Vitamin D: Difference between revisions

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==Deficiency==
==Deficiency==
Low levels of vitamin D are common in medical inpatients<ref name="pmid9504937">{{cite journal |author=Thomas MK, Lloyd-Jones DM, Thadhani RI, ''et al'' |title=Hypovitaminosis D in medical inpatients |journal=N. Engl. J. Med. |volume=338 |issue=12 |pages=777–83 |year=1998 |pmid=9504937 |doi=}}</ref> and some populations of patients with widespread musculoskeletal pain like fibromyalgia<ref name="pmid14661675">{{cite journal |author=Plotnikoff GA, Quigley JM |title=Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain |journal=Mayo Clin. Proc. |volume=78 |issue=12 |pages=1463–70 |year=2003 |pmid=14661675 |doi=}}</ref>.<ref name="pmid18331295">{{cite journal |author=Hicks GE, Shardell M, Miller RR, ''et al'' |title=Associations between vitamin D status and pain in older adults: the Invecchiare in Chianti study |journal=J Am Geriatr Soc |volume=56 |issue=5 |pages=785–91 |year=2008 |month=May |pmid=18331295 |doi=10.1111/j.1532-5415.2008.01644.x |url=http://www.blackwell-synergy.com/openurl?genre=article&sid=nlm:pubmed&issn=0002-8614&date=2008&volume=56&issue=5&spage=785 |issn=}}</ref> However, more recent studies make the associated between Vitamin D and non-specific pain doubtful.<ref name="pmid18431091">{{cite journal |author=Warner AE, Arnspiger SA |title=Diffuse musculoskeletal pain is not associated with low vitamin D levels or improved by treatment with vitamin D |journal=J Clin Rheumatol |volume=14 |issue=1 |pages=12–6 |year=2008 |month=February |pmid=18431091 |doi=10.1097/RHU.0b013e31816356a9 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?an=00124743-200802000-00003 |issn=}}</ref><ref name="pmid18431091">{{cite journal |author=Warner AE, Arnspiger SA |title=Diffuse musculoskeletal pain is not associated with low vitamin D levels or improved by treatment with vitamin D |journal=J Clin Rheumatol |volume=14 |issue=1 |pages=12–6 |year=2008 |month=February |pmid=18431091 |doi=10.1097/RHU.0b013e31816356a9 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?an=00124743-200802000-00003 |issn=}}</ref>
Low levels of vitamin D are common in medical inpatients<ref name="pmid9504937">{{cite journal |author=Thomas MK, Lloyd-Jones DM, Thadhani RI, ''et al'' |title=Hypovitaminosis D in medical inpatients |journal=N. Engl. J. Med. |volume=338 |issue=12 |pages=777–83 |year=1998 |pmid=9504937 |doi=}}</ref> and some populations of patients with widespread musculoskeletal pain like fibromyalgia<ref name="pmid14661675">{{cite journal |author=Plotnikoff GA, Quigley JM |title=Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain |journal=Mayo Clin. Proc. |volume=78 |issue=12 |pages=1463–70 |year=2003 |pmid=14661675 |doi=}}</ref>.<ref name="pmid18331295">{{cite journal |author=Hicks GE, Shardell M, Miller RR, ''et al'' |title=Associations between vitamin D status and pain in older adults: the Invecchiare in Chianti study |journal=J Am Geriatr Soc |volume=56 |issue=5 |pages=785–91 |year=2008 |month=May |pmid=18331295 |doi=10.1111/j.1532-5415.2008.01644.x |url=http://www.blackwell-synergy.com/openurl?genre=article&sid=nlm:pubmed&issn=0002-8614&date=2008&volume=56&issue=5&spage=785 |issn=}}</ref> However, more recent studies make the associated between Vitamin D and non-specific pain doubtful.<ref name="pmid18431091">{{cite journal |author=Warner AE, Arnspiger SA |title=Diffuse musculoskeletal pain is not associated with low vitamin D levels or improved by treatment with vitamin D |journal=J Clin Rheumatol |volume=14 |issue=1 |pages=12–6 |year=2008 |month=February |pmid=18431091 |doi=10.1097/RHU.0b013e31816356a9 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?an=00124743-200802000-00003 |issn=}}</ref><ref name="pmid18431091">{{cite journal |author=Warner AE, Arnspiger SA |title=Diffuse musculoskeletal pain is not associated with low vitamin D levels or improved by treatment with vitamin D |journal=J Clin Rheumatol |volume=14 |issue=1 |pages=12–6 |year=2008 |month=February |pmid=18431091 |doi=10.1097/RHU.0b013e31816356a9 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?an=00124743-200802000-00003 |issn=}}</ref>
About a quarter of older adults have levels below 20 ng/mL.<ref name="pmid19174492">{{cite journal |author=Orwoll E, Nielson CM, Marshall LM, ''et al'' |title=Vitamin D deficiency in older men |journal=J. Clin. Endocrinol. Metab. |volume=94 |issue=4 |pages=1214–22 |year=2009 |month=April |pmid=19174492 |doi=10.1210/jc.2008-1784 |url=http://jcem.endojournals.org/cgi/pmidlookup?view=long&pmid=19174492 |issn=}}</ref>


==Administration==
==Administration==

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Vitamin D is a steroid and is vitamin that "includes both cholecalciferols and ergocalciferols, which have the common effect of preventing or curing rickets in animals. It can also be viewed as a hormone since it can be formed in skin by action of ultraviolet rays upon the precursors, 7-dehydrocholesterol and ergosterol, and acts on vitamin D receptors to regulate calcium in opposition to parathyroid hormone."[1]

Vitamin D serves two classes of functions: (a) an endocrine function, in which a form of vitamin D, calcitriol, produced in the kidneys and secreted into the bloodstream, acts on target organs (gastrointestinal tract, bone, parathyroid glands) in such a way as to regulate aspects of calcium and phosphorus metabolism important to bone health and homeostasis of circulating calcium and phosphorus concentrations; and, (b) an autocrine function, in which the cells of numerous organs and tissues in the body (e.g., parts of the immune system, various epithelial tissues) generate calcitriol that functions in the cells that generate it, in intracellular signaling pathways (e.g., facilitation of the expression of specific genes) important to optimal functioning of those cells.[2] The autocrine mechanisms account for the preponderance of vitamin D utilized by body each day, and therefore tends to set the daily requirement for vitamin D.[2]

Biochemistry

Ergocalciferols (vitamin D2) is formed in plants. Ergocalciferols are "derivatives of ergosterol formed by ultraviolet rays breaking of the C9-C10 bond. They differ from cholecalciferol in having a double bond between C22 and C23 and a methyl group at C24."[3]

Cholecalciferol (vitamin D3) is formed in the skin of animals from 7-dehydrocholesterol by sunlight. Cholecalciferol is a "derivative of 7-dehydroxycholesterol formed by ultraviolet rays breaking of the C9-C10 bond. It differs from ergocalciferol in having a single bond between C22 and C23 and lacking a methyl group at C24."[4]

Vitamin D2 and vitamin D3 are of equal potency.[5]

Vitamin D2 and vitamin D3 are hydroxylated in the liver at the 25 position.[5] This leads to calcitriol (1,25-Dihydroxyvitamin D3). Calcitriol is the "physiologically active form of vitamin D. It is formed primarily in the kidney by enzymatic hydroxylation of 25-hydroxycholecalciferol (calcifediol). Its production is stimulated by low blood calcium levels and parathyroid hormone. Calcitriol increases intestinal absorption of calcium and phosphorus, and in concert with parathyroid hormone increases bone resorption."[6]

Deficiency

Low levels of vitamin D are common in medical inpatients[7] and some populations of patients with widespread musculoskeletal pain like fibromyalgia[8].[9] However, more recent studies make the associated between Vitamin D and non-specific pain doubtful.[10][10]

About a quarter of older adults have levels below 20 ng/mL.[11]

Administration

In health adults, Vitamin D2 and vitamin D3 are equally effective in maintaining serum 25-hydroxyvitamin D levels.[12]

Vitamin D and risk of internal cancers

In 2007 in the American Journal of Clinical Nutrition, Lappe and coworkers published the first population-based, double-blind, randomised, placebo-controlled, interventional trial of cholecalciferol (vitamin D3) taking internal cancer prevention as their principal secondary end point, with fractures as their primary end point.[13] They reported that 1100 IU of vitamin D (cholecalciferol) combined with 1500 mg of calcium per day administered for four years greatly reduced the risk for new cancers compared with placebo controls (p < 0.005). They also noted that the concentrations of serum 25-hydroxy-vitamin D (25[OH]D) levels, both pre-treatment and during treatment independently predicted cancer risk. The treatment group achieved mean concentrations of serum 25-hydroxy-vitamin D (25[OH]D) of 96 nmol/L (38 ng/ml). Natural levels for people who live and work in the sun: ~50-70 ng/ml (~125-175 nmol/L). [14]

References

  1. ↑ Anonymous (2024), Vitamin D (English). Medical Subject Headings. U.S. National Library of Medicine.
  2. ↑ 2.0 2.1 Heaney RP. (2008) 10.2215/CJN.01160308 Vitamin D in Health and Disease. Clin. J. Am. Soc. Nephrol. (first published online June 4, 2008)
  3. ↑ Anonymous (2024), Ergocalciferols (English). Medical Subject Headings. U.S. National Library of Medicine.
  4. ↑ Anonymous (2024), Cholecalciferol (English). Medical Subject Headings. U.S. National Library of Medicine.
  5. ↑ 5.0 5.1 Harper, Harold W.; Murray, Robert F. (2000). “Structure and Function of the Lipid-Soluble Vitamins”, Harper's Biochemistry. Norwalk, CT: Appleton & Lange, 645. ISBN 0-8385-3684-0. 
  6. ↑ Anonymous (2024), Calcitriol (English). Medical Subject Headings. U.S. National Library of Medicine.
  7. ↑ Thomas MK, Lloyd-Jones DM, Thadhani RI, et al (1998). "Hypovitaminosis D in medical inpatients". N. Engl. J. Med. 338 (12): 777–83. PMID 9504937. [e]
  8. ↑ Plotnikoff GA, Quigley JM (2003). "Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain". Mayo Clin. Proc. 78 (12): 1463–70. PMID 14661675. [e]
  9. ↑ Hicks GE, Shardell M, Miller RR, et al (May 2008). "Associations between vitamin D status and pain in older adults: the Invecchiare in Chianti study". J Am Geriatr Soc 56 (5): 785–91. DOI:10.1111/j.1532-5415.2008.01644.x. PMID 18331295. Research Blogging.
  10. ↑ 10.0 10.1 Warner AE, Arnspiger SA (February 2008). "Diffuse musculoskeletal pain is not associated with low vitamin D levels or improved by treatment with vitamin D". J Clin Rheumatol 14 (1): 12–6. DOI:10.1097/RHU.0b013e31816356a9. PMID 18431091. Research Blogging.
  11. ↑ Orwoll E, Nielson CM, Marshall LM, et al (April 2009). "Vitamin D deficiency in older men". J. Clin. Endocrinol. Metab. 94 (4): 1214–22. DOI:10.1210/jc.2008-1784. PMID 19174492. Research Blogging.
  12. ↑ Holick MF, Biancuzzo RM, Chen TC, et al (2008). "Vitamin D2 is as effective as vitamin D3 in maintaining circulating concentrations of 25-hydroxyvitamin D". J. Clin. Endocrinol. Metab. 93 (3): 677-81. DOI:10.1210/jc.2007-2308. PMID 18089691. Research Blogging.
  13. ↑ Lappe,J.M.; Travers-Gustafson,D.; Davies,K.M.; Recker,R.R.; Heaney,R.P. (2007) Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. Am J. Clin Nutr. 85(6):1586-1591. Full Text
    • Abstract: BACKGROUND: Numerous observational studies have found supplemental calcium and vitamin D to be associated with reduced risk of common cancers. However, interventional studies to test this effect are lacking. OBJECTIVE: The purpose of this analysis was to determine the efficacy of calcium alone and calcium plus vitamin D in reducing incident cancer risk of all types. DESIGN: This was a 4-y, population-based, double-blind, randomized placebo-controlled trial. The primary outcome was fracture incidence, and the principal secondary outcome was cancer incidence. The subjects were 1179 community-dwelling women randomly selected from the population of healthy postmenopausal women aged >55 y in a 9-county rural area of Nebraska centered at latitude 41.4 degrees N. Subjects were randomly assigned to receive 1400-1500 mg supplemental calcium/d alone (Ca-only), supplemental calcium plus 1100 IU vitamin D3/d (Ca + D), or placebo. RESULTS: When analyzed by intention to treat, cancer incidence was lower in the Ca + D women than in the placebo control subjects (P < 0.03). With the use of logistic regression, the unadjusted relative risks (RR) of incident cancer in the Ca + D and Ca-only groups were 0.402 (P = 0.01) and 0.532 (P = 0.06), respectively. When analysis was confined to cancers diagnosed after the first 12 mo, RR for the Ca + D group fell to 0.232 (CI: 0.09, 0.60; P < 0.005) but did not change significantly for the Ca-only group. In multiple logistic regression models, both treatment and serum 25-hydroxyvitamin D concentrations were significant, independent predictors of cancer risk. CONCLUSIONS: Improving calcium and vitamin D nutritional status substantially reduces all-cancer risk in postmenopausal women. This trial was registered at clinicaltrials.gov as NCT00352170.
  14. ↑ Vieth R. (2006) What is the optimal vitamin D status for health? Prog. Biophys. Mol. Biol. 92(1):26-32. Full Text
    • Abstract: The most objectively substantiated health-related reason for tanning is that it improves vitamin D status. The serum 25-hydroxyvitamin D concentration (25(OH)D) is the measure of vitamin D nutrition status. Human biology was probably optimized through natural selection for a sun-rich environment that maintained serum 25(OH)D higher than 100 nmol/L. These levels are now only prevalent in people who spend an above-average amount of time outdoors, with the sun high in the sky. The best-characterized criteria for vitamin D adequacy are based on randomized clinical trials that show fracture prevention and preservation of bone mineral density. Based upon these studies, 25(OH)D concentrations should exceed 75 nmol/L. This concentration is near the upper end of the 25(OH)D reference ("normal") range for populations living in temperate climates, or for people who practice sun-avoidance, or who wear head coverings. Officially mandated nutrition guidelines restrict vitamin D intake from fortified food and supplements to less than 25 mcg/day, a dose objectively shown to raise serum 25(OH)D in adults by about 25 nmol/L. The combined effect of current nutrition guidelines and current sun-avoidance advice is to ensure that adults who follow these recommendations will have 25(OH)D concentrations lower than 75 nmol/L. Therefore, advice to avoid UVB light should be accompanied by encouragement to supplement with vitamin D in an amount that will correct for the nutrient deficit that sun-avoidance will cause.
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