressive, then why is there not a higher level of chronic disease and cancer, flu mortality, etc. in these tropical areas? Also, how can you explain away the seasonality of flu and the higher morbidity and mortality rates throughout the fall and winter months? I know your information says that some of these epidemiological studies showing higher incidence of some of these diseases in northern climates are technically flawed– if they are, how so?
3. With regard to the Marshall protocol, or just restriction of Vitamin D intake in general, do you have any data on long term health effects of this popultion wide, or even in specific disease states? This is one of your criticisms of Heaney/Vieth/Cannell/Vitamin D Council et al. You pose the question that since they have no real long term data, i.e. 1-2 decades or more that we cannot really know the true health implications of higher vitamin D supplementation. I would ask the same question– if you have no long term studies regarding the health implications of restricting D3 intake and thus keeping 25D levels low, we cannot really know the true health implications of that either, can we?
4. To expand on point #2, how can something that we’ve evolved with over millennia– our innate ability to produce D3 and thus 25D from the sun, and given that a human can produce nearly 10,000IU per day from sun exposure, how can it be that 25D is deleterious to us? Perhaps there is an optimal level for both sides? i.e. something below the 32 ng/ml threshhold where you suggest 25D is immunosuppressive? Or would people with certain chronic diseases need to be even lower due to the L form bacteria produced proteins also occupying the VDR? If so, how LOW should someone with chronic disease go? To undectable levels of 25D? If so, what are the health implications non related to their chronic disease? Could we help their chronic disease on one hand, but cause other problems on the other? What is the risk/benefit ratio here?
5. From reading your misconceptions on vitamin D page, it was difficult to determine if the studies done demonstrating the immunosuppressive nature of 25D above 32ng/ml were in vitro or in vivo. If they were indeed in vitro studies, is it possible that if you had isolated only the VDR in vitro and introduced 25D that the response could be markedly different than that found in vivo, with the living system and all other substances and enzymes, etc found in the human body? Or do you actually have a double blind placebo controlled study that measured baseline blood levels of anti-microbial peptides as well as baseline 25D and 1,25D levels prior to, during and after supplementation, and do you have concrete proof that 25D above 32ng/ml in humans suppresses the expression of anti-microbial peptides and actually causes their production and blood levels to go down? I don’t believe the other side (Heaney/Vieth/Cannell et al) has a study showing that the levels actually do increase. However, the case reports in facilities and patient populations where patient’s 25D levels are checked and they are supplemented to the other side’s “optimal” levels of 40-60ng/ml are interesting. It does seem like the supplemented populations have less incidence of flu infection compared to surrounding counterparts in the same facility. I know these are clearly not scientific studies, but rather observations that may not even be statistically significant, but there seems to be enough of these case reports independent of each other to show that there may be something to higher vitamin D supplementation and immunity to flu.
6. Your information points out connections of some of the researchers invovled in the D supplementation proponent studies to those in the supplement and/or dairy industries. Some of which disturbed me. However, I believe it is a fair question to ask, what kind of market exists for the Marshall Protocol (independent of the patients actually enrolled in the formal study protocol under the study’s superision), i.e. books, foods, supplements, etc? And if so, what financial benefit if any do Marshall, you and others involved in this work have to gain? Perhaps if not commercial, then maybe private and/or government grants, continued employment, etc.? Your information points out that studies have a funny way of providing the information that is sought by the funder when speaking of those done by Heaney, Vieth et al. I think it is fair to say the same about your work too– could the results of your work be driven to provide information contrary to the other side of the D argument to be different and feed an alternative market?
Please don’t misunderstand me, I don’t mean to be antagonistic. From what I have read, the work you have done looks great and your motives seem genuine– perhaps more genuine than Heaney, Vieth et al. However, I am just trying to get to the truth for me and my sister and others I know that this issue can effect. Guaranteed someone is wrong on either side of this argument and no question there will be damage done. The question is, what side?
Also, you should know, I am not involved at all in supplement production or sales, though I did work for GSK for 6 years up til 2005, primarily selling antibiotics and antidepressants. I now own a business selling medical software– completely unrelated to pharma or supplements. I have been a paramedic for 20 years and have a keen interest in pharmacokinetics and pharmacodynamics, so that is where my medical knowledge and knowledge of study design/methods comes from.
I am really just looking for the truth, and your answers to my questions will help me to get that much closer.
Sincerely,
Bill Kelleher