Vitamin D

The effect of vitamin D2 and vitamin D3 on intestinal calcium absorption in Nigerian children with rickets. Thacher TD, Obadofin MO, O'Brien KO, Abrams SA. J Clin Endocrinol Metab. 2009 Sep;94(9):3314-21. Epub 2009 Jun 30. PMID: 19567516 Conclusions: Despite similar increases in 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D with vitamin D2 or vitamin D3, fractional calcium absorption did not increase, indicating that rickets in Nigerian children is not primarily due to vitamin D-deficient calcium malabsorption

Serum 25-hydroxyvitamin D status of the US population: 1988-1994 compared with 2000-2004. Looker AC, Pfeiffer CM, Lacher DA, Schleicher RL, Picciano MF, Yetley EA. Am J Clin Nutr. 2008 Dec;88(6):1519-27. PMID: 19064511 doi:10.3945/ajcn.2008.26182 Conclusions: Overall, mean serum 25(OH)D was lower in 2000-2004 than 1988-1994. Assay changes unrelated to changes in vitamin D status accounted for much of the difference in most population groups. In an adult subgroup, combined changes in BMI, milk intake, and sun protection appeared to contribute to a real decline in vitamin D status. In summary, age-standardized mean serum 25(OH)D concentrations based on observed values were significantly lower in 2000-2004 than in 1988-1994 in all groups examined. Adjustment for assay changes noticeably reduced the difference between surveys. However, mean serum 25(OH)D concentrations remained significantly lower in males (except Mexican Americans) in NHANES 2000-2004 than in NHANES III, even after adjustment for assay differences. This remaining difference likely represents a real decline in vitamin D status. Changes in BMI, milk intake, and sun protection appeared to contribute to this decline in a subgroup of non-Hispanic white adults. The possibility that trends in overweight, sun protection, and milk intake may continue supports the need to continue monitoring the serum 25(OH)D status of the population

A vitamin D nutritional cornucopia: new insights concerning the serum 25-hydroxyvitamin D status of the US population. Norman AW. Am J Clin Nutr. 2008 Dec;88(6):1455-6. PMID: 19064502 doi:10.3945/ajcn.2008.27049 In summary, the report of Looker et al should be required reading for all nutritionists, clinicians, and vitamin D aficionados who are decision makers with regard to 25(OH)D assays, vitamin D nutritional policy, and the care of patients with vitamin D-related diseases.

Induction of ovarian cancer cell apoptosis by 1,25-dihydroxyvitamin D3 through the down-regulation of telomerase. Jiang F, Bao J, Li P, Nicosia SV, Bai W. J Biol Chem. 2004 Dec 17;279(51):53213-21. Epub 2004 Oct 12. PMID: 15485861 doi: 10.1074/jbc.M410395200 Overall, the study suggests that the down-regulation of telomerase activity by 1,25(OH)2VD3 and the resulting cell death are important components of the response of OCa cells to 1,25(OH)2VD3-induced growth suppression. Progressive shortening of telomere associated with cell divisions limits the life span of normal cells and eventually leads to senescence. To become immortal, human cancers including OCa are invariably associated with activation of mechanism that maintains telomere length. Approximately 85-90% of cancers show reactivation of telomerase. The present study shows that telomerase in OCa cells is down-regulated by 1,25(OH)2VD3. Down-regulation of telomerase is due to decreased stability of hTERT mRNA rather than VDRE-mediated transcriptional repression through the putative VDRE present in the regulatory region of the hTERT gene. It is known that the inhibition of telomerase may lead to a phenotypic lag during which cells would continue to divide until the point at which the telomeres became critically short. This phenomenon may explain why the apoptotic induction by 1,25(OH)2VD3 needs the treatment for more than 6 days. As mentioned in the results, no detectable shortening of telomeric repeats was observed in parental OVCAR3 cells after 9 days of treatment with 1,25(OH)2VD3 (Fig. 4D). This is likely due to the fact that the short telomere (about 3 kb) in OVCAR3 cells is very close to the minimal length required for survival and that cells with detectably shorter telomere may have been selected against apoptosis. It has been shown that transformed human cells enter crisis once the terminal restriction fragment of the telomere reaches a length of about 4 kb. This is insufficient to protect chro

Vitamin D and aging. Tuohimaa P. J Steroid Biochem Mol Biol. 2009 Mar;114(1-2):78-84. Review. PMID: 19444937

Low serum 25-hydroxyvitamin D concentrations are associated with greater all-cause mortality in older community-dwelling women. Semba RD, Houston DK, Ferrucci L, Cappola AR, Sun K, Guralnik JM, Fried LP. Nutr Res. 2009 Aug;29(8):525-30. PMID: 19761886 doi:10.1016/j.nutres.2009.07.007 Older community-dwelling women with low 25(OH)D levels are at an increased risk of death.

Vitamin D and mortality in older men and women. Pilz S, Dobnig H, Nijpels G, Heine RJ, Stehouwer CD, Snijder MB, van Dam RM, Dekker JM. Clin Endocrinol (Oxf). 2009 Nov;71(5):666-72. Epub 2009 Feb 18. PMID: 19226272 DOI: 10.1111/j.1365-2265.2009.03548.x Conclusions Low 25(OH)D levels are associated with all-cause mortality and even more pronounced with cardiovascular mortality, but it remains unclear whether vitamin D deficiency is a cause or a consequence of a poor health status. Therefore, intervention studies are warranted to evaluate whether vitamin D supplementation reduces mortality and cardiovascular diseases.

"Hypervitaminosis D is a state of vitamin D toxicity. The recommended daily allowance is 400 IU per day. Overdose has been observed at 1925 µg/d (77,000 IU per day). Acute overdose requires between 15,000 µg/d (600,000 IU per day) and 42,000 µg/d (1,680,000 IU per day) over a period of several days to months, with a safe intake level being 250 µg/d (10,000 IU per day).[1] Foods contain low levels, and have not been known to cause overdose. Overdose has occurred due to industrial accidents, for example when incorrectly formulated pills were sold or missing industrial concentrate cans misused as cans of milk. Vitamin D toxicity is unlikely except when certain medical conditions are present, such as primary hyperparathyroidism, sarcoidosis, tuberculosis, and lymphoma."

"Hypovitaminosis D is a deficiency of Vitamin D. It can result from: inadequate intake coupled with inadequate sunlight exposure (in particular sunlight with adequate ultra violet B rays), disorders that limit its absorption, conditions that impair conversion of vitamin D into active metabolites, such as liver or kidney disorders, or, rarely, by a number of hereditary disorders.[1] Deficiency results in impaired bone mineralization, and leads to bone softening diseases, rickets in children and osteomalacia in adults, and contributes to osteoporosis.[1] Osteomalacia may also occur rarely as a side-effect of phenytoin use Hypovitaminosis D is typically diagnosed by measuring the concentration in blood of the compound 25-hydroxyvitamin D (calcidiol), which is a precursor to the active form 1,25-dihydroxyvitamin D (calcitriol).[6] One recent review has proposed the following four categories for hypovitaminosis D:[7] * Insufficient 50-100 nmol/L (20-40 ng/mL) * Mild 25-50 nmol/L (10-20 ng/mL) * Moderate 12.5-25.0 nmol/L (5-10 ng/mL) * Severe < 12.5 nmol/L (< 5 ng/mL) Note that 1.0 nmol/L = 0.4 ng/mL for this compound.[8] Other authors have suggested that a 25-hydroxyvitamin D level of 75-80 nmol/L (30-32 ng/mL) may be sufficient

Serum 25-Hydroxyvitamin D Levels Among US Children Aged 1 to 11 Years: Do Children Need More Vitamin D? Mansbach JM, Ginde AA, Camargo CA Jr. Pediatrics. 2009 Nov;124(5):1404-1410. PMID: 19951983 CONCLUSIONS: On the basis of a nationally representative sample of US children aged 1 to 11 years, millions of children may have suboptimal levels of 25(OH)D, especially non-Hispanic black and Hispanic children. More data in children are needed not only to understand better the health implications of specific serum levels of 25(OH)D but also to determine the appropriate vitamin D supplement requirements for children.

The vitamin D-antimicrobial peptide pathway and its role in protection against infection. Gombart AF. Future Microbiol. 2009 Nov;4:1151-65. PMID: 19895218 doi:10.2217/fmb.09.87

"Vitamin D, often referred to as the "sunshine vitamin," is actually a fat-soluble hormone that the body can synthesize naturally. There are several forms, including two that are important to humans: D2 and D3. Vitamin D2 (ergocalciferol) is synthesized by plants, and vitamin D3 (cholecalciferol) is synthesized by humans when skin is exposed to ultraviolet-B (UVB) rays from sunlight. The active form of the vitamin is calcitriol, synthesized from either D2 or D3 in the kidneys. Vitamin D helps to maintain normal blood levels of calcium and phosphorus"

"If you're running low on vitamin D - as an estimated 70 percent of the U.S. population is - your immune system may not be functioning as well as it should. As a result, you may be more vulnerable to infectious diseases than you would if your vitamin D levels were optimal. Worse, you could be at higher than normal risk of a long list of diseases including heart disease and several kinds of cancer. A report recently published journal, Future Microbiology, highlighted research at the Linus Pauling Institute at Oregon State University, which has shown that vitamin D induces expression of an antimicrobial peptide gene called cathelicidin that is the "first line of defense" in the immune system's response to minor wounds, cuts and bacterial and viral infections. The regulation of cathelicidin by vitamin D could help explain its vital role in immune function. The report noted that vitamin D is a key cofactor in reducing inflammation, in blood pressure control and helping to protect against heart disease. Author Adrian Gombart explains that there is still much to explore about D's mechanisms of action, the potential use of synthetic analogs of it in new treatments, and its duty in fighting infection."

"Cathelicidin antimicrobial peptide is a family of polypeptides found in lysosomes in polymorphonuclear leukocytes (PMNs).[1] Members of the cathelicidin family of antimicrobial polypeptides are characterized by a highly conserved region (cathelin domain) and a highly variable cathelicidin peptide domain. Cathelicidin peptides have been isolated from many different species of mammals. Cathelicidins were originally found in neutrophils but have since been found in many other cells including epithelial cells and macrophages activated by bacteria, viruses, fungi, or the hormone 1,25-D"

"Calbindin describes calcium binding proteins first described as the vitamin D-dependent calcium binding proteins in intestine and kidney."

"Vitamin D-dependent calcium binding proteins were discovered in the cytosolic fractions of chicken intestine, and later in mammalian intestine and kidney, by workers including Robert Wasserman of Cornell University. They bound calcium in the micromolar range and were greatly reduced in vitamin D-deficient animals. Expression could be induced by treating these animals with vitamin D metabolites such as calcitriol. They were found to exist in two distant sizes with a molecular weight of approximately 9 kDa and 28 kDa. They were renamed calbindin; calbindin-D9k is found in mammalian intestine and calbindin-D28k in avain intestine and in kidney."

"Numerous studies link Vitamin D and influenza, as well as Vitamin D and respiratory infections more generally. This vitamin up-regulates genetic expression of various endogenous antimicrobial peptides (AMP), which exhibit broad-spectrum microbicidal activity against bacteria, fungi, and viruses. Reports discussed below indicate that susceptibility to influenza is reduced with higher levels of sun exposure or vitamin D supplementation. Seasonal variation of vitamin D levels in humans can help explain the seasonality of flu epidemics."

"Ergocalciferol (Deltalin, Eli Lilly and Company) is a form of vitamin D, also called vitamin D2. It has the systematic name "(3β,5Z,7E,22E)-9,10-secoergosta-5,7,10(19),22-tetraen-3-ol". It is created from viosterol, which in turn is created when ultraviolet light activates ergosterol."

"Cholecalciferol is a form of Vitamin D, also called vitamin D3 or calciol.[1] It is structurally similar to steroids such as testosterone, cholesterol, and cortisol (though vitamin D3 itself is a secosteroid). One gram of pure vitamin D3 is 40 000 000 (40x106) IU, or, in other words, one IU is 0.025 μg. Individuals having a high risk of deficiency should consume 125 μg (5000 IU) of vitamin D daily"

Onko D-vitamiini ihmelääke? Auringosta tai purkista saatavan supervitamiinin väitetään suojaavan syövältä, sydänsairauksilta, sikainfluenssalta, masennukselta ja auttavan jopa laihtumaan. Monet kokevat kaamosmasennuksen helpottavan, kun syövät riittävän korkeita määriä D-vitamiinia. Kuulostaa liian hyvältä ollakseen totta. Vanha tuttu D-vitamiini onkin yhtäkkiä kuin taikajuoma, joka auttaa melkein mihin tahansa. Se laihduttaa, ehkäisee syöpää, laskee verenpainetta, kohottaa mielialaa. Vitamiini tuntuu tekevän melkein mitä tahansa, kunhan se on positiivista. Uusista hyötyvaikutuksista kerrotaan päivittäin. Time-lehti julisti jo pari vuotta sitten D-vitamiinin saannin ja vaikutuksien selvittämisen yhdeksi tieteen tärkeimmistä tutkimuskohteista! "D-vitamiini on hyvä tietokilpailukysymys, kun kysytään, mihin sairauteen sen puute ei näytä jotenkin liittyvän", toteaa Jouni Karhu. Hänet tunnetaan verkkokeskusteluissa väsymättömästi D-vitamiinia suitsuttavana nimimerkki Neonomidena, jonka monipuolisten tietojen innoittamana monet ovat marssineet apteekin vitamiinihyllylle tai tilanneet D-pillereitä verkkokaupasta.