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From the Townsend Letter
January 2009

Reversing Bacteria-Induced Vitamin D Receptor Dysfunction to Treat Chronic Disease: Why Vitamin D Supplementation Can Be Immunosuppressive, Potentially Leading to Pathogen Increase
by J.C. Waterhouse, PhD

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Recent attempts to increase vitamin D supplementation to prevent and treat chronic disease have arisen primarily out of observations of low vitamin D levels (25-D) being associated with a variety of diseases. However, new research indicates that these low vitamin D levels are often the result rather than the cause of the disease process, just as in the autoimmune disease, sarcoidosis. Trevor Marshall, PhD, recently summarized this alternative perspective on vitamin D, in a session he co-chaired at the 6th International Congress on Autoimmunity. He and his colleagues presented in silico* and clinical data from the last eight years, indicating that intraphagocytic bacteria are able to block the vitamin D receptor (VDR), and this leads to abnormally low measured vitamin D levels. A second consequence of the bacteria-induced VDR blockage is inhibition of innate immunity. By blocking the VDR, bacteria are able to cause persistent infection and inflammation and thus cause many chronic diseases. Short-term symptom reduction observed from vitamin D supplementation appears to be due to immune suppression by precursor forms of vitamin D that add to the bacterial blockage of the VDR. In silico data also indicates that high levels of vitamin D metabolites suppress antimicrobial peptide production by binding to other nuclear receptors (e.g., thyroid-alpha-1, glucocorticoid). Increasingly, epidemiological, geographical and clinical data are lending support to this model of disease. Studies using more advanced cell culture and molecular techniques are confirming the presence of previously undetected bacteria, including biofilm and cell wall deficient bacteria, as well as "persisters." A greater understanding of how bacteria resist standard antibiotic approaches is also being gained. A protocol has been developed that is successfully restoring VDR and innate immune function with a VDR agonist and eliminating pathogens with low-dose, pulsed combinations of antibiotics. Immunopathological reactions (a.k.a., Jarisch-Herxheimer reactions) occur due to increased pro-inflammatory cytokines resulting from bacterial killing. The result is an exacerbation of symptoms with each dose of antibiotic, but improvement occurs over the long-term. Remission is being achieved in numerous chronic conditions, including many autoimmune diseases and fibromyalgia, as well as many diseases of aging. Although vitamin D ingestion is avoided as part of this protocol, the evidence indicates that the net result of the protocol is improved vitamin D receptor activation.

* in silico = performed via computer simulation

Vitamin D is a topic of increasing interest and has been implicated in many physiological processes beyond its initially recognized role in calcium absorption and metabolism.1 Vitamin D is found in supplements and a few foods (e.g., fish, liver, egg yolk, fortified products). The majority of vitamin D is produced in the skin when exposed to UV radiation from sunlight. But some have begun advocating consumption of levels of vitamin D above the RDA, and some advocate very high levels, ranging from 1,000 to 5,000 IU or more daily.2 Vitamin D is a secosteroid, with a close resemblance in structure to immunosuppressive steroids. Levels of the various vitamin D metabolites are the result of complex feedback mechanisms involving multiple enzymes and receptors, indicating that it is regulated more like a steroid than a nutrient.1

Short-term symptom reduction has sometimes been observed through increases in sun exposure 3,4 or vitamin D supplementation.5 However, this appears to be due to the anti-inflammatory effect arising from immune suppression, analogous to the effect of a steroid, such as prednisone. If one were to assume that the inflammation is purely pathological, this might be considered beneficial, but evidence that has been accumulating over many decades indicates that inflammation in most chronic diseases is occurring in response to undetected chronic bacterial infection (see below). Since immune suppression can promote the increase of pathogens, the effect of vitamin D supplementation is not likely to be harmless in this situation, but appears to have long-term effects associated with increased levels of bacterial pathogens. The role of this microbiota in producing the inflammation and oxidative stress observed in so many diseases will be discussed near the end of this article.6-8

Vitamin D from food or sun is first converted to 25-D (25-hydroxyvitamin-D) and then converted in a second step to the active 1,25D form (1,25-dihydroxyvitamin-D) that is able to activate the vitamin D receptor (VDR). The type of vitamin D usually measured in the blood is the precursor form, 25-D, rather than 1,25-D, the form that activates the receptor. Activation of the vitamin D receptor is extremely important, as it has numerous effects, including effects on the immune system1 and cancer.9,10 However, recent research indicates that increasing vitamin D via supplementation or sun exposure is not the way to achieve more VDR activation in chronic disease, due to blockage of the VDR by bacterial products.6 This insight has been put to use in a new model of chronic disease and a new protocol.6,8,11-14

A New Perspective on Vitamin D and a New Treatment Approach
Trevor Marshall, PhD, (Murdoch University, Australia) has developed a model of chronic autoimmune and inflammatory diseases in which intraphagocytic bacteria cause disease by producing a substance that binds to and blocks the VDR.1 One such substance has been already identified providing proof of principle.1 The VDR is important for adequate innate immune function, including the production of numerous antimicrobial peptides.15 These include cathelicidin and beta-defensin, two of the body's own arsenal of internally produced antibiotics. Thus, VDR blockage would seem to be an excellent bacterial strategy, as it would lead to poor innate immune system function and further growth of bacteria and other pathogens. A functioning VDR also appears to be important in controlling cell growth and metastasis, so as to help prevent and control cancerous growths.9,10

A protocol based on this model of disease has been achieving a high rate of improvement/remissions in a wide array of conditions.6,11-14,16-18 It involves the use of a VDR agonist, olmesartan, which is able to activate the VDR effectively and safely. In addition, low dosages of combinations of select pulsed antibiotics are used to eliminate the bacteria, which also helps restore VDR functioning. The protocol also involves avoidance of vitamin D supplementation. When faced with VDR dysfunction, the evidence indicates that attempting to increase 25-D only adds to the dysregulation of the vitamin D metabolites without being able to adequately overcome the bacteria-induced VDR blockage.6,8

Too much vitamin D can be harmful in two ways, according to Marshall's work.1,6 In silico data from highly sophisticated molecular modeling shows that high vitamin D levels can block the VDR and thus block innate immune function.18 In addition, high levels of various vitamin D metabolites can affect thyroid-alpha-1, glucorticoid, and androgen receptors and disrupt hormonal control and further affect innate immune function.1 Thus, any short-term symptom reduction from high levels of vitamin D that may occur is probably occurring at the cost of long-term pathogen increase. This has been supported by observations of patient's responses over time. In the short-term, even for ten years or more in some cases, the person may feel better with high vitamin D intake. But in the long-term, the chronic infection progresses, because the high 25-D is only adding to the bacterial blockage of the VDR and the suppression of bacterial killing.18

Symptoms increase when the immune system is better able to kill the pathogens, due to the high levels of inflammatory cytokine levels that occur. This is called the immunopathological reaction or Jarisch-Herxheimer reaction.6,11 The symptoms range from pain and fatigue to cognitive impairment and depression, but include numerous other symptoms characteristic of the underlying inflammatory condition.6,11 By suppressing the immune response, vitamin D supplementation may suppress these symptoms in the short-term and may even result in a sort of dependence on vitamin D supplementation or sun exposure to keep the symptoms at bay.

The long-term efficacy of the protocol (sometimes called the Marshall Protocol or MP) in activating the VDR is also supported by improved or stabilized bone density, which is typical in patients on the protocol, if the RDA of calcium is consumed. The protocol replaces vitamin D supplementation with use of the VDR agonist olmesartan (120 to 160 mg in divided doses) and reduces the level of bacteria blocking the VDR with antibiotics and, in this way, is apparently effective in activating the VDR.6,12

Marshall proposes that vitamin D receptor blockage results in the low levels of 25-D that have been observed in numerous diseases. The precursor, 25-D form is the form that is most frequently measured. The VDR blockage typically leads to dysregulation of metabolite levels, and one effect is down-regulation of the conversion of vitamin D to 25-D.1 Thus, according to this perspective, low 25-D levels are the result, not a cause, of the disease process. It follows that a low serum 25-D is not indicative of a true vitamin D deficiency in this situation. Both laboratory19 and clinical findings20 have supported the existence of an apparently similar type of down-regulation of conversion to 25-D.

At the same time that low 25-D is observed, high 1,25-D levels are also usually observed. In fact, elevated 1,25-D has been shown to be a good indicator of inflammatory and autoimmune disease.13,16 When interpreting the results, however, it should be remembered that samples must be frozen until analyzed for accurate 1,25-D results. And occasionally, in cases of quite advanced disease or elderly patients, 1,25-D will be low as well, yet still be consistent with VDR blockage and inflammatory disease.21

Marshall's protocol was first used to treat sarcoidosis. It is well established that a dysregulation of vitamin D levels, often with very high 1,25-D and low 25-D, occurs in this condition.22 Marshall's and other's work has confirmed that this dysregulation also occurs in a wide range of other diseases.12,13,23,24 This pattern of high 1,25-D and low 25-D also exists in VDR knockout mice.25 These mice are genetically engineered to lack a VDR, a situation analogous to a bacteria-blocked VDR.

The very complex relationships among genes, metabolites, enzymes, and receptors that Marshall recently summarized1,6 show that vitamin D is not a mere nutrient. In fact, the active form is a secosteroid transcriptional factor. It is part of a highly regulated and complex system influencing many aspects of metabolism and immune function. There are several feedback and feedforward pathways that influence the levels of various vitamin D forms that Marshall reviewed in depth.1

Marshall was recently invited to co-chair a session on vitamin D at the 6th Annual International Autoimmunity Conference, and he gave one of the keynote presentations of the session.6 Several other presentations were given that support the protocol and model. For example, Perez presented data on treatment response in 20 autoimmune conditions that support Marshall's model.11 The autoimmune diseases successfully treated in this open-label trial include rheumatoid arthritis, systemic lupus erythematosis, diabetes type 1 and 2, psoriasis, Hashimoto's thyroiditis, Sjogren's syndrome, scleroderma, uveitis, myasthenia gravis, and ankylosing spondylitis. Chronic fatigue syndrome and fibromyalgia were shown to respond to the protocol in another presentation.17 And another study indicated that dysregulation of nuclear receptors in the endometrium by vitamin D, along with chronic bacterial infection, can help explain the higher prevalence of some autoimmune diseases in women.26

Epidemiological and Short-Term Clinical and Experimental Data
The in silico and clinical data discussed above provide strong evidence for Marshall's model, and some might argue it is more reliable than epidemiological and short-term evidence. It is widely recognized that there are many limitations inherent in epidemiological and short-term experimental data due to difficulties in obtaining relevant and accurate results. Confounding factors and the inability to assess the effects of long-term immune suppression from high levels of vitamin D make the results less reliable.13,21 Experiments using animal models have the problem of genetic differences and different disease causation methods.1,13 Studies of supplementation are often not randomized and thus are subject to unknown confounding factors that may affect the choice to take vitamin D supplements.13 Furthermore, sun exposure is hard to quantify and is often left out of the analyses. Any of the above can lead to invalid conclusions.

Despite this, a number of recent studies that may be relevant will be discussed here to show that there is much independent support for Marshall's model among these types of studies. In addition, some lesser-known aspects of some of the studies used to support a high vitamin D intake will be reviewed, which cast doubt on some of their conclusions.

Cancer and All-Cause Mortality
In the case of cancer prevention, a recent randomized controlled trial of calcium and vitamin D by Lappe et al.27 is used to support vitamin D supplementation. However, it has a number of serious limitations. One problem is the assumption that removing the data from the first year is justified. If one looks at Figure 1, in the article by Lappe et al,27 in which the data from the first year was included, there is very little difference between calcium and vitamin D vs. calcium alone throughout the study period. No group of patients was given vitamin D alone. Also, there is not yet long-term data on incidence, since the study lasted only four years. Any reduced incidence may reflect delay in diagnosis. In addition, long-term survival may not ultimately improve. In fact, patients taking vitamin D might even die sooner (see below). In addition to the above critique, a number of published comments have also taken issue with this trial, pointing to other problems and limitations.9,28

Another recent study29 reported finding barely significant lower cancer rates in premenopausal women (95% confidence interval, 0.42-1.0) who consumed more vitamin D. However, they found a marginally significant higher rate of moderately differentiated tumors in postmenopausal women who had higher vitamin D intake. And since postmenopausal women make up a much higher proportion of breast cancer cases, this is particularly concerning. This is just one example of the rather inconclusive, mixed data on vitamin D supplementation that becomes apparent when the vitamin D studies are looked at as a whole (see Discussion section in ref. 29). Even the benefit for premenopausal women is questionable. Bertone-Johnson et al.30 pointed out a quite plausible rationale for the existence of a bias toward low estrogen in those who choose to take vitamin D supplements.

A number of limitations found in the other studies are used as a basis for supporting vitamin D supplementation. For instance, the data is rarely long-term enough and rarely covers all the effects possible. Although there may be an appearance of benefit in the short-term or for subsets of the populations studied, a large, long-term prospective study showed no effect of 25-D on the overall cancer mortality rate in the long-term.31 Freedman et al.31 even showed a suggestion of a negative effect of higher vitamin D levels. There was a non-significant increase in overall mortality in the two groups with 25-D at higher levels (80 to <100 nmol/L: Risk Ratio = 1.21, 95% CI =0.83 to 1.78; =100 nmol/L: Risk Ratio = 1.35; 95% CI = 0.78 to 2.31, where 100 nmol/L corresponds to about 40 ng/ml).

This is in accord with a study in prostate cancer32 (also see discussion in ref. 21) and one in pancreatic cancer33 that found higher cancer rates when 25-D was high. Cancer rates increased among patients with a 25-D level above approximately 32 ng/ml. Evidence regarding solar radiation and geographical/latitudinal analyses are also used as evidence, yet solar radiation has many other effects besides raising 25-D.34,35 Many other relevant factors, such as pathogen distributions, climate effects on pathogen spread36,37 and host susceptibility,38 diet, and pollution levels also vary with geographical location.

It was recently pointed out in the Bulletin of the World Health Organization that high 25-D has been found to be associated with greater cancer risk in some studies.39 Studies mentioned, included one that found that there was a higher rate of many internal cancers in patients who have a type of skin cancer that is considered to be the best indicator of long-term sun exposure.40 Another study discussed failed to find a geographical pattern that would support a protective effect of increased 25-D.41 On the whole, in these epidemiological studies, the data is mixed and inconsistent, which is to be expected when there are so many unknown confounding factors affecting 25-D levels and disease incidence that may bias the results.13 In addition, a recent large prospective study presented evidence suggesting that circulating 25-D concentrations may be associated with increased risk of aggressive prostate cancer.42 For all types of prostate cancer, the data failed to support the hypothesis that higher vitamin D decreases prostate cancer risk.42

Studies looking at overall mortality benefits of vitamin D are sometimes misleading at first glance. In the large meta-analysis done recently on the effect of vitamin D and calcium on mortality rates,43 the abstract attributes reduced mortality to vitamin D, yet the only statistically significant results were for calcium together with vitamin D. Another serious problem is that most of the studies analyzed in the meta-analysis were only a few years in duration, so long-term effects on mortality and morbidity could not be accurately assessed.

Bone Density, Parathyroid Hormone
Another area that should be re-evaluated is the negative association between parathyroid hormone and 25-D levels. This association is often used to assert that high levels of 25-D (e.g., 40 –50 ng/ml or more) are optimal. Aloia et al.44 has pointed out that the studies that conclude these high levels of vitamin D are needed fail to require adequate calcium intake, and that is why such high levels are suggested. It should also be considered whether both low 25-D and high PTH are due to the disease process rather than the low 25-D causing the elevated PTH. In addition, only a small percentage of patients with low 25-D have elevated PTH. The low 25-D may be indicating a systemic chronic bacterial infection, and the abnormally high PTH levels in a small percentage of patients may merely be pointing to those cases in which bacteria have infected the parathyroid gland to a greater degree.

In a study comparing vitamin D supplementation with calcium supplementation,45 "the effect of calcium on bone loss was blunted in subjects with the highest levels of serum 25OH vitamin D [25-D]." This last finding is supportive of Marshall's in silico work indicating that high 25-D actually blocks the VDR.6,18 The largest meta-analysis so far clearly showed benefit from calcium supplementation; however, benefit for vitamin D was much less clear.46 No significant benefit for fracture risk was found when comparing vitamin D and calcium to calcium alone, though some differences were found between vitamin D levels.

Another factor that needs to be considered is whether immune suppression is the cause of bone density improvement when high vitamin D levels are used. Immunosuppressive drugs that lower TNF-alpha using antibodies can improve bone density by reducing inflammation.47 High levels of vitamin D supplementation can also lower TNF-alpha48 and suppress the immune response. Thus, it is possible that an increase in bone density from vitamin D supplementation could be the result of immune suppression via TNF reduction, rather than correction of a vitamin D deficiency. TNF-lowering drugs such as infliximab (Remicade) increase risk of cancer and tuberculosis. Thus, the desirability of improving bone density through immune suppression is questionable. This immunosuppressive effect of vitamin D may even explain what seems to be a beneficial effect on falls and muscle strength of elevating vitamin D through supplementation.21 This may be only a symptom reduction in the short-term and may be harmful in the long-term due to the immune suppression.

Autoimmune Disease
In the area of autoimmune disease, the data is equally mixed, and sometimes the larger, more recent studies fail to show any effect of vitamin D levels. For example, a recent large study failed to find an association between serum 25-D levels and the incidence of systemic lupus erythematosis and rheumatoid arthritis.49 Research has found that the average age at which patients acquired rheumatoid arthritis is 12 years earlier in Mexico than in Canada and pointed to the possible role of infectious agents in causing the disease.50 And clearly this study does not support the idea that sun exposure is beneficial for rheumatoid arthritis, since Mexico gets far more sun than Canada.

Although some studies in type 2 diabetes have indicated vitamin D supplementation may be preventive,51 these studies were not randomized and thus are subject to many known and unknown confounding factors affecting a parent's decision to give a child supplemental vitamin D.13 And even if it were clearly established that vitamin D supplementation reduced the incidence of diabetes in infants and small children, that would not mean that it would help in established disease or older patients, nor would it necessarily mean it is the optimal way to achieve diabetes prevention and long-term health. The positive response of both type 1 and type 2 diabetes patients to the Marshall Protocol11 indicates research on the role of bacteria in diabetes should be a priority.

Influenza and Colds
It has been proposed that vitamin D levels' decline in winter best accounts for the seasonality of colds and influenza52 and that this potentially supports the need for increased supplementation.52,53 However, new evidence indicates that changes in the viral coat properties can account for the seasonal outbreaks at higher latitudes.36,37 Effects on the airways in dry, cold climates also appear to increase susceptibility to viral and bacterial infections in winter and could contribute to higher winter prevalence of respiratory infections in cold climates.38

Another important point is that the patients being followed on the Marshall Protocol include a number of individuals who report that during the worst period of their chronic illness, they had few or no colds or flu-like illnesses, sometimes for many years at a time. And sometimes this low rate of colds was apparent even years before their illness. This has also been reported in Parkinson's disease, with the decrease in viral respiratory infections also occurring several years before the disease was diagnosed.54 Thus, even if future research were to establish that vitamin D supplementation reduced colds and influenza, this is by no means an adequate argument for its use. The above observations in chronically ill patients indicate that observing a reduction in respiratory viral infections is not always a sign of good overall health.

Indications of Long-Term Negative Effects of Vitamin D Supplementation
Brannon et al.55 pointed out in a recent report from a roundtable discussion of vitamin D data needs that many studies so far have not yet adequately investigated potential negative consequences such as soft tissue calcification. Vitamin D has been implicated in arterial calcification in the past56 as well as other negative effects.13 The report by the roundtable of vitamin D experts expressed concern that many studies may be shortsighted with regard to adverse outcomes.55

A disturbing new study showed a highly significant correlation (p=0.007) between increased vitamin D intake from food and supplements and the volume of brain lesions shown by MRI in elderly adults.57 In the multivariable regression model, vitamin D intake retained its significant correlation with brain lesion volume even after the effects of calcium were statistically removed. However, calcium did not retain a significant independent correlation with the lesions when the study controlled for vitamin D. Thus, the analysis points to vitamin D supplementation as the key factor in higher lesion volume in this study. These types of brain lesions have been linked to adverse effects in many studies, e.g., stroke,58 psychiatric disorders,59,60 brain atrophy,61 and earlier death.62 Interestingly, the levels of vitamin D intake were not particularly high by some standards, with the highest intake estimated at 1015 mg daily (mean of 341 mg), about half coming from supplements and the rest from food.

The correlation between vitamin D intake and brain lesions seems to lend further support to Marshall's work. In another study, the finding that over a three-year period, a small percentage of patients were found to have a slight regression of their brain lesions,63 leaves room for hope that the lesions are potentially reversible. Reversibility would be in accord with the improvement of depression and cognitive deficits and other neurological symptoms reported in patients on the Marshall Protocol.6,64

Elusive Bacterial Pathogens Are Detected with Improved Methods
Over many decades, researchers have reported evidence that hard-to-detect bacterial infections are the cause of many diseases,65,66 including autoimmune disease,65-68 cardiovascular disease,69-71 and even cancer.72-77 Some have noted the recent trend toward finding more infectious causes of disease and suggested this is likely to increase in the coming years.6,71,77-80

Recently, Barry Marshall received the Nobel Prize for discovering that the bacteria Helicobacter pylori causes ulcers. And it is now known that H. pylori is a causal factor in stomach cancer.77

New techniques using 16s ribosomal RNA shotgun sequencing,81,82 as well as more advanced culturing and observational techniques65,66,80,83-85 are suggesting that, up until now, most microbiologists have failed to detect a large percentage of potential disease-causing agents. "Persister" cells have been identified that escape antibiotic treatment.86 Cell wall deficient organisms have long been studied,65-66 and just recently, advances have been made in understanding their structure and in culturing techniques.80 Research is also indicating that a bacterial biofilm-like microbiota of multiple species even exists within human cells.6,8

Bacteria that grow on a surface in a multi-species community, protected by both a biofilm and the combined effect of their individual resistance strategies, have been a growing area of research.79 Bacterial biofilms have been found to cause the non-healing ulcers in diabetics and may be successfully treated using novel approaches, thus reducing the need for limb amputation.88

Other examples of studies detecting unexpected bacterial pathogens include work linking pathogens in amniotic fluid to pre-term birth89 and research showing numerous previously undetected species in the biofilms that coat prosthetic hip joints.82 Many species of bacteria have been in wounds that were previously undetected using older techniques.81 Macfarlane et al.90 used a combination of more advanced techniques to study bacteria in biofilm communities in patients with Barrett's esophagus, a pre-cancerous condition. Their methods revealed significant differences between patients and controls in the types and numbers of bacterial species, differences that were previously undetected using older techniques.

Increasingly, inflammation is observed in chronic diseases ranging from depression to cardiovascular disease and cancer.87 The above trends, when combined with observations of bacteria in numerous diseases6,13,65,66,71,91 and the success of the anti-bacterial protocol developed by Marshall6,8,11,13 suggest an extensive role for previously unidentified chronic bacterial infections.

Research is also supporting the ineffectiveness of most standard antibiotic protocols against these bacteria70 and suggesting why other approaches may work better. For instance, some antibiotics target cell walls, and this actually promotes the production of cell wall deficient forms of bacteria that resist many antibiotics.80 Furthermore, many antibiotics are known to inhibit phagocytosis and other aspects of the immune response when taken at high, constant dosages.92

The ability of bacteriostatic antibiotics such as clindamycin to be effective at low doses has been documented.93,94 The survival of "persister" cells mean that pulsed antibiotics are likely to be more effective.86 And fascinating investigations of biofilm communities have revealed many ways in which bacteria can resist antibiotics when used in traditional ways.95 The existence of communities of many bacterial species means that combinations of antibiotics are probably needed to be effective against all the species present. Thus, there is increasing support for the use of pulsed, low dosages of combinations of bacteriostatic antibiotics as used in the anti-bacterial protocol discussed here.

What is particularly encouraging is that the effectiveness of Marshall's protocol in many systemic chronic disease indicates that these elusive pathogens do respond to select currently available bacteriostatic antibiotics when innate immune function is restored through restoring vitamin D receptor function.6,11 Not only do the bacterial infections appear to resolve, the evidence so far suggests that the improved immune response leads to reduced viral, fungal, and protozoal infections as well.

In silico and clinical data indicate that it is likely that associations between low vitamin D levels and chronic diseases are not evidence of deficiency, but result from a bacteria-induced blockage of the vitamin D receptor, leading to down-regulation of 25-D levels.1,6 According to this model of chronic disease, the short-term benefits sometimes perceived with high vitamin D levels are not due to correction of a vitamin D deficiency but due to suppression of bacterial killing and the immunopathological reaction that accompanies it. Data on reversal of a range of inflammatory and autoimmune diseases through an anti-bacterial protocol that includes vitamin D avoidance and a VDR agonist support this view.6,11

As discussed in detail above, it appears that increasing vitamin D supplementation is not the answer to these chronic diseases and is likely to be counter-productive. Other researchers have also raised concerns regarding vitamin D supplementation's potential adverse effects. Potential dangers include increased aortic calcification55,56 and brain lesions shown by MRI57 (also see above). In addition, some studies have even found evidence of increased danger from cancer in association with higher levels of vitamin D.32,33,39,40,42

Many have been attracted to the area of vitamin D research, recognizing interesting patterns and responses to supplementation that at first seemed to indicate widespread deficiency and, at the very least, indicate that vitamin D plays a powerful role in physiological processes. Great strides have been made in the last 30 years by scientists with a range of perspectives, and this has led to great excitement and a laudable commitment to use that knowledge to help patients.

However, new genomic and molecular research and the positive response to a new anti-bacterial protocol that involves the avoidance of vitamin D indicate the need for a reappraisal of the data gathered so far. It appears that attempting to raise 25-D through vitamin D supplementation or sun exposure is not the right approach to many, if not most, common chronic diseases. Instead, as discussed above, the evidence supports the effectiveness of a new protocol in restoring vitamin D receptor function, which appears to be a crucial factor in recovery.

One of the most commendable attributes of a truly objective scientist is the willingness to be open to changing long-held positions in the light of new evidence. It will be interesting to see how many have this all-too-rare quality, as research and discussion of vitamin D and the VDR continues. It is to be hoped that the tremendous healing potential likely to be available from eliminating the pathogens that cause chronic disease will inspire an especially high level of open-minded discussion and cooperation.

Caution: The immunopathological reactions from killing the high levels of bacteria that have accumulated in chronically ill patients can be severe and even life-threatening, and thus the Marshall Protocol must be done very carefully and slowly, according to the guidelines.7,96 For the sake of safety, antibiotics must be started at quite low dosages, starting with only one antibiotic. Health care providers are responsible for the use of this information. Neither Autoimmunity Research, Inc., nor the author assume responsibility for the use or misuse of this protocol.

Note: Neither the author, Prof. Marshall, nor the non-profit Autoimmunity Research, Inc. have any financial connection with any product or lab mentioned with regard to the Marshall Protocol. The information needed to implement the Marshall Protocol is available free of charge from

Joyce Waterhouse, PhD, graduated from the University of California, Irvine, cum laude and Phi Beta Kappa, with a bachelor's in Biology. Dr. Waterhouse received a PhD in Systems Ecology with a minor in Statistics from the University of Tennessee, Knoxville. She then pursued postdoctoral research at Oak Ridge National Laboratory. Since 1997, she has written for and edited an online newsletter focused on chronic illness: CISRA's Synergy Health Newsletter ( She has written a number of articles for peer-reviewed journals, written a chapter in the book, Vitamin D: New Research, and is currently a volunteer Research Scientist with the non-profit Autoimmunity Research, Inc.

(For further links to Dr. Marshall's papers and presentations and those of his colleagues, see:

(1) Marshall TG. Vitamin D discovery outpaces FDA decision making.
Bioessays. 2008; 30:173-82. Available at:
(2) Kimball SM, Ursell MR, O'Connor P, Vieth R. Safety of vitamin D3 in adults with multiple sclerosis.
Am J Clin Nutr. 2007;86(3):645-51.
(3) Cutolo M, Otsa K, Laas K, Yprus M, Lehtme R, Secchi ME, Sulli A, Paolino S, Seriolo B. Circannual vitamin D serum levels and disease activity in rheumatoid arthritis: Northern versus Southern Europe.
Clin Exp Rheumatol. 2006 Nov-Dec;24(6):702-4.
(4) Cutolo M. Vitamin D and autoimmune rheumatic diseases. 6th International Congress on Autoimmunity, Porto, Portugal, 2008.
(5) Goldberg P, Fleming MC, Picard EH. Multiple sclerosis: decreased relapse rate through dietary supplementation with calcium, magnesium and vitamin D.
Med Hypotheses. 1986 Oct;21(2):193-200.
(6) Marshall TG. Presentation. VDR receptor competence induces recovery from chronic autoimmune disease, 6th International Congress on Autoimmunity, Porto, Portugal. 2008, (video: available at:
(7) Waterhouse JC. The Marshall Protocol for Lyme disease and other chronic inflammatory conditions: Part One. Overview and implementation.
Townsend Letter. 2007 Mar;285:85-92. (8) Waterhouse JC. The Marshall Protocol for Lyme disease and other chronic inflammatory conditions, Part Two: Scientific background, data, and case histories. Townsend Letter. 2007 Apr;286:84-90.
(9) Davis CD. Vitamin D and cancer: current dilemmas and future research needs.
Am J Clin Nutr. 2008 Aug;88(2):565S-569S.
(10) Mordan-McCombs S, Valrance M, Zinser G, Tenniswood M, Welsh J. Calcium, vitamin D and the vitamin D receptor: impact on prostate and breast cancer in preclinical models.
Nutr Rev. 2007 Aug;65(8 Pt 2):S131-3.
(11) Waterhouse JC, Perez TH, Albert P, Proal A. Presentation. Bacteria-induced vitamin D receptor dysfunction in autoimmune disease: theoretical and practical implications for interpretation of serum vitamin D metabolite levels, 6th International Congress on Autoimmunity, Porto, Portugal, 2008. (Video: Available at: Data: Available at :
(12) Marshall TG, Marshall FE. Sarcoidosis succumbs to antibiotics – Implications for autoimmune disease.
Autoimmun Rev. 2004; 3(4):295-300.
(13) Waterhouse JC, Marshall TG, Fenter B, Mangin M, Blaney G. High levels of active 1,25-dihydroxyvitamin D despite low levels of the 25-hydroxyvitamin D precursor – Implications of dysregulated vitamin D for diagnosis and treatment of chronic disease. In: Stoltz VD, ed.
Vitamin D: New Research. New York: Nova Science Publishers; 2006:1-23.
(14) Arasaki K. Presentation. Report on a case of systemic sarcoidosis treated according to the Marshall Protocol. The 26th Conference of the Japan Society of Sarcoidosis and Other Granulomatous Diseases. Oct. 2006, Available at:
(15) Brahmachary M, Schönbach C, Yang L, Huang E, Tan SL, Chowdhary R, Krishnan SP, Lin CY, Hume DA, Kai C, Kawai J, Carninci P, Hayashizaki Y, Bajic VB. Computational promoter analysis of mouse, rat and human antimicrobial peptide-coding genes.
BMC Bioinformatics. 2007; 18;7 Suppl 5:S8.
(16) Blaney GP. Presentation. Vitamin D metabolites as clinical markers in autoimmune and chronic illness, 6th International Congress on Autoimmunity, Porto, Portugal, 2008. (Video: Available at:
(17) Mangin M. Presentation. Monitoring recovery from autoimmune disease with an interactive, internet-based clinical trial based on a molecular model of chronic disease. 6th International Congress on Autoimmunity, Porto, Portugal, 2008.
(18) Marshall TG. VDR nuclear receptor competence is the key to recovery from chronic inflammatory and autoimmune disease. Presentation. Days of Molecular Medicine 2006. Available at:
(19) Reinholz GG, DeLuca HF. Inhibition of 25-hydroxyvitamin D3 production by 1, 25-dihydroxyvitamin D3 in rats.
Arch Biochem Biophys. 1998;355:77-83.
(20) Bell NH, Shaw S, Turner RT. Evidence that 1,25-dihydroxyvitamin D3 inhibits the hepatic production of 25-hydroxyvitamin D in man.
J Clin Invest. 1984 Oct;74(4):1540-4.
(21) Waterhouse JC. Vitamins D in chronic disease. Presentation. Recovery from Chronic Disease Conference, Autoimmunity Research Inc., Los Angeles, California, 2006. Available at:
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