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Is the MP Treatment for Sarcoidosis Helpful for Other Chronic Diseases? MP's Vitamin D Theories Are Not Supported by Lab Studies. Updated July 2, 2008 "The MP treatment plan was originally designed to treat an inflammatory condition known as sarcoidosis. The treatment consists of using the drug Benicar, combined with the avoidance of all sources of vitamin D, and eventually adding various antibiotics, especially minocycline. After being used by sarcoidosis patients for some years, it was then theorized and claimed that the treatment could treat other inflammatory conditions. Eventually it was also claimed that it could treat fibromyalgia and CFS, conditions which are not recognized by the medical literature as being inflammatory in nature. "

Measurement of vitamin D levels in inflammatory bowel disease patients reveals a subset of Crohn's disease patients with elevated 1,25-dihydroxyvitamin D and low bone mineral density. Abreu MT, Kantorovich V, Vasiliauskas EA, Gruntmanis U, Matuk R, Daigle K, Chen S, Zehnder D, Lin YC, Yang H, Hewison M, Adams JS. Gut. 2004 Aug;53(8):1129-36. PMID: 15247180 doi: 10.1136/gut.2003.036657. Conclusions: These data demonstrate that elevated 1,25(OH)2D is more common in CD than previously appreciated and is independently associated with low bone mineral density. The source of the active vitamin D may be the inflamed intestine. Treatment of the underlying inflammation may improve metabolic bone disease in this subgroup of patients.

Vitamin D and calcium insufficiency-related chronic diseases: molecular and cellular pathophysiology. Peterlik M, Cross HS. Eur J Clin Nutr. 2009 Dec;63(12):1377-86. Epub 2009 Sep 2. PMID: 19724293 doi:10.1038/ejcn.2009.105 A compromised vitamin D status, characterized by low 25-hydroxyvitamin D (25-(OH)D) serum levels, and a nutritional calcium deficit are widely encountered in European and North American countries, independent of age or gender. Both conditions are linked to the pathogenesis of many degenerative, malignant, inflammatory and metabolic diseases. Studies on tissue-specific expression and activity of vitamin D metabolizing enzymes, 25-(OH)D-1alpha-hydroxylase and 25-(OH)D-24-hydroxylase, and of the extracellular calcium-sensing receptor (CaR) have led to the understanding of how, in non-renal tissues and cellular systems, locally produced 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) and extracellular Ca2+ act jointly as key regulators of cellular proliferation, differentiation and function. Impairment of cooperative signalling from the 1,25-(OH)2D3-activated vitamin D receptor (VDR) and from the CaR in vitamin D and calcium insufficiency causes cellular dysfunction in many organs and biological systems, and, therefore, increases the risk of diseases, particularly of osteoporosis, colorectal and breast cancer, inflammatory bowel disease, insulin-dependent diabetes mellitus type I, metabolic syndrome, diabetes mellitus type II, hypertension and cardiovascular disease. Understanding the underlying molecular and cellular processes provides a rationale for advocating adequate intake of vitamin D and calcium in all populations, thereby preventing many chronic diseases worldwide.

[Low levels of 25-hydroxyvitamin D (25OHD) in patients with inflammatory bowel disease and its correlation with bone mineral density] Souza HN, Lora FL, Kulak CA, Mañas NC, Amarante HM, Borba VZ. Arq Bras Endocrinol Metabol. 2008 Jun;52(4):684-91. Portuguese. PMID: 18604382

A German group has now shown that the important inflammatory marker, tumor necrosis factor (TNF), is also reduced by vitamin D supplementation. Many studies have implicated increased TNF levels in promoting cancer. In this study, a modest vitamin D dose of 3320 units (83 micrograms) was given vs. placebo. The 25-hydroxy D level reached in the treated group was 34.2 ng/ml (85.5 nmol/L), which resulted in a 26.5% reduction in TNF compared with 18.7% reduction (?) in the placebo group.

Vitamin D in preventive medicine: are we ignoring the evidence? Zittermann A. Br J Nutr. 2003 May;89(5):552-72. Review. PMID: 12720576 Vitamin D is metabolised by a hepatic 25-hydroxylase into 25-hydroxyvitamin D (25(OH)D) and by a renal 1alpha-hydroxylase into the vitamin D hormone calcitriol. Calcitriol receptors are present in more than thirty different tissues. Apart from the kidney, several tissues also possess the enzyme 1alpha-hydroxylase, which is able to use circulating 25(OH)D as a substrate. Serum levels of 25(OH)D are the best indicator to assess vitamin D deficiency, insufficiency, hypovitaminosis, adequacy, and toxicity. European children and young adults often have circulating 25(OH)D levels in the insufficiency range during wintertime. Elderly subjects have mean 25(OH)D levels in the insufficiency range throughout the year. In institutionalized subjects 25(OH)D levels are often in the deficiency range. There is now general agreement that a low vitamin D status is involved in the pathogenesis of osteoporosis. Moreover, vitamin D insufficiency can lead to a disturbed muscle function. Epidemiological data also indicate a low vitamin D status in tuberculosis, rheumatoid arthritis, multiple sclerosis, inflammatory bowel diseases, hypertension, and specific types of cancer. Some intervention trials have demonstrated that supplementation with vitamin D or its metabolites is able: (i) to reduce blood pressure in hypertensive patients; (ii) to improve blood glucose levels in diabetics; (iii) to improve symptoms of rheumatoid arthritis and multiple sclerosis. The oral dose necessary to achieve adequate serum 25(OH)D levels is probably much higher than the current recommendations of 5-15 microg/d.

Serum 25-hydroxyvitamin D3 concentrations and carotid artery intima-media thickness among type 2 diabetic patients. Targher G, Bertolini L, Padovani R, Zenari L, Scala L, Cigolini M, Arcaro G. Clin Endocrinol (Oxf). 2006 Nov;65(5):593-7. PMID: 17054459 DOI: 10.1111/j.1365-2265.2006.02633.x CONCLUSIONS: Hypovitaminosis D is highly prevalent in type 2 diabetic adults and is strongly and independently associated with increased carotid IMT. Further investigation into whether vitamin D may play a role in the prevention of atherosclerosis appears to be warranted. In conclusion, our results show that type 2 diabetic adults have significant reductions in serum 25(OH)D concentrations (vs matched controls) that predict preclinical atherosclerosis, independent of classical risk factors, renal function tests, inflammatory markers, use of medications and presence of the metabolic syndrome. These findings suggest the need for ongoing evaluation of the possible protective role of vitamin D3 supplementation in the development of atherosclerosis.

Now a new and controversial book by an American doctor suggests that taking even higher levels of the vitamin - 10 to 15 times the recommended amounts - can work wonders. Dr James Dowd, who works at the Arthritis Institute of Michigan, has been prescribing vitamin D to people suffering from chronic disorders such as arthritis, back pain and headaches and the result, he claims, is a huge improvement in their symptoms. In his book, The Vitamin D Cure, Dr Dowd describes a number of success stories using this approach. One of his patients, Barbara, for instance, was obese, and suffered from arthritis in one leg as well as high blood pressure. As Dowd explains: "In the past I would have given her anti-inflammatory drugs, pain medication, a pill to lose weight and drug treatment for hypertension."

Conclusion We demonstrated that the VDRE in the CAMP gene originated from the exaptation of an AluSx SINE in the lineage leading to humans, apes, OWMs and NWMs and remained under purifying selection for the last 55-60 million years. We present convincing evidence of an evolutionarily fixed, Alu-mediated divergence in steroid hormone nuclear receptor gene regulation between humans/primates and other mammals. Evolutionary selection to place the primate CAMP gene under regulation of the vitamin D pathway potentiates the innate immune response and may counter the anti-inflammatory properties of vitamin D. Exaptation of an ancient Alu short interspersed element provides a highly conserved vitamin D-mediated innate immune response in humans and primates. Gombart AF, Saito T, Koeffler HP. BMC Genomics. 2009 Jul 16;10:321. PMID: 19607716 doi:10.1186/1471-2164-10-321

Serum tumor necrosis factor-alpha concentrations are negatively correlated with serum 25(OH)D concentrations in healthy women. Peterson CA, Heffernan ME. J Inflamm (Lond). 2008 Jul 24;5:10. PMID: 18652680 doi:10.1186/1476-9255-5-10 Conclusion Serum 25(OH)D status is inversely related to TNF-α concentrations in healthy women, which may in part explain this vitamin's role in the prevention and treatment of inflammatory diseases. Results gleaned from this investigation also support the need to re-examine the biological basis for determining optimal vitamin D status.

Hypovitaminosis D among rheumatology outpatients in clinical practice.\nMouyis M, Ostor AJ, Crisp AJ, Ginawi A, Halsall DJ, Shenker N, Poole KE.\nRheumatology (Oxford). 2008 Sep;47(9):1348-51. Epub 2008 May 22.\nPMID: 18499714 \ndoi:10.1093/rheumatology/ken203

I stumbled on one of the growing number of local media stories on the power of vitamin D. \nIn one story, a purported "expert" was talking about the benefits of "high-dose" vitamin D, meaning up to 1000, even 2000 units per day. \nI regard this as high-dose---for an infant. \nJudging by my experiences, now numbering well over 1000 patients over three years time, I'd regard this dose range not as "high dose," nor moderate dose, perhaps not even low dose. I'd regard it as barely adequate.