m_ob
New Member
I was up in the 70s without supplementation during the summer working as a lifeguard. I believe the best way to get it is to let your body convert it from cholesterol.
MESO-Rx
Anabolic Steroids
Vitamin D
- Thread starter Michael Scally MD
- Start date
Vitamin D toxicity is a known cause of hypercalcemia. This report describes nine hypercalcemic patients found to have vitamin D toxicity due to an oral remedy available over the counter and manufactured in the Dominican Republic. All patients were ambulatory, with normal serum calcium levels (range, 8.7–9.2 mg/dl) before ingestion of this preparation, although in many cases they harbored a disorder that can be associated with hypercalcemia.
Lowe H, Cusano NE, Binkley N, Blaner WS, Bilezikian JP. Vitamin D Toxicity due to a Commonly Available "Over the Counter" Remedy from the Dominican Republic. J Clin Endocrinol Metab:jc.2010-1999.
Context: Hypercalcemia in ambulatory patients is occasionally caused by vitamin D toxicity.
Objective: We report nine patients presenting to Columbia University Medical Center with hypercalcemia due to a supplement from the Dominican Republic containing massive amounts of vitamin D.
Methods: Case histories and laboratory evaluation (calcium, PTH, vitamin D metabolites) are discussed in the context of other published cases of vitamin D toxicity. The supplement was analyzed by HPLC to quantitate vitamin D and A content.
Results: Nine patients presented with hypercalcemia (range, 10.8-17.2 mg/dl; normal, 8.4-9.8 mg/dl), suppressed PTH (range, <3 to 11 pg/ml), and elevated 25-hydroxyvitamin D (range, 94-525 ng/ml; normal, 30-80 ng/ml) levels. All reported recently taking an over-the-counter vitamin supplement called Soladek readily available in the Dominican Republic and in Upper Manhattan. Although serum calcium values before the ingestion of Soladek were not elevated (baseline serum calcium range, 8.7-9.2 mg/dl), most had a disorder that can be associated with hypercalcemia [squamous cell cancer (n = 1), Pneumocystis or mycobacterial infection (n = 3), lymphoma (n = 1), granulomatous disease (n = 1), hyperthyroidism (n = 2)]. According to the manufacturer's label, each 5-ml vial of Soladek contains vitamin D (600,000 IU), vitamin A (120,000 IU), and vitamin E (5 mg). Laboratory analysis by HPLC revealed that the supplement actually contained vitamin D3 (864,000 IU) and vitamin A (predominantly retinyl palmitate 123,500 IU) per vial.
Conclusion: Although hypercalcemia due to exogenous use of vitamin D is unusual, it is important to consider it in the differential diagnosis, particularly among individuals with access to Soladek.
Lowe H, Cusano NE, Binkley N, Blaner WS, Bilezikian JP. Vitamin D Toxicity due to a Commonly Available "Over the Counter" Remedy from the Dominican Republic. J Clin Endocrinol Metab:jc.2010-1999.
Context: Hypercalcemia in ambulatory patients is occasionally caused by vitamin D toxicity.
Objective: We report nine patients presenting to Columbia University Medical Center with hypercalcemia due to a supplement from the Dominican Republic containing massive amounts of vitamin D.
Methods: Case histories and laboratory evaluation (calcium, PTH, vitamin D metabolites) are discussed in the context of other published cases of vitamin D toxicity. The supplement was analyzed by HPLC to quantitate vitamin D and A content.
Results: Nine patients presented with hypercalcemia (range, 10.8-17.2 mg/dl; normal, 8.4-9.8 mg/dl), suppressed PTH (range, <3 to 11 pg/ml), and elevated 25-hydroxyvitamin D (range, 94-525 ng/ml; normal, 30-80 ng/ml) levels. All reported recently taking an over-the-counter vitamin supplement called Soladek readily available in the Dominican Republic and in Upper Manhattan. Although serum calcium values before the ingestion of Soladek were not elevated (baseline serum calcium range, 8.7-9.2 mg/dl), most had a disorder that can be associated with hypercalcemia [squamous cell cancer (n = 1), Pneumocystis or mycobacterial infection (n = 3), lymphoma (n = 1), granulomatous disease (n = 1), hyperthyroidism (n = 2)]. According to the manufacturer's label, each 5-ml vial of Soladek contains vitamin D (600,000 IU), vitamin A (120,000 IU), and vitamin E (5 mg). Laboratory analysis by HPLC revealed that the supplement actually contained vitamin D3 (864,000 IU) and vitamin A (predominantly retinyl palmitate 123,500 IU) per vial.
Conclusion: Although hypercalcemia due to exogenous use of vitamin D is unusual, it is important to consider it in the differential diagnosis, particularly among individuals with access to Soladek.
knucklehead
New Member
I have read phds level people saying that the metabolic effects of d3 cholecalciferol are possibly detrimintal. '
Specifically I have heard that thyroid issues can potentially be worsened as well as autoimmmune. secondly, I believe d3 upregulates thyroid, which would down regulate testosterone in most people?
My concern is 2nd hypogonadism. Levels d3 are low normal. however when I take it I feel sped up and assume this is going to interfere with test.
Can anyone with a scientific background speak to this claims?
Specifically I have heard that thyroid issues can potentially be worsened as well as autoimmmune. secondly, I believe d3 upregulates thyroid, which would down regulate testosterone in most people?
My concern is 2nd hypogonadism. Levels d3 are low normal. however when I take it I feel sped up and assume this is going to interfere with test.
Can anyone with a scientific background speak to this claims?
Wehr E, Pilz S, Boehm BO, März W, Obermayer-Pietsch B. Association of vitamin D status with serum androgen levels in men. Clinical Endocrinology 2010;73(2):243-8. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2265.2009.03777.x/abstract
Objective - Studies in rodents indicate a role of vitamin D in male reproduction, but the relationship between vitamin D and androgen levels in men is largely unexplored. We aimed to investigate the association of 25-hydroxyvitamin D [25(OH)D] levels with testosterone, free androgen index (FAI) and SHBG. Moreover, we examined whether androgen levels show a similar seasonal variation to 25(OH)D.
Design - In this cross-sectional study, 25(OH)D, testosterone and SHBG levels were assessed by immunoassay in 2299 men who were routinely referred for coronary angiography (1997–2000).
Measurements - Main outcome measures were associations of 25(OH)D levels with testosterone, SHBG and FAI. FAI was calculated as testosterone (nmol/l)/SHBG (nmol/l) × 100.
Results - Men with sufficient 25(OH)D levels (?30 ?g/l) had significantly higher levels of testosterone and FAI and significantly lower levels of SHBG when compared to 25(OH)D insufficient (20–29•9 ?g/l) and 25(OH)D-deficient (<20 ?g/l) men (P < 0•05 for all). In linear regression analyses adjusted for possible confounders, we found significant associations of 25(OH)D levels with testosterone, FAI and SHBG levels (P < 0•05 for all). 25(OH)D, testosterone and FAI levels followed a similar seasonal pattern with a nadir in March (12•2 ?g/l, 15•9 nmol/l and 40•8, respectively) and peak levels in August (23•4 ?g/l, 18•7 nmol/l and 49•7, respectively) (P < 0•05 for all).
Conclusion - Androgen levels and 25(OH)D levels are associated in men and reveal a concordant seasonal variation. Randomized controlled trials are warranted to evaluate the effect of vitamin D supplementation on androgen levels.
Objective - Studies in rodents indicate a role of vitamin D in male reproduction, but the relationship between vitamin D and androgen levels in men is largely unexplored. We aimed to investigate the association of 25-hydroxyvitamin D [25(OH)D] levels with testosterone, free androgen index (FAI) and SHBG. Moreover, we examined whether androgen levels show a similar seasonal variation to 25(OH)D.
Design - In this cross-sectional study, 25(OH)D, testosterone and SHBG levels were assessed by immunoassay in 2299 men who were routinely referred for coronary angiography (1997–2000).
Measurements - Main outcome measures were associations of 25(OH)D levels with testosterone, SHBG and FAI. FAI was calculated as testosterone (nmol/l)/SHBG (nmol/l) × 100.
Results - Men with sufficient 25(OH)D levels (?30 ?g/l) had significantly higher levels of testosterone and FAI and significantly lower levels of SHBG when compared to 25(OH)D insufficient (20–29•9 ?g/l) and 25(OH)D-deficient (<20 ?g/l) men (P < 0•05 for all). In linear regression analyses adjusted for possible confounders, we found significant associations of 25(OH)D levels with testosterone, FAI and SHBG levels (P < 0•05 for all). 25(OH)D, testosterone and FAI levels followed a similar seasonal pattern with a nadir in March (12•2 ?g/l, 15•9 nmol/l and 40•8, respectively) and peak levels in August (23•4 ?g/l, 18•7 nmol/l and 49•7, respectively) (P < 0•05 for all).
Conclusion - Androgen levels and 25(OH)D levels are associated in men and reveal a concordant seasonal variation. Randomized controlled trials are warranted to evaluate the effect of vitamin D supplementation on androgen levels.
Effect of Vitamin D Supplementation on Testosterone Levels in Men
"The male reproductive tract has been identified as a target tissue for vitamin D, and previous data suggest an association of 25-hydroxyvitamin D [25(OH)D] with testosterone levels in men. We therefore aimed to evaluate whether vitamin D supplementation influences testosterone levels in men. Healthy overweight men undergoing a weight reduction program who participated in a randomized controlled trial were analyzed for testosterone levels. The entire study included 200 nondiabetic subjects, of whom 165 participants (54 men) completed the trial. Participants received either 83??g (3?332?IU) vitamin D daily for 1 year (n=31) or placebo (n=23). Initial 25(OH)D concentrations were in the deficiency range (<50?nmol/l) and testosterone values were at the lower end of the reference range (9.09-55.28?nmol/l for males aged 20-49 years) in both groups. Mean circulating 25(OH)D concentrations increased significantly by 53.5?nmol/l in the vitamin D group, but remained almost constant in the placebo group. Compared to baseline values, a significant increase in total testosterone levels (from 10.7±3.9?nmol/l to 13.4±4.7?nmol/l; p<0.001), bioactive testosterone (from 5.21±1.87?nmol/l to 6.25±2.01?nmol/l; p=0.001), and free testosterone levels (from 0.222±0.080?nmol/l to 0.267±0.087?nmol/l; p=0.001) were observed in the vitamin D supplemented group. By contrast, there was no significant change in any testosterone measure in the placebo group. Our results suggest that vitamin D supplementation might increase testosterone levels. Further randomized controlled trials are warranted to confirm this hypothesis."
Copied from Pubmed
"The male reproductive tract has been identified as a target tissue for vitamin D, and previous data suggest an association of 25-hydroxyvitamin D [25(OH)D] with testosterone levels in men. We therefore aimed to evaluate whether vitamin D supplementation influences testosterone levels in men. Healthy overweight men undergoing a weight reduction program who participated in a randomized controlled trial were analyzed for testosterone levels. The entire study included 200 nondiabetic subjects, of whom 165 participants (54 men) completed the trial. Participants received either 83??g (3?332?IU) vitamin D daily for 1 year (n=31) or placebo (n=23). Initial 25(OH)D concentrations were in the deficiency range (<50?nmol/l) and testosterone values were at the lower end of the reference range (9.09-55.28?nmol/l for males aged 20-49 years) in both groups. Mean circulating 25(OH)D concentrations increased significantly by 53.5?nmol/l in the vitamin D group, but remained almost constant in the placebo group. Compared to baseline values, a significant increase in total testosterone levels (from 10.7±3.9?nmol/l to 13.4±4.7?nmol/l; p<0.001), bioactive testosterone (from 5.21±1.87?nmol/l to 6.25±2.01?nmol/l; p=0.001), and free testosterone levels (from 0.222±0.080?nmol/l to 0.267±0.087?nmol/l; p=0.001) were observed in the vitamin D supplemented group. By contrast, there was no significant change in any testosterone measure in the placebo group. Our results suggest that vitamin D supplementation might increase testosterone levels. Further randomized controlled trials are warranted to confirm this hypothesis."
Copied from Pubmed
Re: Effect of Vitamin D Supplementation on Testosterone Levels in Men
Pilz S, Frisch S, Koertke H, et al. Effect of Vitamin D Supplementation on Testosterone Levels in Men. Horm Metab Res. Effect of Vitamin D Supplementation on Testosteron... [Horm Metab Res. 2010] - PubMed result
Pilz S, Frisch S, Koertke H, et al. Effect of Vitamin D Supplementation on Testosterone Levels in Men. Horm Metab Res. Effect of Vitamin D Supplementation on Testosteron... [Horm Metab Res. 2010] - PubMed result
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Several studies have reported on the relative potencies of cholecalciferol (D3) and ergocalciferol (D2), as assessed by their effect on elevating or sustaining serum 25(OH)D concentration. Several reports found cholecalciferol to be superior to ergocalciferol by this criterion, with the potency of the two compounds varying by factors ranging up to four fold. At least one other study reported that the two calciferols were essentially equipotent. Aside from the fact that the doses and dosing regimens in these studies differed considerably, the reason for this discordance is unclear. In an attempt to clarify this issue, this study was designed to specifically test the hypothesis of the superiority of cholecalciferol (D3) over ergocalciferol (D2) in a randomized, controlled trial, using change in total serum 25(OH)D as the primary outcome variable, and change in adipose tissue fat content of the calciferols as a secondary outcome. Their conclusion is D3 is approximately 87% more potent in raising and maintaining serum 25(OH)D concentrations and produces 2- to 3-fold greater storage of vitamin D than does equimolar D2.
Heaney RP, Recker RR, Grote J, Horst RL, Armas LAG. Vitamin D3 Is More Potent Than Vitamin D2 in Humans. J Clin Endocrinol Metab:jc.2010-230.
Background: Current unitage for the calciferols suggests that equimolar quantities of vitamins D2 (D2) and D3 (D3) are biologically equivalent. Published studies yield mixed results.
Objective: The aim of the study was to compare the potencies of D2 and D3.
Design: The trial used a single-blind, randomized design in 33 healthy adults. Calciferols were dosed at 50,000 IU/wk for 12 wk. Principal outcome variables were area under the curve for incremental total 25-hydroxyvitamin D [25(OH)D] and change in calciferol content of sc fat.
Results: Incremental mean (SD) 25(OH)D area under the curve at 12 wk was 1366 ng {middle dot} d/ml (516) for the D2-treated group and 2136 (606) for the D3 (P < 0.001). Mean (SD) steady-state 25(OH)D increments showed similar differences: 24 ng/ml for D2 (10.3) and 45 ng/ml (16.2) for D3 (P <0.001). Subcutaneous fat content of D2 rose by 50 g/kg in the D2-treated group, and D3 content rose by 104 g/kg in the D3-treated group. Total calciferol in fat rose by only 33 ng/kg in the D2-treated, whereas it rose by 104 g/kg in the D3-treated group. Extrapolating to total body fat D3, storage amounted to just 17% of the administered dose.
Conclusion: D3 is approximately 87% more potent in raising and maintaining serum 25(OH)D concentrations and produces 2- to 3-fold greater storage of vitamin D than does equimolar D2. For neither was there evidence of sequestration in fat, as had been postulated for doses in this range. Given its greater potency and lower cost, D3 should be the preferred treatment option when correcting vitamin D deficiency.
Heaney RP, Recker RR, Grote J, Horst RL, Armas LAG. Vitamin D3 Is More Potent Than Vitamin D2 in Humans. J Clin Endocrinol Metab:jc.2010-230.
Background: Current unitage for the calciferols suggests that equimolar quantities of vitamins D2 (D2) and D3 (D3) are biologically equivalent. Published studies yield mixed results.
Objective: The aim of the study was to compare the potencies of D2 and D3.
Design: The trial used a single-blind, randomized design in 33 healthy adults. Calciferols were dosed at 50,000 IU/wk for 12 wk. Principal outcome variables were area under the curve for incremental total 25-hydroxyvitamin D [25(OH)D] and change in calciferol content of sc fat.
Results: Incremental mean (SD) 25(OH)D area under the curve at 12 wk was 1366 ng {middle dot} d/ml (516) for the D2-treated group and 2136 (606) for the D3 (P < 0.001). Mean (SD) steady-state 25(OH)D increments showed similar differences: 24 ng/ml for D2 (10.3) and 45 ng/ml (16.2) for D3 (P <0.001). Subcutaneous fat content of D2 rose by 50 g/kg in the D2-treated group, and D3 content rose by 104 g/kg in the D3-treated group. Total calciferol in fat rose by only 33 ng/kg in the D2-treated, whereas it rose by 104 g/kg in the D3-treated group. Extrapolating to total body fat D3, storage amounted to just 17% of the administered dose.
Conclusion: D3 is approximately 87% more potent in raising and maintaining serum 25(OH)D concentrations and produces 2- to 3-fold greater storage of vitamin D than does equimolar D2. For neither was there evidence of sequestration in fat, as had been postulated for doses in this range. Given its greater potency and lower cost, D3 should be the preferred treatment option when correcting vitamin D deficiency.
There is an emerging consensus that serum 25-OHD3 levels of about 75 nmol/l are optimal for bone health and extraskeletal effects. However, there is no consensus on how to achieve this target rapidly. In the USA, ergocalciferol (vitamin D2) is recommended at a dose of 50 000 IU/week for 8 weeks, irrespective of the degree of vitamin D deficiency or body weight. In Europe, cholecalciferol (vitamin D3) is mainly used to treat vitamin D deficiency. Usually, this is done with daily supplementation using tablets. The cholecalciferol loading dose required to reach the serum 25-OHD3 target level of 75 nmol/l can be calculated as follows: dose (IU) = 40 x (75-serum 25-OHD3) x body weight. [Vitamin D - 25-Hydroxyvitamin D: ng/mL X 2.496 = nmol/L]
van Groningen L, Opdenoordt S, van Sorge A, Telting D, Giesen A, de Boer H. Cholecalciferol loading dose guideline for vitamin D-deficient adults. Eur J Endocrinol 2010;162(4):805-11. http://www.ncbi.nlm.nih.gov/pubmed/20139241
Introduction - Severe vitamin D deficiency is very common. Evidence-based guidelines for rapid correction with high-dose oral cholecalciferol are not yet available.
Objective - To develop a practical cholecalciferol loading dose regimen. Materials and methodsA total of 208 vitamin D-deficient subjects (serum 25-hydroxyvitamin D3 (25-OHD3) level <50 nmol/l), aged 18-88 years, were treated with solubilized cholecalciferol, 50 000 IU/ml. They received either 25 000 IU every fortnight for 8 weeks (total dose 100 000 IU), 25 000 IU every week for 6 weeks (total dose 150 000 IU), or 25 000 IU every week for 8 weeks (total dose 200 000 IU). Blood samples were collected at baseline and 10 days after the final dose of cholecalciferol.
Results - Most patients were severely vitamin D deficient: 76% had a serum 25-OHD3 level <30 nmol/l at baseline. Cholecalciferol in a cumulative dose of 100 000, 150 000, and 200 000 IU increased mean serum 25-OHD3 level by 29 nmol/l (95% confidence interval (CI): 23-35 nmol/l), 43 nmol/l (95% CI: 36-50 nmol/l), and 69 nmol/l (95% CI: 64-75 nmol/l) respectively. The change in 25-OHD3 ({Delta}25-OHD3) was related to the dose per kilogram body weight (R2=0.38, P<0.0001), and is described by the equation: {Delta}25-OHD3=0.025x(dose per kg body weight).
Conclusion - The cholecalciferol loading dose required to reach the serum 25-OHD3 target level of 75 nmol/l can be calculated as follows: dose (IU) = 40 x (75-serum 25-OHD3) x body weight.
van Groningen L, Opdenoordt S, van Sorge A, Telting D, Giesen A, de Boer H. Cholecalciferol loading dose guideline for vitamin D-deficient adults. Eur J Endocrinol 2010;162(4):805-11. http://www.ncbi.nlm.nih.gov/pubmed/20139241
Introduction - Severe vitamin D deficiency is very common. Evidence-based guidelines for rapid correction with high-dose oral cholecalciferol are not yet available.
Objective - To develop a practical cholecalciferol loading dose regimen. Materials and methodsA total of 208 vitamin D-deficient subjects (serum 25-hydroxyvitamin D3 (25-OHD3) level <50 nmol/l), aged 18-88 years, were treated with solubilized cholecalciferol, 50 000 IU/ml. They received either 25 000 IU every fortnight for 8 weeks (total dose 100 000 IU), 25 000 IU every week for 6 weeks (total dose 150 000 IU), or 25 000 IU every week for 8 weeks (total dose 200 000 IU). Blood samples were collected at baseline and 10 days after the final dose of cholecalciferol.
Results - Most patients were severely vitamin D deficient: 76% had a serum 25-OHD3 level <30 nmol/l at baseline. Cholecalciferol in a cumulative dose of 100 000, 150 000, and 200 000 IU increased mean serum 25-OHD3 level by 29 nmol/l (95% confidence interval (CI): 23-35 nmol/l), 43 nmol/l (95% CI: 36-50 nmol/l), and 69 nmol/l (95% CI: 64-75 nmol/l) respectively. The change in 25-OHD3 ({Delta}25-OHD3) was related to the dose per kilogram body weight (R2=0.38, P<0.0001), and is described by the equation: {Delta}25-OHD3=0.025x(dose per kg body weight).
Conclusion - The cholecalciferol loading dose required to reach the serum 25-OHD3 target level of 75 nmol/l can be calculated as follows: dose (IU) = 40 x (75-serum 25-OHD3) x body weight.
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Wang Y, DeLuca HF. Is the Vitamin D Receptor Found in Muscle? Endocrinology:en.2010-1109. Is the Vitamin D Receptor Found in Muscle? -- Wang and DeLuca, 10.1210/en.2010-1109 -- Endocrinology
The active form of vitamin D, 1{alpha},25-dihydroxyvitamin D3, is critical for the regulation of serum calcium and phosphorus levels that in turn support bone mineralization and neuromuscular activity. It is well known that vitamin D deficiency causes rachitic/osteomalacic myopathy and cardiac disorder and the provision of vitamin D can reverse the symptoms. However, the underlying mechanisms remain unclear. The question of whether the vitamin D receptor is found in muscle has been debated but not settled. We recently studied all available antibodies against the vitamin D receptor and found that most antibodies used detect proteins other than the vitamin D receptor, and therefore, the utility of these antibodies may generate the false-positive results. Using antibodies that do not detect proteins in tissues from vitamin D receptor null mice, we have developed a specific and sensitive immunohistochemical assay. The results from this investigation show that the vitamin D receptor is undetectable in skeletal, cardiac, and smooth muscle, suggesting that the function of vitamin D on muscle is either of an indirect nature or does not involve the known receptor.
The active form of vitamin D, 1{alpha},25-dihydroxyvitamin D3, is critical for the regulation of serum calcium and phosphorus levels that in turn support bone mineralization and neuromuscular activity. It is well known that vitamin D deficiency causes rachitic/osteomalacic myopathy and cardiac disorder and the provision of vitamin D can reverse the symptoms. However, the underlying mechanisms remain unclear. The question of whether the vitamin D receptor is found in muscle has been debated but not settled. We recently studied all available antibodies against the vitamin D receptor and found that most antibodies used detect proteins other than the vitamin D receptor, and therefore, the utility of these antibodies may generate the false-positive results. Using antibodies that do not detect proteins in tissues from vitamin D receptor null mice, we have developed a specific and sensitive immunohistochemical assay. The results from this investigation show that the vitamin D receptor is undetectable in skeletal, cardiac, and smooth muscle, suggesting that the function of vitamin D on muscle is either of an indirect nature or does not involve the known receptor.
In this study, Vitamin D deficiency was below 30 ng/mL (75 nm/L). While this is becoming the accepted standard, many use a lower value. Vitamin D toxicity is rare. It would be prudent for anyone to have their Vitamin D status checked.
Choi HS, Oh HJ, Choi H, et al. Vitamin D Insufficiency in Korea--A Greater Threat to Younger Generation: The Korea National Health and Nutrition Examination Survey (KNHANES) 2008. J Clin Endocrinol Metab:jc.2010-133. Vitamin D Insufficiency in Korea--A Greater Threat to Younger Generation: The Korea National Health and Nutrition Examination Survey (KNHANES) 2008 -- Choi et al., 10.1210/jc.2010-2133 -- Journal of Clinical Endocrinology & Metabolism
Context: Vitamin D status in the Korean population has not been adequately determined.
Objective: To investigate the vitamin D status and the prevalence of vitamin D insufficiency in the Korean population, and also identify the predictors for vitamin D insufficiency in Korea.Design and Setting: The Fourth Korea National Health and Nutrition Examination Surveys (KNHANES IV) in the Korean population conducted in 2008.
Participants: 3,047 males and 3,878 females aged 10 years and older selected in all the 16 administrative districts of South Korea.Main Outcome Measures: Serum 25-hydroxyvitamin D [25(OH)D] levels and the prevalence of vitamin D insufficiency defined as serum 25(OH)D level of less than 20 ng/ml.
Results: Vitamin D insufficiency was found in 47.3% of males and 64.5% of females, whereas only 13.2% of male and 6.7% of female population had a serum 25(OH)D level of greater than 30 ng/ml. Vitamin D insufficiency was most prevalent in the age of 20-29, with a rate of 65.0% in males and 79.9% in females, and least prevalent in the age of 60-69 in males and 50-59 in females. Those who work usually indoors were more predisposed to vitamin D insufficiency. In the adult population, predictors for vitamin D insufficiency included young age groups, spring and winter seasons, living in an urban area, and indoor occupations.
Conclusions: Vitamin D insufficiency is very common, and it is now a greater threat to the younger generation in Korea. Current recommendations for vitamin D intakes for Koreans are inadequate, especially for the youth.
Choi HS, Oh HJ, Choi H, et al. Vitamin D Insufficiency in Korea--A Greater Threat to Younger Generation: The Korea National Health and Nutrition Examination Survey (KNHANES) 2008. J Clin Endocrinol Metab:jc.2010-133. Vitamin D Insufficiency in Korea--A Greater Threat to Younger Generation: The Korea National Health and Nutrition Examination Survey (KNHANES) 2008 -- Choi et al., 10.1210/jc.2010-2133 -- Journal of Clinical Endocrinology & Metabolism
Context: Vitamin D status in the Korean population has not been adequately determined.
Objective: To investigate the vitamin D status and the prevalence of vitamin D insufficiency in the Korean population, and also identify the predictors for vitamin D insufficiency in Korea.Design and Setting: The Fourth Korea National Health and Nutrition Examination Surveys (KNHANES IV) in the Korean population conducted in 2008.
Participants: 3,047 males and 3,878 females aged 10 years and older selected in all the 16 administrative districts of South Korea.Main Outcome Measures: Serum 25-hydroxyvitamin D [25(OH)D] levels and the prevalence of vitamin D insufficiency defined as serum 25(OH)D level of less than 20 ng/ml.
Results: Vitamin D insufficiency was found in 47.3% of males and 64.5% of females, whereas only 13.2% of male and 6.7% of female population had a serum 25(OH)D level of greater than 30 ng/ml. Vitamin D insufficiency was most prevalent in the age of 20-29, with a rate of 65.0% in males and 79.9% in females, and least prevalent in the age of 60-69 in males and 50-59 in females. Those who work usually indoors were more predisposed to vitamin D insufficiency. In the adult population, predictors for vitamin D insufficiency included young age groups, spring and winter seasons, living in an urban area, and indoor occupations.
Conclusions: Vitamin D insufficiency is very common, and it is now a greater threat to the younger generation in Korea. Current recommendations for vitamin D intakes for Koreans are inadequate, especially for the youth.
[The following commentary critiques the recent IOM recommendations for Vitamin D intake. IMO, the commentary is correct. They suggest a lower level of 50 ng/mL. They also recommend a higher daily intake of Vitamin D.]
Heaney RP, Holick MF. Why the IOM recommendations for vitamin D are deficient. Journal of Bone and Mineral Research. Why the IOM recommendations for vitamin D are deficient - Heaney - Journal of Bone and Mineral Research - Wiley Online Library
In the past two years, vitamin D supplement sales to consumers have increased by more than 100% per year. Now, following the publication of the report on Dietary Reference Intakes (DRIs) for calcium and vitamin D by the Institute of Medicine (IOM), many physicians report that they are decreasing their vitamin D recommendations to patients. Members of the IOM panel in their various media statements explicitly proposed this change. While a small fraction of consumers may well have all the vitamin D they need, on balance we consider a general downward trend to be harmful for the health of the public.
Both of the authors of this Perspective served as members of the panel that drafted the 1997 report of the IOM on the DRIs for calcium and vitamin D. That report was the first issued by the IOM under the then new evidence-based guidelines for evaluating studies and making recommendations. We are thus familiar with the process and, most importantly, with vitamin D itself. Based on this experience, we respectfully dissent from many of the findings and recommendations in the current report and we set forth here a small fraction of the reasons for that dissent.
The IOM report (and its presentation to the media) stressed that its recommendations for vitamin D were based primarily on the intake [and serum 25(OH)D concentration] needed to ensure skeletal health and that, in the panel’s judgement, there was insufficient evidence to make any recommendations in respect to non-skeletal benefits, if any. Second, the report concluded that a serum level for 25(OH)D of 20 ng/mL was sufficient to ensure bone health. And third, they concluded that, since the bulk of the American public had 25(OH)D values that were above 20 ng/mL, most individuals were getting all of the vitamin D they needed and had no reason for further supplementation.
These conclusions fail on three grounds: logic, science, and guidance.
First, logic. Since the panel, in its judgement, concluded that it did not know whether there might be non-skeletal benefits (or at what blood level they could be ensured), then it is patently incorrect to say that they know that people are getting enough. The most the panel could logically have said was “Here’s what you need for bone; most people get that much; we do not know whether more would confer possible non-skeletal benefits.” That, at least, would have been an honest communication of the state of the issue as the panel apparently understands it. But to state publicly that the general public does not need more goes well beyond what the panel admits it knows.
Second, science. The statement that skeletal health can be assured at serum 25(OH)D levels of 20 ng/mL is simply incorrect. Without going into an exhaustive recital of all of the evidence pointing to a skeletal need for higher levels, we cite here three illustrative observations which, in our collective judgement, indicate that, instead of 20, a serum level of 30 ng/mL is closer to the bottom end of the acceptable range for skeletal health. First, there is the large randomized controlled trial in the UK which raised serum 25(OH)D level from 21 ng/mL to 29 ng/mL, and produced a 33% reduction in all major osteoporotic fractures combined. The fact that other trials, with less good compliance, failed to reproduce that effect does not negate the evidence of a well-conducted trial. Second, there are the many meta-analyses of Bischoff-Ferrari and her colleagues demonstrating that, taken overall, fracture reduction with vitamin D does not reproducibly occur below serum 25(OH)D levels of 30, and for some fractures even 40 ng/mL. Finally, there is the demonstration, in a large German autopsy series (strangely misinterpreted by the panel) that osteoid seam width – the histological hallmark of vitamin D deficiency – does not reach fully normal values until serum 25(OH)D levels are above 30 ng/mL. [N.B.: Of 33 cases with 25(OH)D values between 20 and 30 ng/mL, more than half (18) had elevated osteoid volume. An RDA, by definition, meets the need of 97.5% of the population.] In a closely related finding investigators from South Australia showed seasonal variation in osteoid seam width and mineral appositional rate, reflecting variations in serum 25(OH)D precisely within the 20–30 ng/mL range, i.e., above the IOM panel’s “adequate” level.
Additionally, there is an apparent inconsistency between the recommended intake (600 IU/d for all individuals up through age 70) and the bottom end of the acceptable 25(OH)D serum concentration range (let alone higher values). As virtually universal experience with vitamin D supplementation demonstrates, 600 IU/d, if the body’s sole input of vitamin D, would not be enough to produce a value of even 10 ng/mL, let alone 20 or above. There is a generally recognized “rule of thumb” to the effect that each additional 100 IU of vitamin D/day, raises serum 25(OH)D by approximately 1 ng/mL. That is, in fact, a “rounding up” for convenience of calculation. Several studies indicate that the response increment is closer to 0.7 ng/mL/100 IU. Either way, 600 IU/d will not suffice without appreciable solar and dietary input. Furthermore, as is also widely recognized, 600 IU/d produces barely perceptible changes in individuals who are overweight or obese (now better than 50% of the US adult population). Hence the increase from the 1997 DRIs, while welcome, and certainly in the right direction, is simply inconsistent with current professional experience. It not only is inadequate, by itself, to meet even the panel’s recommended serum levels, but this internal inconsistency detracts from the credibility of the whole report inasmuch as it flies in the face of the everyday experience of clinicians who recommend supplements to their patients and measure the resulting responses.
Finally, guidance. At already noted, the panel indicated that it was uncertain about extra-skeletal benefits – benefits that might accrue at intakes above the new intake recommendations. At the same time, the panel raised the upper level intake “TUIL” to 4,000 IU/d. (The report acknowledges that intakes up to 10,000 IU/d are probably safe for everyone, and applied an uncertainty factor to that 10,000 IU figure to generate the 4,000 IU TUIL. It is important to stress that the TUIL is not a “limit” and, instead, constitutes an assurance of safety for such an intake.) One should have thought that even a very simplistic, game-theory approach would have led to a guidance statement such as the following: “We do not know whether taking more vitamin D than we are currently recommending will help you, but it could, and we can assure you that supplemental intakes up to at least 4,000 IU per day are safe.” Such a statement couched, perhaps, in less straightforward language, would nevertheless provide guidance that both the public and governmental agencies could find useful. Instead, we now have only a confused public.
But beyond these errors and inconsistencies, serious as they are, lies a much deeper flaw in the approach taken by the panel, exemplified by a quote from one of the panel members to the New York Times at the time of the release of the report. The statement was simply that the “onus” (i.e., burden of proof) fell on anyone who claimed benefits for intakes higher than the panel’s current recommendations. This is an approach that is correct for drugs, which are foreign chemicals and which do carry an appropriately heavy requirement for proof. For drugs, the position of privilege is given to the placebo. And in the current IOM report, the privilege is given to a serum 25(OH)D level that is effectively the status quo. We judge that that is exactly backward for nutrients. The privilege must instead be given to the intake that prevailed during the evolution of human physiology, the intake to which, presumably, that physiology is fine-tuned. So far as can be judged from numerous studies documenting the magnitude of the effect of sun exposure, the primitive intake would have been at least 4000 IU/d, and probably two to three times that level, with corresponding serum 25(OH)D levels ranging from 40 to 80 ng/mL. The fact that primitive levels would have been higher than current IOM recommendations does not, of course, prove their necessity today. But such intakes should be given the presumption of correctness, and the burden of proof must be placed on those who propose that lower intakes (and lower serum levels) are without risk of preventable dysfunction or disease. The IOM, in its report, has utterly failed to recognize or meet that standard.
Finally, we commend the IOM panel for their concern about safety, certainly an appropriate posture for a body crafting public policy. However, the standards adopted by the panel for taking into evidence papers indicating possible risk were, we note, far lower than those the panel required to indicate benefit. Additionally, many of the purported risks were, on their face, implausible and inconsistent with the experience of population subgroups that routinely have serum levels in the range mentioned by the panel as possibly risky (e.g., ~50 ng/mL). We note that one of the widely accepted Hill criteria for acceptance of observational data is precisely biological plausibility. Furthermore, we consider it highly implausible that serum levels such as prevailed during hominid evolution could carry more risk than benefit for the populations concerned. Had that been the case, one should have expected that natural selection would have eliminated those prone to such risks.
In this Perspective, we have deliberately avoided a mind-numbing laundry list of the vast number of factual inaccuracies and misinterpretations in the report. We are informed that there is a request, through the Freedom of Information Act, to obtain the external review comments submitted to the IOM in response to a prepublication draft. When those materials become available, those interested can review the many problems with the IOM report in detail. For now, our recommendation to the American public is that the IOM report should be taken with a grain of salt (another nutrient the IOM finds risky).
Heaney RP, Holick MF. Why the IOM recommendations for vitamin D are deficient. Journal of Bone and Mineral Research. Why the IOM recommendations for vitamin D are deficient - Heaney - Journal of Bone and Mineral Research - Wiley Online Library
In the past two years, vitamin D supplement sales to consumers have increased by more than 100% per year. Now, following the publication of the report on Dietary Reference Intakes (DRIs) for calcium and vitamin D by the Institute of Medicine (IOM), many physicians report that they are decreasing their vitamin D recommendations to patients. Members of the IOM panel in their various media statements explicitly proposed this change. While a small fraction of consumers may well have all the vitamin D they need, on balance we consider a general downward trend to be harmful for the health of the public.
Both of the authors of this Perspective served as members of the panel that drafted the 1997 report of the IOM on the DRIs for calcium and vitamin D. That report was the first issued by the IOM under the then new evidence-based guidelines for evaluating studies and making recommendations. We are thus familiar with the process and, most importantly, with vitamin D itself. Based on this experience, we respectfully dissent from many of the findings and recommendations in the current report and we set forth here a small fraction of the reasons for that dissent.
The IOM report (and its presentation to the media) stressed that its recommendations for vitamin D were based primarily on the intake [and serum 25(OH)D concentration] needed to ensure skeletal health and that, in the panel’s judgement, there was insufficient evidence to make any recommendations in respect to non-skeletal benefits, if any. Second, the report concluded that a serum level for 25(OH)D of 20 ng/mL was sufficient to ensure bone health. And third, they concluded that, since the bulk of the American public had 25(OH)D values that were above 20 ng/mL, most individuals were getting all of the vitamin D they needed and had no reason for further supplementation.
These conclusions fail on three grounds: logic, science, and guidance.
First, logic. Since the panel, in its judgement, concluded that it did not know whether there might be non-skeletal benefits (or at what blood level they could be ensured), then it is patently incorrect to say that they know that people are getting enough. The most the panel could logically have said was “Here’s what you need for bone; most people get that much; we do not know whether more would confer possible non-skeletal benefits.” That, at least, would have been an honest communication of the state of the issue as the panel apparently understands it. But to state publicly that the general public does not need more goes well beyond what the panel admits it knows.
Second, science. The statement that skeletal health can be assured at serum 25(OH)D levels of 20 ng/mL is simply incorrect. Without going into an exhaustive recital of all of the evidence pointing to a skeletal need for higher levels, we cite here three illustrative observations which, in our collective judgement, indicate that, instead of 20, a serum level of 30 ng/mL is closer to the bottom end of the acceptable range for skeletal health. First, there is the large randomized controlled trial in the UK which raised serum 25(OH)D level from 21 ng/mL to 29 ng/mL, and produced a 33% reduction in all major osteoporotic fractures combined. The fact that other trials, with less good compliance, failed to reproduce that effect does not negate the evidence of a well-conducted trial. Second, there are the many meta-analyses of Bischoff-Ferrari and her colleagues demonstrating that, taken overall, fracture reduction with vitamin D does not reproducibly occur below serum 25(OH)D levels of 30, and for some fractures even 40 ng/mL. Finally, there is the demonstration, in a large German autopsy series (strangely misinterpreted by the panel) that osteoid seam width – the histological hallmark of vitamin D deficiency – does not reach fully normal values until serum 25(OH)D levels are above 30 ng/mL. [N.B.: Of 33 cases with 25(OH)D values between 20 and 30 ng/mL, more than half (18) had elevated osteoid volume. An RDA, by definition, meets the need of 97.5% of the population.] In a closely related finding investigators from South Australia showed seasonal variation in osteoid seam width and mineral appositional rate, reflecting variations in serum 25(OH)D precisely within the 20–30 ng/mL range, i.e., above the IOM panel’s “adequate” level.
Additionally, there is an apparent inconsistency between the recommended intake (600 IU/d for all individuals up through age 70) and the bottom end of the acceptable 25(OH)D serum concentration range (let alone higher values). As virtually universal experience with vitamin D supplementation demonstrates, 600 IU/d, if the body’s sole input of vitamin D, would not be enough to produce a value of even 10 ng/mL, let alone 20 or above. There is a generally recognized “rule of thumb” to the effect that each additional 100 IU of vitamin D/day, raises serum 25(OH)D by approximately 1 ng/mL. That is, in fact, a “rounding up” for convenience of calculation. Several studies indicate that the response increment is closer to 0.7 ng/mL/100 IU. Either way, 600 IU/d will not suffice without appreciable solar and dietary input. Furthermore, as is also widely recognized, 600 IU/d produces barely perceptible changes in individuals who are overweight or obese (now better than 50% of the US adult population). Hence the increase from the 1997 DRIs, while welcome, and certainly in the right direction, is simply inconsistent with current professional experience. It not only is inadequate, by itself, to meet even the panel’s recommended serum levels, but this internal inconsistency detracts from the credibility of the whole report inasmuch as it flies in the face of the everyday experience of clinicians who recommend supplements to their patients and measure the resulting responses.
Finally, guidance. At already noted, the panel indicated that it was uncertain about extra-skeletal benefits – benefits that might accrue at intakes above the new intake recommendations. At the same time, the panel raised the upper level intake “TUIL” to 4,000 IU/d. (The report acknowledges that intakes up to 10,000 IU/d are probably safe for everyone, and applied an uncertainty factor to that 10,000 IU figure to generate the 4,000 IU TUIL. It is important to stress that the TUIL is not a “limit” and, instead, constitutes an assurance of safety for such an intake.) One should have thought that even a very simplistic, game-theory approach would have led to a guidance statement such as the following: “We do not know whether taking more vitamin D than we are currently recommending will help you, but it could, and we can assure you that supplemental intakes up to at least 4,000 IU per day are safe.” Such a statement couched, perhaps, in less straightforward language, would nevertheless provide guidance that both the public and governmental agencies could find useful. Instead, we now have only a confused public.
But beyond these errors and inconsistencies, serious as they are, lies a much deeper flaw in the approach taken by the panel, exemplified by a quote from one of the panel members to the New York Times at the time of the release of the report. The statement was simply that the “onus” (i.e., burden of proof) fell on anyone who claimed benefits for intakes higher than the panel’s current recommendations. This is an approach that is correct for drugs, which are foreign chemicals and which do carry an appropriately heavy requirement for proof. For drugs, the position of privilege is given to the placebo. And in the current IOM report, the privilege is given to a serum 25(OH)D level that is effectively the status quo. We judge that that is exactly backward for nutrients. The privilege must instead be given to the intake that prevailed during the evolution of human physiology, the intake to which, presumably, that physiology is fine-tuned. So far as can be judged from numerous studies documenting the magnitude of the effect of sun exposure, the primitive intake would have been at least 4000 IU/d, and probably two to three times that level, with corresponding serum 25(OH)D levels ranging from 40 to 80 ng/mL. The fact that primitive levels would have been higher than current IOM recommendations does not, of course, prove their necessity today. But such intakes should be given the presumption of correctness, and the burden of proof must be placed on those who propose that lower intakes (and lower serum levels) are without risk of preventable dysfunction or disease. The IOM, in its report, has utterly failed to recognize or meet that standard.
Finally, we commend the IOM panel for their concern about safety, certainly an appropriate posture for a body crafting public policy. However, the standards adopted by the panel for taking into evidence papers indicating possible risk were, we note, far lower than those the panel required to indicate benefit. Additionally, many of the purported risks were, on their face, implausible and inconsistent with the experience of population subgroups that routinely have serum levels in the range mentioned by the panel as possibly risky (e.g., ~50 ng/mL). We note that one of the widely accepted Hill criteria for acceptance of observational data is precisely biological plausibility. Furthermore, we consider it highly implausible that serum levels such as prevailed during hominid evolution could carry more risk than benefit for the populations concerned. Had that been the case, one should have expected that natural selection would have eliminated those prone to such risks.
In this Perspective, we have deliberately avoided a mind-numbing laundry list of the vast number of factual inaccuracies and misinterpretations in the report. We are informed that there is a request, through the Freedom of Information Act, to obtain the external review comments submitted to the IOM in response to a prepublication draft. When those materials become available, those interested can review the many problems with the IOM report in detail. For now, our recommendation to the American public is that the IOM report should be taken with a grain of salt (another nutrient the IOM finds risky).
Grant WB. Is the Institute of Medicine Report on Calcium and Vitamin D Good Science? Biol Res Nurs. 2011 Jan 10.
The Institute of Medicine (IOM) of the National Academies released its new Dietary Reference Intakes for Calcium and Vitamin D report on November 30, 2010 (IOM, 2011), which is summarized in Ross et al. (2010). [See: https://thinksteroids.com/community/posts/736236 ] The IOM report found that the only health benefit of vitamin D supported by the rigorous scientific studies they reviewed was for the bones. The report set recommended dietary allowances of 600 IU/day for those aged 1–70 years and 800 IU/day for those aged 71 or older, under conditions of minimal sun exposure. It also stated that a serum 25-hydroxyvitamin D (25[OH]D) level of 20 ng/ml was adequate. However, the authors noted that no adverse effects such as hypercalcemia or acute toxicity had been documented for oral intakes of up to 10,000 IU/day for adults; regardless, they set the upper-level intake at between 1,000 IU/day for infants (aged 0–6 months) and 4,000 IU/day for those older than 9 years. While this report is a step forward, it is disappointing that no nonbony benefits emerged from this review.
Continue Reading – See Attachment
The Institute of Medicine (IOM) of the National Academies released its new Dietary Reference Intakes for Calcium and Vitamin D report on November 30, 2010 (IOM, 2011), which is summarized in Ross et al. (2010). [See: https://thinksteroids.com/community/posts/736236 ] The IOM report found that the only health benefit of vitamin D supported by the rigorous scientific studies they reviewed was for the bones. The report set recommended dietary allowances of 600 IU/day for those aged 1–70 years and 800 IU/day for those aged 71 or older, under conditions of minimal sun exposure. It also stated that a serum 25-hydroxyvitamin D (25[OH]D) level of 20 ng/ml was adequate. However, the authors noted that no adverse effects such as hypercalcemia or acute toxicity had been documented for oral intakes of up to 10,000 IU/day for adults; regardless, they set the upper-level intake at between 1,000 IU/day for infants (aged 0–6 months) and 4,000 IU/day for those older than 9 years. While this report is a step forward, it is disappointing that no nonbony benefits emerged from this review.
Continue Reading – See Attachment
Re: OnLine First
Vitamin D deficiency is endemic in the general population; however, there is much to be learned about the vitamin D status of athletes.
Halliday T, Peterson N, Thomas J, Kleppinger K, Hollis B, Larson-Meyer D. Vitamin D Status Relative to Diet, Lifestyle, Injury and Illness in College Athletes. Med Sci Sports Exerc. Vitamin D Status Relative to Diet, Lifestyle, Inju... [Med Sci Sports Exerc. 2010] - PubMed result
PURPOSE:: To assess the prevalence of vitamin D insufficiency in collegiate athletes and determine whether 25(OH)D concentrations are related to vitamin D intake, sun exposure, body composition, and risk for illness or athletic injury.
METHODS:: 25(OH) vitamin D concentrations were measured in 41 (18 male/23 female) athletes (12 indoor/29 outdoor) throughout the academic year. Dietary intake and lifestyle habits were assessed via questionnaire, bone density was measured by DEXA and injury and illness were documented as part of routine care.
RESULTS:: 25(OH)D concentrations changed across time (P=0.001) and averaged 49.0+/-16.6, 30.5+/-9.4 and 41.9+/-14.6 ng/mL in the fall, winter and spring, respectively, and were higher in outdoor versus indoor athletes in the fall (P <0.05). Using 40 ng/mL as the cutoff for optimal status, 75.6 %, 15.2% and 36.0% of athletes had optimal status in the fall, winter and spring, respectively. 25(OH)D concentrations were significantly (P <0.05) correlated with multivitamin intake in the winter (r=0.39) and tanning bed use in the spring (r=0.48), however, status was otherwise not related to intake, lifestyle factors or body composition. 25(OH)D concentrations in the spring (r=-0.40; P=0.048) was correlated with frequency of illness.
CONCLUSION:: Our results suggest that collegiate athletes can maintain sufficient status during the fall and spring but would benefit from supplementation during the winter to prevent seasonal decreases in 25(OH)D concentrations. Results further suggest that insufficient vitamin D status may increase risk for frequent illness. Future research is needed to identify whether vitamin D status influences injury risk during athletic training/competition.
Vitamin D deficiency is endemic in the general population; however, there is much to be learned about the vitamin D status of athletes.
Halliday T, Peterson N, Thomas J, Kleppinger K, Hollis B, Larson-Meyer D. Vitamin D Status Relative to Diet, Lifestyle, Injury and Illness in College Athletes. Med Sci Sports Exerc. Vitamin D Status Relative to Diet, Lifestyle, Inju... [Med Sci Sports Exerc. 2010] - PubMed result
PURPOSE:: To assess the prevalence of vitamin D insufficiency in collegiate athletes and determine whether 25(OH)D concentrations are related to vitamin D intake, sun exposure, body composition, and risk for illness or athletic injury.
METHODS:: 25(OH) vitamin D concentrations were measured in 41 (18 male/23 female) athletes (12 indoor/29 outdoor) throughout the academic year. Dietary intake and lifestyle habits were assessed via questionnaire, bone density was measured by DEXA and injury and illness were documented as part of routine care.
RESULTS:: 25(OH)D concentrations changed across time (P=0.001) and averaged 49.0+/-16.6, 30.5+/-9.4 and 41.9+/-14.6 ng/mL in the fall, winter and spring, respectively, and were higher in outdoor versus indoor athletes in the fall (P <0.05). Using 40 ng/mL as the cutoff for optimal status, 75.6 %, 15.2% and 36.0% of athletes had optimal status in the fall, winter and spring, respectively. 25(OH)D concentrations were significantly (P <0.05) correlated with multivitamin intake in the winter (r=0.39) and tanning bed use in the spring (r=0.48), however, status was otherwise not related to intake, lifestyle factors or body composition. 25(OH)D concentrations in the spring (r=-0.40; P=0.048) was correlated with frequency of illness.
CONCLUSION:: Our results suggest that collegiate athletes can maintain sufficient status during the fall and spring but would benefit from supplementation during the winter to prevent seasonal decreases in 25(OH)D concentrations. Results further suggest that insufficient vitamin D status may increase risk for frequent illness. Future research is needed to identify whether vitamin D status influences injury risk during athletic training/competition.
The use of a target level of 75 nM/L (30 ng/mL) is NOT optimal. IMO, you should be shooting for 125 nM/L (50 ng/mL).
Supplementation to achieve adequate levels - Available higher-level evidence provides some guidance on vitamin D intakes for health maintenance:
• 400 IU daily is sufficient to prevent rickets in children and osteomalacia in adults, but is insufficient to achieve adequate serum levels of 25(OH)D.
• 700 to 1000 IU daily is the minimum required to reduce risk of falling in the elderly.
• 400 to 800 IU daily is the minimum required to reduce risk of fracture in the elderly.
• 500 to 1500 IU daily reduced cancer mortality and all-cause mortality in various studies.
• 2000 IU daily reduced the incidence of type 1 diabetes in young children.
• 1000 IU daily is required to bring 50% of adults to 25(OH)D levels above 75 nmol/L (considered adequate).
• 2000 IU daily is required to bring 85% to 90% of the adult population to 25(OH)D levels above 75 nmol/L.
Bosomworth NJ. Mitigating epidemic vitamin D deficiency: The agony of evidence. Can Fam Physician 2011;57(1):16-20. Mitigating epidemic vitamin D deficiency: The agony of evidence -- Bosomworth 57 (1): 16 -- Canadian Family Physician
Supplementation to achieve adequate levels - Available higher-level evidence provides some guidance on vitamin D intakes for health maintenance:
• 400 IU daily is sufficient to prevent rickets in children and osteomalacia in adults, but is insufficient to achieve adequate serum levels of 25(OH)D.
• 700 to 1000 IU daily is the minimum required to reduce risk of falling in the elderly.
• 400 to 800 IU daily is the minimum required to reduce risk of fracture in the elderly.
• 500 to 1500 IU daily reduced cancer mortality and all-cause mortality in various studies.
• 2000 IU daily reduced the incidence of type 1 diabetes in young children.
• 1000 IU daily is required to bring 50% of adults to 25(OH)D levels above 75 nmol/L (considered adequate).
• 2000 IU daily is required to bring 85% to 90% of the adult population to 25(OH)D levels above 75 nmol/L.
Bosomworth NJ. Mitigating epidemic vitamin D deficiency: The agony of evidence. Can Fam Physician 2011;57(1):16-20. Mitigating epidemic vitamin D deficiency: The agony of evidence -- Bosomworth 57 (1): 16 -- Canadian Family Physician
Couple of thoughts. And I just read through this ENTIRE F'n Thread... With some look at the articles... Its a good thread..
1. I understood in the past the sun/skin derived vitamin D is due to a light interaction with CHolesterol in the skin. I have not really seen that addressed here yet... So whick spectrum of light radiation is involved precisesly, and what gives with the cholesterol? Clearly different folks exhibit different amounts of cholesterol on the surface of the skin. So how do factors like cleanliness play in.?? Myself, I could be oiled back down by 10am, but I have that type skin. What about dry skin that is "overcleaned". Or am I off base...?
2. I dont really understand the diff between the 3 diffrent Vit D classifications here. Hve not really researched. But recently got my wife a D sup & w/potassium seems like?
3. To the guys out there MEGADosing supplements. Obviously the body is a complex symphony. Dont you think maybe something else is the missing link?? To get the stuff in, OR maybe slow it down.
4.I still testify that serum counts are going to be the end of us. Its the ephitemy of the glass is half empty/full argument...
1. I understood in the past the sun/skin derived vitamin D is due to a light interaction with CHolesterol in the skin. I have not really seen that addressed here yet... So whick spectrum of light radiation is involved precisesly, and what gives with the cholesterol? Clearly different folks exhibit different amounts of cholesterol on the surface of the skin. So how do factors like cleanliness play in.?? Myself, I could be oiled back down by 10am, but I have that type skin. What about dry skin that is "overcleaned". Or am I off base...?
2. I dont really understand the diff between the 3 diffrent Vit D classifications here. Hve not really researched. But recently got my wife a D sup & w/potassium seems like?
3. To the guys out there MEGADosing supplements. Obviously the body is a complex symphony. Dont you think maybe something else is the missing link?? To get the stuff in, OR maybe slow it down.
4.I still testify that serum counts are going to be the end of us. Its the ephitemy of the glass is half empty/full argument...
Re: OnLine First
[Email me for the full-text article.]
Vitamin D receptors and metabolizing enzymes have been found in several human brain areas, including the prefrontal cortex, hippocampus, cingulate gyrus, thalamus, hypothalamus, and substantia nigra where autocrine and paracrine activity has been suggested. Vitamin D has been implicated in the regulation of behavior, stimulation of neurotrophin release, and protection of the brain by buffering antioxidant and antiinflammatory defenses. Hypovitaminosis D is prevalent in psychiatric patients and several studies suggest an association between hypovitaminosis D and basic and executive cognitive functions, depression, and schizophrenia. In regions that have historically suffered from hypovitaminosis D, an impact on personality dimensions, lower mean levels of sociosexuality, extraversion, and openness have been reported. This study explored whether the multifunctional 1,25 (OH)2D3 might be associated with basic personality traits finding Vitamin D might influence personality traits, promoting extrovert and open behavior.
Ubbenhorst A, Striebich S, Lang F, Lang UE. Exploring the relationship between vitamin D and basic personality traits. Psychopharmacology (Berl). Exploring the relationship between vitamin D and b... [Psychopharmacology (Berl). 2011] - PubMed result
RATIONALE: Several studies suggest an association between hypovitaminosis D and basic and executive cognitive functions, depression, bipolar disorder, and schizophrenia. A recent study confirms neophobic responses in vitamin D receptor mutant mice. We explored whether the plasma levels of 1,25-dihydroxyvitamin D (1,25(OH)(2)D(3)), the active form of vitamin D, are correlated with basic personality traits.
METHODS: A total of 206 healthy unrelated volunteers (108 male, 98 female, age 31 +/- 13 years) completed the German version of the NEO Five-Factor Inventory (NEO-FFI), which allows reliable and valid assessment of personality along the dimensions neuroticism, extraversion, openness to new experiences, agreeableness and conscientiousness.
RESULTS: We found a significant correlation between 1,25(OH)(2)D(3) concentration and the factor extraversion (n = 206, r = 0.202, p = 0.004) and the factor openness (n = 206, r = 0.148, p = 0.034).
CONCLUSION: The possible mechanisms by which 1,25(OH)(2)D(3) acts on the brain might include Ca(2+) signaling, buffering antioxidant, and anti-inflammatory defenses against vascular injury, stimulating neurotrophins and improving metabolic and cardiovascular function. In conclusion, we suggest that 1,25(OH)(2)D(3) might influence personality traits, promoting extrovert and open behavior.
[Email me for the full-text article.]
Vitamin D receptors and metabolizing enzymes have been found in several human brain areas, including the prefrontal cortex, hippocampus, cingulate gyrus, thalamus, hypothalamus, and substantia nigra where autocrine and paracrine activity has been suggested. Vitamin D has been implicated in the regulation of behavior, stimulation of neurotrophin release, and protection of the brain by buffering antioxidant and antiinflammatory defenses. Hypovitaminosis D is prevalent in psychiatric patients and several studies suggest an association between hypovitaminosis D and basic and executive cognitive functions, depression, and schizophrenia. In regions that have historically suffered from hypovitaminosis D, an impact on personality dimensions, lower mean levels of sociosexuality, extraversion, and openness have been reported. This study explored whether the multifunctional 1,25 (OH)2D3 might be associated with basic personality traits finding Vitamin D might influence personality traits, promoting extrovert and open behavior.
Ubbenhorst A, Striebich S, Lang F, Lang UE. Exploring the relationship between vitamin D and basic personality traits. Psychopharmacology (Berl). Exploring the relationship between vitamin D and b... [Psychopharmacology (Berl). 2011] - PubMed result
RATIONALE: Several studies suggest an association between hypovitaminosis D and basic and executive cognitive functions, depression, bipolar disorder, and schizophrenia. A recent study confirms neophobic responses in vitamin D receptor mutant mice. We explored whether the plasma levels of 1,25-dihydroxyvitamin D (1,25(OH)(2)D(3)), the active form of vitamin D, are correlated with basic personality traits.
METHODS: A total of 206 healthy unrelated volunteers (108 male, 98 female, age 31 +/- 13 years) completed the German version of the NEO Five-Factor Inventory (NEO-FFI), which allows reliable and valid assessment of personality along the dimensions neuroticism, extraversion, openness to new experiences, agreeableness and conscientiousness.
RESULTS: We found a significant correlation between 1,25(OH)(2)D(3) concentration and the factor extraversion (n = 206, r = 0.202, p = 0.004) and the factor openness (n = 206, r = 0.148, p = 0.034).
CONCLUSION: The possible mechanisms by which 1,25(OH)(2)D(3) acts on the brain might include Ca(2+) signaling, buffering antioxidant, and anti-inflammatory defenses against vascular injury, stimulating neurotrophins and improving metabolic and cardiovascular function. In conclusion, we suggest that 1,25(OH)(2)D(3) might influence personality traits, promoting extrovert and open behavior.
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The dissent by Heaney and Hollick is a gem, Dr. Scally. Thank you for posting it.
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Re: OnLine First
[Email me for the full-text article.]
The purposes of this 1-yr, randomized, double-blind, placebo-controlled prospective trial in adults age 65 and over were to evaluate the effect of vitamin D2 or D3, 1,600 IU daily vs. 50,000 IU monthly, on the serum 25(OH)D concentration and serum and urinary calcium concentration, while concurrently investigating the potential importance of measuring trough 25(OH)D values.
Binkley N, Gemar D, Engelke J, et al. Evaluation of Ergocalciferol or Cholecalciferol Dosing, 1,600 IU Daily or 50,000 IU Monthly in Older Adults. J Clin Endocrinol Metab:jc.2010-0015. Evaluation of Ergocalciferol or Cholecalciferol Dosing, 1,600 IU Daily or 50,000 IU Monthly in Older Adults -- Binkley et al., 10.1210/jc.2010-0015 -- Journal of Clinical Endocrinology & Metabolism
Context: Whether ergocalciferol (D2) and cholecalciferol (D3) are equally effective to increase and maintain serum 25-hydroxyvitamin D [25(OH)D] concentration is controversial.
Objective: The aim of the study was to evaluate the effect of daily and once monthly dosing of D2 or D3 on circulating 25(OH)D and serum and urinary calcium.
Design, Setting and Participants: In a university clinical research setting, 64 community dwelling adults age 65+ were randomly assigned to receive daily (1,600 IU) or once-monthly (50,000 IU) D2 or D3 for 1 yr.
Main Outcome Measures: Serum 25(OH)D, serum calcium, and 24-h urinary calcium were measured at months 0, 1, 2, 3, 6, 9, and 12. Serum PTH, bone-specific alkaline phosphatase, and N-telopeptide were measured at months 0, 3, 6, and 12.
Results: Serum 25(OH)D was less than 30 ng/ml in 40% of subjects at baseline; after 12 months of vitamin D dosing, levels in 19% of subjects (n = 12, seven receiving daily doses and five monthly doses) remained low, despite compliance of more than 91%. D2 dosing increased 25(OH)D2 but produced a decline (P < 0.0001) in 25(OH)D3. Substantial between-individual variation in 25(OH)D response was observed for both D2 and D3. The highest 25(OH)D observed was 72.5 ng/ml. Vitamin D administration did not alter serum calcium, PTH, bone-specific alkaline phosphatase, N-telopeptide, or 24-h urine calcium.
Conclusions: Overall, D3 is slightly, but significantly, more effective than D2 to increase serum 25(OH)D. One year of D2 or D3 dosing (1,600 IU daily or 50,000 IU monthly) does not produce toxicity, and 25(OH)D levels of less than 30 ng/ml persist in approximately 20% of individuals. Substantial between-individual response to administered vitamin D2 or D3 is observed.
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The purposes of this 1-yr, randomized, double-blind, placebo-controlled prospective trial in adults age 65 and over were to evaluate the effect of vitamin D2 or D3, 1,600 IU daily vs. 50,000 IU monthly, on the serum 25(OH)D concentration and serum and urinary calcium concentration, while concurrently investigating the potential importance of measuring trough 25(OH)D values.
Binkley N, Gemar D, Engelke J, et al. Evaluation of Ergocalciferol or Cholecalciferol Dosing, 1,600 IU Daily or 50,000 IU Monthly in Older Adults. J Clin Endocrinol Metab:jc.2010-0015. Evaluation of Ergocalciferol or Cholecalciferol Dosing, 1,600 IU Daily or 50,000 IU Monthly in Older Adults -- Binkley et al., 10.1210/jc.2010-0015 -- Journal of Clinical Endocrinology & Metabolism
Context: Whether ergocalciferol (D2) and cholecalciferol (D3) are equally effective to increase and maintain serum 25-hydroxyvitamin D [25(OH)D] concentration is controversial.
Objective: The aim of the study was to evaluate the effect of daily and once monthly dosing of D2 or D3 on circulating 25(OH)D and serum and urinary calcium.
Design, Setting and Participants: In a university clinical research setting, 64 community dwelling adults age 65+ were randomly assigned to receive daily (1,600 IU) or once-monthly (50,000 IU) D2 or D3 for 1 yr.
Main Outcome Measures: Serum 25(OH)D, serum calcium, and 24-h urinary calcium were measured at months 0, 1, 2, 3, 6, 9, and 12. Serum PTH, bone-specific alkaline phosphatase, and N-telopeptide were measured at months 0, 3, 6, and 12.
Results: Serum 25(OH)D was less than 30 ng/ml in 40% of subjects at baseline; after 12 months of vitamin D dosing, levels in 19% of subjects (n = 12, seven receiving daily doses and five monthly doses) remained low, despite compliance of more than 91%. D2 dosing increased 25(OH)D2 but produced a decline (P < 0.0001) in 25(OH)D3. Substantial between-individual variation in 25(OH)D response was observed for both D2 and D3. The highest 25(OH)D observed was 72.5 ng/ml. Vitamin D administration did not alter serum calcium, PTH, bone-specific alkaline phosphatase, N-telopeptide, or 24-h urine calcium.
Conclusions: Overall, D3 is slightly, but significantly, more effective than D2 to increase serum 25(OH)D. One year of D2 or D3 dosing (1,600 IU daily or 50,000 IU monthly) does not produce toxicity, and 25(OH)D levels of less than 30 ng/ml persist in approximately 20% of individuals. Substantial between-individual response to administered vitamin D2 or D3 is observed.
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