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Breastfeeding does not protect against urinary tract infection in the first 3 months of life, but vitamin D supplementation increases the risk by 76%. Katikaneni R, Ponnapakkam T, Ponnapakkam A, Gensure R. Clin Pediatr (Phila). 2009 Sep;48(7):750-5. Epub 2009 Mar 4. PMID: 19264720 DOI: 10.1177/0009922809332588 The relative risk of UTI with breastfeeding versus formula feeding was 1.03 (0.58-1.82), and any breastfeeding versus no breastfeeding was 0.92 (0.58-1.45). Vitamin D supplementation increased the UTI risk, with a relative risk of 1.76 (1.07-2.91, P < .05). However, only formula-fed infants showed an increased risk of UTI after vitamin D supplementation.

Plasma 25-hydroxyvitamin D levels and risk of incident hypertension among young women. Forman JP, Curhan GC, Taylor EN. Hypertension. 2008 Nov;52(5):828-32. Epub 2008 Oct 6. PMID: 18838623 doi: 10.1161/HYPERTENSIONAHA.108.117630 Women in the lowest compared with highest quartile of plasma 25(OH)D had an adjusted odds ratio for incident hypertension of 1.66 (95% CI: 1.11 to 2.48; P for trend=0.01). Compared with women with sufficient levels, those with vitamin D deficiency (<30 ng/mL; 65.7% of the study population) had a multivariable odds ratio of 1.47 (95% CI: 1.10 to 1.97). Plasma 25(OH)D levels are inversely and independently associated with the risk of developing hypertension.

Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Hyppönen E, Läärä E, Reunanen A, Järvelin MR, Virtanen SM. Lancet. 2001 Nov 3;358(9292):1500-3. PMID: 11705562 doi:10.1016/S0140-6736(01)06580-1 INTERPRETATION: Dietary vitamin D supplementation is associated with reduced risk of type 1 diabetes. Ensuring adequate vitamin D supplementation for infants could help to reverse the increasing trend in the incidence of type 1 diabetes.

High-dose vitamin D3 supplementation in a cohort of breastfeeding mothers and their infants: a 6-month follow-up pilot study. Wagner CL, Hulsey TC, Fanning D, Ebeling M, Hollis BW. Breastfeed Med. 2006 Summer;1(2):59-70. PMID: 17661565 doi:10.1089/bfm.2006.1.59. Objective: To examine the effect of high-dose maternal vitamin D3 (vitD) supplementation on the nutritional vitD status of breastfeeding (BF) women and their infants compared with maternal and infant controls receiving 400 and 300 IU vitD/day, respectively. Design: Fully lactating women (n = 19) were enrolled at 1-month postpartum into a randomized- control pilot trial. Each mother received one of two treatments for a 6-month study period: 0 or 6000 IU vitD3 plus a prenatal vitamin containing 400 IU vitD3. The infants of mothers assigned to the control group received 300 IU vitD3/day; those infants of mothers in the high-dose group received 0 IU (placebo). Maternal serum and milk vitD and 25(OH)D were measured at baseline then monthly; infant serum vitD and 25(OH)D were measured at baseline, and months 4 and 7. Urinary calcium/creatinine ratios were measured monthly in both mothers and infants. Dietary and BF history and outdoor activity questionnaires were completed at each visit. Changes in skin pigmentation were measured by spectrophotometry. Data were analyzed using chi-square, t-test, and analysis of variance (ANOVA) on an intent-to-treat basis. Conclusion: With limited sun exposure, an intake of 400 IU/day vitamin D3 did not sustain circulating maternal 25(OH)D levels, and thus, supplied only extremely limited amounts of vitamin D to the nursing infant via breast milk. Infant levels achieved exclusively through maternal supplementation were equivalent to levels in infants who received oral vitamin D supplementation. Thus, a maternal intake of 6400 IU/day vitamin D elevated circulating 25(OH)D in both mother and nursing infant.

25-hydroxyvitamin D, IGF-1, and metabolic syndrome at 45 years of age: a cross-sectional study in the 1958 British Birth Cohort. Hyppönen E, Boucher BJ, Berry DJ, Power C. Diabetes. 2008 Feb;57(2):298-305. Epub 2007 Nov 14. PMID: 18003755 doi: 10.2337/db07-1122 CONCLUSIONS-Serum 25(OH)D is inversely associated with metabolic syndrome, whereas the inverse association with IGF-1 was found only among those without hypovitaminosis D. These results suggest that metabolic syndrome prevalence is the lowest when both 25(OH)D and IGF-1 are high.

"Retinol-induced Intestinal Tumorigenesis in Min/+ Mice and Importance of Vitamin D Status. Hetland RB, Alexander J, Berg JP, Svendsen C, Paulsen JE. Anticancer Res. 2009 Nov;29(11):4353-60. PMID: 20032378 The effects of life-long dietary exposure, starting in utero, to high retinol, low vitamin D, or high retinol in combination with low vitamin D on intestinal tumorigenesis in Min/+ mice were investigated. In males, high retinol alone significantly increased the number (2.6-fold) and size (1.3-fold) of small intestinal tumours; in females no significant increase in tumour number or size was seen. In both genders, low vitamin D intake alone did not affect intestinal tumorigenesis. In males, intake of the combined high retinol/low vitamin D diet did not further increase the effects caused by high retinol alone. In females, however, the high retinol/low vitamin D-induced increase in tumour number (3.1-fold) and tumour size (1.5-fold) exceeded that of high retinol alone. In conclusion, a high dietary intake of retinol stimulated intestinal tumorigenesis in Min/+ mice. Furthermore, the results indicate a combined effect of high retinol and low vitamin D on tumorigenesis in females"

Vitamin D receptor gene polymorphisms influence susceptibility to type 1 diabetes mellitus in the Taiwanese population. Chang TJ, Lei HH, Yeh JI, Chiu KC, Lee KC, Chen MC, Tai TY, Chuang LM. Clin Endocrinol (Oxf). 2000 May;52(5):575-80. PMID: 10792336 DOI: 10.1046/j.1365-2265.2000.00985.x CONCLUSIONS Vitamin D receptor gene polymorphisms were associated with type 1 diabetes in a Taiwanese population. However, functional studies are needed to establish the role of the vitamin D receptor in the pathogenesis of type 1 diabetes mellitus.

Statins and vitamin D. Aloia JF, Li-Ng M, Pollack S. Am J Cardiol. 2007 Oct 15;100(8):1329. Epub 2007 Jul 5. No abstract available. PMID: 17920383 A total of 208 women were randomized to receive vitamin D3 (n=104) or placebo (n=104). 51 women were on statins. At baseline, the subjects on statins had a significantly higher 25-OHD level than the subjects who were not on statins (51.2 ± 20.1 nmol/L versus 43.2 ± 18.0 nmol/L respectively, p=0.008). This was also true when averaging 25-OHD levels across the 3-year study period and looking at active and placebo patients separately. 185 subjects had follow-up 25-OHD levels drawn every 6 months during the study. Higher levels were seen in the statin use subgroup whether they were on placebo or active vitamin D (Figure 1Figure 1). There was no interaction seen between vitamin D use and statin use, i.e. the impacts are additive (p=0.5502). This significant difference is comparable to the increase in 25-OHD levels seen in Pérez-Castrillón's study (41 ± 19 versus 47 ± 19 nmol/L, p=0.003) [1]. Although Pérez-Castrillón et al found a statistically significant relation between total cholesterol and 25-OHD (r=0.277, p=0.002), we did not find a significant relation between total cholesterol and 25-OHD in our study population.

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.

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

The calcitriol receptor, also known as the vitamin D receptor (VDR) and also known as NR1I1 (nuclear receptor subfamily 1, group I, member 1), is a member of the nuclear receptor family of transcription factors.[1] Upon activation by vitamin D, the VDR forms a heterodimer with the retinoid-X receptor and binds to hormone response elements on DNA resulting in expression or transrepression of specific geneproducts. In humans, the vitamin D receptor is encoded by the VDR gene.[2]

Diagnosis and treatment of vitamin D deficiency. Cannell JJ, Hollis BW, Zasloff M, Heaney RP. Expert Opin Pharmacother. 2008 Jan;9(1):107-18. PMID: 18076342 DOI 10.1517/14656566.9.1.107

Why "Vitamin D" is not a hormone, and not a synonym for 1,25-dihydroxy-vitamin D, its analogs or deltanoids. Vieth R. J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):571-3. PMID: 15225841 doi:10.1016/j.jsbmb.2004.03.037

Kalsiumaineenvaihdunnan häiriöt ilmenevät hyper- tai hypokalsemiana, hyperkalsiuriana tai luuston aineenvaihduntahäiriöinä (osteoporoosi, osteomalasia, riisitauti, renaalinen osteodystrofia, Pagetin tauti). Epäiltäessä kalsiumaineenvaihdunnan häiriöitä voidaan käyttää seuraavanlaisia tutkimuksia: seerumin ja virtsan kalsium, seerumin ionosoitu kalsium, seerumin fosfaatti, albumiini, alkaalinen fosfataasi ja tarvittaessa sen isoentsyymit, kreatiniini, kloridi ja PTH. PTH:sta on mahdollista määrittää intakti PTH sekä sen keskimolekyyli- ja N-terminaalifragmentti. Luun aineenvaihdunnan biokemiallisia mittareita voidaan käyttää kuvantamaan luun hajoamista ja/tai rakentumista. Luun rakentumisen seerumimarkkereita ovat osteokalsiini ja tyypin 1 prokollageenin aminoterminaalinen propeptidi (PINP). Vastaavasti luunhajoamista kuvastavat virtsan ja seerumin tyypin 1 kollageenin aminoterminaalinen telopeptidi (NTx) sekä seerumin tartraattiresistentti alkalinen fosfataasi (TRAP). Luuston tilaa voidaan selvittää röntgenologisesti natiivikuvin (destruktiot, murtumat ja valemurtumat, resorptio- ja osteoskleroosipesäkkeet). Luun mineraalipitoisuuden määrittämisessä käytetään tiheysmittareita. Koepalan otto luustosta tulee kyseeseen erikoistilanteissa histologisen diagnoosin saamiseksi. Hyperkalsemia Hyperkalsemia on monasti sattumalöydös varsin vähäoireisella epämääräisiä vaivoja valittavalla potilaalla. Tavallisimmat oireet on esitetty taulukossa 1. Tyypillinen hyperkalsemiapotilas on epämääräisistä neuropsykiatrisista oireista kärsivä henkilö. Aikaisemmin tyypilliset munuaiskivipotilaat ovat jäämässä selvään vähemmistöön. Vanhuksilla hyperkalsemia voi aiheuttaa dementian kaltaisen sekavuustilan. Mikäli S-Ca on alle 3 mmol/l, voidaan potilas tutkia rauhassa polikliinisesti. Mikäli arvo sen sijaan on selvästi yli 3 mmol/l ja se vielä nousee perättäisissä mittauksissa, on tutkimuksia kiirehdittävä. Kalsiumarvon

"Hypovitaminosis D is a deficiency of Vitamin D. It can result from: inadequate intake coupled with inadequate sunlight exposure (in particular sunlight with adequate ultra violet B rays), disorders that limit its absorption, conditions that impair conversion of vitamin D into active metabolites, such as liver or kidney disorders, or, rarely, by a number of hereditary disorders.[1] Deficiency results in impaired bone mineralization, and leads to bone softening diseases, rickets in children and osteomalacia in adults, and contributes to osteoporosis.[1] Osteomalacia may also occur rarely as a side-effect of phenytoin use Hypovitaminosis D is typically diagnosed by measuring the concentration in blood of the compound 25-hydroxyvitamin D (calcidiol), which is a precursor to the active form 1,25-dihydroxyvitamin D (calcitriol).[6] One recent review has proposed the following four categories for hypovitaminosis D:[7] * Insufficient 50-100 nmol/L (20-40 ng/mL) * Mild 25-50 nmol/L (10-20 ng/mL) * Moderate 12.5-25.0 nmol/L (5-10 ng/mL) * Severe < 12.5 nmol/L (< 5 ng/mL) Note that 1.0 nmol/L = 0.4 ng/mL for this compound.[8] Other authors have suggested that a 25-hydroxyvitamin D level of 75-80 nmol/L (30-32 ng/mL) may be sufficient

Vitamin D content in Alaskan Arctic zooplankton, fishes, and marine mammals. David E. Kenny 1, Todd M. O'Hara, Tai C. Chen, Zhiren Lu, Xiao Tian, Michael F. Holick. Zoo Biology Volume 23 Issue 1, Pages 33 - 43 Published Online: 13 Feb 2004 Doi: 10.1002/zoo.10104

Use of cod liver oil during the first year of life is associated with lower risk of childhood-onset type 1 diabetes: a large, population-based, case-control study. Stene LC, Joner G; Norwegian Childhood Diabetes Study Group. Am J Clin Nutr. 2003 Dec;78(6):1128-34. PMID: 14668274 Conclusion: Cod liver oil may reduce the risk of type 1 diabetes, perhaps through the antiinflammatory effects of long-chain n-3 fatty acids.

Review article: vitamin D acquisition and breast cancer risk. Pérez-López FR, Chedraui P, Haya J. Reprod Sci. 2009 Jan;16(1):7-19. Review. PMID: 19144887 DOI: 10.1177/1933719108327595 Conclusions: Although there are controversial results, it seems plausible that sufficient endogenous vitamin D levels may have a protective function on mammary cells, reducing breast cancer risk.

A critical review of Vitamin D and cancer: A report of the IARC Working Group on vitamin D William B. Grant Dermato-Endocrinology. Volume 1, Issue 1 January/February 2009 Pages: 25 - 33 The International Agency for Research on Cancer (IARC) released a report, Vitamin D and Cancer, on November 25, 2008. The report focused on the current state of knowledge and level of evidence of a causal association between vitamin D status and cancer risk. Although presenting and evaluating evidence for the beneficial role of UVB and vitamin D in reducing the risk of cancer, it discounted or omitted important evidence in support of the efficacy of vitamin D. The report largely dismissed or ignored ecological studies on the grounds that confounding factors might have affected the findings. The report accepted a preventive role of vitamin D in colorectal cancer but not for breast cancer.

Diagnosis and treatment of vitamin D deficiency. Cannell JJ, Hollis BW, Zasloff M, Heaney RP. Expert Opin Pharmacother. 2008 Jan;9(1):107-18. PMID: 18076342 DOI 10.1517/14656566.9.1.107