More likely the quality on the brand of drops went to shit.
MESO-Rx
Anabolic Steroids
Vitamin D
- Thread starter Michael Scally MD
- Start date
More likely the quality on the brand of drops went to shit.
Olson ML, Maalouf NM, Oden JD, White PC, Hutchison MR. Vitamin D Deficiency in Obese Children and Its Relationship to Glucose Homeostasis. Journal of Clinical Endocrinology & Metabolism. Vitamin D Deficiency in Obese Children and Its Relationship to Glucose Homeostasis
Objectives: The aim of the study was to compare the prevalence of vitamin D deficiency in obese and non-overweight children in North Texas, to examine relationships between dietary habits and 25-hydroxyvitamin D [25(OH)D] level in obese children, and to examine the relationship between 25(OH)D level and markers of abnormal glucose metabolism and blood pressure.
Patients and Methods: Using a cross-sectional design, systolic and diastolic blood pressure, dietary information, serum 25(OH)D, fasting glucose and insulin, 2-h glucose from oral glucose tolerance test, hemoglobin A1c, and homeostasis model assessment of insulin resistance were recorded for 411 obese subjects (6–16 yr old) at an obesity referral clinic. 25(OH)D was also obtained from 87 control non-overweight subjects (6–16 yr old).
Results: Ninety-two percent of obese subjects had a 25(OH)D level below 75 nmol/liter, and 50% were below 50 nmol/liter. Among non-overweight subjects, these frequencies were 68 and 22%, respectively (both P < 0.01 compared with obese subjects). 25(OH)D was negatively associated with soda intake (P < 0.001), juice intake (P = 0.009), and skipping breakfast (P < 0.001). 25(OH)D was negatively correlated with homeostasis model assessment of insulin resistance (r = ?0.19; P = 0.001) and 2-h glucose (r = ?0.12; P = 0.04) after adjustment for body mass index and age but was not correlated with hemoglobin A1c, systolic blood pressure Z score, or diastolic blood pressure Z score.
Conclusions: Vitamin D deficiency is common in children in this southern United States location and is significantly more prevalent in obese children. Lower 25(OH)D level is associated with risk factors for type 2 diabetes in obese children.
Objectives: The aim of the study was to compare the prevalence of vitamin D deficiency in obese and non-overweight children in North Texas, to examine relationships between dietary habits and 25-hydroxyvitamin D [25(OH)D] level in obese children, and to examine the relationship between 25(OH)D level and markers of abnormal glucose metabolism and blood pressure.
Patients and Methods: Using a cross-sectional design, systolic and diastolic blood pressure, dietary information, serum 25(OH)D, fasting glucose and insulin, 2-h glucose from oral glucose tolerance test, hemoglobin A1c, and homeostasis model assessment of insulin resistance were recorded for 411 obese subjects (6–16 yr old) at an obesity referral clinic. 25(OH)D was also obtained from 87 control non-overweight subjects (6–16 yr old).
Results: Ninety-two percent of obese subjects had a 25(OH)D level below 75 nmol/liter, and 50% were below 50 nmol/liter. Among non-overweight subjects, these frequencies were 68 and 22%, respectively (both P < 0.01 compared with obese subjects). 25(OH)D was negatively associated with soda intake (P < 0.001), juice intake (P = 0.009), and skipping breakfast (P < 0.001). 25(OH)D was negatively correlated with homeostasis model assessment of insulin resistance (r = ?0.19; P = 0.001) and 2-h glucose (r = ?0.12; P = 0.04) after adjustment for body mass index and age but was not correlated with hemoglobin A1c, systolic blood pressure Z score, or diastolic blood pressure Z score.
Conclusions: Vitamin D deficiency is common in children in this southern United States location and is significantly more prevalent in obese children. Lower 25(OH)D level is associated with risk factors for type 2 diabetes in obese children.
Nimptsch K, Platz EA, Willett WC, Giovannucci E. Association between plasma 25-OH vitamin D and testosterone levels in men. Clinical Endocrinology. Association between plasma 25-OH vitamin D and testosterone levels in men - Nimptsch - Clinical Endocrinology - Wiley Online Library
Objective:? A small randomized controlled trial suggested that vitamin D might increase the production of testosterone in men, which is supported by experimental studies in animals and a cross-sectional study showing positive associations between plasma 25-hydroxyvitamin D [25(OH)D] and testosterone and concordant seasonal variation of both biomarkers.
Design and Measurements:? We investigated the cross-sectional association of plasma 25(OH)D levels and total and free testosterone measured by immunoassay in 1,362 male participants of the Health Professionals Follow-up Study who were selected for a nested case-control study on prostate cancer using multivariate adjusted linear and restricted cubic spline regression models.
Results:? 25(OH)D was positively associated with total and free testosterone levels. From the lowest to the highest 25(OH)D quintile, multivariate adjusted means (95% confidence interval) were 18.5 (17.7; 19.4), 19.4 (18.6; 20.2), 19.6 (18.8; 20.4), 20.1 (19.3; 20.9) and 20.0 (19.1; 20.8); p-trend=0.003) for total testosterone and 97.7 (93.9; 101.5), 98.2 (94.1; 102.2), 99.2 (95.2; 103.2), 100.7 (96.9; 104.5) and 101.5 (97.6; 105.4; p-trend=0.03) for free testosterone. The shapes of the dose-response curves indicate that the association between 25(OH)D and total and free testosterone is linear at lower levels of 25(OH)D (below approximately 75-85 nmol/l), reaching a plateau at higher levels. Unlike for 25(OH)D, we did not observe any seasonal variation of testosterone concentrations.
Conclusion:? This study supports previously reported positive associations between vitamin D and testosterone although we did not observe parallel seasonal variation patterns. Possible causality and direction of the vitamin D-testosterone association deserve further scientific investigation.
Objective:? A small randomized controlled trial suggested that vitamin D might increase the production of testosterone in men, which is supported by experimental studies in animals and a cross-sectional study showing positive associations between plasma 25-hydroxyvitamin D [25(OH)D] and testosterone and concordant seasonal variation of both biomarkers.
Design and Measurements:? We investigated the cross-sectional association of plasma 25(OH)D levels and total and free testosterone measured by immunoassay in 1,362 male participants of the Health Professionals Follow-up Study who were selected for a nested case-control study on prostate cancer using multivariate adjusted linear and restricted cubic spline regression models.
Results:? 25(OH)D was positively associated with total and free testosterone levels. From the lowest to the highest 25(OH)D quintile, multivariate adjusted means (95% confidence interval) were 18.5 (17.7; 19.4), 19.4 (18.6; 20.2), 19.6 (18.8; 20.4), 20.1 (19.3; 20.9) and 20.0 (19.1; 20.8); p-trend=0.003) for total testosterone and 97.7 (93.9; 101.5), 98.2 (94.1; 102.2), 99.2 (95.2; 103.2), 100.7 (96.9; 104.5) and 101.5 (97.6; 105.4; p-trend=0.03) for free testosterone. The shapes of the dose-response curves indicate that the association between 25(OH)D and total and free testosterone is linear at lower levels of 25(OH)D (below approximately 75-85 nmol/l), reaching a plateau at higher levels. Unlike for 25(OH)D, we did not observe any seasonal variation of testosterone concentrations.
Conclusion:? This study supports previously reported positive associations between vitamin D and testosterone although we did not observe parallel seasonal variation patterns. Possible causality and direction of the vitamin D-testosterone association deserve further scientific investigation.
Heijboer AC, Blankenstein MA, Kema IP, Buijs MM. Accuracy of 6 Routine 25-Hydroxyvitamin D Assays; Influence of Vitamin D Binding Protein Concentration. Clin Chem. Accuracy of 6 Routine 25-Hydroxyvitamin D Assays; Influence of Vitamin D Binding Protein Concentration
BACKGROUND: Recent recognition of its broad pathophysiological importance has triggered an increased interest in 25-hydroxyvitamin D [25(OH)D]. By consequence, throughput in 25(OH)D testing has become an issue for clinical laboratories, and several automated assays for measurement of 25(OH)D are now available. The aim of this study was to test the accuracy and robustness of these assays by comparing their results to those of an isotope dilution/online solid-phase extraction liquid chromatography/tandem mass spectrometry (ID-XLC-MS/MS) method. We put specific focus on the influence of vitamin D-binding protein (DBP) by using samples with various concentrations of DBP.
METHODS: We used 5 automated assays (Architect, Centaur, iSYS, Liaison, and Elecsys), 1 RIA (Diasorin) preceded by extraction, and an ID-XLC-MS/MS method to measure 25(OH)D concentrations in plasma samples of 51 healthy individuals, 52 pregnant women, 50 hemodialysis patients, and 50 intensive care patients. Using ELISA, we also measured DBP concentrations in these samples.
RESULTS: Most of the examined 25(OH)D assays showed significant deviations in 25(OH)D concentrations from those of the ID-XLC-MS/MS method. As expected, DBP concentrations were higher in samples of pregnant women and lower in samples of IC patients compared to healthy controls. In 4 of the 5 fully automated 25(OH)D assays, we observed an inverse relationship between DBP concentrations and deviations from the ID-XLC-MS/MS results.
CONCLUSIONS:25(OH)D measurements performed with most immunoassays suffer from inaccuracies that are DBP concentration dependent. Therefore, when interpreting results of 25(OH)D measurements, careful consideration of the measurement method is necessary.
BACKGROUND: Recent recognition of its broad pathophysiological importance has triggered an increased interest in 25-hydroxyvitamin D [25(OH)D]. By consequence, throughput in 25(OH)D testing has become an issue for clinical laboratories, and several automated assays for measurement of 25(OH)D are now available. The aim of this study was to test the accuracy and robustness of these assays by comparing their results to those of an isotope dilution/online solid-phase extraction liquid chromatography/tandem mass spectrometry (ID-XLC-MS/MS) method. We put specific focus on the influence of vitamin D-binding protein (DBP) by using samples with various concentrations of DBP.
METHODS: We used 5 automated assays (Architect, Centaur, iSYS, Liaison, and Elecsys), 1 RIA (Diasorin) preceded by extraction, and an ID-XLC-MS/MS method to measure 25(OH)D concentrations in plasma samples of 51 healthy individuals, 52 pregnant women, 50 hemodialysis patients, and 50 intensive care patients. Using ELISA, we also measured DBP concentrations in these samples.
RESULTS: Most of the examined 25(OH)D assays showed significant deviations in 25(OH)D concentrations from those of the ID-XLC-MS/MS method. As expected, DBP concentrations were higher in samples of pregnant women and lower in samples of IC patients compared to healthy controls. In 4 of the 5 fully automated 25(OH)D assays, we observed an inverse relationship between DBP concentrations and deviations from the ID-XLC-MS/MS results.
CONCLUSIONS:25(OH)D measurements performed with most immunoassays suffer from inaccuracies that are DBP concentration dependent. Therefore, when interpreting results of 25(OH)D measurements, careful consideration of the measurement method is necessary.
I recently ran 2 Vitamin D tests on myself.
I'm a slightly brown skinned white guy.
When I ran my first test I was literally dark brown from slow and steady Sun exposure all last summer. It was rare for me to be anywhere near this dark.
My normal diet also includes several Vitamin D sources including 2 Organic eggs every morning, a glass of chocolate milk (fortified milk and Ovaltime) after my workouts, and a fair bit of salmon and tuna. (2-3x per week)
I tested at 31. The healthy range was from 30-100 I believe. The test also broke down the units of Vit d by their source and all 31 units was from 'natural' and it showed none from supplementation.
I then added 5000 units of vitamin d supplementation. Furthermore cooler weather came and I completely lost my tan. I retested and was at 60 units. The test showed something like 25 units from supplementation. I know some of those breakdowns don't make sense but that is what it said.
It's also worth noting that because of my rather extreme lifestyle I've broken approximately 20 bones throwout my life. Now some of them it wasn't surprising at all that I broke some bones. But several of those breaks I was pretty shocked that the X-ray showed a fracture. It's also worth noting that from a very young ago I was taught to avoid Sun exposure and did exactly that very effectively for about 20 years.
I'm of the opinion that proper Vitamin D supplementation and Sun exposure could have lowered my number of injuries substantially and furthmore could have altered my entire racing career. Alas, what's done is done.
I'm a slightly brown skinned white guy.
When I ran my first test I was literally dark brown from slow and steady Sun exposure all last summer. It was rare for me to be anywhere near this dark.
My normal diet also includes several Vitamin D sources including 2 Organic eggs every morning, a glass of chocolate milk (fortified milk and Ovaltime) after my workouts, and a fair bit of salmon and tuna. (2-3x per week)
I tested at 31. The healthy range was from 30-100 I believe. The test also broke down the units of Vit d by their source and all 31 units was from 'natural' and it showed none from supplementation.
I then added 5000 units of vitamin d supplementation. Furthermore cooler weather came and I completely lost my tan. I retested and was at 60 units. The test showed something like 25 units from supplementation. I know some of those breakdowns don't make sense but that is what it said.
It's also worth noting that because of my rather extreme lifestyle I've broken approximately 20 bones throwout my life. Now some of them it wasn't surprising at all that I broke some bones. But several of those breaks I was pretty shocked that the X-ray showed a fracture. It's also worth noting that from a very young ago I was taught to avoid Sun exposure and did exactly that very effectively for about 20 years.
I'm of the opinion that proper Vitamin D supplementation and Sun exposure could have lowered my number of injuries substantially and furthmore could have altered my entire racing career. Alas, what's done is done.
Risks: When Too Much Vitamin D Is Too Much
http://www.nytimes.com/2012/01/17/health/research/risks-when-too-much-vitamin-d-is-too-much.html
January 12, 2012
By NICHOLAS BAKALAR
Too much vitamin D may be just as bad as too little, a recent study suggests.
Vitamin D supplements reduce blood levels of C-reactive protein, or CRP, an indicator of inflammation that is linked to cardiovascular disease. But supplements help only up to a point.
In a study of more than 15,000 adults ages 18 to 85, researchers at Johns Hopkins University found that after blood levels exceeded 21 nanograms per milliliter — the lower end of what is usually considered normal — any additional vitamin D led to an increase in CRP.
The association held after the researchers accounted for the effects of factors like obesity, smoking, cholesterol and high blood pressure. There was also a dose-response relationship: Above 21 units, each 10-unit increase in vitamin D was accompanied by an increase of 0.06 milligrams per deciliter in CRP.
“Vitamin D is good to a certain level,” said the lead author, Dr. Muhammad Amer, an assistant professor of medicine at Johns Hopkins. “But don’t just keep on taking it. Have your blood drawn and your levels checked.”
Previous studies of vitamin D supplementation have produced inconsistent results, with some trials showing a decrease in inflammatory markers and others showing no effect. The finding that the benefit is apparent only at lower levels of vitamin D, the authors write, may help explain these conflicting findings.
The study was published online in The American Journal of Cardiology.
Amer M, Qayyum R. Relation Between Serum 25-Hydroxyvitamin D and C-Reactive Protein in Asymptomatic Adults (From the Continuous National Health and Nutrition Examination Survey 2001 to 2006). The American journal of cardiology 2012;109(2):226-30. Elsevier
The inverse relation between vitamin D supplementation and inflammatory biomarkers among asymptomatic adults is not settled. We hypothesized that the inverse relation is present only at lower levels and disappears at higher serum levels of vitamin D. We examined the relation between 25-hydroxyvitamin D [25(OH)D] and C-reactive protein (CRP) using the continuous National Health and Nutrition Examination Survey data from 2001 to 2006. Linear spline [single knot at median serum levels of 25(OH)D] regression models were used. The median serum 25(OH)D and CRP level was 21 ng/ml (interquartile range 15 to 27) and 0.21 mg/dl (interquartile range 0.08 to 0.5), respectively. On univariate linear regression analysis, CRP decreased [geometric mean CRP change 0.285 mg/dl for each 10-ng/ml change in 25(OH)D, 95% confidence interval [CI] ?0.33 to ?0.23] as 25(OH)D increased ?21 ng/ml. However, an increase in 25(OH)D to >21 ng/ml was not associated with any significant decrease [geometric mean CRP change 0.05 mg/dl for each 10-ng/ml change in 25(OH)D, 95% CI ?0.11 to 0.005) in CRP. The inverse relation between 25(OH)D below its median and CRP remained significant [geometric mean CRP change 0.11 mg/dl for each 10-ng/ml change in 25(OH)D, 95% CI 0.16 to ?0.04] on multivariate linear regression analysis. Additionally, we observed a positive relation between 25(OH)D above its median and CRP [geometric mean CRP change 0.06 mg/dl for each 10-ng/ml change in 25(OH)D, 95% CI 0.02 to 0.11) after adjusting for traditional cardiovascular risk factors. In conclusion, from this cohort of asymptomatic adults, independent of traditional cardiovascular risk factors, we observed a statistically significant inverse relation between 25(OH)D at levels <21 ng/ml and CRP. We found that 25(OH)D at a level ?21 ng/ml is associated with an increase in serum CRP. It is possible that the role of vitamin D supplementation to reduce inflammation is beneficial only among those with a lower serum 25(OH)D.
http://www.nytimes.com/2012/01/17/health/research/risks-when-too-much-vitamin-d-is-too-much.html
January 12, 2012
By NICHOLAS BAKALAR
Too much vitamin D may be just as bad as too little, a recent study suggests.
Vitamin D supplements reduce blood levels of C-reactive protein, or CRP, an indicator of inflammation that is linked to cardiovascular disease. But supplements help only up to a point.
In a study of more than 15,000 adults ages 18 to 85, researchers at Johns Hopkins University found that after blood levels exceeded 21 nanograms per milliliter — the lower end of what is usually considered normal — any additional vitamin D led to an increase in CRP.
The association held after the researchers accounted for the effects of factors like obesity, smoking, cholesterol and high blood pressure. There was also a dose-response relationship: Above 21 units, each 10-unit increase in vitamin D was accompanied by an increase of 0.06 milligrams per deciliter in CRP.
“Vitamin D is good to a certain level,” said the lead author, Dr. Muhammad Amer, an assistant professor of medicine at Johns Hopkins. “But don’t just keep on taking it. Have your blood drawn and your levels checked.”
Previous studies of vitamin D supplementation have produced inconsistent results, with some trials showing a decrease in inflammatory markers and others showing no effect. The finding that the benefit is apparent only at lower levels of vitamin D, the authors write, may help explain these conflicting findings.
The study was published online in The American Journal of Cardiology.
Amer M, Qayyum R. Relation Between Serum 25-Hydroxyvitamin D and C-Reactive Protein in Asymptomatic Adults (From the Continuous National Health and Nutrition Examination Survey 2001 to 2006). The American journal of cardiology 2012;109(2):226-30. Elsevier
The inverse relation between vitamin D supplementation and inflammatory biomarkers among asymptomatic adults is not settled. We hypothesized that the inverse relation is present only at lower levels and disappears at higher serum levels of vitamin D. We examined the relation between 25-hydroxyvitamin D [25(OH)D] and C-reactive protein (CRP) using the continuous National Health and Nutrition Examination Survey data from 2001 to 2006. Linear spline [single knot at median serum levels of 25(OH)D] regression models were used. The median serum 25(OH)D and CRP level was 21 ng/ml (interquartile range 15 to 27) and 0.21 mg/dl (interquartile range 0.08 to 0.5), respectively. On univariate linear regression analysis, CRP decreased [geometric mean CRP change 0.285 mg/dl for each 10-ng/ml change in 25(OH)D, 95% confidence interval [CI] ?0.33 to ?0.23] as 25(OH)D increased ?21 ng/ml. However, an increase in 25(OH)D to >21 ng/ml was not associated with any significant decrease [geometric mean CRP change 0.05 mg/dl for each 10-ng/ml change in 25(OH)D, 95% CI ?0.11 to 0.005) in CRP. The inverse relation between 25(OH)D below its median and CRP remained significant [geometric mean CRP change 0.11 mg/dl for each 10-ng/ml change in 25(OH)D, 95% CI 0.16 to ?0.04] on multivariate linear regression analysis. Additionally, we observed a positive relation between 25(OH)D above its median and CRP [geometric mean CRP change 0.06 mg/dl for each 10-ng/ml change in 25(OH)D, 95% CI 0.02 to 0.11) after adjusting for traditional cardiovascular risk factors. In conclusion, from this cohort of asymptomatic adults, independent of traditional cardiovascular risk factors, we observed a statistically significant inverse relation between 25(OH)D at levels <21 ng/ml and CRP. We found that 25(OH)D at a level ?21 ng/ml is associated with an increase in serum CRP. It is possible that the role of vitamin D supplementation to reduce inflammation is beneficial only among those with a lower serum 25(OH)D.
Zhao G, Ford ES, Li C, Croft JB. Serum 25-hydroxyvitamin D levels and all-cause and cardiovascular disease mortality among US adults with hypertension: the NHANES linked mortality study. J Hypertens 2012;30(2):284-9. Serum 25-hydroxyvitamin D levels and all-cause a... [J Hypertens. 2012] - PubMed - NCBI
OBJECTIVES: Research suggests that serum concentrations of 25-hydroxyvitamin D [25(OH)D] are inversely associated with hypertension incidence. This study examined whether concentrations of 25(OH)D are inversely associated with mortality risk among US adults with hypertension.
METHODS: We analyzed data from the 2001-2004 National Health and Nutrition Examination Survey with mortality data obtained through 2006. Hazard ratios with 95% confidence intervals (CIs) for all-cause and cardiovascular disease (CVD) mortality were estimated using Cox proportional hazard models.
RESULTS: Of 2609 participants with hypertension, 191 died (including 68 CVD deaths) during an average of 3.7-year follow-up. Compared with participants with 25(OH)D concentrations in the highest quartile (?29?ng/ml), the hazard ratios for all-cause mortality were 1.93 (95% CI 1.06-3.49), 1.32 (95% CI 0.85-2.04), and 1.36 (95% CI 0.84-2.22), respectively (P for trend <0.05), and the hazard ratios for CVD mortality were 3.21 (95% CI 1.14-8.99), 2.42 (95% CI 0.85-6.90), and 2.33 (95% CI 0.88-6.12), respectively (P for trend <0.05), in the first (<17?ng/ml), second (17-<23?ng/ml) and third (23-<29?ng/ml) quartiles of 25(OH)D after adjustment for potential confounding variables. Additionally, concentrations of 25(OH)D as a continuous variable were linearly and inversely associated with the risk of mortality from all causes (P?=?0.012) and from CVD (P?=?0.010). These relationships were not affected much by adjustment for baseline blood pressure and use of antihypertension medications.
CONCLUSION: Concentrations of 25(OH)D were inversely associated with all-cause and CVD mortality among adults with hypertension in the US. Enhancing vitamin D intake may contribute to a lower risk for premature death.
OBJECTIVES: Research suggests that serum concentrations of 25-hydroxyvitamin D [25(OH)D] are inversely associated with hypertension incidence. This study examined whether concentrations of 25(OH)D are inversely associated with mortality risk among US adults with hypertension.
METHODS: We analyzed data from the 2001-2004 National Health and Nutrition Examination Survey with mortality data obtained through 2006. Hazard ratios with 95% confidence intervals (CIs) for all-cause and cardiovascular disease (CVD) mortality were estimated using Cox proportional hazard models.
RESULTS: Of 2609 participants with hypertension, 191 died (including 68 CVD deaths) during an average of 3.7-year follow-up. Compared with participants with 25(OH)D concentrations in the highest quartile (?29?ng/ml), the hazard ratios for all-cause mortality were 1.93 (95% CI 1.06-3.49), 1.32 (95% CI 0.85-2.04), and 1.36 (95% CI 0.84-2.22), respectively (P for trend <0.05), and the hazard ratios for CVD mortality were 3.21 (95% CI 1.14-8.99), 2.42 (95% CI 0.85-6.90), and 2.33 (95% CI 0.88-6.12), respectively (P for trend <0.05), in the first (<17?ng/ml), second (17-<23?ng/ml) and third (23-<29?ng/ml) quartiles of 25(OH)D after adjustment for potential confounding variables. Additionally, concentrations of 25(OH)D as a continuous variable were linearly and inversely associated with the risk of mortality from all causes (P?=?0.012) and from CVD (P?=?0.010). These relationships were not affected much by adjustment for baseline blood pressure and use of antihypertension medications.
CONCLUSION: Concentrations of 25(OH)D were inversely associated with all-cause and CVD mortality among adults with hypertension in the US. Enhancing vitamin D intake may contribute to a lower risk for premature death.
Amrein K, Worm HC, Schilcher G, Krisper P, Dobnig H. A Challenging Case of Hypocalcemia Supporting the Concept That 25-Hydroxyvitamin D Status Is Important for Intestinal Calcium Absorption. Journal of Clinical Endocrinology & Metabolism. A Challenging Case of Hypocalcemia Supporting the Concept That 25-Hydroxyvitamin D Status Is Important for Intestinal Calcium Absorption
Context: Intestinal mucosa seems to be responsive not only to circulating calcitriol but also to serum 25-hydroxyvitamin D concentrations.
Objective: We report a complex patient with chronic kidney disease who presented with symptomatic hypocalcemia (ionized calcium, 0.77 mmol/liter) despite regular calcitriol and calcium supplementation.
Methods: Case history, laboratory evaluation, and bone biopsies are discussed.
Results: Only vigorous treatment with im cholecalciferol led to a significant improvement of serum calcium, a decrease in PTH levels, and histological improvement of osteomalacic bone disease. However, oral anticoagulation became necessary for advanced peripheral artery disease, which precluded further im injections. Therefore, UVB phototherapy was initiated to treat vitamin D deficiency.
Conclusion: This case is clinically relevant because it demonstrates that efficient calcium absorption is markedly reduced in profound vitamin D deficiency, even with normal active vitamin D levels. An important consequence is to stay aware of vitamin D deficiency in patients with compromised kidney function irrespective of regular calcitriol replacement. Second, when both parenteral and oral vitamin D administration are contraindicated, ineffective, or unavailable, UVB phototherapy is an effective option to treat vitamin D deficiency. Third, this case underlines the importance of obtaining regular 25-hydroxyvitamin D levels in complex clinical cases when prediction of individual response is unreliable.
Context: Intestinal mucosa seems to be responsive not only to circulating calcitriol but also to serum 25-hydroxyvitamin D concentrations.
Objective: We report a complex patient with chronic kidney disease who presented with symptomatic hypocalcemia (ionized calcium, 0.77 mmol/liter) despite regular calcitriol and calcium supplementation.
Methods: Case history, laboratory evaluation, and bone biopsies are discussed.
Results: Only vigorous treatment with im cholecalciferol led to a significant improvement of serum calcium, a decrease in PTH levels, and histological improvement of osteomalacic bone disease. However, oral anticoagulation became necessary for advanced peripheral artery disease, which precluded further im injections. Therefore, UVB phototherapy was initiated to treat vitamin D deficiency.
Conclusion: This case is clinically relevant because it demonstrates that efficient calcium absorption is markedly reduced in profound vitamin D deficiency, even with normal active vitamin D levels. An important consequence is to stay aware of vitamin D deficiency in patients with compromised kidney function irrespective of regular calcitriol replacement. Second, when both parenteral and oral vitamin D administration are contraindicated, ineffective, or unavailable, UVB phototherapy is an effective option to treat vitamin D deficiency. Third, this case underlines the importance of obtaining regular 25-hydroxyvitamin D levels in complex clinical cases when prediction of individual response is unreliable.
My last D test came back at 25.
I had a doctor who was giving me D injections but I can't see him any more because he stopped taking my insurance.
I notice the oral Vitamin D upsets my stomach.
Im thinking go just buying the lamp thing
I had a doctor who was giving me D injections but I can't see him any more because he stopped taking my insurance.
I notice the oral Vitamin D upsets my stomach.
Im thinking go just buying the lamp thing
Neyestani TR, Nikooyeh B, Alavi-Majd H, et al. Improvement of Vitamin D Status via Daily Intake of Fortified Yogurt Drink Either with or without Extra Calcium Ameliorates Systemic Inflammatory Biomarkers, including Adipokines, in the Subjects with Type 2 Diabetes. Journal of Clinical Endocrinology & Metabolism. Improvement of Vitamin D Status via Daily Intake of Fortified Yogurt Drink Either with or without Extra Calcium Ameliorates Systemic Inflammatory Biomarkers, including Adipokines, in the Subjects with Type 2 Diabetes
Context: Systemic inflammation is thought to have a central role in diabetic long-term complications.
Objective: The aim of this study was to investigate the effects of vitamin D either with or without extra calcium on certain inflammatory biomarkers in the subjects with type 2 diabetes (T2D).
Design, Setting, and Participants: This was a double-blind, randomized, controlled trial conducted over 12 wk in 90 T2D subjects aged 30–60 yr from both sexes.
Intervention: Subjects were randomly allocated to one of three groups to receive two 250-ml bottles a day of plain Persian yogurt drink or doogh (PD, containing 150 mg calcium and no detectable vitamin D3/250 ml), vitamin D-fortified doogh (DD, containing 500 IU vitamin D3 and 150 mg calcium/250 ml), or calcium + vitamin D3-fortified doogh (CDD, containing 500 IU vitamin D3 and 250 mg calcium/250 ml).
Outcome Measures: The changes in inflammatory markers were evaluated.
Results: Compared to the baseline values, highly sensitive C-reactive protein, IL-1?, IL-6, fibrinogen, and retinol binding protein-4 concentrations significantly decreased in both the DD and CDD groups. Although the decrement in highly sensitive C-reactive protein and fibrinogen was more in CDD compared to DD (?4.0 ± 8.5 vs. ?1.3 ± 2.8 mg/liter, and ?0.40 ± 0.74 and ?0.20 ± 0.52 mg/liter, respectively), the differences were not significant. There was a significant increase in serum adiponectin in both the DD and CDD groups (51.3 ± 65.3 vs. 57.1 ± 33.8 ?g/liter; P < 0.05). Mean adiponectin changes in CDD were significantly higher than in PD (P = 0.021).
Conclusions: Daily intake of vitamin D-fortified doogh improved inflammatory markers in T2D subjects, and extra calcium conferred additional benefit only for the antiinflammatory adipokine, i.e. adiponectin.
Context: Systemic inflammation is thought to have a central role in diabetic long-term complications.
Objective: The aim of this study was to investigate the effects of vitamin D either with or without extra calcium on certain inflammatory biomarkers in the subjects with type 2 diabetes (T2D).
Design, Setting, and Participants: This was a double-blind, randomized, controlled trial conducted over 12 wk in 90 T2D subjects aged 30–60 yr from both sexes.
Intervention: Subjects were randomly allocated to one of three groups to receive two 250-ml bottles a day of plain Persian yogurt drink or doogh (PD, containing 150 mg calcium and no detectable vitamin D3/250 ml), vitamin D-fortified doogh (DD, containing 500 IU vitamin D3 and 150 mg calcium/250 ml), or calcium + vitamin D3-fortified doogh (CDD, containing 500 IU vitamin D3 and 250 mg calcium/250 ml).
Outcome Measures: The changes in inflammatory markers were evaluated.
Results: Compared to the baseline values, highly sensitive C-reactive protein, IL-1?, IL-6, fibrinogen, and retinol binding protein-4 concentrations significantly decreased in both the DD and CDD groups. Although the decrement in highly sensitive C-reactive protein and fibrinogen was more in CDD compared to DD (?4.0 ± 8.5 vs. ?1.3 ± 2.8 mg/liter, and ?0.40 ± 0.74 and ?0.20 ± 0.52 mg/liter, respectively), the differences were not significant. There was a significant increase in serum adiponectin in both the DD and CDD groups (51.3 ± 65.3 vs. 57.1 ± 33.8 ?g/liter; P < 0.05). Mean adiponectin changes in CDD were significantly higher than in PD (P = 0.021).
Conclusions: Daily intake of vitamin D-fortified doogh improved inflammatory markers in T2D subjects, and extra calcium conferred additional benefit only for the antiinflammatory adipokine, i.e. adiponectin.
Lerchbaum E, Obermayer-Pietsch BR. Vitamin D and fertility-a systematic review. European Journal of Endocrinology. http://www.eje-online.org/content/early/2012/01/24/EJE-11-0984.full.pdf
Background: Vitamin D has been well-known for its function in maintaining calcium and phosphorus homeostasis and promoting bone mineralization. There is some evidence, that in addition to sex steroid hormones, the classic regulators of human reproduction, vitamin D also modulates reproductive processes in women and men.
Aim: The aim of this review was to assess studies that evaluated the relationship between vitamin D and fertility in women and men as well as in animals. Methods: We performed a systematic literature search in Pubmed for relevant English language publications published until October 2011.
Results and Discussion: The vitamin D receptor (VDR) and vitamin D metabolizing enzymes are found in reproductive tissues of women and men. VDR knockout mice have significant gonadal insufficiency, decreased sperm count and motility, and histological abnormalities of testis, ovary and uterus. Moreover, we present evidence that vitamin D is involved in female reproduction including in-vitro fertilization (IVF) outcome (clinical pregnancy rates) and polycystic ovary syndrome (PCOS). In PCOS women, low 25-hydroxyvitamin D (25(OH)D) levels are associated with obesity, metabolic and endocrine disturbances and vitamin D supplementation might improve menstrual frequency and metabolic disturbances in those women. Moreover, vitamin D might influence steroidogenesis of sex hormones (estradiol and progesterone) in healthy women and high 25(OH)D levels might be associated with endometriosis. In men, vitamin D is positively associated with semen quality and androgen status. Moreover, vitamin D treatment might increase testosterone levels. Testiculopathic men show low CYP21R expression, 25(OH)D levels and osteoporosis despite normal testosterone levels.
Background: Vitamin D has been well-known for its function in maintaining calcium and phosphorus homeostasis and promoting bone mineralization. There is some evidence, that in addition to sex steroid hormones, the classic regulators of human reproduction, vitamin D also modulates reproductive processes in women and men.
Aim: The aim of this review was to assess studies that evaluated the relationship between vitamin D and fertility in women and men as well as in animals. Methods: We performed a systematic literature search in Pubmed for relevant English language publications published until October 2011.
Results and Discussion: The vitamin D receptor (VDR) and vitamin D metabolizing enzymes are found in reproductive tissues of women and men. VDR knockout mice have significant gonadal insufficiency, decreased sperm count and motility, and histological abnormalities of testis, ovary and uterus. Moreover, we present evidence that vitamin D is involved in female reproduction including in-vitro fertilization (IVF) outcome (clinical pregnancy rates) and polycystic ovary syndrome (PCOS). In PCOS women, low 25-hydroxyvitamin D (25(OH)D) levels are associated with obesity, metabolic and endocrine disturbances and vitamin D supplementation might improve menstrual frequency and metabolic disturbances in those women. Moreover, vitamin D might influence steroidogenesis of sex hormones (estradiol and progesterone) in healthy women and high 25(OH)D levels might be associated with endometriosis. In men, vitamin D is positively associated with semen quality and androgen status. Moreover, vitamin D treatment might increase testosterone levels. Testiculopathic men show low CYP21R expression, 25(OH)D levels and osteoporosis despite normal testosterone levels.
Vaidya A, Sun B, Larson C, Forman JP, Williams JS. Vitamin D3 Therapy Corrects the Tissue Sensitivity to Angiotensin II Akin to the Action of a Converting Enzyme Inhibitor in Obese Hypertensives: An Interventional Study. Journal of Clinical Endocrinology & Metabolism. Vitamin D3 Therapy Corrects the Tissue Sensitivity to Angiotensin II Akin to the Action of a Converting Enzyme Inhibitor in Obese Hypertensives: An Interventional Study
Context: Vitamin D deficiency and obesity are associated with increased tissue renin-angiotensin system (RAS) activity.
Objective: The objective of the study was to evaluate whether vitamin D3 therapy in obesity reduces tissue-RAS activity, as indicated by an increase in tissue sensitivity to angiotensin II (AngII).
Participants: Participants included obese subjects with hypertension and 25-hydroxyvitamin D less than 25 ng/ml.
Design: Subjects were studied before and after 1 month of vitamin D3 15,000 IU/d, while in dietary sodium balance, and off all interfering medications. Fourteen subjects successfully completed all study procedures.
Setting: The study was conducted at a clinical research center.
Outcome Measures: At each study visit, tissue sensitivity to AngII was assessed by measuring renal plasma flow (RPF), mean arterial pressure (MAP), and adrenal secretion of aldosterone during an infusion of AngII. Subjects were then given captopril, and a second AngII infusion to evaluate the effect of captopril on tissue-RAS activity.
Results: Vitamin D3 therapy increased 25-hydroxyvitamin D (18 to 52 ng/ml) and basal RPF (+5%) and lowered supine MAP (?3%) (all P < 0.01). There was a greater decline in RPF and higher stimulation of aldosterone with AngII infusion after vitamin D3 therapy (both P < 0.05). As anticipated, captopril increased the renal-vascular, MAP, and adrenal sensitivity to AngII, but this effect was much smaller after vitamin D3 therapy, indicating that vitamin D3 therapy corrected the tissue sensitivity to AngII akin to captopril.
Conclusions: Vitamin D3 therapy in obese hypertensives modified RPF, MAP, and tissue sensitivity to AngII similar to converting enzyme inhibition. Whether chronic vitamin D3 therapy abrogates the development of diseases associated with excess RAS activity warrants investigation.
Context: Vitamin D deficiency and obesity are associated with increased tissue renin-angiotensin system (RAS) activity.
Objective: The objective of the study was to evaluate whether vitamin D3 therapy in obesity reduces tissue-RAS activity, as indicated by an increase in tissue sensitivity to angiotensin II (AngII).
Participants: Participants included obese subjects with hypertension and 25-hydroxyvitamin D less than 25 ng/ml.
Design: Subjects were studied before and after 1 month of vitamin D3 15,000 IU/d, while in dietary sodium balance, and off all interfering medications. Fourteen subjects successfully completed all study procedures.
Setting: The study was conducted at a clinical research center.
Outcome Measures: At each study visit, tissue sensitivity to AngII was assessed by measuring renal plasma flow (RPF), mean arterial pressure (MAP), and adrenal secretion of aldosterone during an infusion of AngII. Subjects were then given captopril, and a second AngII infusion to evaluate the effect of captopril on tissue-RAS activity.
Results: Vitamin D3 therapy increased 25-hydroxyvitamin D (18 to 52 ng/ml) and basal RPF (+5%) and lowered supine MAP (?3%) (all P < 0.01). There was a greater decline in RPF and higher stimulation of aldosterone with AngII infusion after vitamin D3 therapy (both P < 0.05). As anticipated, captopril increased the renal-vascular, MAP, and adrenal sensitivity to AngII, but this effect was much smaller after vitamin D3 therapy, indicating that vitamin D3 therapy corrected the tissue sensitivity to AngII akin to captopril.
Conclusions: Vitamin D3 therapy in obese hypertensives modified RPF, MAP, and tissue sensitivity to AngII similar to converting enzyme inhibition. Whether chronic vitamin D3 therapy abrogates the development of diseases associated with excess RAS activity warrants investigation.
Sorenson M, Grant WB. Does vitamin D deficiency contribute to erectile dysfunction? Dermato-Endocrinology 2012;4(2):1. Landes Bioscience Journals: Dermato-Endocrinology
Erectile dysfunction (ED) is a multifactorial disease, and its causes can be neurogenic, psychogenic, hormonal and vascular. ED is often an important indicator of cardiovascular disease (CVD) and a powerful early marker for asymptomatic CVD. Erection is a vascular event, and ED is often a vascular disease caused by endothelial damage and subsequent inhibition of vasodilation. We show here that risk factors associated with a higher CVD risk also associate with a higher ED risk. Such factors include diabetes mellitus, hypertension, arterial calcification and Inflammation in the vascular endothelium. Vitamin D deficiency is one of several dynamics that associates with increased CVD risk, but to our knowledge, it has not been studied as a possible contributor to ED. Here we examine research linking ED and CVD and discuss how vitamin D influences CVD and its classic risk factors—factors that also associate to increased ED risk. We also summarize research indicating that vitamin D associates with reduced risk of several nonvascular contributing factors for ED. We conclude that VDD contributes to ED. This hypothesis should be tested through observational and intervention studies.
Erectile dysfunction (ED) is a multifactorial disease, and its causes can be neurogenic, psychogenic, hormonal and vascular. ED is often an important indicator of cardiovascular disease (CVD) and a powerful early marker for asymptomatic CVD. Erection is a vascular event, and ED is often a vascular disease caused by endothelial damage and subsequent inhibition of vasodilation. We show here that risk factors associated with a higher CVD risk also associate with a higher ED risk. Such factors include diabetes mellitus, hypertension, arterial calcification and Inflammation in the vascular endothelium. Vitamin D deficiency is one of several dynamics that associates with increased CVD risk, but to our knowledge, it has not been studied as a possible contributor to ED. Here we examine research linking ED and CVD and discuss how vitamin D influences CVD and its classic risk factors—factors that also associate to increased ED risk. We also summarize research indicating that vitamin D associates with reduced risk of several nonvascular contributing factors for ED. We conclude that VDD contributes to ED. This hypothesis should be tested through observational and intervention studies.
[MON-346] Prevalence and Associations of Vitamin D Deficiency in Medical Outpatients and Inpatients
http://www.abstracts2view.com/endo/view.php?nu=ENDO12L_MON-346
Marianne Ghobrial, Katayoun Edalat-Parsi, Evelina Svrdlan, Ivance Pugoy, Abhishek Sawant, Paul K Mills, Soe Naing. UCSF Fresno Center for Medical Education and Research, Fresno, CA; Community Regional Medical Center, Fresno, CA; Fresno Medical Education Program, University of California, San Francisco, Fresno, CA.
Aim: To determine the prevalence of vitamin D deficiency (VDD) and associations between VDD and clinical parameters in medical outpatients (OP) and inpatients (IP)
Method: This retrospective study was conducted at a community hospital in Fresno, California. The medical OP and IP, who had serum 25 hydroxyvitamin D [25(OH)D] measured from July 2009 to June 2011 for any reason, were included in the study.
Results: We studied a total of 1548 patients: 536 OP (mean age 55 years, 62% female, 55% Hispanics, mean 25(OH)D 19.4 mg/dl) and 862 IP (mean age 59 years, 49% female, 41% Hispanics, mean 25(OH)D 16.3 mg/dl).
16.4% of OP and 30.4% of IP had severe VDD (<10mg/dl) whereas 56.6% OP and 70.1% IP had VDD (<20).
In both groups, those with VDD were younger (OP 54 vs 57 years; IP 58 vs 63),
had higher body weight (OP 188 vs 181 lbs; IP 175 vs 162),
lower total calcium (OP 9.3 vs 9.5 mg/dl; IP 8.5 vs 8.8),
higher HbA1c (OP 7.2 vs 6.6%; IP 6.8 vs 6.0),
lower hemoglobin (Hb) (OP 12.2 vs 12.8 mg/dl; IP 10.3 vs 10.8),
higher triglyceride (OP 170 vs 135 mg/dl; IP 139 vs 121),
higher LDL (OP 103 vs 93 mg/dl; IP 82 vs 75),
higher TSH (OP 5.5 vs 2.1 mU/L;IP 4.4 vs 3.8),
higher PTH (OP 129 vs 113 mg/dl; IP 219 vs 141), than those without VDD.
In multivariate regression analysis, the presence of DM (OR 4.25; 95% CI 1.46-12.39), higher LDL (OR 1.025; 95% CI 1.00-1.04) and lower Hb (OR 0.61; 95% CI 0.44-0.85) levels in OP and younger age (OR 0.969; 95% CI 0.945-0.994), lower albumin (OR 0.374; CI 0.198-0.708) and higher PTH (OR 1.003; CI 1.000-1.006) levels in IP were independently associated with VDD.
Discussion: Prevalence of VDD is surprisingly high though there is abundant sunlight in Fresno at Central California (36.7° N latitude and 267 total days with sun). Old age is considered to be one of the major risk factors for VDD in general population. However, in our study, those with VDD were significantly younger than those without. The prevalence of VDD was much higher and mean 25(OH)D level was significantly lower in IP than in OP, that may suggest that acute medical conditions or exacerbation of chronic diseases may associate with higher risk of VDD.
Conclusion: VDD was highly prevalent in both medical OP and IP in this sunny region. Prevalence of severe VDD was about 2 times higher in IP than in OP. The presence of DM, elevated LDL and low Hb levels were significantly associated with VDD in OP whereas younger age, lower albumin and higher PTH levels were independently correlated with VDD in IP.
http://www.abstracts2view.com/endo/view.php?nu=ENDO12L_MON-346
Marianne Ghobrial, Katayoun Edalat-Parsi, Evelina Svrdlan, Ivance Pugoy, Abhishek Sawant, Paul K Mills, Soe Naing. UCSF Fresno Center for Medical Education and Research, Fresno, CA; Community Regional Medical Center, Fresno, CA; Fresno Medical Education Program, University of California, San Francisco, Fresno, CA.
Aim: To determine the prevalence of vitamin D deficiency (VDD) and associations between VDD and clinical parameters in medical outpatients (OP) and inpatients (IP)
Method: This retrospective study was conducted at a community hospital in Fresno, California. The medical OP and IP, who had serum 25 hydroxyvitamin D [25(OH)D] measured from July 2009 to June 2011 for any reason, were included in the study.
Results: We studied a total of 1548 patients: 536 OP (mean age 55 years, 62% female, 55% Hispanics, mean 25(OH)D 19.4 mg/dl) and 862 IP (mean age 59 years, 49% female, 41% Hispanics, mean 25(OH)D 16.3 mg/dl).
16.4% of OP and 30.4% of IP had severe VDD (<10mg/dl) whereas 56.6% OP and 70.1% IP had VDD (<20).
In both groups, those with VDD were younger (OP 54 vs 57 years; IP 58 vs 63),
had higher body weight (OP 188 vs 181 lbs; IP 175 vs 162),
lower total calcium (OP 9.3 vs 9.5 mg/dl; IP 8.5 vs 8.8),
higher HbA1c (OP 7.2 vs 6.6%; IP 6.8 vs 6.0),
lower hemoglobin (Hb) (OP 12.2 vs 12.8 mg/dl; IP 10.3 vs 10.8),
higher triglyceride (OP 170 vs 135 mg/dl; IP 139 vs 121),
higher LDL (OP 103 vs 93 mg/dl; IP 82 vs 75),
higher TSH (OP 5.5 vs 2.1 mU/L;IP 4.4 vs 3.8),
higher PTH (OP 129 vs 113 mg/dl; IP 219 vs 141), than those without VDD.
In multivariate regression analysis, the presence of DM (OR 4.25; 95% CI 1.46-12.39), higher LDL (OR 1.025; 95% CI 1.00-1.04) and lower Hb (OR 0.61; 95% CI 0.44-0.85) levels in OP and younger age (OR 0.969; 95% CI 0.945-0.994), lower albumin (OR 0.374; CI 0.198-0.708) and higher PTH (OR 1.003; CI 1.000-1.006) levels in IP were independently associated with VDD.
Discussion: Prevalence of VDD is surprisingly high though there is abundant sunlight in Fresno at Central California (36.7° N latitude and 267 total days with sun). Old age is considered to be one of the major risk factors for VDD in general population. However, in our study, those with VDD were significantly younger than those without. The prevalence of VDD was much higher and mean 25(OH)D level was significantly lower in IP than in OP, that may suggest that acute medical conditions or exacerbation of chronic diseases may associate with higher risk of VDD.
Conclusion: VDD was highly prevalent in both medical OP and IP in this sunny region. Prevalence of severe VDD was about 2 times higher in IP than in OP. The presence of DM, elevated LDL and low Hb levels were significantly associated with VDD in OP whereas younger age, lower albumin and higher PTH levels were independently correlated with VDD in IP.
Giallauria F, Milaneschi Y, Tanaka T, et al. Arterial Stiffness and Vitamin D Levels: the Baltimore Longitudinal Study of Aging. Journal of Clinical Endocrinology & Metabolism. Arterial Stiffness and Vitamin D Levels: the Baltimore Longitudinal Study of Aging
Context: The importance of vitamin D for bone health has long been acknowledged. Recent evidence suggests that vitamin D can also play a role in reducing the risk of several other diseases, including cardiovascular disease.
Objective: The aim of this study is to test the hypothesis that 25-hydroxyvitamin D (25-OH D) is an independent cross-sectional correlate of central arterial stiffness in a normative aging study population.
Design and Settings: We conducted a cross-sectional analysis.
Subjects: We studied 1228 healthy volunteers (50% males; age, 70 ± 12 yr) of the Baltimore Longitudinal Study of Aging.
Main Outcome Measures: We measured carotid-femoral pulse wave velocity (PWV) and 25-OH D levels.
Results: We found a significant inverse association between PWV and 25-OH D levels (adjusted r2 = 0.27; ? = ?0.43; P = 0.001). After adjusting for age, gender, ethnicity, season of blood draw, estimated glomerular filtration rate, physical activity level, cardiovascular risk factors score (smoking, visceral obesity, hypercholesterolemia, hypertension, and diabetes), calcium/vitamin D supplementation, serum calcium, and PTH levels, the association between PWV and 25-OH D levels was only slightly reduced and remained statistically significant (adjusted r2 = 0.34; ? = ?0.34; P = 0.04).
Conclusions: Vitamin D levels are inversely associated with increased arterial stiffness in a normative aging population, irrespective of traditional risk factor burden. Further research is needed to understand the mechanism of this association and to test the hypothesis that vitamin D supplementation can reduce arterial stiffness.
Context: The importance of vitamin D for bone health has long been acknowledged. Recent evidence suggests that vitamin D can also play a role in reducing the risk of several other diseases, including cardiovascular disease.
Objective: The aim of this study is to test the hypothesis that 25-hydroxyvitamin D (25-OH D) is an independent cross-sectional correlate of central arterial stiffness in a normative aging study population.
Design and Settings: We conducted a cross-sectional analysis.
Subjects: We studied 1228 healthy volunteers (50% males; age, 70 ± 12 yr) of the Baltimore Longitudinal Study of Aging.
Main Outcome Measures: We measured carotid-femoral pulse wave velocity (PWV) and 25-OH D levels.
Results: We found a significant inverse association between PWV and 25-OH D levels (adjusted r2 = 0.27; ? = ?0.43; P = 0.001). After adjusting for age, gender, ethnicity, season of blood draw, estimated glomerular filtration rate, physical activity level, cardiovascular risk factors score (smoking, visceral obesity, hypercholesterolemia, hypertension, and diabetes), calcium/vitamin D supplementation, serum calcium, and PTH levels, the association between PWV and 25-OH D levels was only slightly reduced and remained statistically significant (adjusted r2 = 0.34; ? = ?0.34; P = 0.04).
Conclusions: Vitamin D levels are inversely associated with increased arterial stiffness in a normative aging population, irrespective of traditional risk factor burden. Further research is needed to understand the mechanism of this association and to test the hypothesis that vitamin D supplementation can reduce arterial stiffness.
Anyone see the studies released this morning on 8000 ius or whatever reducing old fart fractures by 30%!?!
Kabadi SM, Lee BK, Liu L. Joint Effects of Obesity and Vitamin D Insufficiency on Insulin Resistance and Type 2 Diabetes. Diabetes Care. Joint Effects of Obesity and Vitamin D Insufficiency on Insulin Resistance and Type 2 Diabetes
OBJECTIVE The possible interaction of serum 25-hydroxyvitamin D [25(OH)D] and obesity in regard to type 2 diabetes and insulin resistance has not been well studied. To explore the effect modification of obesity on the association between 25(OH)D and insulin resistance/type 2 diabetes, data were examined from a nationally representative sample.
RESEARCH DESIGN AND METHODS The analytic sample for the type 2 diabetes analysis (n = 12,900) was limited to participants from the National Health and Nutrition Examination Survey (NHANES) 2001–2006 over 20 years of age. Participants >20 years of age assigned to the morning session and free of diabetes were limited to the insulin resistance analysis (n = 5,806). Multiplicative interaction was assessed through a cross-product interaction term in a multiple logistic regression model. The presence of additive interaction between insufficient 25(OH)D and obesity (indicated by BMI or waist circumference) was evaluated by calculation of the relative excess risk due to interaction (RERI) and attributable proportion due to interaction (AP).
RESULTS There was no multiplicative interaction of insufficient 25(OH)D and obesity on type 2 diabetes or insulin resistance. Furthermore, none of the RERI or AP values were statistically significant in the diabetes analysis. However, there was strong additive interaction between abdominal obesity and insufficient 25(OH)D (RERI 6.45 [95% CI 1.03–11.52]) in regard to insulin resistance. In addition, 47% of the increased odds of insulin resistance can be explained by interaction between insufficient 25(OH)D and high BMI (AP 0.47 [95% CI 0.08–0.87]).
CONCLUSIONS Within a cross-sectional, nationally representative sample, abdominal obesity and insufficient 25(OH)D interact to synergistically influence the risk of insulin resistance.
OBJECTIVE The possible interaction of serum 25-hydroxyvitamin D [25(OH)D] and obesity in regard to type 2 diabetes and insulin resistance has not been well studied. To explore the effect modification of obesity on the association between 25(OH)D and insulin resistance/type 2 diabetes, data were examined from a nationally representative sample.
RESEARCH DESIGN AND METHODS The analytic sample for the type 2 diabetes analysis (n = 12,900) was limited to participants from the National Health and Nutrition Examination Survey (NHANES) 2001–2006 over 20 years of age. Participants >20 years of age assigned to the morning session and free of diabetes were limited to the insulin resistance analysis (n = 5,806). Multiplicative interaction was assessed through a cross-product interaction term in a multiple logistic regression model. The presence of additive interaction between insufficient 25(OH)D and obesity (indicated by BMI or waist circumference) was evaluated by calculation of the relative excess risk due to interaction (RERI) and attributable proportion due to interaction (AP).
RESULTS There was no multiplicative interaction of insufficient 25(OH)D and obesity on type 2 diabetes or insulin resistance. Furthermore, none of the RERI or AP values were statistically significant in the diabetes analysis. However, there was strong additive interaction between abdominal obesity and insufficient 25(OH)D (RERI 6.45 [95% CI 1.03–11.52]) in regard to insulin resistance. In addition, 47% of the increased odds of insulin resistance can be explained by interaction between insufficient 25(OH)D and high BMI (AP 0.47 [95% CI 0.08–0.87]).
CONCLUSIONS Within a cross-sectional, nationally representative sample, abdominal obesity and insufficient 25(OH)D interact to synergistically influence the risk of insulin resistance.
Similar threads
