请输入您要查询的百科知识：

　

词条 Hypervitaminosis D
释义

  1. Signs and symptoms

  2. Recommended supplement limits

     Suggested tolerable upper intake level (UL) 

  3. Long-term effects of supplementary oral intake

      Cardiovascular disease   Ethnic differences  Premature aging 

  4. See also

  5. References

  6. External links

{{Infobox medical condition (new)
| name = Hypervitaminosis D
| image = Cholecalciferol.svg
| caption = Cholecalciferol (shown above) and ergocalciferol are the two major forms of Vitamin D.
| pronounce =
| field = Endocrinology, toxicology
| synonyms =
| symptoms =
| complications =
| onset =
| duration =
| types =
| causes =
| risks =
| diagnosis =
| differential =
| prevention =
| treatment =
| medication =
| prognosis =
| frequency =
| deaths =
}}Hypervitaminosis D is a state of vitamin D toxicity. The normal range for blood concentration is 30.0 to 74.0 nanograms per milliliter (ng/mL).[1]

Signs and symptoms

An excess of vitamin D causes abnormally high blood concentrations of calcium, which can cause overcalcification of the bones, soft tissues, heart and kidneys. In addition, hypertension can result.[2] Symptoms of vitamin D toxicity may include the following:

  • Dehydration
  • Vomiting
  • Decreased appetite
  • Irritability
  • Constipation
  • Fatigue
  • Muscle weakness
  • Metastatic calcification of the soft tissues

Hypervitaminosis D symptoms appear several months after excessive doses of vitamin D are administered. In almost every case, a low-calcium diet combined with corticosteroid drugs will allow for a full recovery within a month. It is possible that some of the symptoms of vitamin D toxicity are actually due to vitamin K depletion. One animal experiment has demonstrated that co-consumption with vitamin K reduced adverse effects, but this has not been tested in humans.[3]

Recommended supplement limits

The U.S Institute of Medicine has established a Tolerable Upper Intake Level (UL) to protect against vitamin D toxicity. These levels in microgram (mcg or µg) and International Units (IU) for both males and females are:

(Conversion : 1 µg = 40 IU and 0.025 µg = 1 IU.[4])

  • 0–6 months: 25 µg (1000 IU)
  • 7–12 months: 38 µg (1500 IU)
  • 1–3 years: 63 µg (2500 IU)
  • 4–8 years:75 µg (3000 IU)
  • 9+ years:100 µg (4000 IU)
  • Pregnant and Lactating: 100 µg (4000 IU)

The recommended dietary allowance is 15 µg/d (600 IU per day; 800 IU for those over 70 years). Overdose has been observed at 1,925 µg/d (77,000 IU per day).{{citation needed|date=March 2019}} 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.

Suggested tolerable upper intake level (UL)

Based on risk assessment, a safe upper intake level of 250 µg (10,000 IU) per day in healthy adult has been suggested by non-government authors.[5][6] However, no government has a UL higher than 4,000 IU.

Long-term effects of supplementary oral intake

Excessive exposure to sunlight poses no risk in vitamin D toxicity through overproduction of vitamin D precursor, cholecalciferol, regulating vitamin D production. During ultraviolet exposure, the concentration of vitamin D precursors produced in the skin reach an equilibrium, and any further vitamin D that is produced is degraded.[7] This process is less efficient with increased melanin pigmentation in the skin. Endogenous production with full body exposure to sunlight is comparable to taking an oral dose between 250 µg and 625 µg (10,000 IU and 25,000 IU) per day.[7][8]

Vitamin D oral supplementation and skin synthesis have a different effect on the transport form of vitamin D, plasma calcifediol concentrations. Endogenously synthesized vitamin D3 travels mainly with vitamin D-binding protein (DBP), which slows hepatic delivery of vitamin D and the availability in the plasma.[9] In contrast, orally administered vitamin D produces rapid hepatic delivery of vitamin D and increases plasma calcifediol.[9]

It has been questioned whether to ascribe a state of sub-optimal vitamin D status when the annual variation in ultraviolet will naturally produce a period of falling levels, and such a seasonal decline has been a part of Europeans' adaptive environment for 1000 generations.[10][11] Still more contentious is recommending supplementation when those supposedly in need of it are labeled healthy and serious doubts exist as to the long-term effect of attaining and maintaining serum 25(OH)D of at least 80nmol/L by supplementation.[12]

Current theories of the mechanism behind vitamin D toxicity (starting at a plasmatic concentration of ≈750 nmol/L[13]) propose that:

  • Intake of vitamin D raises calcitriol concentrations in the plasma and cell
  • Intake of vitamin D raises plasma calcifediol concentrations which exceed the binding capacity of the DBP, and free calcifediol enters the cell
  • Intake of vitamin D raises the concentration of vitamin D metabolites which exceed DBP binding capacity and free calcitriol enters the cell

All of which affect gene transcription and overwhelm the vitamin D signal transduction process, leading to vitamin D toxicity.[14]

Cardiovascular disease

Evidence suggests that dietary vitamin D may be carried by lipoprotein particles into cells of the artery wall and atherosclerotic plaque, where it may be converted to active form by monocyte-macrophages.[9][15][16] This raises questions regarding the effects of vitamin D intake on atherosclerotic calcification and cardiovascular risk as it may be causing vascular calcification.[17] Calcifediol is implicated in the etiology of atherosclerosis, especially in non-Caucasians.[18][19]

The levels of the active form of vitamin D, calcitriol, are inversely correlated with coronary calcification.[20] Moreover, the active vitamin D analog, alfacalcidol, seems to protect patients from developing vascular calcification.[21][22] Serum vitamin D has been found to correlate with calcified atherosclerotic plaque in African Americans as they have higher active serum vitamin D levels compared to Euro-Americans.[19][23][24][25] Higher levels of calcidiol positively correlate with aorta and carotid calcified atherosclerotic plaque in African Americans but not with coronary plaque, whereas individuals of European descent have an opposite, negative association.[19] There are racial differences in the association of coronary calcified plaque in that there is less calcified atherosclerotic plaque in the coronary arteries of African-Americans than in whites.[26]

Among descent groups with heavy sun exposure during their evolution, taking supplemental vitamin D to attain the 25(OH)D level associated with optimal health in studies done with mainly European populations may have deleterious outcomes.[12] Despite abundant sunshine in India, vitamin D status in Indians are low and suggests a public health need to fortify Indian foods with vitamin D. However, the levels found in India are consistent with many other studies of tropical populations which have found that even an extreme amount of sun exposure, does not raise 25(OH)D levels to the levels typically found in Europeans.[27][28][29][30]

Recommendations stemming for a single standard for optimal serum 25(OH)D concentrations ignores the differing genetically mediated determinates of serum 25(OH)D and may result in ethnic minorities in Western countries having the results of studies done with subjects not representative of ethnic diversity applied to them. Vitamin D levels vary for genetically mediated reasons as well as environmental ones.[31][32][33][34]

Ethnic differences

Possible ethnic differences in physiological pathways for ingested vitamin D, such as the Inuit, may confound across the board recommendations for vitamin D levels. Inuit compensate for lower production of vitamin D by converting more of this vitamin to its most active form.[35]

A Toronto study of young Canadians of diverse ancestry applied a standard of serum 25(OH)D levels that was significantly higher than official recommendations.[36][37] These levels were described to be 75 nmol/L as "optimal", between 75 nmol/L and 50 nmol/L as "insufficient" and < 50 nmol/L as "deficient". 22% of individuals of European ancestry had 25(OH)D levels less than the 40 nmol/L cutoff, comparable to the values observed in previous studies (40nmol/L is 15 ng/mL). 78% of individuals of East Asian ancestry and 77% of individuals of South Asian ancestry had 25(OH)D concentrations lower than 40 nmol/L. The East Asians in the Toronto sample had low 25(OH)D levels when compared to whites. In a Chinese population at particular risk for esophageal cancer and with the high serum 25(OH)D concentrations have a significantly increased risk of the precursor lesion.[38]

Studies on the South Asian population uniformly point to low 25(OH)D levels, despite abundant sunshine.[39] Rural men around Delhi average 44 nmol/L. Healthy Indians seem have low 25(OH)D levels which are not very different from healthy South Asians living in Canada. Measuring melanin content to assess skin pigmentation showed an inverse relationship with serum 25(OH)D.[36] The uniform occurrence of very low serum 25(OH)D in Indians living in India and Chinese in China does not support the hypothesis that the low levels seen in the more pigmented are due to lack of synthesis from the sun at higher latitudes.

Premature aging

Complex regulatory mechanisms control metabolism. Recent epidemiologic evidence suggests that there is a narrow range of vitamin D levels in which vascular function is optimized. Levels above or below this range increased mortality.[15] Animal research suggests that both excess and deficiency of vitamin D appears to cause abnormal functioning and premature aging.[40][41][42][43]

See also

  • Hypervitaminosis

References

1. ^{{MedlinePlusEncyclopedia|003569|25-hydroxy vitamin D test}}
2. ^{{MerckManual|01|004|k||Vitamin D}}
3. ^{{cite journal |vauthors=Elshama SS, et al. |title = Comparison between the protective effects of vitamin K and vitamin A on the modulation of hypervitaminosis D3 short-term toxicity in adult albino rats |journal=Turk J Med Sci |volume=46 |issue=2 |pages=524–38 |year=2016 |pmid=27511521 |doi=10.3906/sag-1411-6 |url=}}
4. ^{{cite web|url = http://dietarysupplementdatabase.usda.nih.gov/ingredient_calculator/help.php#q9|title = Dietary Reference Intakes Tables [Health Canada, 2005]|accessdate = 21 July 2011|deadurl = yes|archiveurl = https://web.archive.org/web/20110721054856/http://dietarysupplementdatabase.usda.nih.gov/ingredient_calculator/help.php#q9|archivedate = 21 July 2011|df = }}
5. ^{{cite journal | vauthors = Hathcock JN, Shao A, Vieth R, Heaney R | title = Risk assessment for vitamin D | journal = The American Journal of Clinical Nutrition | volume = 85 | issue = 1 | pages = 6–18 | date = January 2007 | pmid = 17209171 |doi=10.1093/ajcn/85.1.6 |doi-access=free}}
6. ^{{cite journal | vauthors = Vieth R | title = Vitamin D toxicity, policy, and science | journal = Journal of Bone and Mineral Research | volume = 22 Suppl 2 | pages = V64-8 | date = December 2007 | pmid = 18290725 | doi = 10.1359/jbmr.07s221 }}
7. ^1 {{cite journal | vauthors = Holick MF | title = Environmental factors that influence the cutaneous production of vitamin D | journal = The American Journal of Clinical Nutrition | volume = 61 | issue = 3 Suppl | pages = 638S-645S | date = March 1995 | pmid = 7879731 | url = http://www.ajcn.org/cgi/pmidlookup?view=long&pmid=7879731 }}
8. ^[Effects Of Vitamin D and the Natural selection of skin colour:how much vitamin D nutrition are we talking about http://www.direct-ms.org/pdf/VitDVieth/Vieth%20Anthropology%20vit%20D.pdf]{{full|date=December 2016}}
9. ^1 2 {{cite journal | vauthors = Haddad JG, Matsuoka LY, Hollis BW, Hu YZ, Wortsman J | title = Human plasma transport of vitamin D after its endogenous synthesis | journal = The Journal of Clinical Investigation | volume = 91 | issue = 6 | pages = 2552–5 | date = June 1993 | pmid = 8390483 | pmc = 443317 | doi = 10.1172/JCI116492 }}
10. ^{{cite journal | vauthors = Kull M, Kallikorm R, Tamm A, Lember M | title = Seasonal variance of 25-(OH) vitamin D in the general population of Estonia, a Northern European country | journal = BMC Public Health | volume = 9 | pages = 22 | date = January 2009 | pmid = 19152676 | pmc = 2632995 | doi = 10.1186/1471-2458-9-22 }}
11. ^{{cite journal | vauthors = Hoffecker JF | title = Out of Africa: modern human origins special feature: the spread of modern humans in Europe | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 106 | issue = 38 | pages = 16040–5 | date = September 2009 | pmid = 19571003 | pmc = 2752585 | doi = 10.1073/pnas.0903446106 | bibcode = 2009PNAS..10616040H | jstor = 40485016 }}
12. ^1 {{cite journal |first=Lisa |last=Tseng |year=2003 |title=Controversies in Vitamin D Supplementation |journal=Nutrition Bytes |volume=9 |issue=1 |url=http://escholarship.org/uc/item/4m84d4fn}}
13. ^{{cite journal | vauthors = Jones G | title = Pharmacokinetics of vitamin D toxicity | journal = The American Journal of Clinical Nutrition | volume = 88 | issue = 2 | pages = 582S-586S | date = August 2008 | pmid = 18689406 | url = http://www.ajcn.org/cgi/pmidlookup?view=long&pmid=18689406 | doi=10.1093/ajcn/88.2.582s}}
14. ^{{cite journal | vauthors = Jones G | title = Pharmacokinetics of vitamin D toxicity | journal = The American Journal of Clinical Nutrition | volume = 88 | issue = 2 | pages = 582S-586S | date = August 2008 | pmid = 18689406 | url = http://www.ajcn.org/cgi/pmidlookup?view=long&pmid=18689406 | doi=10.1093/ajcn/88.2.582s}}
15. ^1 {{cite journal | vauthors = Hsu JJ, Tintut Y, Demer LL | title = Vitamin D and osteogenic differentiation in the artery wall | journal = Clinical Journal of the American Society of Nephrology | volume = 3 | issue = 5 | pages = 1542–7 | date = September 2008 | pmid = 18562594 | pmc = 4571147 | doi = 10.2215/CJN.01220308 }}
16. ^{{cite journal | vauthors = Speeckaert MM, Taes YE, De Buyzere ML, Christophe AB, Kaufman JM, Delanghe JR | title = Investigation of the potential association of vitamin D binding protein with lipoproteins | journal = Annals of Clinical Biochemistry | volume = 47 | issue = Pt 2 | pages = 143–50 | date = March 2010 | pmid = 20144976 | doi = 10.1258/acb.2009.009018 }}
17. ^{{cite journal | vauthors = Demer LL, Tintut Y | title = Vascular calcification: pathobiology of a multifaceted disease | journal = Circulation | volume = 117 | issue = 22 | pages = 2938–48 | date = June 2008 | pmid = 18519861 | pmc = 4431628 | doi = 10.1161/CIRCULATIONAHA.107.743161 }}
18. ^{{cite journal | vauthors = Fraser DR | title = The physiological economy of vitamin D | journal = Lancet | volume = 1 | issue = 8331 | pages = 969–72 | date = April 1983 | pmid = 6132277 | doi = 10.1016/S0140-6736(83)92090-1 }}
19. ^1 2 {{cite journal | vauthors = Freedman BI, Wagenknecht LE, Hairston KG, Bowden DW, Carr JJ, Hightower RC, Gordon EJ, Xu J, Langefeld CD, Divers J | title = Vitamin d, adiposity, and calcified atherosclerotic plaque in african-americans | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 95 | issue = 3 | pages = 1076–83 | date = March 2010 | pmid = 20061416 | pmc = 2841532 | doi = 10.1210/jc.2009-1797 }}
20. ^{{cite journal | vauthors = Watson KE, Abrolat ML, Malone LL, Hoeg JM, Doherty T, Detrano R, Demer LL | title = Active serum vitamin D levels are inversely correlated with coronary calcification | journal = Circulation | volume = 96 | issue = 6 | pages = 1755–60 | date = September 1997 | pmid = 9323058 | doi = 10.1161/01.cir.96.6.1755 }}
21. ^{{cite journal | vauthors = Brandi L | title = 1alpha(OH)D3 One-alpha-hydroxy-cholecalciferol--an active vitamin D analog. Clinical studies on prophylaxis and treatment of secondary hyperparathyroidism in uremic patients on chronic dialysis | journal = Danish Medical Bulletin | volume = 55 | issue = 4 | pages = 186–210 | date = November 2008 | pmid = 19232159 | url = http://www.danmedj.dk/dmb_2008/0408/0408-disputatser/dmb4040.htm }}
22. ^{{cite journal | vauthors = Ogawa T, Ishida H, Akamatsu M, Matsuda N, Fujiu A, Ito K, Ando Y, Nitta K | title = Relation of oral 1alpha-hydroxy vitamin D3 to the progression of aortic arch calcification in hemodialysis patients | journal = Heart and Vessels | volume = 25 | issue = 1 | pages = 1–6 | date = January 2010 | pmid = 20091391 | doi = 10.1007/s00380-009-1151-4 }}
23. ^{{cite journal | vauthors = Bell NH, Greene A, Epstein S, Oexmann MJ, Shaw S, Shary J | title = Evidence for alteration of the vitamin D-endocrine system in blacks | journal = The Journal of Clinical Investigation | volume = 76 | issue = 2 | pages = 470–3 | date = August 1985 | pmid = 3839801 | pmc = 423843 | doi = 10.1172/JCI111995 }}
24. ^{{cite journal | vauthors = Cosman F, Nieves J, Dempster D, Lindsay R | title = Vitamin D economy in blacks | journal = Journal of Bone and Mineral Research | volume = 22 Suppl 2 | pages = V34-8 | date = December 2007 | pmid = 18290719 | doi = 10.1359/jbmr.07s220 }}
25. ^{{cite journal | vauthors = Dawson-Hughes B | title = Racial/ethnic considerations in making recommendations for vitamin D for adult and elderly men and women | journal = The American Journal of Clinical Nutrition | volume = 80 | issue = 6 Suppl | pages = 1763S-6S | date = December 2004 | pmid = 15585802 | url = http://www.ajcn.org/cgi/pmidlookup?view=long&pmid=15585802 }}
26. ^{{cite journal | vauthors = Tang W, Arnett DK, Province MA, Lewis CE, North K, Carr JJ, Pankow JS, Hopkins PN, Devereux RB, Wilk JB, Wagenknecht L | title = Racial differences in the association of coronary calcified plaque with left ventricular hypertrophy: the National Heart, Lung, and Blood Institute Family Heart Study and Hypertension Genetic Epidemiology Network | journal = The American Journal of Cardiology | volume = 97 | issue = 10 | pages = 1441–8 | date = May 2006 | pmid = 16679080 | doi = 10.1016/j.amjcard.2005.11.076 }}
27. ^{{cite journal | vauthors = Goswami R, Kochupillai N, Gupta N, Goswami D, Singh N, Dudha A | title = Presence of 25(OH) D deficiency in a rural North Indian village despite abundant sunshine | journal = The Journal of the Association of Physicians of India | volume = 56 | pages = 755–7 | date = October 2008 | pmid = 19263699 }}
28. ^{{cite journal | vauthors = Lips P | title = Worldwide status of vitamin D nutrition | journal = The Journal of Steroid Biochemistry and Molecular Biology | volume = 121 | issue = 1–2 | pages = 297–300 | date = July 2010 | pmid = 20197091 | doi = 10.1016/j.jsbmb.2010.02.021 }}
29. ^{{cite journal | vauthors = Schoenmakers I, Goldberg GR, Prentice A | title = Abundant sunshine and vitamin D deficiency | journal = The British Journal of Nutrition | volume = 99 | issue = 6 | pages = 1171–3 | date = June 2008 | pmid = 18234141 | doi = 10.1017/S0007114508898662 | pmc=2758994}}
30. ^{{cite journal | vauthors = Hagenau T, Vest R, Gissel TN, Poulsen CS, Erlandsen M, Mosekilde L, Vestergaard P | title = Global vitamin D levels in relation to age, gender, skin pigmentation and latitude: an ecologic meta-regression analysis | journal = Osteoporosis International | volume = 20 | issue = 1 | pages = 133–40 | date = January 2009 | pmid = 18458986 | doi = 10.1007/s00198-008-0626-y }}
31. ^{{cite journal | vauthors = Engelman CD, Fingerlin TE, Langefeld CD, Hicks PJ, Rich SS, Wagenknecht LE, Bowden DW, Norris JM | title = Genetic and environmental determinants of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D levels in Hispanic and African Americans | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 93 | issue = 9 | pages = 3381–8 | date = September 2008 | pmid = 18593774 | pmc = 2567851 | doi = 10.1210/jc.2007-2702 }}
32. ^{{cite journal | vauthors = Creemers PC, Du Toit ED, Kriel J | title = DBP (vitamin D binding protein) and BF (properdin factor B) allele distribution in Namibian San and Khoi and in other South African populations | journal = Gene Geography | volume = 9 | issue = 3 | pages = 185–9 | date = December 1995 | pmid = 8740896 }}
33. ^{{cite journal | vauthors = Lips P | title = Vitamin D status and nutrition in Europe and Asia | journal = The Journal of Steroid Biochemistry and Molecular Biology | volume = 103 | issue = 3–5 | pages = 620–5 | date = March 2007 | pmid = 17287117 | doi = 10.1016/j.jsbmb.2006.12.076 }}
34. ^{{cite journal | vauthors = Borges CR, Rehder DS, Jarvis JW, Schaab MR, Oran PE, Nelson RW | title = Full-length characterization of proteins in human populations | journal = Clinical Chemistry | volume = 56 | issue = 2 | pages = 202–11 | date = February 2010 | pmid = 19926773 | doi = 10.1373/clinchem.2009.134858 }}
35. ^{{cite journal | vauthors = Rejnmark L, Jørgensen ME, Pedersen MB, Hansen JC, Heickendorff L, Lauridsen AL, Mulvad G, Siggaard C, Skjoldborg H, Sørensen TB, Pedersen EB, Mosekilde L | title = Vitamin D insufficiency in Greenlanders on a westernized fare: ethnic differences in calcitropic hormones between Greenlanders and Danes | journal = Calcified Tissue International | volume = 74 | issue = 3 | pages = 255–63 | date = March 2004 | pmid = 14708040 | doi = 10.1007/s00223-003-0110-9 }}
36. ^1 {{cite journal | vauthors = Gozdzik A, Barta JL, Wu H, Wagner D, Cole DE, Vieth R, Whiting S, Parra EJ | title = Low wintertime vitamin D levels in a sample of healthy young adults of diverse ancestry living in the Toronto area: associations with vitamin D intake and skin pigmentation | journal = BMC Public Health | volume = 8 | pages = 336 | date = September 2008 | pmid = 18817578 | doi = 10.1186/1471-2458-8-336 | pmc=2576234}}
37. ^Scientific Advisory Committee on Nutrition (2007) Update on Vitamin D Position Statement by the Scientific Advisory Committee on Nutrition 2007 {{ISBN|978-0-11-243114-5}}{{pn|date=December 2016}}
38. ^{{cite journal | vauthors = Abnet CC, Chen W, Dawsey SM, Wei WQ, Roth MJ, Liu B, Lu N, Taylor PR, Qiao YL | title = Serum 25(OH)-vitamin D concentration and risk of esophageal squamous dysplasia | journal = Cancer Epidemiology, Biomarkers & Prevention | volume = 16 | issue = 9 | pages = 1889–93 | date = September 2007 | pmid = 17855710 | pmc = 2812415 | doi = 10.1158/1055-9965.EPI-07-0461 }}
39. ^{{cite web|url=http://www.japi.org/january_2009/R-1.html|title=Vitamin D Status in India – Its Implications and Remedial Measures|website=www.JAPI.org|access-date=22 January 2018}}
40. ^{{cite journal | vauthors = Tuohimaa P | title = Vitamin D and aging | journal = The Journal of Steroid Biochemistry and Molecular Biology | volume = 114 | issue = 1–2 | pages = 78–84 | date = March 2009 | pmid = 19444937 | doi = 10.1016/j.jsbmb.2008.12.020 }}
41. ^{{cite journal | vauthors = Keisala T, Minasyan A, Lou YR, Zou J, Kalueff AV, Pyykkö I, Tuohimaa P | title = Premature aging in vitamin D receptor mutant mice | journal = The Journal of Steroid Biochemistry and Molecular Biology | volume = 115 | issue = 3–5 | pages = 91–7 | date = July 2009 | pmid = 19500727 | doi = 10.1016/j.jsbmb.2009.03.007 }}
42. ^{{cite journal | vauthors = Tuohimaa P, Keisala T, Minasyan A, Cachat J, Kalueff A | title = Vitamin D, nervous system and aging | journal = Psychoneuroendocrinology | volume = 34 Suppl 1 | pages = S278-86 | date = December 2009 | pmid = 19660871 | doi = 10.1016/j.psyneuen.2009.07.003 }}
43. ^{{Cite journal|last=Lanske|first=B|last2=Razzaque|first2=M|date=December 2007|title=Vitamin D and aging: old concepts and new insights|url=https://linkinghub.elsevier.com/retrieve/pii/S0955286307000605|journal=The Journal of Nutritional Biochemistry|language=en|volume=18|issue=12|pages=771–777|doi=10.1016/j.jnutbio.2007.02.002|pmc=2776629|pmid=17531460|via=}}

External links

{{Medical resources
| ICD10 = {{ICD10|E|67|3|e|65}}
| ICD9 = {{ICD9|278.4}}
| ICDO =
| OMIM =
| DiseasesDB = 13939
| MedlinePlus = 001594
| eMedicineSubj =
| eMedicineTopic =
}}{{Nutritional pathology}}

3 : Vitamin D|Effects of external causes|Hypervitaminosis
随便看

　

开放百科全书收录14589846条英语、德语、日语等多语种百科知识，基本涵盖了大多数领域的百科知识，是一部内容自由、开放的电子版国际百科全书。

　

Copyright © 2023 OENC.NET All Rights Reserved
京ICP备2021023879号 更新时间：2024/11/12 4:20:01