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Conclusion The data point to a critical role for the VDR and 1,25(OH)2D3 in control of innate immunity and the response of the colon to chemical injury. Vitamin D and the vitamin D receptor are critical for control of the innate immune response to colonic injury. Froicu M, Cantorna MT. BMC Immunol. 2007 Mar 30;8:5. PMID: 17397543 doi:10.1186/1471-2172-8-5

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

Vitamin D signaling, infectious diseases, and regulation of innate immunity. White JH. Infect Immun. 2008 Sep;76(9):3837-43. Epub 2008 May 27. Review. PMID: 18505808 doi:10.1128/IAI.00353-08

The vitamin D-antimicrobial peptide pathway and its role in protection against infection. Gombart AF. Future Microbiol. 2009 Nov;4:1151-65. PMID: 19895218 Vitamin D deficiency has been correlated with increased rates of infection. Since the early 19th century, both environmental (i.e., sunlight) and dietary sources (cod liver) of vitamin D have been identified as treatments for TB. The recent discovery that vitamin D induces antimicrobial peptide gene expression explains, in part, the 'antibiotic' effect of vitamin D and has greatly renewed interest in the ability of vitamin D to improve immune function. Subsequent work indicates that this regulation is biologically important for the response of the innate immune system to wounds and infection and that deficiency may lead to suboptimal responses toward bacterial and viral infections. The regulation of the cathelicidin antimicrobial peptide gene is a human/primate-specific adaptation and is not conserved in other mammals. The capacity of the vitamin D receptor to act as a high-affinity receptor for vitamin D and a low-affinity receptor for secondary bile acids and potentially other novel nutritional compounds suggests that the evolutionary selection to place the cathelicidin gene under control of the vitamin D receptor allows for its regulation under both endocrine and xenobiotic response systems. Future studies in both humans and humanized mouse models will elucidate the importance of this regulation and lead to the development of potential therapeutic applications

Vitamin D in defense of the human immune response.\nAdams JS, Liu PT, Chun R, Modlin RL, Hewison M.\nAnn N Y Acad Sci. 2007 Nov;1117:94-105. Epub 2007 Jul 26. Review.\nPMID: 17656563\nDOI: 10.1196/annals.1402.03

Vitamin D A Key Player In Overall Health Of Several Body Organs, Says Biochemist In a paper published in the August issue of the American Journal of Clinical Nutrition, Norman identifies vitamin D's potential for contributions to good health in the adaptive and innate immune systems, the secretion and regulation of insulin by the pancreas, the heart and blood pressure regulation, muscle strength and brain activity. In addition, access to adequate amounts of vitamin D is believed to be beneficial towards reducing the risk of cancer. Norman also lists 36 organ tissues in the body whose cells respond biologically to vitamin D. The list includes bone marrow, breast, colon, intestine, kidney, lung, prostate, retina, skin, stomach and the uterus.

"I recently received an email from the Vitamin D Council regarding recent evidence that having adequate serum Vitamin D levels could be very important to avoiding illness from the H1N1 (swine) flu that is making the rounds. That will seem intuitive to those of you who read my earlier post about D, but it's good to see some real evidence. Some of you may have seen this information already on other blogs, including Richard's, but I have some new information and some comments to add."

Vitamin D may suppress infections which lead to development of Multiple Sclerosis Steven R Brenner, None (16 August 2007) J Neurol Neurosurg Psychiatry 2008 I read the article with reference to the inverse relationship between multiple sclerosis clinical activity and deficiency of vitamin D by Soilu-Hannienen (1) with interest, and was considering what mechanism could be in play to cause such a relationship. 25-hydroxylated metabolites of vitamin D act as intracellular regulators of the synthesis and action of defensin (2) molecules against bacterial antigens, defensin being an endogenously synthesized antimicrobial substance (2). Human cathelicidin antimicrobial peptide gene is a target of vitamin D receptor and is strongly up-regulated by 1,25-dihydroxyvitamin D3, indicating vitamin D receptor and the 1,25-dihydroxyvitaminD3 regulate primate innate immunity (3)

"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."

"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.!

'Vitamin D Induces Innate Antibacterial Responses in Human Trophoblasts via an Intracrine Pathway.\nLiu N, Kaplan AT, Low J, Nguyen L, Liu GY, Equils O, Hewison M.\nBiol Reprod. 2009 Mar;80(3):398-406. Epub 2008 Nov 12.\nPMID: 19005165DOI: 10.1095/biolreprod.108.073577

A new study has concluded that one key part of the immune system, the ability of vitamin D to regulate anti-bactericidal proteins, is so important that is has been conserved through almost 60 million years of evolution and is shared only by primates, including humans - but no other known animal species.

Vitamin D deficiency is a very serious health problem. Most people tend to think of it only in terms of skeletal problems; however, it is much more than that. Vitamin D deficiency has now been linked with a multitude of neoplasms, autoimmune dysfunction, compromised innate immunity and neurodevelopment in utero. Vitamin D is made in huge amounts when we go into intense sun. A fair-skinned individual can produce approximately 20,000 IU in 10 minutes' time with a total body exposure. A person with significant pigmentation will require up to 10 times the exposure to make an equivalent amount. In the winter at the latitude of Chicago, even a fair person cannot photo-produce vitamin D from mid-October through March. Thus, it is VERY important to have a realistic vitamin D recommendation as the current 200 IU/day recommendation is a joke

On the epidemiology of influenza. Cannell JJ, Zasloff M, Garland CF, Scragg R, Giovannucci E. Virol J. 2008 Feb 25;5:29. Review. PMID: 18298852 doi:10.1186/1743-422X-5-29

Bikle DD. What is new in vitamin D: 2006-2007. Curr Opin Rheumatol. 2007 Jul;19(4):383-8. PMID: 17551371 [PubMed - in process]

Association Between Serum 25-Hydroxyvitamin D Level and Upper Respiratory Tract Infection. \nAdit A. Ginde, MD, MPH; Jonathan M. Mansbach, MD; Carlos A. Camargo Jr, MD, DrPH . \nArch Intern Med. 2009;169(4):384-390\n

P.T. Liu, S. Stenger, H. Li, L. Wenzel, B.H. Tan, S.R. Krutzik, M.T. Ochoa, J. Schauber, K. Wu, C. Meinken, et al.\nVitamin D3-Triggered Antimicrobial Response--Another Pleiotropic Effect beyond Mineral and Bone Metabolism: Toll-Like Receptor Triggering of a Vitamin D-Mediated Human Antimicrobial Response. Science 311: 1770-1773, 2006\nJ. Am. Soc. Nephrol., November 1, 2006; 17(11): 2949 - 2953.

Back to the future: a new look at 'old' vitamin D. Chun RF, Adams JS, Hewison M. J Endocrinol. 2008 Aug;198(2):261-9. Epub 2008 May 21. PMID: 18495944 DOI: 10.1677/JOE-08-0170

Cutting edge: vitamin D-mediated human antimicrobial activity against Mycobacterium tuberculosis is dependent on the induction of cathelicidin.\nLiu PT, Stenger S, Tang DH, Modlin RL.\nJ Immunol. 2007 Aug 15;179(4):2060-3.\nPMID: 1767546

Vitamin D supplementation to prevent infections: a sub-study of a randomised placebo-controlled trial in older people (RECORD trial, ISRCTN 51647438).\nAvenell A, Cook JA, Maclennan GS, Macpherson GC.\nAge Ageing. 2007 Sep;36(5):574-7. Epub 2007 Aug 15. No abstract available.\nPMID: 17702768 \ndoi:10.1093/ageing/afm091