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Use of vitamin D in clinical practice. Cannell JJ, Hollis BW. Altern Med Rev. 2008 Mar;13(1):6-20. PMID: 18377099 The recent discovery--from a meta-analysis of 18 randomized controlled trials--that supplemental cholecalciferol (vitamin D) significantly reduces all-cause mortality emphasizes the medical, ethical, and legal implications of promptly diagnosing and adequately treating vitamin D deficiency. Not only are such deficiencies common, and probably the rule, vitamin D deficiency is implicated in most of the diseases of civilization. Vitamin D's final metabolic product is a potent, pleiotropic, repair and maintenance, seco-steroid hormone that targets more than 200 human genes in a wide variety of tissues, meaning it has as many mechanisms of action as genes it targets. One of the most important genes vitamin D up-regulates is for cathelicidin, a naturally occurring broad-spectrum antibiotic. Natural vitamin D levels, those found in humans living in a sun-rich environment, are between 40-70 ng per ml, levels obtained by few modern humans. Assessing serum 25-hydroxy-vitamin D (25(OH)D) is the only way to make the diagnosis and to assure treatment is adequate and safe. Three treatment modalities exist for vitamin D deficiency: sunlight, artificial ultraviolet B (UVB) radiation, and vitamin D3 supplementation. Treatment of vitamin D deficiency in otherwise healthy patients with 2,000-7,000 IU vitamin D per day should be sufficient to maintain year-round 25(OH)D levels between 40-70 ng per mL. In those with serious illnesses associated with vitamin D deficiency, such as cancer, heart disease, multiple sclerosis, diabetes, autism, and a host of other illnesses, doses should be sufficient to maintain year-round 25(OH)D levels between 55 -70 ng per mL. Vitamin D-deficient patients with serious illness should not only be supplemented more aggressively than the well, they should have more frequent monitoring of serum 25(OH)D and serum calcium. Vitamin D should always be

Vitamin D in preventive medicine: are we ignoring the evidence? Zittermann A. Br J Nutr. 2003 May;89(5):552-72. Review. PMID: 12720576 Vitamin D is metabolised by a hepatic 25-hydroxylase into 25-hydroxyvitamin D (25(OH)D) and by a renal 1alpha-hydroxylase into the vitamin D hormone calcitriol. Calcitriol receptors are present in more than thirty different tissues. Apart from the kidney, several tissues also possess the enzyme 1alpha-hydroxylase, which is able to use circulating 25(OH)D as a substrate. Serum levels of 25(OH)D are the best indicator to assess vitamin D deficiency, insufficiency, hypovitaminosis, adequacy, and toxicity. European children and young adults often have circulating 25(OH)D levels in the insufficiency range during wintertime. Elderly subjects have mean 25(OH)D levels in the insufficiency range throughout the year. In institutionalized subjects 25(OH)D levels are often in the deficiency range. There is now general agreement that a low vitamin D status is involved in the pathogenesis of osteoporosis. Moreover, vitamin D insufficiency can lead to a disturbed muscle function. Epidemiological data also indicate a low vitamin D status in tuberculosis, rheumatoid arthritis, multiple sclerosis, inflammatory bowel diseases, hypertension, and specific types of cancer. Some intervention trials have demonstrated that supplementation with vitamin D or its metabolites is able: (i) to reduce blood pressure in hypertensive patients; (ii) to improve blood glucose levels in diabetics; (iii) to improve symptoms of rheumatoid arthritis and multiple sclerosis. The oral dose necessary to achieve adequate serum 25(OH)D levels is probably much higher than the current recommendations of 5-15 microg/d.

BACKGROUND: To determine the effect of vitamin D binding protein (DBP) genotypes on 25-hydroxyvitamin D [25(OH)D] changes with vitamin D supplements, we studied 98 adults receiving 600 or 4000 IU/d vitamin D(3) for one year. METHODS: The DBP functional variant, T436K, was genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). RESULTS: Mean 25(OH)D increases were 97% for TT (n=48), 151% for TK (n=31) and 307% (n=6) for KK genotypes (p=.004). CONCLUSIONS: As with baseline 25(OH)D, T436K genotype predicts 25(OH)D changes after long-term vitamin D supplementation. Common genetic variants of the vitamin D binding protein (DBP) predict differences in response of serum 25-hydroxyvitamin D [25(OH)D] to vitamin D supplementation. Fu L, Yun F, Oczak M, Wong BY, Vieth R, Cole DE. Clin Biochem. 2009 Jul;42(10-11):1174-7. Epub 2009 Mar 18. PMID: 19302999

D-vitamiini on yksi ihmisen tarvitsemista rasvaliukoisista vitamiineista. D-vitamiinin muotoja ovat kolekalsiferoli (D3) ja ergokalsiferoli (D2). Ihminen pystyy itsekin tuottamaan D-vitamiinia riittävässä auringonvalossa UVB-säteilyn vaikutuksesta. D-vitamiini on steroidihormoni, jonka esimuotoa muodostuu ihossa tai saadaan ruoasta. D-vitamiinin vaikutukset välittyvät vitamiinireseptorin (VDR) kautta. Reseptoreita on kaikissa soluissa keskushermosto mukaan lukien. Useat kliiniset ja kokeelliset tulokset osoittavat D-vitamiinin vaikuttavan aivojen toimintaan. D-vitamiini voi vähentää riskiä sairastua tyypin 2 diabetekseen[6]. Kansanterveyslaitoksen tutkijat seurasivat 17 vuotta noin 4000 suomalaisen naisen ja miehen terveydentilaa. Niillä henkilöillä, joiden veressä oli eniten D-vitamiinia, oli 40 % pienempi sairastumisriski verrattuna niihin, joiden veressä vitamiinia oli vähiten. Maailman terveysjärjestön (WHO:n) syöväntutkimuslaitos IARC Lyonissa analysoi 18 suurta D-vitamiinitutkimusta, joihin oli osallistunut 57 311 ihmistä[7]. Heidän terveydentilaansa oli seurattu lähes kuusi vuotta. Sinä aikana 4 777 heistä kuoli. D-vitamiinia ravintolisänä käyttäneiden kuolleisuus oli kahdeksan prosenttia pienempi kuin muiden. D-vitamiinilisän päiväannos vaihteli 7,5:stä 50 µg:aan; keskimäärin se oli 14 µg. D-vitamiinilisää käyttävien ihmisten veressä oli 1,5-5,2 kertaa enemmän tätä vitamiinia kuin muilla[8]. Lontoon King's Collegessa tehdyn tutkimuksen mukaan D-vitamiini lisää keuhkoissa tulehdusta vaimentavan tulehdussytokiinin, interleukiini 10:n (IL10:n) tuotantoa. Silloin astman oireet vähenevät, jopa sellaisilla potilailla, joihin kortisoni (deksametasoni) ei ole tehonnut[

"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 and breast cancer. Bertone-Johnson ER. Ann Epidemiol. 2009 Jul;19(7):462-7. Epub 2009 Feb 20. Review. PMID: 19230714 Though the relationship between vitamin D and breast cancer remains unclear, a growing body of evidence suggests that vitamin D may modestly reduce risk. A large number of in vitro studies indicate that vitamin D can inhibit cell proliferation and promote apoptosis and cell differentiation in breast tumor tissue. Results from analytic studies of sunlight exposure and dietary intake have been inconsistent but together generally support a modestly protective role of vitamin D, at least in some population subgroups. Studies using blood vitamin D metabolites to assess vitamin D status may be less prone to misclassification than those of diet and sunlight exposure. Overall, the two prospective and four case-control studies of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D tend to support a protective effect in older women. The relationship between common vitamin D receptor polymorphisms and risk remains unclear. Many questions about this relationship clearly remain, including the utility of assessing vitamin D through diet and sunlight exposure, the relationship between plasma metabolites, and the potential modifying effects of age, menopausal status and tumor characteristics. Given that vitamin D status is modifiable, additional prospective studies are necessary to determine if vitamin D may have important potential for breast cancer prevention.

Improved cholecalciferol nutrition in rats is noncalcemic, suppresses parathyroid hormone and increases responsiveness to 1, 25-dihydroxycholecalciferol. Vieth R, Milojevic S, Peltekova V. J Nutr. 2000 Mar;130(3):578-84. PMID: 10702588 We conclude suppression of 1,25(OH)(2)D and PTH, and higher renal VDR mRNA and 24-hydroxylase did not involve higher free 1,25(OH)(2)D concentration or a first pass effect at the gut. Thus, 25(OH)D or a metabolite other than 1,25(OH)(2)D is a physiological, transcriptionally and biochemically active, noncalcemic vitamin D metabolite. When viewed from a perspective that starts with higher vitamin D nutrition, the results indicate that low vitamin D nutrition may bring about a form of resistance to 1,25(OH)2D. This situation would explain why, in humans, nutritional rickets and osteomalacia are commonly associated with normal or increased levels of 1,25(OH)2D (Chesney et al. 1981Citation , Eastwood et al. 1979Citation , Garabedian et al. 1983Citation ,Rasmussen et al. 1980Citation )-these are not like the low hormone levels associated with any other endocrine-deficiency disorder. A connection between lower vitamin D nutrition and vitamin D resistance helps to explain why the supposedly inactive compound 25(OH)D is more relevant in diagnosing nutritional rickets than is the active hormone 1,25(OH)2D. If the features of improved vitamin D nutrition shown here were demonstrated for any newly synthesized compound, the compound would be classified as a noncalcemic 1,25(OH)2D analogue (Brown et al. 1989Citation , Finch et al. 1999Citation , Goff et al. 1993Citation , Koshizuka et al. 1999Citation ). Thus, we contend that 25(OH)D or a metabolite of it other than 1,25(OH)2D exists as a physiological and biologically-active noncalcemic vitamin D metabolite whose effects require further examination, particularly in relationship to studies involving the synthetic analogs of 1,25(OH)2D.

Effectiveness and safety of vitamin D in relation to bone health. Cranney A, Horsley T, O'Donnell S, Weiler H, Puil L, Ooi D, Atkinson S, Ward L, Moher D, Hanley D, Fang M, Yazdi F, Garritty C, Sampson M, Barrowman N, Tsertsvadze A, Mamaladze V. Evid Rep Technol Assess (Full Rep). 2007 Aug;(158):1-235. Review. PMID: 18088161 CONCLUSIONS: The results highlight the need for additional high quality studies in infants, children, premenopausal women, and diverse racial or ethnic groups. There was fair evidence from studies of an association between circulating 25(OH)D concentrations with some bone health outcomes (established rickets, PTH, falls, BMD). However, the evidence for an association was inconsistent for other outcomes (e.g., BMC in infants and fractures in adults). It was difficult to define specific thresholds of circulating 25(OH)D for optimal bone health due to the imprecision of different 25(OH)D assays. Standard reference preparations are needed so that serum 25(OH)D can be accurately and reliably measured, and validated. In most trials, the effects of vitamin D and calcium could not be separated. Vitamin D(3) (>700 IU/day) with calcium supplementation compared to placebo has a small beneficial effect on BMD, and reduces the risk of fractures and falls although benefit may be confined to specific subgroups. Vitamin D intake above current dietary reference intakes was not reported to be associated with an increased risk of adverse events. However, most trials of higher doses of vitamin D were not adequately designed to assess long-term harms.

Effectiveness and safety of vitamin D in relation to bone health. Cranney A, Horsley T, O'Donnell S, Weiler H, Puil L, Ooi D, Atkinson S, Ward L, Moher D, Hanley D, Fang M, Yazdi F, Garritty C, Sampson M, Barrowman N, Tsertsvadze A, Mamaladze V. Evid Rep Technol Assess (Full Rep). 2007 Aug;(158):1-235. Review. PMID: 18088161 CONCLUSIONS: The results highlight the need for additional high quality studies in infants, children, premenopausal women, and diverse racial or ethnic groups. There was fair evidence from studies of an association between circulating 25(OH)D concentrations with some bone health outcomes (established rickets, PTH, falls, BMD). However, the evidence for an association was inconsistent for other outcomes (e.g., BMC in infants and fractures in adults). It was difficult to define specific thresholds of circulating 25(OH)D for optimal bone health due to the imprecision of different 25(OH)D assays. Standard reference preparations are needed so that serum 25(OH)D can be accurately and reliably measured, and validated. In most trials, the effects of vitamin D and calcium could not be separated. Vitamin D(3) (>700 IU/day) with calcium supplementation compared to placebo has a small beneficial effect on BMD, and reduces the risk of fractures and falls although benefit may be confined to specific subgroups. Vitamin D intake above current dietary reference intakes was not reported to be associated with an increased risk of adverse events. However, most trials of higher doses of vitamin D were not adequately designed to assess long-term harms.

"Vitamiinilisissä kannattaa suosia D3-vitamiinia On ilmeistä, että suomalaiset eivät saa ruoasta ja auringonvalosta riittävästi D-vitamiinia, niinpä onkin turvauduttava D-vitamiinilisiin. Kannattaa huomioida, että D-vitamiineissa on eroja. D2-valmisteet ovat tehottomampia kuin D3-valmisteet. D-vitamiinitason nostaminen kannattaa. Useissa tutkimuksissa on osoitettu, että jo pelkällä D-vitamiinilla pystytään vähentämään murtumia, kun potilaan D-vitamiinitaso saadaan yli 75 nmol/l. Tärkeä syy D-vitamiinin käyttöön on myös se, että D-vitamiinilla voidaan vähentää kaatumisia. D-vitamiinin on todettu parantavan ikäihmisillä lihasvoimaa ja tasapainoa ja sitä kautta vaikuttavan kaatumisriskiä pienentävästi. Erityishuomiota vaativat myös potilaat, joilta on poistettu mahalaukku tai joilla on imeytymishäiriöitä aiheuttava suolistosairaus. Heillä, kuten myös kirroosi- ja keliakiapotilailla, vaste ravinnosta saatuun D-vitamiiniin on muita huonompi. D-vitamiinilisän annosta voidaan joutua heidän kohdallaan nostamaan huomattavasti."

Severe vitamin D deficiency in Swiss hip fracture patients. Bischoff-Ferrari HA, Can U, Staehelin HB, Platz A, Henschkowski J, Michel BA, Dawson-Hughes B, Theiler R. Bone. 2008 Mar;42(3):597-602. Epub 2007 Nov 28. PMID: 18180211 BACKGROUND: Most clinical guidelines for the prevention of hip fractures recommend 800 IU vitamin D per day. This dose shifted serum 25-hydroxyvitamin D levels (25(OH)D) in previous studies to between 60 and 100 nmol/l. AIM: To measure 25(OH)D levels and prevalence of vitamin D supplementation in individuals age 65+ with acute hip fracture. METHODS: 222 consecutive hip fracture patients were investigated over a 12 month period. Mean age of patients was 86 years and 77% were women. RESULTS: Mean serum 25(OH)D levels were low among hip fracture patients admitted from home (34.6 nmol/l), from assisted living (27.7 nmol/l), and from nursing homes (24 nmol/l). Severe vitamin D deficiency below 30 nmol/l was present in 60%, 80% were below 50 nmol/l, and less than 4% reached desirable levels of at least 75 nmol/l. Consistently, only 10% of hip fracture patients had any vitamin D supplementation on admission to acute care with significantly higher 25(OH)D levels among individuals supplemented with 800-880 IU/day (63.5 nmol/l). Controlling for age and gender, vitamin D supplementation, type of dwelling, and season were independently and significantly associated with 25(OH)D levels. CONCLUSION: These data provide evidence that current guidelines for the prevention of hip fractures need further effort to be translated into clinical practice.

Circulating vitamin D3 and 25-hydroxyvitamin D in humans: An important tool to define adequate nutritional vitamin D status. Hollis BW, Wagner CL, Drezner MK, Binkley NC. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):631-4. Epub 2007 Jan 10. PMID: 17218096 In the present study, we sought to investigate what circulating 25(OH)D levels would result in populations exhibiting no substrate limitations to the vitamin D-25-hydroxylase. To perform this, we chose two distinct populations. The first were individuals from a year-found sunny environment who spent a good deal of time outdoors. The second were a group of lactating women receiving a substantial daily oral dose of vitamin D3. Surprisingly, a study such as this previously had not been undertaken. There are several reasons for this. First, finding a group of sun-exposed individuals is not an easy task; in fact, we had to go to Hawaii to find them. Secondly, very few studies have been performed where subjects actually received adequate vitamin D3 supplementation to make them replete. Finally, it is very difficult and costly to measure circulating vitamin D3 and relate it to circulating 25(OH)D. The results of our study are far-reaching. This study also demonstrates that individuals can be vitamin D deficient with significant sun exposure if the skin area exposed is limited as was suggested several years ago (19). Finally, whether one receives their vitamin D3 orally or through UV exposure, the vitamin D-25-hydroxylase appears to handle it in an equivalent fashion with respect to maintaining circulating 25(OH)D levels. Thus, we believe that the relationship between circulating vitamin D and 25(OH)D may define adequate nutritional vitamin D status.

Vitamin D: a D-Lightful health perspective. Holick MF. Nutr Rev. 2008 Oct;66(10 Suppl 2):S182-94. Review. PMID: 18844847 DOI: 10.1111/j.1753-4887.2008.00104.x Sunlight provides most humans with their vitamin D requirement. Adequate vitamin D(3) by synthesis in the skin or from dietary and supplemental sources is essential for bone health throughout life. Vitamin D deficiency is defined as a 25(OH)D concentration 30 ng/mL (75 nmol/L), and insufficiency as 21-29 ng/mL. Vitamin D deficiency and insufficiency has been linked to a wide variety of chronic diseases including common cancers, autoimmune, cardiovascular, and infectious diseases. Healthcare professionals need to be aware of the vitamin D deficiency pandemic. Guidelines for sensible sun exposure and supplemental vitamin D of 800-1000 IU/day are needed.

"D-vitamiini on nyt valtavan suosittu ravintolisä. Tähän asti tämän vitamiinin yliannostelun vaaroilla on peloteltu, mutta nyttemmin on käynyt ilmeiseksi, että pelottelu on ollut turhaa ja suorastaan turmiollista kansanterveydelle ja -taloudelle. Maailman johtavat sveitsiläiset ja amerikkalaiset D-vitamiinitutkijat esittävät arvionsa D-vitamiinin hyödyistä ja riskeistä luukadon ehkäisyssä. Voimassa olevat D-vitamiinin päivittäiset saantisuositukset - jotka vaihtelevat eri maissa 5 ja 15 mikrogramman (µg) välillä - voivat olla liian pienet tämän vitamiinin monipuolisten vaikutusten kannalta monien eri tautien ehkäisyssä, toteavat tutkijat kirjoituksensa alussa. He arvioivat suosituksia suurempien D-vitamiiniannosten hyötyjä ja punnitsivat mahdollisia riskejä erityisesti seerumin D-vitamiinin pitoisuuden (25-OHD, S-D-25) valossa. Arviointi perustuu satunnaistettuihin kaksoissokkokokeisiin, joista 8 käsitteli ikääntyvien ihmisten kaatumisia (N=2426) ja 12 luunmurtumia (N=42279). Tulokset osoittivat, että mitä suurempi S-D-25 oli, sitä vähemmän oli kaatumisia ja murtumia. Tosiin sanoen, suuri S-D-25 ehkäisee ikäihmisillä sekä kaatumisia että luunmurtumia. Ihanteellinen S-D-25 näyttää olevan 75-110 nmol/l, johon on mahdollista päästä nauttimalla ruoan lisänä D-vitamiinia 17,5-25 µg, päättelivät tutkijat edellä mainittujen poikkileikkaustutkimusten valossa. "

"Kuluttajille on eräillä keskustelufoorumeilla yritelty uskotella, että öljypohjaiset D-vitamiinivalmisteet omaavat paremman biologisen hyväksikäytettävyyden kuin D-vitamiinitabletit, mutta tälle väitteelle ei löydy mitään tukea tieteellisestä kirjallisuudesta. Norjalaistutkimuksessa verrattiin D3-vitamiinia sisältävät multivitamiinitabletin ja D3-vitamiinia sisältävän kalaöljykapselin vaikutuksia seerumin (veren) 25-OH-D-vitamiinipitoisuuteen (S-25(OH)D). Koehenkilöt saivat neljän viikon ajan 10 mikrogrammaa D3-vitamiinia joko tableteista tai öljykapseleista. Tablettiryhmässä S-25(OH)D-pitoisuus nousi keskimäärin 35,8 nmol/l ja kapseliryhmässä 32,3 nmol/l. "We conclude that fish oil capsules and multivitamin tablets containing 10 microg cholecalciferol administered over a 4-week period produced a similar mean increase in s-25(OH)D concentration", päättelivät tutkijat. Vuotta aiemmin julkaistussa suomalaistutkimuksessa havaittiin, että D3-vitamiini imeytyy erilaisista leivistä samalla tehokkuudella kuin D-vitamiinivalmisteesta. Kanadalaistutkijat raportoivat juuston osalta samanlaisia tuloksia. Vuonna 2003 jenkkitutkijat totesivat, että "fat is not required for vitamin D to be bioavailable." Mainittakoon lopuksi, että D3-vitamiinitabletteihin lisätään yleensä D3-vitamiinivalmistetta, jossa on öljy jo valmiina. Ainesosaluetteloissa lukee lähes säännönmukaisesti "D3-vitamiinivalmiste" ja sen jälkeen suluissa pelkkä aktiiviaine eli "kolekalsiferoli" tai "sisältää mm. kolekalsiferolia ja soijaöljyä" tai jotain vastaavaa. Tämä D3-vitamiinivalmiste on sitten ympäröity täyteaineilla, jotka eivät vaikuta D3-vitamiinin imeytymiseen millään tavalla. Tabletti hajoaa hyvin nopeasti maha-suolikanavassa."

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.

Suomalaisten ravitsemussuositusten mukaan päivittäisen D-vitamiinisaannin tulisi olla ennen 70 ikävuotta 7,5 µg/VRK ja 10 µg/VRK sen jälkeen. Tällaisella saannilla elimistön D-vitamiinin tarve ei tule koskaan turvattua ilman riittäviä erillisiä D-vitamiinilisiä tai "etelän aurinkolomia". Valtion Ravitsemusneuvottelukunnan vuonna 2004 laatimat suositukset ovatkin aikansa eläneitä eivätkä nykytiedon mukaan turvaa väestön D-vitamiinin tarvetta. D-vitamiinireseptoreita, jotka yhdessä D-vitamiinin kanssa toimivat solun sisäisinä säätelijöinä, on mm aivoissa, eturauhasessa, rintarauhasessa, paksussa suolessa ja vasta-aineita tuottavissa soluissa. D-vitamiini säätelee yli 200 geeniä, joista osa säätelee solujen lisääntymistä, erilaistumista, kuolemaa ja verisuonten syntyä. Riittävän D-vitamiinin saanti vähentää tutkimustiedon mukaan selvästi riskiä sairastua eturauhasen, rintarauhasen ja imukudoksen syöpiin, diabetekseen ja sydän- ja verisuonisairauksiin - siis sairauksiin, jotka ovat suomalaisten suuria terveysongelmia. Lisätietoja: Olli Simonen, Suomen Osteoporoosiliiton pj puh 044-3080306 ( D-vitamiinin puute kansanterveyshaasteena) Christel Lamberg-Allardt, professori, puh 09-19158266 tai 040-5769500 (väestön D-vitamiinin tarve ja saanti) Hannu Aro, professori puh 040-353 7644 (osteoporoosin, -malasian ja murtumien diagnostiikka ja hoito)

Vitamin D and skin physiology: a D-lightful story. Holick MF, Chen TC, Lu Z, Sauter E. J Bone Miner Res. 2007 Dec;22 Suppl 2:V28-33. PMID: 18290718 doi: 10.1359/jbmr.07s211 Very few foods naturally contain vitamin D, and those that do have a very variable vitamin D content. Recently it was observed that wild caught salmon had between 75% and 90% more vitamin D(3) compared with farmed salmon. The associations regarding increased risk of common deadly cancers, autoimmune diseases, infectious diseases, and cardiovascular disease with living at higher latitudes and being prone to vitamin D deficiency should alert all health care professionals about the importance of vitamin D for overall health and well being. Humans have depended on sunlight for their vitamin D requirement. The impact of season, time of day, and latitude on vitamin D synthesis is well documented.(2,3) We now report that altitude also has a dramatic influence on vitamin D3 production and that living at altitudes above 3500 m permits previtamin D3 production at a time when very little is produced at latitudes below 3400 m. It was surprising that, at 27° N in Agra (169 M), little previtamin D3 production was observed. However, there was significant air pollution that caused a haze over the city. It is likely the ozone and other UVB-absorbing pollutants in the air prevented the solar UVB photons from reaching the earth's surface to produce previtamin D3.

Diagnosis and treatment of vitamin D deficiency. Cannell JJ, Hollis BW, Zasloff M, Heaney RP. Expert Opin Pharmacother. 2008 Jan;9(1):107-18. PMID: 18076342 The recent discovery - in a randomised, controlled trial - that daily ingestion of 1100 IU of colecalciferol (vitamin D) over a 4-year period dramatically reduced the incidence of non-skin cancers makes it difficult to overstate the potential medical, social and economic implications of treating vitamin D deficiency. Not only are such deficiencies common, probably the rule, vitamin D deficiency stands implicated in a host of diseases other than cancer. The metabolic product of vitamin D is a potent, pleiotropic, repair and maintenance, secosteroid hormone that targets > 200 human genes in a wide variety of tissues, meaning it has as many mechanisms of action as genes it targets. A common misconception is that government agencies designed present intake recommendations to prevent or treat vitamin D deficiency. They did not. Instead, they are guidelines to prevent particular metabolic bone diseases. Official recommendations were never designed and are not effective in preventing or treating vitamin D deficiency and in no way limit the freedom of the physician - or responsibility - to do so. At this time, assessing serum 25-hydroxy-vitamin D is the only way to make the diagnosis and to assure that treatment is adequate and safe. The authors believe that treatment should be sufficient to maintain levels found in humans living naturally in a sun-rich environment, that is, > 40 ng/ml, year around. Three treatment modalities exist: sunlight, artificial ultraviolet B radiation or supplementation. All treatment modalities have their potential risks and benefits. Benefits of all treatment modalities outweigh potential risks and greatly outweigh the risk of no treatment. As a prolonged 'vitamin D winter', centred on the winter solstice, occurs at many temperate latitudes, ≤ 5000 IU (125 μg) of vitamin D/d

"TAMPEREEN YLIOPISTO TIEDOTTAA 15.12.2009 "D-vitamiini hidastaa vanhenemista ja lisää terveitä elinvuosia. D-vitamiinin riittävällä annostelulla voitaisiin saada 2-5 tervettä elinvuotta lisää. Suomessa, jossa D-vitamiinin vajaus talvella on yleistä, olisi syytä kokonaan uudelleen arvioida D-vitamiinin terveydelliset vaikutukset. Siitä voi olla hyötyä jopa kausi-influenssan torjunnassa, mutta suurimmat kansainterveydelliset vaikutukset saataisiin kroonisten vanhuuteen liittyvien sairauksien ehkäisyssä. Eri arvioiden mukaan D-vitamiinin riittävällä annostelulla voitaisiin saada 2-5 tervettä elinvuotta lisää", sanotaan yliopiston tiedotteessa. D-vitamiini näyttäisi suojaavan keskushermoston rappeutumissairauksilta. Viime vuosien aikana on saatu lisävalaistusta normaaliin elimistön vanhenemiseen, kun on selvinnyt, että vanhenemista jarruttavan hormonin (FGF-23) vaikutus perustuu D-vitamiiniin. Sekä koe-eläimillä että ihmisillä on todettu, että FGF-23 jarruttaa D-vitamiinin hormonaalisten muotojen tuottoa. Siten FGF-23:n toimintaa häiritsevät mutaatiot saavat aikaan D-vitamiinin yliaktiivisuuden ja nopeuttavat vanhenemista."