Patients who have been on IT (or a similar treatment) for several years should monitor 1,25-D annually to make sure it hasn't become too low due to avoidance of vitamin D sources. A reasonable level of 25-D (8-15 ng/ml) should be maintained to ensure adequate production of 1,25-D (23-37 pg/ml) which is essential for many essential metabolic functions.

We hope you find our latest newsletter helpful, whether you're on Inflammation Therapy (IT) or still exploring your treatment options.

IT is tailored to individual patient response, in order to increase treatment effectiveness and safety. At CIR, we're always looking for ways to make the recovery process easier for both medical practitioners and patients.

Our Physician's Guide to Inflammation Therapy is available to your doctor free of charge upon request via email, fax or toll-free phone number. Visit our website for details.

Our Patient's Introduction to Inflammation Therapy helps patients manage their own day-to-day care. For information on obtaining a copy, please see 'CIR Library Access' in the sidebar of this newsletter.

Being responsive to the needs of both medical practitioners and

patients is important to us. If you'd like to provide us with feedback or suggestions about IT and/or CIR, please send us an email.

We'd love to hear from you.

Warm regards,

Optimal Level of Vitamin D

Vitamin D (i.e., 25-hydroxyvitamin-D or 25OHD or 25-D) is synthesized in the kerotinocytes of the skin in reaction to sunlight.  25-D may also be obtained from naturally occurring dietary sources, processed foods that are supplemented with vitamin D, and vitamin D supplements.

There is no Recommended Daily Allowance (RDA) for vitamin D because it is endogenously produced by humans in the presence of a few minutes of sunlight. The alternative Recommended Dietary Intake (RDI) of nutritional vitamin D is based on the absence of adequate sunlight. However, as long as humans have access to minimal sunlight several months of the year, they will not become deficient in vitamin D because the body stores it for later use and it has a half-life of 2-6 months.  

Kimlin et al. (2007), using computer modeling, concluded it may no longer be correct to assume that vitamin D levels in populations follow latitude gradients.  Geophysical surveys have shown that UVB penetration over 24 hours, during the summer months at Canadian north latitudes when there are many hours of sunlight, equals or exceeds UVB penetration at the equator. [1.]

Sunscreens are used to protect the skin from ultraviolet radiation (UVA and UVB) waveband exposure that is associated with deoxyribonucleic acid (DNA) damage-the same UVB exposure that is needed for vitamin D synthesis.  Experimental studies (Misra et al., 2008) suggest that sunscreens can decrease cutaneous vitamin D synthesis. However, emerging evidence (Diehl and Chiu, 2010 and Springbett et al., 2010) suggests that although sunscreens are effective, many may not actually be blocking UVB radiation because they are improperly or inadequately applied. Thus, sunscreen use may not actually diminish vitamin D synthesis in real world use, although further study is needed to verify its actual impact. [2.]  

According to a 2011 report from the Food and Nutrition Board,

"Of great concern recently have been the reports of widespread vitamin D deficiency in the North American population. Based on this committee's work and as discussed below, the concern is not well founded. In fact, the cut-point values used to define deficiency, or as some have suggested, "insufficiency," have not been established systematically using data from studies of good quality. Nor have values to be used for such determinations been agreed upon by consensus within the scientific community."  [3.]   

An association between low vitamin D levels and disease states has been noted, but no cause-and-effect relationship has been found. Unfortunately, doctors and scientists have misinterpreted the results of epidemiological studies because they just measure the inert form of vitamin D (25-D). Only a study that measures both 25-D and 1,25-dyhydroxyvitamin-D (the active metabolite), with an understanding of their relationship to each other in health and disease, will yield pertinent results.

Researchers fail to recognize that vitamin D metabolism can be dysregulated by intra-phagocytic bacteria. These L-forms and biofilms produce substances which inactivate the Vitamin D Receptor (VDR), a key component of the innate immune system, so they can proliferate undetected inside cellular cytoplasm.

In an attempt to activate the VDR and kill the bacteria, infected macrophages release inflammatory cytokines which transcribe Protein Kinase A (PKA) to activate the enzyme CYP27b1 which causes 25-D to be converted into 1,25-D; the result is low (depleted) 25-D and elevated (excess) 1,25-D. Thus, the disease process causes low 25-D; low 25-D doesn't cause disease.

Supplementation with vitamin D to try to prevent diseases or resolve inflammatory symptoms is an alarming trend; emerging evidence suggests that vitamin D may be harmful at levels which can be reached through the use of supplements. A United States Institute of Medicine report states: "Outcomes related to cancer, cardiovascular disease and hypertension, diabetes and metabolic syndrome, falls and physical performance, immune functioning and autoimmune disorders, infections, neuropsychological functioning, and preeclampsia could not be linked reliably with calcium or vitamin D intake and were often conflicting." [4.]   

A recent study found that if blood contains less than 2.5 ng/mL of 25-D (6.24 nmol/L), mortality is 2.31 times higher. However, if the blood contains more than 56 ng/mL of 25-D (139.7 nmol/L), mortality is higher by a factor of 1.42. Both values were compared to 20 ng/mL of 25-D (49.9 nmol/L), where the scientists saw the lowest mortality rate. [5.]

Patients in both categories are statistically more likely to succumb to chronic illness.