Vitamin D

Plasma 25-hydroxyvitamin D levels and risk of incident hypertension among young women. Forman JP, Curhan GC, Taylor EN. Hypertension. 2008 Nov;52(5):828-32. Epub 2008 Oct 6. PMID: 18838623 doi: 10.1161/HYPERTENSIONAHA.108.117630 Women in the lowest compared with highest quartile of plasma 25(OH)D had an adjusted odds ratio for incident hypertension of 1.66 (95% CI: 1.11 to 2.48; P for trend=0.01). Compared with women with sufficient levels, those with vitamin D deficiency (<30 ng/mL; 65.7% of the study population) had a multivariable odds ratio of 1.47 (95% CI: 1.10 to 1.97). Plasma 25(OH)D levels are inversely and independently associated with the risk of developing hypertension.

Seasonal affective disorder (SAD) is a type of winter-time depression experienced by people those who live in northern latitudes such as those of New York, Seattle, all of Canada, and Northern Europe. I believe it is primarily a disorder of sunlight/vitamin D deficiency. Vitamin D, when administered in late winter, produces a positive effect on mood in only five days.[1] One theory for this is that vitamin D stimulates the brain to produce more serotonin. In a wintertime experiment, serum vitamin D levels doubled in six months through supplementation and dramatically increased scores on a wellbeing assessment.[2] Two groups were given either 1,000 IU or 4,000 IU of vitamin D daily. And although both groups improved, the higher dose produced better results.

Influenssan leviämisen vuodenaikatekijää on haettu 80-luvulta lähtien (Hope-Simpson 1987). Auringon valon saantia ja elimistön D-vitamiinitasojen vaihtelua on jo pitkään epäilty täksi vuodenaikatekijäksi. Viime vuosina tämä yhteys on jo hyvin pitkälle varmistunut kun seerumin D-vitamiinitasoja on opittu mittaaman ja sen myötä on voitu todeta että väestön D-vitamiinitasot elimistössä laskevat voimakkaasti syksyllä ja talvella samanaikaisesti kun influenssa leviää. Lisäksi kun viime vuosina on selvinnyt D-vitamiinin merkittävä asema elimistön immuunipuolustuksen säätelijänä, niin yhteyttä voidaan pitää ainakin suurelta osin selvitettynä eli laskevien D-vitamiinitasojen huonontama immuniteetti altistaa ihmiset influenssalle kuten ilmeisesti monille muillekin infektioille (Cannell 2008).

Professor Robert P. Heaney's talk about vitamin D deficiency and what actions should be taken

Vitamin D and Diabetes-Can We Prevent it? Frank C. Garland

Connection with Vitamin D and Cancer by Dr. Donald L. Trump

Vitamin D and Cardiovascular Disease Prevention by Dr. David C. Sane

Vitamin D and Prevention of Chronic Diseases. A presentation by professor Michael F. Holick

YouTube - Vitamin D and Cancer Prevention. A presentation by Dr. Cedric Garland.

Vitamin D Good For The Heart? CBS NEws about Harvard Study

Vitamin D: It's Not Just For Bones Anymore. A presentation professor David Feldman

Vitamin D levels in healthy men in eastern Saudi Arabia. Sadat-Ali M, AlElq A, Al-Turki H, Al-Mulhim F, Al-Ali A. Ann Saudi Med. 2009 Sep-Oct;29(5):378-82. PMID: 19700896

25-Hydroxyvitamin D levels in serum at the onset of multiple sclerosis. Soilu-Hänninen M, Airas L, Mononen I, Heikkilä A, Viljanen M, Hänninen A. Mult Scler. 2005 Jun;11(3):266-71. PMID: 15957505 DOI: 10.1191/1352458505ms1157oa

A longitudinal study of serum 25-hydroxyvitamin D and intact parathyroid hormone levels indicate the importance of vitamin D and calcium homeostasis regulation in multiple sclerosis. Soilu-Hänninen M, Laaksonen M, Laitinen I, Erälinna JP, Lilius EM, Mononen I. J Neurol Neurosurg Psychiatry. 2008 Feb;79(2):152-7. Epub 2007 Jun 19. PMID: 17578859 doi:10.1136/jnnp.2006.105320 Conclusions: The endocrine circuitry regulating serum calcium may be altered in MS. There is an inverse relationship between serum vitamin D level and MS clinical activity. The role of vitamin D in MS must be explored further.

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)

Higher levels of 25-hydroxyvitamin D are associated with a lower incidence of multiple sclerosis only in women. Kragt J, van Amerongen B, Killestein J, Dijkstra C, Uitdehaag B, Polman Ch, Lips P. Mult Scler. 2009 Jan;15(1):9-15. Epub 2008 Aug 13. PMID: 18701572 DOI: 10.1177/1352458508095920 CONCLUSIONS: Our data suggest that higher circulating levels of 25(OH)D are associated with a lower incidence of MS and MS-related disability in women. This may imply clues to the pathogenesis of the sex difference in risk and to the nature of the environmental factors involved in MS.

Why would vitamin D be prescribed when vitamin D3 is available over-the-counter? Let's review the known differences between vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol): --D3 is the human form; D2 is the non-human form found in plants. --Dose for dose, D3 is more effective at raising blood levels of 25-hydroxy vitamin D than D2. It requires roughly twice to 250% of the dose of D2 to match that of D3 (Trang H et al 1998). --D2 blood levels don't yield long-term sustained levels of 25-hydroxy vitamin D as does D3. When examined as a 28-day area under the curve (AUC--a superior measure of biologic exposure), D3 yields better than a 300% increased potency compared to D2. This means that it requires around 50,000 units D2 to match the effects of 15,000 units D3 (Armas LA et al 2004). --D2 has lower binding affinity for vitamin D-binding protein, compared to D3 --Mitochondrial vitamin D 25-hydroxylase converts D3 to the 25-hydroxylated form five times more rapidly than D2. --As we age, the ability to metabolize D2 is dramatically reduced, while D3 is not subject to this phenomenon

This month, the authoritative International Agency for Research into Cancer (IARC) have weighed in on the issue. By gathering a group of expert scientists, they have looked at all the available evidence and published a detailed report on vitamin D and cancer. The massive tome weighs in at 465 pages, but we'll take a look at the key points in the first of two posts looking at the vitamin D debate. It is impossible for us to get more than about five percent of the vitamin D we need from our diet - unless, like Eskimos, we eat oily fish three times a day.

Not enough vitamin D: health consequences for Canadians. Schwalfenberg G. Can Fam Physician. 2007 May;53(5):841-54. Review PMID: 17872747 Conclusion Low levels of VTD are considered a major public health problem in Canada, especially during the winter. Those with risk factors should be screened for low 25(OH)D levels and repletion therapy instituted if needed. Researchers have estimated that the oral dose of vitamin D3 to attain and maintain 25(OH)D levels >80 nmol/L is 2200 IU/d if baseline levels are 20 to 40 nmol/L, 1800 IU/d if levels are 40 to 60 nmol/L, and 1160 IU/d if levels are between 60 and 80 nmol/L.64 We need to ensure that patients have healthy blood levels of 25(OH)D to prevent levels of parathyroid hormone from rising and to maximize absorption of calcium, magnesium, and phosphate. Positive effects on bone are marginal at best unless patients consume at least 800 IU/d of VTD. The emerging and exciting role of the VTD receptor and the actions of VTD in maintaining health in other cell types have become more apparent during the last decade.

Vitamin D supplementation. Eveleigh B. Can Fam Physician. 2007 Sep;53(9):1435; author reply 1435. PMID: 17872869 My concern regarding vitamin D2 is that it is a synthetic analogue and might interact with the vitamin D receptor differently in various cell systems. It has been reported that vitamin D3 might improve glycemic control.7 Vitamin D2 has been reported to cause worsening of glycemic control in people of East Indian descent.8 Is this because of vitamin D receptor polymorphism, or because of enhanced 24-hydroxylase enzyme activation, or is it due to how vitamin D2 interacts with the receptor? Until this has been sorted out, I feel safest using vitamin D3. There are about 2000 synthetic analogues of vitamin D. The search is on for one that can cross the blood-brain barrier to treat certain types of brain cancers without causing hypercalcemia.9 But then again, what other effects would this compound have? There are still so many unknowns