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Development of a model for optimal food fortification: vitamin D among adults in Finland. Hirvonen T, Sinkko H, Valsta L, Hannila ML, Pietinen P. Eur J Nutr. 2007 Aug;46(5):264-70. Epub 2007 May 18. PMID: 17514377

Duration of vitamin D synthesis from weather model data for use in prospective epidemiological studies. Edvardsen K, Engelsen O, Brustad M. Int J Biometeorol. 2009 Sep;53(5):451-9. Epub 2009 May 15. PMID: 19444487

Vitamin D production in human skin occurs only when UV radiation exceeds a threshold. From simulations of UV irradiances, the VitD-ez www page ( http://zardoz.nilu.no/~olaeng/fastrt/VitD-ez.html) computes the daily duration of dermal vitamin D production at midday when UV radiation exceeds the required threshold. The VitD-ez www page is a simplified version of the more complex VitD web page ( http://zardoz.nilu.no/~olaeng/fastrt/VitD.html). The simplified VitD-ez www page is convenient for users unfamiliar to radiative transfer modelling, because the model input is limited and more intuitive.

An acknowledged benefit of exposure to ultraviolet radiation is synthesis of vitamin D in human skin. Here we have defined a standard vitamin D dose based upon recommended requirements for vitamin D, and present a simplified web-based tool that enables the user to calculate associated exposure times for any time and place ( http://nadir.nilu.no/~olaeng/fastrt/VitD-ez_quartMED.html). This www page is a simplified version of the more complex web tool ( http://nadir.nilu.no/~olaeng/fastrt/VitD_quartMED.html). The simplified www page is convenient for users unfamiliar to radiative transfer modelling, because the model input is limited and more intuitive.

Serum 25-hydroxyvitamin D concentration and subsequent risk of type 2 diabetes. Mattila C, Knekt P, Männistö S, Rissanen H, Laaksonen MA, Montonen J, Reunanen A. Diabetes Care. 2007 Oct;30(10):2569-70. Epub 2007 Jul 12. PMID: 17626891 doi: 10.2337/dc07-0292 We found a significant inverse association between serum 25OHD and risk of type 2 diabetes in the simple model. However, the association was attenuated in the multivariate analysis, adjusting for potential risk factors of type 2 diabetes. To our knowledge, this is the first cohort study investigating the association between serum 25OHD and incidence of type 2 diabetes. Our results are in line with those from the Nurses' Health Study (5), where an inverse association was observed for the intake of vitamin D supplements. We could not differentiate whether the results depended on the effect of vitamin D deficiency on β-cell function or on insulin resistance. In summary, the results are in line with the hypothesis that a high serum 25OHD concentration may reduce the risk of type 2 diabetes. Further research is needed to confirm the association and to distinguish between the independent role of vitamin D and the role of healthy dietary and lifestyle patterns in reducing the risk of type 2 diabetes.

Vitamin D treatment in multiple sclerosis. Myhr KM. J Neurol Sci. 2009 Jun 22. [Epub ahead of print] PMID: 19549608 doi:10.1016/j.jns.2009.05.002 Epidemiological evidence combined with clinical and laboratory analyses, and experimental animal models, suggest a possible influence of vitamin D on MS susceptibility as well as clinical disease activity. Supplement with vitamin D may reduce the risk of developing MS. An intervention may also reduce the risk of conversion from a first clinical event suggestive of MS to clinical definite MS, as well as reduce the relapse rate among patients with relapsing remitting MS. More studies are, however, needed to determine optimal dose and serum level for vitamin D, as well as target populations and optimal timing for intervention.

Role of vitamin D in the pathogenesis of type 2 diabetes mellitus. Palomer X, González-Clemente JM, Blanco-Vaca F, Mauricio D. Diabetes Obes Metab. 2008 Mar;10(3):185-97. Review. PMID: 18269634 DOI: 10.1111/j.1463-1326.2007.00710.x Vitamin D deficiency has been shown to alter insulin synthesis and secretion in both humans and animal models. It has been reported that vitamin D deficiency may predispose to glucose intolerance, altered insulin secretion and type 2 diabetes mellitus. Vitamin D replenishment improves glycaemia and insulin secretion in patients with type 2 diabetes with established hypovitaminosis D, thereby suggesting a role for vitamin D in the pathogenesis of type 2 diabetes mellitus.

"I discussed in my last post how Dr Vieth has a model of tissue 1,25(OH)2D synthesis and degradation in which the level of active substance is pretty well independent of blood vitamin D level, provided the level is either rising or stable. I think it is also worth pointing out that he is talking, hypothetically, about tissue 1,25(OH)2D, not plasma level... As we know, almost nothing is known about tissue 1,25(OH)2D control. By Vieth's hypothesis tissue 1,25(OH)2D is OK so long as there is at least SOME vitamin D present in plasma and the level dose not vary too much. Obviously there is a level below which you can have as much of the enzyme for converting vitamin D to the active form as you like, if there is no vitamin D in your blood you can't make any 1,25(OH)2D in your tissues, or in your kidneys for export to your blood to control calcium levels. At the lower extremes we have rickets and osteomalacia. These are clear cut, unarguable markers of vitamin D deficiency, in the absence of confounding factors (there are a few)."

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

"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.!