Vitamin D controls over 75% of the human genome, playing a major role as the master gene regulator of nuclear receptors, including the vitamin D receptor (VDR). The VDR is suppressed by the high stored vitamin 25(OH) D3 levels found in supplements and vitamin D enriched food supplies in the U.S. It is now proposed that these resulting elevated vitamin D levels are leading to the current epidemic in chronic degenerative diseases, including autoimmune disease, heart disease, cancer and obesity.

Vitamin D from sunshine does not have the same immunosuppressive effect. Low levels of 25 (OH)D (31.6 ng/ml is found among healthy young adult Hawaiian surfers (Binkley et al., 2007).

It takes relatively little sunlight exposure to acquire adequate stores of vitamin D. Ten to 15 minutes of sunlight to a small area of skin twice a week, without sunscreen supplies all the vitamin D necessary for health. Vitamin D is a fat soluble vitamin and stores easily for the times it is not actively being produced by UV exposure. 27 (National Institutes of Health, 2014). Over 90% of UV rays penetrate clouds (Rehfuess & World Health Organization., 2002) and UV-B penetration equals or exceeds penetration at the equator, refuting a 1988 study (Webb, Kline, & Holick, 1988) often cited to support that latitude influences the amount of solar radiation   available to synthesize vitamin D3 (Rehfuess & World Health Organization., 2002).

Rickets is often cited as a condition linked to low vitamin D. However, adequate calcium is equally important because low calcium leads to hyperparathyroidism and high loss of phosphorus (Tiosano & Hochberg, 2009). Children in developing countries develop rickets if poverty prevents them from eating enough calcium rich foods (Lerch & Meissner, 2007). Rickets occurs in sunny countries due to poor calcium intake and is cured with increased nutritional calcium intake (Pettifor, 2004).


Vitamin D3 dysregulation can be identified by rising levels of active vitamin D (1-25 D) and lower levels of inactive vitamin D (25-D).

(Blaney, Albert, & Proal, 2009)


Low levels of stored vitamin D3 designated as 25OH D is found in both healthy persons and those with autoimmune or chronic inflammatory diseases. Assessing vitamin D3 status requires the additional measurement of 1, 25 (OH) 2 D. In the absence of disease, the low stored form 25OH D is normal (Mangin et al., 2014). This exposes a common faulty medical assumption that “association equals causation”, leading to the erroneous diagnosis that low levels of stored vitamin D3 are the cause of Vitamin D related disease conditions. Trevor Marshall PhD, and many other medical researchers, are demonstrating the overlooked role of elevated levels of active 1, 25 (OH) 2 D3 in suppressing the immune system and worsening existing infections. The ongoing rapid conversion of active vitamin D3 to stored vitamin D3 keeps the commonly measured stored vitamin D levels low.

Vitamin D plays a dual role in VDR control, acting as either stimulatory or suppressive. The active form, 1, 25 (OH) 2D3 regulates the vitamin D receptors in the small intestine, reabsorption of calcium by the kidneys, and resorption of calcium in bones. Elevated active D3 may cause calcium and phosphorus absorption to be impaired (Boden & Kaplan, 1990). Elevated 1, 25 (OH) 2 D3 therefore leads to bone loss. Above 42 pg/mL 1,OH)2D stimulates osteoclasts leading to osteoporosis, dental fractures (Brot, Jørgensen, Madsen, Jensen, & Sørensen, 1999), and  a combination of high 1,25(OH)2D and low 25(OH)Vit D is associated with the poorest bone health (Vanderschueren et al., 2013).

Normal levels of active vitamin 1, 25 (OH) 2 D3 act as a potent activator of the innate immune system. Innate immunity represents the first line of defense against microbial invasion. You need this form of Vitamin D to be doing its job (Quraishi & Camargo, 2012). On the other hand, high levels of active D3 inhibit adaptive immunity through both T and B lymphocytes needed to balance and reduce the severity of inflammatory and autoimmune disease (J. H. White, 2012).

A clinical sign of dysregulated vitamin D metabolism is elevated  active D3/1,25(OH)2D, often accompanied by reduced stored D3/ 25(OH)D reflecting that the immune system is competing with parasitic microbes such as L forms for VDR dominance. Failure of the immune system to mount an effective anti-microbial response results in chronic long term intracellular infection. The resultant  inflammation (immunopathology) causes tissue damage and disease symptoms  (Mangin et al., 2014).


Vitamin D is a secosteroid molecule with a chemical structure almost identical to cholesterol, closely resembling the structure of the immune suppressing steroids.

Vitamin D3 is regulated more like a steroid than a nutrient (Pérez-López, 2007). The short term benefits of taking high doses of vitamin D are a result of further suppression of the immune reaction of killing pathological bacteria. Increasing vitamin D supplementation is likely to be counter-productive, allowing pathogens to proliferate and cause further inflammation.

D3 it is rapidly broken down by the enzyme 24-hydroxylase, making it clinically unmeasurable at normal physiological conditions. During immune suppression, high levels of active D3 seep into the blood stream and therefore these levels are measurably elevated.

Vitamin D dysregulation can be measured by rising levels of the active level of active D3, abbreviated at vitamin D (1-25 D) and lower levels of inactive vitamin D3, abbreviated as D(25-D) (Blaney et al., 2009). The resulting elevated levels of active vitamin D can interfere with receptors for male hormones, corticosteroids and thyroid hormones (Proal, Albert, & Marshall, 2009). Profound immune suppression results as the ability of these receptors are no longer able to express antimicrobial proteins as a result of VDR regulation (Brahmachary et al., 2006).


Many of the pathogens that contribute to chronic inflammatory disease live inside immune cells such as macrophages. These intracellular microbes directly interfere with Vitamin D nuclear receptor biology. This compromising of DNA function drives the systemic breakdown of the immune system, resulting in inflammatory disease (Xu et al., 2003).

Blocking of the VDRs results in high active Vitamin 1-25(OH) 2 D3 in the circulating blood. (Blaney et al., 2009).


Infected tissues become inflamed and attempt to overcome the blockage of the VDR by increasing enzymatic transformation of stored D3 referred to as 25(OH)2 into active D3/1-25(OH)2D to overcome the VDR suppression. The active vitamin D3 levels of the steroidal form of vitamin D3 will rise to toxic levels, seeping into the blood steam at measurable increases. The elevated titers of active D3 are now suppressing the immune system. Since the active form of D3 is not typically measured by blood tests, this condition is not properly diagnosed or treated. A weakened immune system and the use of antibiotics both lead to the formation of the L-form bacteria is creating a growing concern for the current epidemic of chronic disease in the U.S. The inability to raise inactive vitamin D levels indicates problems with active D3 and L form bacteria. Health care providers are therefore well advised to always test both types of vitamin 25 OH and 1-25 OH2 D3.

Medical conditions resulting from damaged vitamin D receptors (VDRs) adapted from (Sundar & Rahman, 2011).


Vitamin D is implicated in many disease states including chronic muscular skeletal pains, diabetes I and II, MS, cardiovascular disease, osteoporosis, breast cancer, prostate and colon cancer. Most cells and tissues in the body have vitamin D receptors (VDRs) that stimulate the nuclear transcription of various genes to alter cellular function or provide a rapid response in cellular membrane.

VDR dysregulation is reflected in rising levels of the active 1, 25(OH)2D3 and lower levels of the inactive 25(OH)2 D3 (Blaney et al., 2009), as the stored vitamin is converted to the active form.

If the VDR receptor is blocked by L- form bacteria or is mutated genetically, your health is seriously impacted.

The illustration below describes how environmental assaults affect the VDR and in turn result in many of our chronic diseases.



Vitamin D proponents have failed to recognize that many of the positive effects of vitamin D are due to the immunosuppressive effect of elevated 25(OH) D3or to make the connection with the fact that immunosuppression is contraindicated because of the probable presence of intracellular infection underlying autoimmune disorders. When the immune system is suppressed, clinical disease markers and symptoms are reduced but immunosuppression does not address an underlying cause of persistent bacteria, thus relapse is common (H. M. Kim, Chung, & Chung, 2010).

Much of current research focuses on finding drugs to suppress inflammation associated with autoimmune disease (Collins, 2011), 95 % of these studies have failed to find drugs to suppress inflammation. It seems clear a better direction is needed. Immunotherapy which restores VDR competence, corrects dysregulated vitamin D metabolism and eliminates intracellular bacteria could be the answer.

Studies report that Vitamin D appears to have a positive effect on autoimmune disease due to immune system suppression (Griffin, Xing, & Kumar, 2003).

Immune suppression is behind the proposed positive effect, as vitamin D inhibits LPS bacterial activation and cytokine production in monocytes/macrophages (Y. Zhang et al., 2012).

Encouraging use of vitamin D and touting the benefits of Immune suppression, is still considered by “experts” to be therapeutically beneficial for autoimmune diseases (Böhm, Luger, Schneider, Schwarz, & Kuhn, 2006).

The current medical model buys into these studies, causing poor treatment protocols and widening the gap between treatment and effective outcome. Vitamin D is frequently prescribed by rheumatologists to prevent and treat osteoporosis. Several observations have shown that vitamin D inhibits proinflammatory processes by suppressing the enhanced activity of immune cells that take part in the autoimmune reaction (Ishizawa et al., 2008).

This information supports a health restoration protocol that includes the discontinuance of vitamin D3 supplements in the treatment of these conditions.


The current recommendations for adequate vitamin D3 and lab normal ranges are based on levels found in unhealthy populations. These populations are over supplemented, overweight, undernourished, immune suppressed and toxic study subjects. This “madness” must be ended if we are to change healthcare and the poor outcomes of our overpriced so called healthcare system. New research is now revising the current medically recommended levels.

Vitamin D supplementation makes autoimmune disease worse due to its steroidal suppressive effect on the immune system (Y. Zhang et al., 2012). However, vitamin D proponents have failed to recognize that these suppressive effects are due to the immunosuppressive effect of elevated 25(OH) D and seemingly fail to grasp the scientifically backed fact this very same immunosuppression is contraindicated because of the probable presence of intracellular infection. When the immune system is suppressed, clinical disease markers and symptoms are reduced but immunosuppression does not address an underlying cause of persistent bacteria, thus relapse is common (H. M. Kim et al., 2010). Unfortunately, immune suppression is considered therapeutically beneficial for autoimmune diseases (Arnson, Amital, & Shoenfeld, 2007).

High levels, not low levels of Vitamin D are associated with autoimmune disease which does not follow our model for Vitamin D being protective. Elevated levels of serum Vitamin D3 were found in 85% of patients in the Pacific Northwest diagnosed with autoimmune disease. The treatment of inflammatory disease had poor result with the use of vitamin D supplementation over long periods of time (Blaney et al., 2009).

This can be explained as the result of the presence of L forms. High levels of 1,25-D result when dysregulation of the VDR by bacterial ligands prevents the receptor from expressing enzymes necessary to keep 1,25-D in a normal range (Blaney et al., 2009).



Why are levels of Vitamin D3 often elevated in patients with autoimmune diagnosis when we expect them to be low? When inflammation goes down, we see that the active levels of vitamin drop into a normal range. The active 1,25-D rather than  the stored 25-D serves as a more accurate measure of a chronic inflammatory disease state (Blaney et al., 2009).  In the presence of L-form bacteria and a compromised immune system, the tissues start to convert any stored D3 to active D3, making the active D3 elevated in the blood as overflows from the tissues. Unlike a healthy state, this tissue dominance of D3 production, in not regulated by the kidneys and requires a unique approach to measurement and analysis.

This is the result of tissue cells producing high levels of the steroid active vitamin D in an effort to stimulate the VDR which are blocked by the L-form bacteria, the stored form of vitamin D can be low or negligible. It is important to measure the active vitamin D3 as well as the stored vitamin D count. An abnormal ratio of stored to active D3 ratio will tell the story. Do not supplement Vitamin D until ratios normalize as steroidal vitamin D suppresses the immune system and leads to higher levels of infection (Blaney et al., 2009).