Athletic performance and vitamin D.
Cannell JJ, Hollis BW, Sorenson MB, Taft TN, Anderson JJ.
Med Sci Sports Exerc. 2009 May;41(5):1102-10. Review.
PMID: 19346976
doi: 10.1249/MSS.0b013e3181930c2b
Conclusions: Vitamin D may improve athletic performance in vitamin D-deficient athletes. Peak athletic performance may occur when 25(OH)D levels approach those obtained by natural, full-body, summer sun exposure, which is at least 50 ng·mL-1. Such 25(OH)D levels may also protect the athlete from several acute and chronic medical conditions.
Calcium and vitamin D intakes may be positively associated with brain lesions in depressed and nondepressed elders.
Payne ME, Anderson JJ, Steffens DC.
Nutr Res. 2008 May;28(5):285-92.
PMID: 19083421
doi: 10.1016/j.nutres.2008.02.013
In conclusion, calcium and vitamin D consumption were associated with brain lesions in elderly subjects even after controlling for potentially explanatory variables. These associations may be due to vascular calcification or other mechanism. The possibility of adverse effects of high intakes of calcium and vitamin D needs to be further explored in longitudinal studies of elderly subjects.
Food chain as origin of vitamin D in fish
D. Sunita Rao and N. Raghuramulu.
Comparative Biochemistry and Physiology Part A: Physiology
Volume 114, Issue 1, May 1996, Pages 15-19
doi:10.1016/0300-9629(95)02024-1
Plankton, the chief food source of fish, was assessed as the possible dietary origin of vitamin D in fish. The presence of vitamin D compounds were examined in fresh water phytoplankton and zooplankton employing a series of chromatographic procedures. Abundant amounts of provitamins D and vitamins D (D2 and D3) were found in the fresh water plankton. The high amount of vitamin D observed may be due to exposure of plankton to sunlight because the plankton were caught during the summer month. Thus, plankton may be an important contributor to vitamin D in fish.
Supplements of vitamin D at 'critical time periods' may be key to reducing the risk of multiple sclerosis, according to a new study from the UK and Canada.
Researchers report that vitamin D may interact with a specific genetic component called HLA-DRB1*1501 that is known to increase the risk of multiple sclerosis by three-fold
Vitamin D Deficiency in the Morbidly Obese.
Buffington C, Walker B, Cowan GS Jr, Scruggs D.
Obes Surg. 1993 Nov;3(4):421-424.
PMID: 10757956
These data suggest that low vitamin D may be associated with obesity per se. Hypovitaminosis D, when it is found in post-bariatric surgery patients, may not be caused by the surgery since it may have been present to some degree pre-operatively.
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.
Serum vitamin D concentration and prostate cancer risk: a nested case-control study.
Ahn J, Peters U, Albanes D, Purdue MP, Abnet CC, Chatterjee N, Horst RL, Hollis BW, Huang WY, Shikany JM, Hayes RB; Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial Project Team.
J Natl Cancer Inst. 2008 Jun 4;100(11):796-804. Epub 2008 May 27.
PMID: 18505967
doi:10.1093/jnci/djn152
CONCLUSION: The findings of this large prospective study do not support the hypothesis that vitamin D is associated with decreased risk of prostate cancer; indeed, higher circulating 25(OH)D concentrations may be associated with increased risk of aggressive disease.
In summary, results from this large prospective study of men who underwent standardized prostate cancer screening in the context of a screening trial do not support the hypothesis that higher serum vitamin D status is associated with decreased risk of prostate cancer. The study showed no association of vitamin D level with nonaggressive disease; however, it raises the possibility that higher vitamin D level may be associated with increased risks for aggressive disease, although a clear monotonic dose-response relationship was lacking. Along with recent reports of adverse associations for higher vitamin D status and risk of pancreatic (32) and esophageal (33,34) cancer, caution should be taken in recommending high doses of vitamin D or sunlight exposure to the general public for prostate cancer prevention. Future analyses are warranted to confirm these results and to further clarify the effects of vitamin D on aggressive prostate cancer.
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.
"Study Shows Vitamin D Supplements May Be Useful in Preventing Heart Disease
Nov. 16, 2009 (Orlando, Fla.) -- Some men with low levels of vitamin D in their blood are at particularly high risk of developing heart disease and weakened bones that can lead to osteoporosis, researchers report.
In a study of more than 1,000 men, those with low levels of both vitamin D and the sex hormone estrogen were at significantly increased risk of having cardiovascular disease, says study head Erin Michos, MD, a cardiologist at Johns Hopkins.
"They were also at dramatically increased risk of osteopenia," or bone loss that can lead to osteoporosis, she says.
"Our results suggest that vitamin D supplements, which are already prescribed to treat osteoporosis, may also be useful in preventing heart disease," Michos tells WebMD.
Men with low levels of vitamin D and testosterone, on the other hand, were not at heightened risk for heart disease or osteopenia."
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
Amsterdam, The Netherlands, May 26, 2009 - There are several risk factors for the development of Alzheimer's disease and vascular dementia. Based on an increasing number of studies linking these risk factors with Vitamin D deficiency, an article in the current issue of the Journal of Alzheimer's Disease (May 2009) by William B. Grant, PhD of the Sunlight, Nutrition, and Health Research Center (SUNARC) suggests that further investigation of possible direct or indirect linkages between Vitamin D and these dementias is needed.
Low serum levels of 25-hydroxyvitamin D [25(OH)D] have been associated with increased risk for cardiovascular diseases, diabetes mellitus, depression, dental caries, osteoporosis, and periodontal disease, all of which are either considered risk factors for dementia or have preceded incidence of dementia. In 2008, a number of studies reported that those with higher serum 25(OH)D levels had greatly reduced risk of incidence or death from cardiovascular diseases
ScienceDaily (Apr. 8, 2009) - Deficiency in vitamin D has been widely regarded as contributing to autoimmune disease, but a review appearing in Autoimmunity Reviews explains that low levels of vitamin D in patients with autoimmune disease may be a result rather than a cause of disease and that supplementing with vitamin D may actually exacerbate autoimmune disease.
Long-term vitamin D3 supplementation may have adverse effects on serum lipids during postmenopausal hormone replacement therapy.
Heikkinen AM, Tuppurainen MT, Niskanen L, Komulainen M, Penttilä I, Saarikoski S.
Eur J Endocrinol. 1997 Nov;137(5):495-502.
PMID: 9405029
CONCLUSIONS: Our results confirm the positive long-term effect of HRT with sequential estradiol valerate and cyproterone acetate on serum lipid concentrations. In addition, the results suggest that vitamin D3 supplementation may have unfavorable effects on lipids in postmenopausal women. Pure vitamin D3 treatment was associated with increased serum LDL cholesterol. Furthermore, the beneficial effects of HRT on serum LDL cholesterol content were reduced when estradiol valerate was combined with vitamin D3. However, the relevance of these associations to cardiovascular morbidity remains to be established.
The role of vitamin D and calcium in type 2 diabetes. A systematic review and meta-analysis.
Pittas AG, Lau J, Hu FB, Dawson-Hughes B.
J Clin Endocrinol Metab. 2007 Jun;92(6):2017-29. Epub 2007 Mar 27. Review.
PMID: 17389701
.CONCLUSIONS: Vitamin D and calcium insufficiency may negatively influence glycemia, whereas combined supplementation with both nutrients may be beneficial in optimizing glucose metabolism.
25-hydroxyvitamin D levels inversely associate with risk for developing coronary artery calcification.
de Boer IH, Kestenbaum B, Shoben AB, Michos ED, Sarnak MJ, Siscovick DS.
J Am Soc Nephrol. 2009 Aug;20(8):1805-12. Epub 2009 May 14.
PMID: 19443637
doi: 10.1681/ASN.2008111157
"In conclusion, lower 25-hydroxyvitamin D concentrations associate with increased risk for incident CAC. Accelerated development of atherosclerosis may underlie, in part, the increased cardiovascular risk associated with vitamin D deficiency."
Fracture prevention with vitamin D supplementation: a meta-analysis of randomized controlled trials.
Bischoff-Ferrari HA, Willett WC, Wong JB, Giovannucci E, Dietrich T, Dawson-Hughes B.
JAMA. 2005 May 11;293(18):2257-64. Review.
PMID: 15886381
Conclusions Oral vitamin D supplementation between 700 to 800 IU/d appears to reduce the risk of hip and any nonvertebral fractures in ambulatory or institutionalized elderly persons. An oral vitamin D dose of 400 IU/d is not sufficient for fracture prevention.
Geographic variation in breast cancer mortality in the United States: a hypothesis involving exposure to solar radiation.
Garland FC, Garland CF, Gorham ED, Young JF.
Prev Med. 1990 Nov;19(6):614-22.
PMID: 2263572
doi:10.1016/0091-7435(90)90058-R
Vitamin D from sunlight exposure may be associated with low risk for fatal breast cancer, and differences in ultraviolet light reaching the United States population may account for the striking regional differences in breast cancer mortality. The ecological nature of this study is emphasized, and the possibility that an indirect association with dietary and socioeconomic factors could explain these findings is discussed.
Prospective study of predictors of vitamin D status and cancer incidence and mortality in men.
Giovannucci E, Liu Y, Rimm EB, Hollis BW, Fuchs CS, Stampfer MJ, Willett WC.
J Natl Cancer Inst. 2006 Apr 5;98(7):451-9.
PMID: 16595781
doi:10.1093/jnci/djj101
Conclusions: Low levels of vitamin D may be associated with increased cancer incidence and mortality in men, particularly for digestive-system cancers. The vitamin D supplementation necessary to achieve a 25(OH)D increment of 25 nmol/L may be at least 1500 IU/day.
ncident invasive breast cancer, geographic location of residence, and reported average time spent outside.
Millen AE, Pettinger M, Freudenheim JL, Langer RD, Rosenberg CA,
Mossavar-Rahmani Y, Duffy CM, Lane DS, McTiernan A, Kuller LH, Lopez AM, Wactawski-Wende J.
Cancer Epidemiol Biomarkers Prev. 2009 Feb;18(2):495-507. Epub 2009 Feb 3.
PMID: 19190147
doi: 10.1158/1055-9965.EPI-08-0652
In conclusion, region of residence and geographic solar irradiance are not consistently related to risk of breast cancer and may not be sufficient proxy measures for sunlight/vitamin D exposure. The observed association between time spent outside and breast cancer risk support the hypothesis that vitamin D may protect against breast cancer.
Relation of body fat indexes to vitamin D status and deficiency among obese adolescents.
Lenders CM, Feldman HA, Von Scheven E, Merewood A, Sweeney C, Wilson DM, Lee PD, Abrams SH, Gitelman SE, Wertz MS, Klish WJ, Taylor GA, Chen TC, Holick MF; Elizabeth Glaser Pediatric Research Network Obesity Study Group.
Am J Clin Nutr. 2009 Sep;90(3):459-67. Epub 2009 Jul 29.
PMID: 19640956
RESULTS: The mean (+/-SD) age of the adolescents was 14.9 +/- 1.4 y; 38 (66%) were female, and 8 (14%) were black. The mean (+/-SD) body mass index (in kg/m(2)) was 36 +/- 5, FM was 40.0 +/- 5.5%, and VAT was 12.4 +/- 4.3%. Seventeen of the adolescents were vitamin D deficient, but none had elevated PTH concentrations. Bone mineral content and bone mineral density were within 2 SDs of national standards. In a multivariate analysis, 25(OH)D decreased by 0.46 +/- 0.22 ng/mL per 1% increment in FM (beta +/- SE, P = 0.05), whereas PTH decreased by 0.78 +/- 0.29 pg/mL per 1% increment in VAT (P = 0.01). CONCLUSIONS: To the best of our knowledge, our results show for the first time that obese adolescents with 25(OH)D deficiency, but without elevated PTH concentrations, have a bone mass within the range of national standards (+/-2 SD). The findings provide initial evidence that the distribution of fat may be associated with vitamin D status, but this relation may be dependent on metabolic factors