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Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient - a randomised, placebo-controlled trial. von Hurst PR, Stonehouse W, Coad J. Br J Nutr. 2009 Sep 28:1-7. [Epub ahead of print] PMID: 19781131 In conclusion, improving vitamin D status in insulin resistant women resulted in improved IR and sensitivity, but no change in insulin secretion. Optimal vitamin D concentrations for reducing IR were shown to be 80-119 nmol/l, providing further evidence for an increase in the recommended adequate levels. Registered Trial No. ACTRN12607000642482.

Baseline serum 25-hydroxy vitamin d is predictive of future glycemic status and insulin resistance: the Medical Research Council Ely Prospective Study 1990-2000. Forouhi NG, Luan J, Cooper A, Boucher BJ, Wareham NJ. Diabetes. 2008 Oct;57(10):2619-25. Epub 2008 Jun 30. PMID: 18591391 doi: 10.2337/db08-0593 CONCLUSIONS: This prospective study reports inverse associations between baseline serum 25(OH)D and future glycemia and insulin resistance. These associations are potentially important in understanding the etiology of abnormal glucose metabolism and warrant investigation in larger, specifically designed prospective studies and randomized controlled trials of supplementation.

Plasma 25-hydroxyvitamin d is associated with markers of the insulin resistant phenotype in nondiabetic adults. Liu E, Meigs JB, Pittas AG, McKeown NM, Economos CD, Booth SL, Jacques PF. J Nutr. 2009 Feb;139(2):329-34. Epub 2008 Dec 23. PMID: 19106328 doi:10.3945/jn.108.093831 After adjusting for age and sex, plasma 25(OH)D was positively associated with ISI(0,120), plasma adiponectin, and HDL cholesterol and inversely associated with plasma triacylglycerol, but these associations were no longer significant after further adjustment for BMI, waist circumference, and current smoking status. 25(OH)D and 2-h post-OGTT glucose were not associated. Among adults without diabetes, vitamin D status was inversely associated with surrogate fasting measures of insulin resistance. These results suggest that vitamin D status may be an important determinant for type 2 diabetes mellitus.

Hypovitaminosis D is associated with insulin resistance and beta cell dysfunction. Chiu KC, Chu A, Go VL, Saad MF. Am J Clin Nutr. 2004 May;79(5):820-5. PMID: 15113720 Conclusions: The data show a positive correlation of 25(OH)D concentration with insulin sensitivity and a negative effect of hypovitaminosis D on ß cell function. Subjects with hypovitaminosis D are at higher risk of insulin resistance and the metabolic syndrome. Further studies are required to explore the underlying mechanisms.

Vitamin D replacement in Asians with diabetes may increase insulin resistance. Taylor AV, Wise PH. Postgrad Med J. 1998 Jun;74(872):365-6. PMID: 9799895 We report three cases of vitamin D replacement in British Asians with vitamin D deficiency and non-insulin-dependent diabetes mellitus. In all cases, replacement resulted in an increase in insulin resistance and a deterioration of glycaemic control

A New Zealand study has found that South Asian women with insulin resistance improved markedly after taking vitamin D supplements Nutrition researcher Pamela von Hurst of the Institute of Food, Nutrition and Human Health at Albany, said while diet and exercise played a major part in the onset of type-2 diabetes, her findings reinforced the importance of vitamin D from the sun and supplements to prevent type-2 diabetes. Initial screening of 235 Auckland women from India, Pakistan and Sri Lanka aged 20 and older, revealed 47 per cent were insulin deficient and 84 per cent were vitamin D deficient. The 81 recruited for the study were split into two groups for a randomised controlled trial and given a vitamin D supplement or placebo. As well as an improvement in insulin resistance among those who took vitamin D for six months, Ms Von Hurst said post-menopausal women in the study also showed a reduced rate of bone breakdown.

"Women from India, Pakistan and Sri Lanka with insulin resistance showed marked improvement after taking vitamin D supplements, says a study. Von Hurst, nutrition lecturer at the Institute of Food, Nutrition and Human Health at Albany, conducted the study for her doctoral thesis. Insulin resistance is largely symptom-free and sufferers are unaware of their condition. 'Once it has fully developed into type-2 diabetes, it can be treated, but not cured,' says Von Hurst. Von Hurst says that while diet and exercise play a major part in the onset of type-2 diabetes, her findings reinforce the importance of vitamin D from the sun and supplements to prevent type-2 diabetes. She also found evidence of vitamin D increasing bone strength in older women. "

Improved cholecalciferol nutrition in rats is noncalcemic, suppresses parathyroid hormone and increases responsiveness to 1, 25-dihydroxycholecalciferol. Vieth R, Milojevic S, Peltekova V. J Nutr. 2000 Mar;130(3):578-84. PMID: 10702588 We conclude suppression of 1,25(OH)(2)D and PTH, and higher renal VDR mRNA and 24-hydroxylase did not involve higher free 1,25(OH)(2)D concentration or a first pass effect at the gut. Thus, 25(OH)D or a metabolite other than 1,25(OH)(2)D is a physiological, transcriptionally and biochemically active, noncalcemic vitamin D metabolite. When viewed from a perspective that starts with higher vitamin D nutrition, the results indicate that low vitamin D nutrition may bring about a form of resistance to 1,25(OH)2D. This situation would explain why, in humans, nutritional rickets and osteomalacia are commonly associated with normal or increased levels of 1,25(OH)2D (Chesney et al. 1981Citation , Eastwood et al. 1979Citation , Garabedian et al. 1983Citation ,Rasmussen et al. 1980Citation )-these are not like the low hormone levels associated with any other endocrine-deficiency disorder. A connection between lower vitamin D nutrition and vitamin D resistance helps to explain why the supposedly inactive compound 25(OH)D is more relevant in diagnosing nutritional rickets than is the active hormone 1,25(OH)2D. If the features of improved vitamin D nutrition shown here were demonstrated for any newly synthesized compound, the compound would be classified as a noncalcemic 1,25(OH)2D analogue (Brown et al. 1989Citation , Finch et al. 1999Citation , Goff et al. 1993Citation , Koshizuka et al. 1999Citation ). Thus, we contend that 25(OH)D or a metabolite of it other than 1,25(OH)2D exists as a physiological and biologically-active noncalcemic vitamin D metabolite whose effects require further examination, particularly in relationship to studies involving the synthetic analogs of 1,25(OH)2D.

Maghbooli Z, Hossein-Nezhad A, Karimi F, Shafaei AR, Larijani B. Correlation between vitamin D(3) deficiency and insulin resistance in pregnancy. Diabetes Metab Res Rev. 2007 Jul 2; [Epub ahead of print] PMID: 17607661 [PubMed - as supplied by publish

In conclusion, genetic variations of DBP are associated with insulin resistance in Japanese with normal glucose tolerance, which might contribute to the development of type 2 diabetes. Variations in vitamin D-binding protein (group-specific component protein) are associated with fasting plasma insulin levels in Japanese with normal glucose tolerance. Hirai M, Suzuki S, Hinokio Y, Hirai A, Chiba M, Akai H, Suzuki C, Toyota T. J Clin Endocrinol Metab. 2000 May;85(5):1951-3. PMID: 10843180

Vitamin D and type 2 diabetes: are we ready for a prevention trial? Scragg R. Diabetes. 2008 Oct;57(10):2565-6. PMID: 18820212 doi: 10.2337/db08-0879 Despite evidence from the current article (3) and the Finnish study (17), doubts still remain about whether low vitamin status is a cause of type 2 diabetes. Further cohort studies are required, assessing baseline vitamin D status using blood 25(OH)D to be sure that the Ely and Finnish studies are not false-positive results. Glucose clamp studies are also required because we are still not sure of the mechanism influenced by vitamin D-whether it is insulin resistance, secretion, or both. But most importantly, given that nearly three decades have passed since the first studies linking vitamin D with insulin metabolism (6,7), well-designed clinical trials of the effect of vitamin D supplementation on glycemia status and diabetes risk are urgently required to settle this question. And they need to prevent past mistakes. In particular, the vitamin D dose given in such trials needs to be high enough-above 2,000 IU per day (19)-to raise blood 25(OH)D levels above 80 nmol/l because diabetes risk is lowest at this level (9,20). If well-designed trials are carried out and confirm a protective effect from vitamin D, it could be used by the general population as a simple and cheap solution to help prevent the diabetes epidemic.

Serum 25-hydroxyvitamin D concentration and subsequent risk of type 2 diabetes. Mattila C, Knekt P, Männistö S, Rissanen H, Laaksonen MA, Montonen J, Reunanen A. Diabetes Care. 2007 Oct;30(10):2569-70. Epub 2007 Jul 12. PMID: 17626891 doi: 10.2337/dc07-0292 We found a significant inverse association between serum 25OHD and risk of type 2 diabetes in the simple model. However, the association was attenuated in the multivariate analysis, adjusting for potential risk factors of type 2 diabetes. To our knowledge, this is the first cohort study investigating the association between serum 25OHD and incidence of type 2 diabetes. Our results are in line with those from the Nurses' Health Study (5), where an inverse association was observed for the intake of vitamin D supplements. We could not differentiate whether the results depended on the effect of vitamin D deficiency on β-cell function or on insulin resistance. In summary, the results are in line with the hypothesis that a high serum 25OHD concentration may reduce the risk of type 2 diabetes. Further research is needed to confirm the association and to distinguish between the independent role of vitamin D and the role of healthy dietary and lifestyle patterns in reducing the risk of type 2 diabetes.

Lääkäri Juha-Petri Ruoholan väitöskirjan mukaan liian vähäinen D-vitamiinin saanti voi altistaa rasitusmurtumien syntymiselle urheilijoille. Tutkimuksen mukaan murtumapotilailla oli selkeästi normaalia alhaisemmat D-vitamiinitasot. On olemassa erityinen TRACP5b-entsyymi (tartrate-resistant acid phosphatase 5b), joka antaa aika selvän kuvan luun hajotuksen määrästä elimistössä. Tätä entsyymiä mitataan osteoporoosin (luukato) diagnostiikassa ja yllätyksettömästi sama entsyymi soveltui myös rasitusmurtumien osoittamiseen. Kohonnut seerumin TRACP5b-arvo nosti murtuman todennäköisyyden kahdeksankertaiseksi verrokkeihin nähden näissä Ruoholan tutkimuksissa. D-vitamiinia voi siis lämpimästi suositella urheilijoille varsinkin talvikuukausina, jolloin auringon kautta saatava D-vitamiinivaikutus on Suomessa lähes olematon.

Pittas AG, Harris SS, Stark PC, Dawson-Hughes B. The Effects of Calcium and Vitamin D Supplementation on Blood Glucose and Markers of Inflammation in Non-diabetic Adults. Diabetes Care. 2007 Feb 2; [Epub ahead of print] PMID: 17277040 [PubMed - as sup

Zittermann A. Vitamin D and disease prevention with special reference to cardiovascular disease. Prog Biophys Mol Biol. 2006 Sep;92(1):39-48. Epub 2006 Feb 28. Review. PMID: 16600341 [PubMed - indexed for MEDLINE]

Reinehr T, de Sousa G, Alexy U, Kersting M, Andler W. Vitamin D status and parathyroid hormone in obese children before and after weight loss. Eur J Endocrinol. 2007 Aug;157(2):225-32. PMID: 17656603 [PubMed - in process]