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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.

Vitamin D toxicity redefined: vitamin K and the molecular mechanism. Masterjohn C. Med Hypotheses. 2007;68(5):1026-34. Epub 2006 Dec 4. PMID: 17145139 doi:10.1016/j.mehy.2006.09.051

Vitamin D: the alternative hypothesis. Albert PJ, Proal AD, Marshall TG. Autoimmun Rev. 2009 Jul;8(8):639-44. Epub 2009 Feb 12. Review. PMID: 19393200 Emerging molecular evidence suggests that symptomatic improvements among those administered vitamin D is the result of 25-D's ability to temper bacterial-induced inflammation by slowing VDR activity. While this results in short-term palliation, persistent pathogens that may influence disease progression, proliferate over the long-term.

"Hi! This is Amy Proal. I wrote the article referenced at the start of the thread about vitamin D. Dr. Marshall is not concerned with vitamin D toxicity. Rather his molecular modeling research has clarified the actions of the two vitamin D metabolites 25-D and 1,25-D. The Vitamin D Receptor (VDR) is a fundamental receptor of the body - it controls the expression thousands of genes, as well as the activity of the innate immune system and the antimicrobial peptides. If you think of the VDR as a switch, 25-D (which is a corticosteroid) turns it off (inactivates it) and 1,25-D turn it on (activates it). What is commonly believed among vitamin D researchers is that if people supplement with extra vitamin D it will be converted into 1,25-D and activate the VDR. Unfortunately, Marshall's work revealed that the type of vitamin D derived from supplements and sun remains, for the most part, in it's precursor form 25-D. This means that the extra vitamin D we get from fortified food products and supplements is turning the VDR off, not on. That causes a decrease in immune function and gene transcription."

"Vitamin D-dependent calcium binding proteins were discovered in the cytosolic fractions of chicken intestine, and later in mammalian intestine and kidney, by workers including Robert Wasserman of Cornell University. They bound calcium in the micromolar range and were greatly reduced in vitamin D-deficient animals. Expression could be induced by treating these animals with vitamin D metabolites such as calcitriol. They were found to exist in two distant sizes with a molecular weight of approximately 9 kDa and 28 kDa. They were renamed calbindin; calbindin-D9k is found in mammalian intestine and calbindin-D28k in avain intestine and in kidney."

"Olmesartan (trade names Benicar, Olmetec) is an angiotensin II receptor antagonist used to treat high blood pressure. The prodrug olmesartan medoxomil is marketed worldwide by Daiichi Sankyo, Ltd. and in the United States by Daiichi Sankyo, Inc. and in India by Ranbaxy Laboratories Ltd. under the trade name Olvance. Olmesartan may possess high affinity for the Vitamin D Receptor, based on molecular modeling studies[2], but these results have not been duplicated in clinical trials. Because of the role of the Vitamin D receptor in innate immunity[3], this would indicate that olmesartan has immune modulatory properties. This theory is currently the premise underlying the Marshall Protocol, which uses olmesartan to impose a chemical blockade on 1,25 Vitamin D as part of a treatment of sarcoidosis and other diseases. The Marshall Protocol asserts that, assuming the etiology of these diseases is based on infection by cell-wall-deficient bacteria, restoring proper Vitamin D ratios via olmesartan dosing, combined with pulsed antibiotic dosing, would result in a cure.!

Calcidiol and prostate cancer. Tuohimaa P, Golovko O, Kalueff A, Nazarova N, Qiao S, Syvälä H, Talonpoika R, Lou YR. J Steroid Biochem Mol Biol. 2005 Feb;93(2-5):183-90. Epub 2005 Jan 22. Review. PMID: 15860261

An evaluation of the vitamin D3 content in fish: Is the vitamin D content adequate to satisfy the dietary requirement for vitamin D?\nLu Z, Chen TC, Zhang A, Persons KS, Kohn N, Berkowitz R, Martinello S, Holick MF.\nJ Steroid Biochem Mol Biol. 2007 Mar;103(3-5):642-4. Epub 2007 Jan 30.\nPMID: 17267210 \ndoi:10.1016/j.jsbmb.2006.12.010 \n

Why "Vitamin D" is not a hormone, and not a synonym for 1,25-dihydroxy-vitamin D, its analogs or deltanoids. Vieth R. J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):571-3. PMID: 15225841 doi:10.1016/j.jsbmb.2004.03.037

Lu Z, Chen TC, Zhang A, Persons KS, Kohn N, Berkowitz R, Martinello S, Holick MF. An evaluation of the vitamin D3 content in fish: Is the vitamin D content adequate to satisfy the dietary requirement for vitamin D? J Steroid Biochem Mol Biol. 2007 Mar;

Vitamin D effective ultraviolet wavelengths due to scattering in shade. Turnbull DJ, Parisi AV, Kimlin MG. J Steroid Biochem Mol Biol. 2005 Sep;96(5):431-6. Epub 2005 Jul 6. PMID: 16005208

The role of Vitamin D3 metabolism in prostate cancer. Lou YR, Qiao S, Talonpoika R, Syvälä H, Tuohimaa P. J Steroid Biochem Mol Biol. 2004 Nov;92(4):317-25. Epub 2004 Dec 19. Review. PMID: 15663995 doi:10.1016/j.jsbmb.2004.10.007 In summary, the local metabolism of hormonal Vitamin D seems to play an important role in the development and progression of prostate cancer.

Vitamin D and prostate cancer. Tuohimaa P, Lyakhovich A, Aksenov N, Pennanen P, Syvälä H, Lou YR, Ahonen M, Hasan T, Pasanen P, Bläuer M, Manninen T, Miettinen S, Vilja P, Ylikomi T. J Steroid Biochem Mol Biol. 2001 Jan-Mar;76(1-5):125-34. PMID: 11384870 doi:10.1016/S0960-0760(00)00141-2

25-Hydroxyvitamin D(3) is an agonistic vitamin D receptor ligand. Lou YR, Molnár F, Peräkylä M, Qiao S, Kalueff AV, St-Arnaud R, Carlberg C, Tuohimaa P. J Steroid Biochem Mol Biol. 2009 Nov 26. [Epub ahead of print] PMID: 19944755 doi:10.1016/j.jsbmb.2009.11.011 In conclusion, 25-hydroxyvitamin D3 is an agonistic vitamin D receptor ligand with gene regulatory and anti-proliferative properties.

Vitamin D and prevention of breast cancer: pooled analysis. Garland CF, Gorham ED, Mohr SB, Grant WB, Giovannucci EL, Lipkin M, Newmark H, Holick MF, Garland FC. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):708-11. PMID: 17368188 CONCLUSIONS: Intake of 2000 IU/day of Vitamin D(3), and, when possible, very moderate exposure to sunlight, could raise serum 25(OH)D to 52 ng/ml, a level associated with reduction by 50% in incidence of breast cancer, according to observational studies.

Twice single doses of 100,000 IU of vitamin D in winter is adequate and safe for prevention of vitamin D deficiency in healthy children from Ushuaia, Tierra Del Fuego, Argentina. Tau C, Ciriani V, Scaiola E, Acuña M. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):651-4. Epub 2007 Jan 25. PMID: 17257830 doi:10.1016/j.jsbmb.2006.12.027 These results disclosed that to prevent vitamin D deficiency for children at zones of risk at the south of our country, double supplementation of 100,000 IU of vitamin D during autumn and winter, would be adequate and safe.