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Vitamin D association with estradiol and progesterone in young women. Knight JA, Wong J, Blackmore KM, Raboud JM, Vieth R. Cancer Causes Control. 2009 Nov 15. [Epub ahead of print] PMID: 19916051 Conclusions Higher levels of vitamin D may reduce progesterone and estradiol, providing a potential mechanism for reduction in breast cancer risk from increased vitamin D exposure in young women

Vitamin D and cognitive performance in adults: a systematic review. Annweiler C, Allali G, Allain P, Bridenbaugh S, Schott AM, Kressig RW, Beauchet O. Eur J Neurol. 2009 Oct;16(10):1083-9. Epub 2009 Jul 29. PMID: 19659751 DOI: 10.1111/j.1468-1331.2009.02755.x This systematic review shows that the association between serum 25OHD concentrations and cognitive performance is not yet clearly established. The inconclusive results of the reviewed studies could be due to methodology, types of the cognitive tasks used and/or the cellular mechanisms of vitamin D.

"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."

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, nervous system and aging. P. Tuohimaa, T. Keisala, A. Minasyan, J. Cachat and A. Kalueff. . Psychoneuroendocrinology, Volume 34, Supplement 1, December 2009, Pages S278-S286 NEUROACTIVE STEROIDS: EFFECTS AND MECHANISMS OF ACTION doi:10.1016/j.psyneuen.2009.07.003 This is a mini-review of vitamin D3, its active metabolites and their functioning in the central nervous system (CNS), especially in relation to nervous system pathologies and aging. The vitamin D3 endocrine system consists of 3 active calcipherol hormones: calcidiol (25OHD3), 1α-calcitriol (1α,25(OH)2D3) and 24-calcitriol (24,25(OH)2D3). The impact of the calcipherol hormone system on aging, health and disease is discussed. Low serum calcidiol concentrations are associated with an increased risk of several chronic diseases including osteoporosis, cancer, diabetes, autoimmune disorders, hypertension, atherosclerosis and muscle weakness all of which can be considered aging-related diseases. The relationship of many of these diseases and aging-related changes in physiology show a U-shaped response curve to serum calcidiol concentrations. Clinical data suggest that vitamin D3 insufficiency is associated with an increased risk of several CNS diseases, including multiple sclerosis, Alzheimer's and Parkinson's disease, seasonal affective disorder and schizophrenia. In line with this, recent animal and human studies suggest that vitamin D insufficiency is associated with abnormal development and functioning of the CNS. Overall, imbalances in the calcipherol system appear to cause abnormal function, including premature aging, of the CNS.

My doctor advised us to give Vitamin D to both our children, though our son is more than 4 year old. I decided to find out more about it. I surfed the Internet, read the description of the vitamin (here Canadian Pharmacy site https://www.canadapharmacy.com/ helped me a lot). Finally, I decided to give it to my children. But I didn't know, it is good for adults. Thanks for sharing this information, it is very useful for me!

Vitamin D deficiency: a worldwide problem with health consequences. Holick MF, Chen TC. Am J Clin Nutr. 2008 Apr;87(4):1080S-6S. Review. PMID: 18400738 A reevaluation needs to take place of what the adequate intakes of vitamin D should be for children and adults. The literature over the past decade suggests that the Institute of Medicine recommendations in 1997 (83) are inadequate, and some experts including us suggest that both children and adults should take ≥800-1000 IU vitamin D/d from dietary and supplemental sources (4, 9, 77) when sunlight is unable to provide it. This recommendation, however, has not yet been embraced either by official government or pediatric organizations in the United States, Canada, or Europe for either children or adults.

Vitamin D and intervention trials in prostate cancer: from theory to therapy. Schwartz GG. Ann Epidemiol. 2009 Feb;19(2):96-102. Epub 2008 Jul 10. PMID: 18619854 doi:10.1016/j.annepidem.2008.03.007 This suggests that whereas vitamin D (e.g., cholecalciferol) might prevent prostate cancer, existing prostate tumors likely would require treatment with 1,25(OH)(2)D and/or its analogs. The major obstacle to the use of 1,25(OH)(2)D in patients therapeutically is the risk of hypercalcemia. Several maneuvers to reduce this risk, including pulse dosing and the use of less calcemic 1,25(OH)(2)D analogs, have been explored in Phase I-III clinical trials. Once merely a promise, vitamin D-based therapies for prostate cancer may soon be medical practice.

Back to the future: a new look at 'old' vitamin D. Chun RF, Adams JS, Hewison M. J Endocrinol. 2008 Aug;198(2):261-9. Epub 2008 May 21. PMID: 18495944 DOI: 10.1677/JOE-08-0170