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Vitamin D supplementation and total mortality: a meta-analysis of randomized controlled trials. Autier P, Gandini S. Arch Intern Med. 2007 Sep 10;167(16):1730-7. Review. PMID: 17846391 Conclusions Intake of ordinary doses of vitamin D supplements seems to be associated with decreases in total mortality rates. The relationship between baseline vitamin D status, dose of vitamin D supplements, and total mortality rates remains to be investigated. Population-based, placebo-controlled randomized trials with total mortality as the main end point should be organized for confirming these findings.

Statins and vitamin D. Aloia JF, Li-Ng M, Pollack S. Am J Cardiol. 2007 Oct 15;100(8):1329. Epub 2007 Jul 5. No abstract available. PMID: 17920383 A total of 208 women were randomized to receive vitamin D3 (n=104) or placebo (n=104). 51 women were on statins. At baseline, the subjects on statins had a significantly higher 25-OHD level than the subjects who were not on statins (51.2 ± 20.1 nmol/L versus 43.2 ± 18.0 nmol/L respectively, p=0.008). This was also true when averaging 25-OHD levels across the 3-year study period and looking at active and placebo patients separately. 185 subjects had follow-up 25-OHD levels drawn every 6 months during the study. Higher levels were seen in the statin use subgroup whether they were on placebo or active vitamin D (Figure 1Figure 1). There was no interaction seen between vitamin D use and statin use, i.e. the impacts are additive (p=0.5502). This significant difference is comparable to the increase in 25-OHD levels seen in Pérez-Castrillón's study (41 ± 19 versus 47 ± 19 nmol/L, p=0.003) [1]. Although Pérez-Castrillón et al found a statistically significant relation between total cholesterol and 25-OHD (r=0.277, p=0.002), we did not find a significant relation between total cholesterol and 25-OHD in our study population.

"From 1955 to 1990, all infants in East Germany received 600,000 IU of Vitamin D every three months for a total of 3,600,000 IU at age 18 months. With the 400 IU/day recommendation of the American Pediatric Association in mind, I ran across this amazing paper while surfing Medline for Vitamin D. According to this paper, all infants in the German Democratic Republic (East Germany) received dangerously high doses of Vitamin D every three months in their doctors office. The policy was in place for 35 years. The first 600,000 IU dose was given at three months and then every three months until the child was 18 months of age. This works out to an average of 6,000 IU per day (actually, for several technical reasons it is not equivalent) for 18 months. The authors collected blood before the dose and then 2 weeks after the quarterly dose to obtain 25(OH)D, 1,25(OH)D, and calcium levels on a total of 43 infants. Before the first dose, at 3 months of age, the average infant was extremely deficient (median 25(OH)D of 7 ng/ml). Two weeks after the first dose the average 25(OH)D level was 120 ng/ml, the second dose 170 ng/ml, the third dose, 180 ng/ml, the fourth dose, 144 ng/ml, the fifth dose, 110 ng/ml and after the sixth and final dose, 3.6 million total units, at age 18 months, the children had mean levels of 100 ng/ml. That is, by the 15 and 18 month doses, the children were beginning to effectively handle these massive doses. The highest level recorded in any of the 43 infants was 408 ng/ml at age 9 months, two weeks after the third 600,000 IU dose. Thirty-four percent of the infants had at least one episode of hypercalcemia but only 3 had an elevated serum 1,25(OH)D. The authors reported that all the infants appeared healthy, even the infant with a level of 408 ng/ml, that is, no clinical toxicity was noted in any of these infants."

Daily duration of vitamin D synthesis in human skin with relation to latitude, total ozone, altitude, ground cover, aerosols and cloud thickness. Engelsen O, Brustad M, Aksnes L, Lund E. Photochem Photobiol. 2005 Nov-Dec;81(6):1287-90. PMID: 16354110 Vitamin D production in human skin occurs only when incident UV radiation exceeds a certain threshold. From simulations of UV irradiances worldwide and throughout the year, we have studied the dependency of the extent and duration of cutaneous vitamin D production in terms of latitude, time, total ozone, clouds, aerosols, surface reflectivity and altitude. For clear atmospheric conditions, no cutaneous vitamin D production occurs at 51 degrees latitude and higher during some periods of the year. At 70 degrees latitude, vitamin D synthesis can be absent for 5 months. Clouds, aerosols and thick ozone events reduce the duration of vitamin D synthesis considerably, and can suppress vitamin D synthesis completely even at the equator. A web page allowing the computation of the duration of cutaneous vitamin D production worldwide throughout the year, for various atmospheric and surface conditions, is available on the Internet at http://zardoz.nilu.no/~olaeng/fastrt/VitD.html and http://zardoz.nilu.no/~olaeng/fastrt/VitD-ez.html. The computational methodology is outlined here.

Effects of Atorvastatin on vitamin D levels in patients with acute ischemic heart disease. Pérez-Castrillón JL, Vega G, Abad L, Sanz A, Chaves J, Hernandez G, Dueñas A. Am J Cardiol. 2007 Apr 1;99(7):903-5. Epub 2007 Feb 8. PMID: 17398180 In conclusion, atorvastatin increases vitamin D levels. This increase could explain some of the beneficial effects of atorvastatin at the cardiovascular level that are unrelated to cholesterol levels. The mechanism by which atorvastatin increases vitamin D levels is related to inhibition of 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase. Cholesterol is synthesized from 7-dehydrocholesterol, which is also a precursor of vitamin D3. For this reason, we initially observed a statistically significant relation between total cholesterol and vitamin D. HMG-CoA enzyme reductase is key to the synthesis of cholesterol, whereas ultraviolet radiation causes the formation of 25-hydroxyvitamin D. Inhibition of the enzyme may increase levels of 7-dehydrocholesterol and increase the synthesis of 25-hydroxycholecalciferol, thereby increasing vitamin D levels,10 although we observed no relation between lower cholesterol and increased vitamin D. In addition, 25-hydroxyvitamin D has been shown to inhibit HMG-CoA enzyme reductase activity in in vitro studies.11 A greater concentration of vitamin D could increase enzymatic inhibition, acting in synergy with the statin in decreasing total cholesterol.

Vitamin D receptor (VDR) gene polymorphisms and haplotypes, interactions with plasma 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, and prostate cancer risk. Mikhak B, Hunter DJ, Spiegelman D, Platz EA, Hollis BW, Giovannucci E. Prostate. 2007 Jun 15;67(9):911-23. PMID: 17440943 DOI: 10.1002/pros.20570 RESULTS No association was found between these SNPs or their associated haplotypes and all PC subtypes except that haplotype 2 (A-f-b) with Cdx2 A, Fok1 f, and Bsm1 b alleles and haplotype 3 (A-F-B) with Cdx2 A, Fok1 F and Bsm1 B alleles compared to the most common haplotype (A-F-b), were associated with reduced risk of aggressive PC (high stage or Gleason sum 7; P = 0.02), both with two alleles suspected of being low risk. Carriers of the variant Cdx2 A allele who were deficient in plasma 25-hydroxyvitamin D (15 ng/ml) compared to non-carriers with normal 25-hydroxyvitamin D, had a lower risk of total and poorly differentiated PCs (Gleason sum 7) (P for interaction = 0.02 and 0.04, respectively). Plasma 1,25-dihydroxyvitamin D deficiency (26 pg/ml) was associated with a threefold risk of poorly differentiated PC (P for interaction = 0.01) when comparing carriers of the Cdx2 A allele to non-carriers with normal 1,25-dihydroxyvitamin D. CONCLUSION In this population of men, none of the VDR polymorphisms studied was associated with susceptibility to PC. Carriers of the variant Cdx2 A allele with low plasma 25-hydroxyvitamin D may experience a reduction in risk of total and poorly differentiated prostate cancers compared to non-carriers with adequate 25-hydroxyvitamin D.

Prospective study of serum vitamin D and cancer mortality in the United States. Freedman DM, Looker AC, Chang SC, Graubard BI. J Natl Cancer Inst. 2007 Nov 7;99(21):1594-602. Epub 2007 Oct 30. PMID: 17971526 doi:10.1093/jnci/djm204 CONCLUSIONS: Our results do not support an association between 25(OH)D and total cancer mortality, although there was an inverse relationship between 25(OH)D levels and colorectal cancer mortality.

"Daily duration of vitamin D synthesis in human skin with relation to latitude, total ozone, altitude, ground cover, aerosols and cloud thickness."

Holick, M. F., MacLaughlin, J. A. & Doppelt, S. H. (1981) Factors that influence the cutaneous photosynthesis of previtamin D3. Science 211:590-593 When human skin was exposed to simulated solar ultraviolet radiation, epidermal 7-dehydrocholesterol was converted to previtamin D3. During prolonged exposure to simulated solar ultraviolet radiation, the synthesis of previtamin D3 reached a plateau at about 10 to 15 percent of the original 7-dehydrocholesterol content, and previtamin D3 was photoisomerized to two biologically inert isomers, lumisterol3 and tachysterol3. Increases either in skin melanin concentration or in latitude necessitated increases in the exposure time to simulated solar ultraviolet radiation required to maximize the formation, but not the total content, of previtamin D3. In order of importance, the significant determinants limiting the cutaneous production of previtamin D3 are (i) photochemical regulation, (ii) pigmentation, and (iii) latitude.

Aging decreases the capacity of human skin to produce vitamin D3. MacLaughlin J, Holick MF. J Clin Invest. 1985 Oct;76(4):1536-8. PMID: 2997282 doi:10.1172/JCI112134 An evaluation of surgically obtained skin (age range, 8-92 yr) revealed that there is an age-dependent decrease in the epidermal concentrations of provitamin D3 (7-dehydrocholesterol). To ascertain that aging indeed decreased the capacity of human skin to produce vitamin D3, some of the skin samples were exposed to ultraviolet radiation and the content of previtamin D3 was determined in the epidermis and dermis. The epidermis in the young and older subjects was the major site for the formation of previtamin D3, accounting for greater than 80% of the total previtamin D3 that was produced in the skin. A comparison of the amount of previtamin D3 produced in the skin from the 8- and 18-yr-old subjects with the amount produced in the skin from the 77- and 82-yr-old subjects revealed that aging can decrease by greater than twofold the capacity of the skin to produce previtamin D3. Recognition of this difference may be extremely important for the elderly, who infrequently expose a small area of skin to sunlight and who depend on this exposure for their vitamin D nutritional needs.

Vitamin D status: measurement, interpretation, and clinical application. Holick MF. Ann Epidemiol. 2009 Feb;19(2):73-8. Epub 2008 Mar 10. Review. PMID: 18329892 Conclusion The only way to determine whether a person is vitamin D deficient or sufficient is to measure their circulating level of 25(OH)D. There are a variety of assays used to measure 25(OH)D. The radioimmunoassays and competitive protein binding assays for 25(OH)D are useful in detecting vitamin D deficiency and sufficiency. However, these assays are fraught with technical difficulties, especially if they are not run routinely (Fig. 4) (33). Several reference laboratories have now switched to LC-MS ,which measures both 25(OH)D2 and 25(OH)D3 quantitatively. The total 25(OH)D, i.e., 25(OH)D2 plus 25(OH)D3, is what physicians need to be aware of for their patients. A level >30 ng/mL is

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

Serum levels of free 1,25-dihydroxyvitamin D in vitamin D toxicity. Pettifor JM, Bikle DD, Cavaleros M, Zachen D, Kamdar MC, Ross FP. Ann Intern Med. 1995 Apr 1;122(7):511-3. PMID: 7872586 CONCLUSIONS: Although the patients had normal or near-normal total 1,25-(OH)2D values, most patients had elevated free 1,25-(OH)2D levels. These findings suggest that elevated free 1,25-(OH)2D levels might play a role in the pathogenesis of hypercalcemia in vitamin D toxicity.

Despite inadequacies in information concerning the minimum prophylactic requirement of vitamin D for all age groups beyond infancy, there is no doubt that a total intake of 400 I.U. per day is adequate to prevent vitamin D deficiency in substantially all normal children from birth through adolescence. Evidence derived from the study of idiopathic hypercalcemia suggests that certain infants excessively sensitive to the toxic action of vitamin D may, on rare occasions, be adversely affected by daily intakes of 3,000 to 4,000 I.U. and sometimes considerably less. Because of the prevalent practice of food fortification in the United States and Canada, there is now a definite possibility that the individual, even the young infant, may ingest considerably more than the recommended vitamin D allowance, and intakes of 2,000 to 3,500 I.U. per day are possible, particularly beyond infancy. Although there has been no specific evidence that intakes of this order produce deleterious effects beyond infancy, it is pointed out that the long-term consequences of this new nutritional situation on older children or adults are entirely unknown.

A few researchers are turning their attention to the sunshine vitamin as a culprit, prompted by the experience of immigrants that have moved from their equatorial country to two northern latitude locations As evidence of widespread vitamin D deficiency grows, some scientists are wondering whether the sunshine vitamin-once only considered important in bone health-may actually play a role in one of neurology's most vexing conditions: autism. The idea, although not yet tested or widely held, comes out of preliminary studies in Sweden and Minnesota. Last summer, Swedish researchers published a study in Developmental Medicine and Child Neurology that found the prevalence of autism and related disorders was three to four times higher among Somali immigrants than non-Somalis in Stockholm. The study reviewed the records of 2,437 children, born between 1988 and 1998 in Stockholm, in response to parents and teachers who had raised concerns about whether children with a Somali background were overrepresented in the total group of children with autism

ScienceDaily (Apr. 24, 2009) - New research provides evidence for a link between vitamin D insufficiency and asthma severity. Serum levels of vitamin D in more than 600 Costa Rican children were inversely linked to several indicators of allergy and asthma severity, including hospitalizations for asthma, use of inhaled steroids and total IgE levels, according to a study that will appear in the first issue for May of the American Journal of Respiratory and Critical Care Medicine.

Vitamin D production in human skin occurs only when UV radiation exceeds a threshold. From simulations of UV irradiances, the VitD www page ( http://zardoz.nilu.no/~olaeng/fastrt/VitD.html) computes the daily duration of dermal vitamin D production at midday when UV radiation exceeds the required threshold. The daily duration depends on latitude, time, total ozone, clouds, aerosols, surface reflectivity and altitude all of which can be specified by the user

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 web-based tool that enables the user to calculate associated exposure times for any time and place ( http://nadir.nilu.no/~olaeng/fastrt/VitD_quartMED.html). The recommended UV exposure times depends on latitude, time, total ozone, clouds, aerosols, surface reflectivity and altitude all of which can be specified by the user. A simpler version for non-experts is available at http://nadir.nilu.no/~olaeng/fastrt/VitD-ez_quartMED.html

Optimal serum 25-hydroxyvitamin D levels for multiple health outcomes. Bischoff-Ferrari HA. Adv Exp Med Biol. 2008;624:55-71. Review. PMID: 18348447 DOI: 10.1007/978-0-387-77574-6_5 Recent evidence suggests that higher vitamin D intakes beyond current recommendations may be associated with better health outcomes. In this chapter, evidence is summarized from different studies that evaluate threshold levels for serum 25(OH)D levels in relation to bone mineral density (BMD), lower extremity function, dental health, risk of falls, admission to nursing home, fractures, cancer prevention and incident hypertension. For all endpoints, the most advantageous serum levels for 25(OH)D appeared to be at least 75 nmol/l (30 ng/ml) and for cancer prevention, desirable 25(OH)D levels are between 90-120 nmol/l (36-48 ng/ml). An intake of no less than 1000IU (25 meg) of vitamin D3 (cholecalciferol) per day for all adults may bring at least 50% of the population up to 75 nmol/l. Thus, higher doses of vitamin D are needed to bring most individuals into the desired range. While estimates suggest that 2000 IU vitamin D3 per day may successfully and safely achieve this goal, the implications of 2000 IU or higher doses for the total adult population need to be addressed in future studies.

Serum 25-hydroxyvitamin D levels in vitamin D-insufficient hip fracture patients after supplementation with ergocalciferol and cholecalciferol. Glendenning P, Chew GT, Seymour HM, Gillett MJ, Goldswain PR, Inderjeeth CA, Vasikaran SD, Taranto M, Musk AA, Fraser WD. Bone. 2009 Nov;45(5):870-5. Epub 2009 Jul 23. PMID: 19631774 doi:10.1016/j.bone.2009.07.015 Cholecalciferol supplementation resulted in a 31% greater increase in total HPLC-measured 25OHD (p=0.010) and 52% greater rise in RIA-measured 25OHD (p0.05). In vitamin D-insufficient hip fracture patients, supplementation with cholecalciferol 1000 IU/day for three months was more effective in increasing serum 25OHD than an equivalent dose of ergocalciferol. However, the lack of difference in PTH lowering between calciferol treatments raises questions about the biological importance of this observation.