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Acid-base balance has an effect on bone turnover, especially on the rates of bone resorption and calcium mobilization. Bone mineral participates in the defense against acid-base disturbances, especially against metabolic acidosis (Lemann et al. 1966, Green & Kleeman 1991). The role of the bone mineral is important in the acid-base disorders, as no appreciable change in the intestinal calcium absorption occurs (Bichara et al. 1990). In the mammalian body, mainly three hormones regulate the calcium metabolism and the bone turnover. 1,25-dihydroxycholecalciferol (vitamin D derivative) increases calcium absorption from the intestine and, indirectly, from bone. Parathyroid hormone mobilizes calcium from the bone and increases the urinary phosphate excretion. Calcitonin inhibits bone resorption (Ganong 1981). Used as drugs, these hormones are also capable of inducing acid-base disorders. Calcitonin administration (Escanero et al. 1991) and vitamin D excess (Bichara et al. 1990) have been reported to cause metabolic alkalosis.

Are sunlight deprivation and influenza epidemics associated with the onset of acute leukemia? Timonen T, Näyhä S, Koskela T, Pukkala E. Haematologica. 2007 Nov;92(11):1553-6. PMID: 18024404 doi:10.3324/haematol.10799 Month of diagnosis of 7,423 cases of acute leukemia (AL) in Finland during 1964-2003 were linked with data on influenza and solar radiation. Acute myeloblastic leukemia (AML) showed the highest risk in the dark season. During the light season, the incidence decreased by 58% (95% confidence interval, 16-79%) per 1,000 kJ/m2/d increase of solar radiation. Independent of solar radiation, AML increased by 9% (95% confidence interval, 0-19%) during influenza epidemics. Reoccurring at the same time annually, darkness-related vitamin D deficiency and influenza could cause successive and co-operative mutations leading to AL with a short latency.

Independent association of low serum 25-hydroxyvitamin d and 1,25-dihydroxyvitamin d levels with all-cause and cardiovascular mortality. Dobnig H, Pilz S, Scharnagl H, Renner W, Seelhorst U, Wellnitz B, Kinkeldei J, Boehm BO, Weihrauch G, Maerz W. Arch Intern Med. 2008 Jun 23;168(12):1340-9. PMID: 18574092 Conclusions Low 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D levels are independently associated with all-cause and cardiovascular mortality. A causal relationship has yet to be proved by intervention trials using vitamin D.

Independent association of low serum 25-hydroxyvitamin d and 1,25-dihydroxyvitamin d levels with all-cause and cardiovascular mortality.\nDobnig H, Pilz S, Scharnagl H, Renner W, Seelhorst U, Wellnitz B, Kinkeldei J, Boehm BO, Weihrauch G, Maerz W.\nArch Intern Med. 2008 Jun 23;168(12):1340-9.\nPMID: 18574092

25-hydroxyvitamin D levels and the risk of mortality in the general population. Melamed ML, Michos ED, Post W, Astor B. Arch Intern Med. 2008 Aug 11;168(15):1629-37. PMID: 18695076 Conclusion The lowest quartile of 25(OH)D level (<17.8 ng/mL) is independently associated with all-cause mortality in the general population.

Sunlight regulates the cutaneous production of vitamin D3 by causing its photodegradation. Webb AR, DeCosta BR, Holick MF. J Clin Endocrinol Metab. 1989 May;68(5):882-7. PMID: 2541158 doi:10.1210/jcem-68-5-882 Vitamin D3 proved to be exquisitely sensitive to sunlight, and once formed in the skin, exposure to sunlight resulted in its rapid photodegradation to a variety of photoproducts, including 5,6-transvitamin D3, suprasterol I, and suprasterol II.suprasterol I, and suprasterol II.

Hypocalcemia as a Cause of Reversible Cardiomyopathy with Ventricular Tachycardia Chandrakant B. Chavan, MD, DNB; Kalavakolanu Sharada, MD, DM; Hygriv B. Rao, MD, DM; and Calambur Narsimhan, MD, DM, AB Annals of Internal Medicine, 3 April 2007, Volume

Vitamin D may suppress infections which lead to development of Multiple Sclerosis Steven R Brenner, None (16 August 2007) J Neurol Neurosurg Psychiatry 2008 I read the article with reference to the inverse relationship between multiple sclerosis clinical activity and deficiency of vitamin D by Soilu-Hannienen (1) with interest, and was considering what mechanism could be in play to cause such a relationship. 25-hydroxylated metabolites of vitamin D act as intracellular regulators of the synthesis and action of defensin (2) molecules against bacterial antigens, defensin being an endogenously synthesized antimicrobial substance (2). Human cathelicidin antimicrobial peptide gene is a target of vitamin D receptor and is strongly up-regulated by 1,25-dihydroxyvitamin D3, indicating vitamin D receptor and the 1,25-dihydroxyvitaminD3 regulate primate innate immunity (3)

Vitamin D deficiency and mortality. Zittermann A, Gummert JF, Börgermann J. Curr Opin Clin Nutr Metab Care. 2009 Aug 25. [Epub ahead of print] PMID: 19710612

Low vitamin D status despite abundant sun exposure. Binkley N, Novotny R, Krueger D, Kawahara T, Daida YG, Lensmeyer G, Hollis BW, Drezner MK. J Clin Endocrinol Metab. 2007 Jun;92(6):2130-5. Epub 2007 Apr 10. PMID: 17426097 doi:10.1210/jc.2006-2250 CONCLUSIONS: These data suggest that variable responsiveness to UVB radiation is evident among individuals, causing some to have low vitamin D status despite abundant sun exposure. In addition, because the maximal 25(OH)D concentration produced by natural UV exposure appears to be approximately 60 ng/ml, it seems prudent to use this value as an upper limit when prescribing vitamin D supplementation.

Circulating 25-hydroxyvitamin d levels and survival in patients with colorectal cancer. Ng K, Meyerhardt JA, Wu K, Feskanich D, Hollis BW, Giovannucci EL, Fuchs CS. J Clin Oncol. 2008 Jun 20;26(18):2984-91. PMID: 18565885 DOI: 10.1200/JCO.2007.15.1027 Conclusion Among patients with colorectal cancer, higher prediagnosis plasma 25(OH)D levels were associated with a significant improvement in overall survival. Further study of the vitamin D pathway and its influence on colorectal carcinogenesis and cancer progression is warranted.

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!

25-hydroxyvitamin D levels and the risk of mortality in the general population. Melamed ML, Michos ED, Post W, Astor B. Arch Intern Med. 2008 Aug 11;168(15):1629-37. PMID: 18695076