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Continuous changes in the healthcare reimbursement criteria require executives across the industry to focus on enterprise-wide changes that have a positive effect on supply chain savings. It's a complex problem and it's easy to get distracted on one issue when having the ability to see a clear BIG picture of your entire supply chain is what can lead to the most dramatic results and return on investments. Register for MHS' webinar on November 01 (2:00pm EST) to learn about how their customers experience an average 4:1 ROI with continual savings into the millions and a positive financial impact to their bottom line through inventory reduction, avoidance of obsolete and expired inventory, improved charge capture for each patient, and physician preference card optimization. Click on http://bit.ly/UvD3nq Presenters *Michael Ferris: Co-Founder, MHS with over 30 years of supply chain management experience *Steve Basiliere: Former Director of Supply Chain Services at Saints Medical Center, Lowell, MA *Art Kozyrovicius: Finance and Procurement Systems Support at New York-Presbyterian Hospital, New York, NY WHY ATTEND? Join a unique discussion with healthcare supply chain thought leaders and understand how to drive significant and sustainable supply chain operational improvements. Get a jump on making an immediate and positive impact on your bottom line as you head into 2013. Register by clicking on http://bit.ly/UvD3nq Note: Event will be online, through WebEx Please Register at http://bit.ly/UvD3nq

Serum 25-hydroxyvitamin D status of the US population: 1988-1994 compared with 2000-2004. Looker AC, Pfeiffer CM, Lacher DA, Schleicher RL, Picciano MF, Yetley EA. Am J Clin Nutr. 2008 Dec;88(6):1519-27. PMID: 19064511 doi:10.3945/ajcn.2008.26182 Conclusions: Overall, mean serum 25(OH)D was lower in 2000-2004 than 1988-1994. Assay changes unrelated to changes in vitamin D status accounted for much of the difference in most population groups. In an adult subgroup, combined changes in BMI, milk intake, and sun protection appeared to contribute to a real decline in vitamin D status. In summary, age-standardized mean serum 25(OH)D concentrations based on observed values were significantly lower in 2000-2004 than in 1988-1994 in all groups examined. Adjustment for assay changes noticeably reduced the difference between surveys. However, mean serum 25(OH)D concentrations remained significantly lower in males (except Mexican Americans) in NHANES 2000-2004 than in NHANES III, even after adjustment for assay differences. This remaining difference likely represents a real decline in vitamin D status. Changes in BMI, milk intake, and sun protection appeared to contribute to this decline in a subgroup of non-Hispanic white adults. The possibility that trends in overweight, sun protection, and milk intake may continue supports the need to continue monitoring the serum 25(OH)D status of the population

Pharmacokinetics of a single, large dose of cholecalciferol. Ilahi M, Armas LA, Heaney RP. Am J Clin Nutr. 2008 Mar;87(3):688-91. PMID: 1832660 Conclusions: Cholecalciferol (100 000 IU) is a safe, effective, and simple way to increase calcidiol concentrations. The dosing interval should be ≤2 mo to ensure continuous serum calcidiol concentrations above baseline. Our study highlights that 100 000 IU cholecalciferol is a safe, efficient, and cost-effective means to increase calcidiol concentrations in the elderly. From this study we can safely recommend 100 000 IU cholecalciferol dosed every 2 mo in persons with moderate baseline calcidiol concentrations. However, in those persons with baseline calcidiol concentrations < 20 ng/mL, even this large dose will not adequately raise their calcidiol concentrations.

Robert P. Heaney is John A. Creighton University Professor, Creighton University, Omaha, Nebraska, United States. Hominid evolution took place in an environment (equatorial East Africa) that provided a superabundance of both calcium and vitamin D, the first in available foods and the second through conversion of 7-dehydrocholesterol to pre-vitamin D in the skin, a reaction catalysed by the intense solar ultraviolet (UV) radiation. Seemingly as a consequence, the evolving human physiology incorporated provisions to prevent the potential of toxic excesses of both nutrients. For vitamin D the protection was of two sorts: skin pigmentation absorbed the critical UV wavelengths and thereby limited dermal synthesis of cholecalciferol; and slow delivery of vitamin D from the skin into the bloodstream left surplus vitamin in the skin, where continuing sun exposure led to its photolytic degradation to inert compounds. For calcium, the adaptation consisted of very inefficient calcium absorption, together with poor to absent systemic conservation. The latter is reflected in unregulated dermal calcium losses, a high sensitivity of renal obligatory calcium loss to other nutrients in the diet and relatively high quantities of calcium in the digestive secretions. Today, chimpanzees in the original hominid habitat have diets with calcium nutrient densities in the range of 2 to 2.5 mmol per 100 kcal, and hunter-gatherer humans in Africa, South America and New Guinea still have diets very nearly as high in calcium (1.75 to 2 mmol per 100 kcal) (Eaton and Nelson, 1991). With energy expenditure of 3 000 kcal per day (a fairly conservative estimate for a contemporary human doing physical work), such diets would provide substantially in excess of 50 mmol of calcium per day. By contrast, median intake in women in North America and in many European countries today is under 15 mmol per day. Two factors altered the primitive situation: the migration of humans from Africa to higher latitude

Evidence continues to pile up that the sunshine vitamin protects against much more than bone-softening rickets. Vitamin D, also found in milk and oily fish, is becoming king, from fighting colds to preventing cancer. \n\nInvestigators at the Medical University of South Carolina shut down part of a National Institutes of Health study that left nursing mothers and infants deficient, even though the mothers received the maximum safe amount of vitamin D allowed by the Institute of Medicine.\n\nBut here's the kicker. New research suggests we're not getting nearly enough, and recommended levels may be woefully inadequate.

The Diet-Heart Hypothesis: Subdividing Lipoproteins Two posts ago, we made the rounds of the commonly measured blood lipids (total cholesterol, LDL, HDL, triglycerides) and how they associate with cardiac risk. It's important to keep in mind that many things associate with cardiac risk, not just blood lipids. For example, men with low serum vitamin D are at a 2.4-fold greater risk of heart attack than men with higher D levels. That alone is roughly equivalent to the predictive power of the blood lipids you get measured at the doctor's office. Coronary calcium scans (a measure of blood vessel calcification) also associate with cardiac risk better than the most commonly measured blood lipids. Lipoproteins Can be Subdivided into Several Subcategories In the continual search for better measures of cardiac risk, researchers in the 1980s decided to break down lipoprotein particles into sub-categories. One of these researchers is Dr. Ronald M. Krauss. Krauss published extensively on the association between lipoprotein size and cardiac risk, eventually concluding (source): The plasma lipoprotein profile accompanying a preponderance of small, dense LDL particles (specifically LDL-III) is associated with up to a threefold increase in the susceptibility of developing [coronary artery disease]. This has been demonstrated in case-control studies of myocardial infarction and angiographically documented coronary disease. Krauss found that small, dense LDL (sdLDL) doesn't travel alone: it typically comes along with low HDL and high triglycerides*. He called this combination of factors "lipoprotein pattern B"; its opposite is "lipoprotein pattern A": large, buoyant LDL, high HDL and low triglycerides. Incidentally, low HDL and high triglycerides are hallmarks of the metabolic syndrome, the quintessential modern metabolic disorder. Krauss and his colleagues went on to hypothesize that sdLDL promotes atherosclerosis because of its ability to penetrate the artery wall more easily

"Dr. Jodie Burton is the acting principal investigator (PI) of the dose-escalation trial of oral vitamin D3 with calcium supplementation in patients with multiple sclerosis with Dr. O'Connor. She started the trial as his fellow, while doing an additional 2 years of training in MS specifically after she received her neurology certification. She completed her fellowship training in 2007. Now she is staff doing clinical research and continuing with the vitamin D trial. As of August 2009, she will be Assistant Professor in Neurology in the Department of Clinical Neuroscience in Calgary and at the University of Calgary. She will be part of the MS team there with Dr. Luanne Metz and the MS group. Please scroll down for an abstract of the trial: A Phase I/II dose-escalation trial of oral vitamin D3 with calcium supplementation in patients with multiple sclerosis." Conclusions: High-dose VD3 (~10 000 IU/day, possibly higher) in MS is safe and tolerable, with evidence of clinical improvement."

Urgent action needed to improve vitamin D status among older people in England! Hirani V, Tull K, Ali A, Mindell J. Age Ageing. 2009 Nov 23. [Epub ahead of print] PMID: 19934073 CONCLUSIONS: poor vitamin D status of older people continues to be a public health problem in England. Hypovitaminosis D is associated with many risk factors and poor health outcomes. There is now an urgent need for a uniform policy on assessment and dietary supplementation of vitamin D in older people to prevent poor vitamin D status and its negative consequences

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

The clinical importance of vitamin D (cholecalciferol): a paradigm shift with implications for all healthcare providers. Vasquez A, Manso G, Cannell J. Altern Ther Health Med. 2004 Sep-Oct;10(5):28-36; quiz 37, 94. Review. PMID: 15478784

"A recent article in the New York Times highlighted an ongoing problem with the accuracy of vitamin D testing at the largest commercial clinical laboratory, Quest Diagnostics. It has become clear from shared experience among vitamin D experts, including myself, that Quest Diagnostics has a problem with seemingly random over-estimation of vitamin D levels."