Vitamin D

[Michael Scally MD]

Lucas RM, Ponsonby AL, Dear K, et al. Sun exposure and vitamin D are independent risk factors for CNS demyelination. Neurology 2011;76(6):540-8. http://www.neurology.org/content/76/6/540.abstract

Objectives: To examine whether past and recent sun exposure and vitamin D status (serum 25-hydroxyvitamin D [25(OH)D] levels) are associated with risk of first demyelinating events (FDEs) and to evaluate the contribution of these factors to the latitudinal gradient in FDE incidence in Australia.

Methods: This was a multicenter incident case-control study. Cases (n = 216) were aged 18–59 years with a FDE and resident within one of 4 Australian centers (from latitudes 27°S to 43°S), from November 1, 2003, to December 31, 2006. Controls (n = 395) were matched to cases on age, sex, and study region, without CNS demyelination. Exposures measured included self-reported sun exposure by life stage, objective measures of skin phenotype and actinic damage, and vitamin D status.

Results: Higher levels of past, recent, and accumulated leisure-time sun exposure were each associated with reduced risk of FDE, e.g., accumulated leisure-time sun exposure (age 6 years to current), adjusted odds ratio (AOR) = 0.70 (95% confidence interval [CI] 0.53–0.94) for each ultraviolet (UV) dose increment of 1,000 kJ/m2 (range 508–6,397 kJ/m2). Higher actinic skin damage (AOR = 0.39 [95% CI 0.17–0.92], highest grade vs the lowest) and higher serum vitamin D status (AOR = 0.93 [95% CI 0.86–1.00] per 10 nmol/L increase in 25(OH)D) were independently associated with decreased FDE risk. Differences in leisure-time sun exposure, serum 25(OH)D level, and skin type additively accounted for a 32.4% increase in FDE incidence from the low to high latitude regions.

Conclusions: Sun exposure and vitamin D status may have independent roles in the risk of CNS demyelination. Both will need to be evaluated in clinical trials for multiple sclerosis prevention.

 

[Michael Scally MD]

Re: OnLine First

The purposes of this study were to evaluate the prevalence of vitamin D insufficiency in National Collegiate Athletic Association (NCAA) Division I athletes throughout the academic year and to determine whether circulating concentrations of 25(OH)D are related to vitamin D intake, sun exposure, and body composition. A secondary purpose was to evaluate whether 25(OH)D concentration is linked to bone density, development of overuse or inflammatory injuries, and/or incidence of frequent illness.

Researchers hypothesized that athletes participating in indoor sports would have lower 25(OH)D concentrations compared with those participating in outdoor sports. Within the entire group of athletes, they further hypothesized that sun exposure, sunscreen use, and vitamin D intake (from food and supplements) would be predictive of 25(OH)D concentrations. In addition, they hypothesized that lower concentrations of 25(OH)D at any time point throughout the year would increase risk for low bone density, overuse and/or inflammatory injuries, and frequent illness.


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. 2011] - PubMed result

Vitamin D deficiency is endemic in the general population; however, there is much to be learned about the vitamin D status of athletes.

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.

 

[Michael Scally MD]

See: https://thinksteroids.com/community/posts/751149

 

[Michael Scally MD]

See: https://thinksteroids.com/community/posts/751641

 

[Michael Scally MD]

Re: OnLine First

Vitamin D Insufficiency High Among Patients With Early Parkinson Disease

High prevalence of hypovitaminosis D has been reported in Parkinson Disease (PD). Researchers found a significant decrease in vitamin D levels in patients with PD compared with matched healthy control subjects and patients with Alzheimer disease, but did not find a correlation with duration of disease symptoms. Other previous reports also noted high prevalence of vitamin D deficiency in PD, but in contrast, the prevalence was higher in patients with later-stage PD than in those with early-stage PD, consistent with the possibility that having PD and reduced mobility contributes to this relatively high prevalence. The Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism (DATATOP) cohort is a well-characterized cohort of subjects with early PD. The cohort is well suited for further examining the prevalence of vitamin D insufficiency early in the course of the disease. Subjects in this cohort also experienced clinically significant disease progression, allowing a preliminary examination of whether vitamin D concentration changes as the disease worsens clinically. In this study, they report vitamin D status in patients with early PD and examine changes in 25(OH)D concentration from baseline to the DATATOP study-defined end point or final visit.


Evatt ML, DeLong MR, Kumari M, et al. High Prevalence of Hypovitaminosis D Status in Patients With Early Parkinson Disease. Arch Neurol 2011;68(3):314-9. Arch Neurol -- Abstract: High Prevalence of Hypovitaminosis D Status in Patients With Early Parkinson Disease, March 2011, Evatt et al. 68 (3): 314

Background Vitamin D insufficiency has been reported to be more common in patients with Parkinson disease (PD) than in healthy control subjects, but it is not clear whether having a chronic disease causing reduced mobility contributes to this relatively high prevalence.

Objective To examine the prevalence of vitamin D insufficiency in a cohort of untreated patients with early PD (diagnosed within 5 years of study entry).

Design, Setting, and Patients The Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism (DATATOP) cohort is a well-characterized cohort of subjects with early, nondisabling PD. The cohort is well suited for examining the prevalence of vitamin D insufficiency early in the course of the disease. We conducted a survey study of vitamin D status in stored blood samples from patients with PD enrolled in the placebo group of the DATATOP trial. Samples from baseline visits and end point/final visits (mean [SD], 18.9 [13.1] months) were analyzed for 25-hydroxyvitamin D (25[OH]D) concentration in blinded fashion.

Main Outcome Measures The mean vitamin D concentration and the prevalence of vitamin D insufficiency at baseline and end point/final visits.

Results Among 199 subjects, 170 (85.4%) had samples from the baseline and end point visits available for analysis; 13 were excluded (10 with low probability of having PD and 3 with 25[OH]D concentrations >3 SDs above the mean). In the remaining 157 subjects, the mean (SD) 25(OH)D concentrations at the baseline and end point visits were 26.3 (8.6) ng/mL and 31.3 (9.0) ng/mL, respectively (to convert to nanomoles per liter, multiply by 2.496). The prevalence of vitamin D insufficiency (25[OH]D concentration <30.0 ng/mL) was 69.4% at baseline and 51.6% at the end point.

Conclusions The prevalence of vitamin D insufficiency in patients with early PD was similar to or higher than those reported in previous studies. Vitamin D concentrations did not decline during progression of PD. Further studies are needed to elucidate the natural history and significance of vitamin D insufficiency in PD.

 

[Michael Scally MD]

About one third of Americans are not getting enough vitamin D," according to a National Center for Health Statistics data brief released March 30 by the Centers for Disease Control and Prevention (CDC). The report "parallels what many other studies have suggested in recent years: that a large chunk of the population is at risk for low vitamin D levels." Although approximately "two-thirds had sufficient levels...about a third were in ranges suggesting risk of either inadequate or deficient levels, says report author Anne Looker, a research scientist with the CDC." Products - Data Briefs - Number 59 - March 2011..

 

[Michael Scally MD]

Osteoporosis, defined by a reduction in bone mass and disruption of bone microarchitecture, accounts for the majority of hip fractures among older adults. Epidemiological studies have identified major risk factors for osteoporosis, such as physical inactivity and low body mass. Discovery of novel fracture risk factors remains an important next step in the evaluation and treatment of this disorder.

Vitamin D deficiency and PTH excess are highly prevalent among older adults and are mechanistically linked with osteoporosis and fracture. Bone-specific alkaline phosphatase (BAP) is an enzyme anchored to osteoblasts that can, in part, inform the rate of bone formation. Previous studies of mineral metabolism and fracture have focused on individual biomarkers in isolation and are mainly limited to secondary fracture prevention.

In this study, researchers measured serum concentrations of 25-hydroxyvitamin D (25-OHD), PTH, and BAP in a relatively healthy cohort of 2294 ambulatory older adults who were free of known fracture and cardiovascular disease at baseline. They evaluated associations of mineral metabolism markers individually, and in combination, with incident hip fracture during more than 14 yr of follow-up.


Robinson-Cohen C, Katz R, Hoofnagle AN, et al. Mineral Metabolism Markers and the Long-Term Risk of Hip Fracture: The Cardiovascular Health Study. J Clin Endocrinol Metab:jc.2010-878. http://jcem.endojournals.org/cgi/content/abstract/jc.2010-2878v1?papetoc (Mineral Metabolism Markers and the Long-Term Risk of Hip Fracture: The Cardiovascular Health Study -- Robinson-Cohen et al., 10.1210/jc.2010-2878 -- Journal of Clinical Endocrinology &amp; Metabolism)

Context - Disturbances in mineral metabolism are associated with lower bone mineral density and fracture; however, previous human studies have assessed individual mineral metabolism markers in isolation.

Objective - We assessed serum concentrations of 25-hydroxyvitamin D (25-OHD), PTH, and bone-specific alkaline phosphatase (BAP) concentrations individually, and in combination, in association with the long-term risk of hip fracture among a general population of older adults.

Design and Setting - We studied 2294 participants from the Cardiovascular Health Study (mean age 74 yr) who were ambulatory and free of hip fracture and known cardiovascular disease at baseline. We used proportional hazards models to evaluate associations of baseline serum 25-OHD, PTH, and BAP concentrations with the time to first hospitalized hip fracture.

Results - During a median of 13 yr of follow-up, 242 participants (10.6%) developed an incident hip fracture. Serum 25-OHD concentrations less than 15 ng/ml were associated with a 61% greater adjusted risk of fracture (95% confidence interval 12-132% greater). In contrast, neither serum PTH nor BAP concentrations were significantly associated with fracture risk. The association of 25-OHD deficiency with hip fracture was not significantly altered by either PTH or BAP concentrations.

Conclusions - Serum concentrations of 25-OHD, but not PTH or BAP, are associated with long-term hip fracture risk among ambulatory older adults. These data suggest that 25-OHD is the most relevant mineral metabolism marker of fracture risk among older people.

 

[Michael Scally MD]

See: https://thinksteroids.com/community/posts/759711 [Vitamin D Status, Adiposity, and Lipids in Black American and Caucasian Children]

 

[Michael Scally MD]

Evaluation, Treatment, and Prevention of Vitamin D Deficiency

Noting that vitamin D deficiency is "very common in all age groups," new treatment guidelines call for many Americans to take more vitamin D than is currently recommended.

The guidelines, from the Endocrine Society, offer some contradictory advice. They say that virtually everyone in the U.S. should be taking vitamin D supplements, but that only those at risk for vitamin D deficiency should have their vitamin D blood levels checked.

Only those whose serum 25(OH)D blood levels are above 30 ng/mL are getting enough vitamin D. Lower levels are "insufficient," and those with levels below 20 ng/mL are frankly deficient.

But much higher levels are better, says guideline committee chairman Michael F. Holick, MD, PhD, director of the vitamin D skin and bone research lab at Boston University.

"The committee decided that 30 ng/mL is the minimum level, and recommended 40 to 60 ng/mL for both children and adults," Holick said at an online news conference.


Holick MF, Binkley NC, Bischoff-Ferrari HA, et al. Evaluation, Treatment, and Prevention of Vitamin D Deficiency: an Endocrine Society Clinical Practice Guideline. Journal of Clinical Endocrinology & Metabolism. http://jcem.endojournals.org/content/early/2011/06/03/jc.2011-0385.abstract (Evaluation, Treatment, and Prevention of Vitamin D Deficiency: an Endocrine Society Clinical Practice Guideline)

Objective: The objective was to provide guidelines to clinicians for the evaluation, treatment, and prevention of vitamin D deficiency with an emphasis on the care of patients who are at risk for deficiency.

Participants: The Task Force was composed of a Chair, six additional experts, and a methodologist. The Task Force received no corporate funding or remuneration.

Consensus Process: Consensus was guided by systematic reviews of evidence and discussions during several conference calls and e-mail communications. The draft prepared by the Task Force was reviewed successively by The Endocrine Society's Clinical Guidelines Subcommittee, Clinical Affairs Core Committee, and cosponsoring associations, and it was posted on The Endocrine Society web site for member review. At each stage of review, the Task Force received written comments and incorporated needed changes.

Conclusions: Considering that vitamin D deficiency is very common in all age groups and that few foods contain vitamin D, the Task Force recommended supplementation at suggested daily intake and tolerable upper limit levels, depending on age and clinical circumstances. The Task Force also suggested the measurement of serum 25-hydroxyvitamin D level by a reliable assay as the initial diagnostic test in patients at risk for deficiency. Treatment with either vitamin D2 or vitamin D3 was recommended for deficient patients. At the present time, there is not sufficient evidence to recommend screening individuals who are not at risk for deficiency or to prescribe vitamin D to attain the noncalcemic benefit for cardiovascular protection.

 

[Michael Scally MD]

Vitamin D and Cardiovascular Outcomes

Despite observational and epidemiological evidence, it is unclear whether vitamin D in interventional studies would affect cardiovascular risk. The Endocrine Society assembled a task force of experts to develop clinical practice guidelines regarding the supplementation of vitamin D. To assist in formulating these guidelines, researchers conducted a systematic review of the literature to quantitatively and qualitatively summarize the available evidence regarding the possible cardiovascular harms and benefits of vitamin D.

Researchers conducted a systematic review and meta-analysis to summarize the best available research evidence regarding the effect of vitamin D on patient-important cardiovascular events and other cardiovascular risk factors. Previous systematic reviews of observational studies found significant associations between low vitamin D levels and the risk of cardiovascular disease (of variable definitions across the studies) and overall mortality. Their analysis of randomized trials in which vitamin D was given as an intervention, as opposed to a blood level, did not demonstrate a significant effect on death, stroke, MI, lipid fractions (except a trivial increase in high-density lipoprotein), blood pressure, and blood glucose values. Their estimate for the mortality outcome, although nonsignificant, is in the same direction (i.e. reduction in risk) of that reported in another systematic review by Grandi et al. [Grandi NC, Breitling LP, Brenner H. Vitamin D and cardiovascular disease: systematic review and meta-analysis of prospective studies. Prev Med 2010;51(3-4):228-33. ScienceDirect - Preventive Medicine : Vitamin D and cardiovascular disease: Systematic review and meta-analysis of prospective studies [


Elamin MB, Abu Elnour NO, Elamin KB, et al. Vitamin D and Cardiovascular Outcomes: A Systematic Review and Meta-Analysis. Journal of Clinical Endocrinology & Metabolism. http://jcem.endojournals.org/content/early/2011/06/10/jc.2011-0398.abstract

Context: Several studies found association between vitamin D levels and hypertension, coronary artery calcification, and heart disease.

Objective: The aim of this study was to summarize the evidence on the effect of vitamin D on cardiovascular outcomes.

Design and Methods: We searched electronic databases from inception through August 2010 for randomized trials. Reviewers working in duplicate and independently extracted study characteristics, quality, and the outcomes of interest. Random-effects meta-analysis was used to pool the relative risks (RR) and the weighted mean differences across trials.

Results: We found 51 eligible trials with moderate quality. Vitamin D was associated with nonsignificant effects on the patient-important outcomes of death [RR, 0.96; 95% confidence interval (CI), 0.93, 1.00; P = 0.08], myocardial infarction (RR, 1.02; 95% CI, 0.93, 1.13; P = 0.64), and stroke (RR, 1.05; 95% CI, 0.88, 1.25; P = 0.59). These analyses were associated with minimal heterogeneity. There were no significant changes in the surrogate outcomes of lipid fractions, glucose, or diastolic or systolic blood pressure. The latter analyses were associated with significant heterogeneity, and the pooled estimates were trivial in absolute terms.

Conclusions: Trial data available to date are unable to demonstrate a statistically significant reduction in mortality and cardiovascular risk associated with vitamin D. The quality of the available evidence is low to moderate at best.

 

[Michael Scally MD]

In this review, researchers summarize and discuss current knowledge on the association of vitamin D with CVD and mortality. They start with an overview of vitamin D metabolism, vitamin D`s history in science, and the current prevalence of vitamin D deficiency. Then, they summarize mechanistic and clinical data on the role of vitamin D for the cardiovascular system and for CVD risk factors. Finally, they present epidemiological and interventional data of vitamin D administration, CVD, and mortality and offer some guidance for treating vitamin D deficiency.


Pilz S, Tomaschitz A, März W, et al. Vitamin D, cardiovascular disease and mortality. Clinical Endocrinology. Vitamin D, cardiovascular disease and mortality - Pilz - Clinical Endocrinology - Wiley Online Library

A poor vitamin D status, i.e. low serum levels of 25-hydroxyvitamin D (25[OH]D), is common in the general population. This finding is of concern not only because of the classic vitamin D effects on musculoskeletal outcomes, but also because expression of the vitamin D receptor (VDR) and vitamin D metabolizing enzymes in the heart and blood vessels suggests a role of vitamin D in the cardiovascular system. VDR-knockout mice suffer from cardiovascular disease (CVD) and various experimental studies suggest cardiovascular-protection by vitamin D, including anti-atherosclerotic, anti-inflammatory and direct cardio-protective actions, beneficial effects on classic cardiovascular risk factors as well as suppression of parathyroid hormone (PTH) levels. In epidemiological studies, low levels of 25(OH)D are associated with increased risk of CVD and mortality. Data from randomized controlled trials (RCTs) are sparse and have partially, but not consistently, shown some beneficial effects of vitamin D supplementation on cardiovascular risk factors (e.g. arterial hypertension).

We have insufficient data on vitamin D effects on cardiovascular events, but meta-analyses of RCTs indicate that vitamin D may modestly reduce all-cause mortality. Despite accumulating data suggesting that a sufficient vitamin D status may protect against CVD, we still must wait for results of large-scale RCTs before raising general recommendations for vitamin D in the prevention and treatment of CVD. In current clinical practice the overall risks and costs of vitamin D supplementation should be weighed against the potential adverse consequences of untreated vitamin D deficiency.

 

[Michael Scally MD]

The 2011 Report on Dietary Reference Intake for Vitamin D

In 2008, The North American governments decided that sufficient new evidence for vitamin D had been developed that a new study of the dietary reference intakes (DRI) should be conducted. The Institute of Medicine (IOM) appointed a committee of 14 scientists with a broad background; they were assisted by experienced IOM staff. The scientists were fully vetted by the IOM for conflicts of interest. The IOM committee’s report was critiqued by an independent panel of experts and the responses were adjudicated by a monitor before their submission. The purpose of this review is to briefly summarize the DRI process and background information concerning vitamin D, followed by a summary of the committee’s findings and the reviewer’s opinions about the next steps.


Aloia JF. Review: The 2011 Report on Dietary Reference Intake for Vitamin D: Where Do We Go From Here? Journal of Clinical Endocrinology & Metabolism. http://jcem.endojournals.org/content/early/2011/07/21/jc.2011-0090.abstract (Review: The 2011 Report on Dietary Reference Intake for Vitamin D: Where Do We Go From Here?)

Context: The Institute of Medicine (IOM) report on dietary reference intakes (DRI) for vitamin D is reviewed, along with its implications.

Evidence Acquisition: Evidence-based reviews were completed; the IOM committee conducted its own literature search, an open public workshop, and two open sessions, and maintained a public web site for stakeholder input. The consensus report of the 14 scientists on the committee was reviewed by a panel of experts.

Evidence Synthesis: Only bone health could be used as an indicator for DRI development. Evidence for extraskeletal outcomes was inadequate, inconsistent, or insufficient to develop DRI. The recommended dietary allowance was found to be 600 IU/d for ages 1-70 yr, corresponding on average to a serum 25-hydroxyvitamin D (25OHD) level of at least 50 nmol/liter (20 ng/ml), and 800 IU/d for those older than 70 yr. Comparison with current levels of 25OHD in the National Health and Nutrition Examination Survey population survey revealed that the vitamin D intake in the United States and Canada is adequate. An upper limit was set at 4000 IU/d for adults, corresponding to an average serum 25OHD level of 125 nmol/liter (50 ng/ml).

Conclusion: Previous reports of an epidemic of vitamin D deficiency in North America were based on an overestimation of adequacy. Population screening with serum 25OHD is therefore not warranted. Current laboratory reference ranges for serum 25OHD are overestimated and should be revised. Practice guidelines to treat disease should not be applied to the healthy American population where use of the DRI is appropriate.

 

[Michael Scally MD]

The 25-hydroxyvitamin D (25OHD) responses to supplementation with vitamin D vary widely among individuals. As a result, it is difficult to predict the dose that an individual needs to reach a specified target 25OHD level. Several sources of variability have been identified, including body mass index (BMI), which is inversely associated with change in 25OHD. The starting level of 25OHD is also important. The increment in 25OHD in response to a given dose of vitamin D3 is inversely related to the starting 25OHD level. Genetic factors influence not only ambient 25OHD levels but also the increment in response to supplemental vitamin D3 (2). Researchers found that people with different vitamin D binding protein genotypes have different serum 25OHD responses to a given dose of vitamin D. Together, the known sources account for no more than one third of the variability in 25OHD increment in response to supplemental vitamin D3; the remainder is unexplained.

Some of the variability may be related to the presence or absence of a meal and to the fat content and composition of the meal or the diet. In vivo studies in the rat have shown that greater fatty acid chain length and degree of unsaturation of fatty acids in the gut slowed the rate of vitamin D3 absorption. In an uncontrolled, prospective study in 17 patients, some of whom had malabsorption, serum 25OHD levels increased when the patients were instructed to take their supplements with the largest meal of the day, as opposed to taking them at the time of their choosing. The diets of these patients were not characterized with respect to their content of fat or of other components.

This study was done to explore possible associations of dietary fat content and composition with the increment in plasma 25OHD in response to supplemental vitamin D3. In healthy older men and women who were instructed to take 700 IU supplemental vitamin D3 daily at bedtime, they identified no association of total daily fat intake with 25OHD increment. In contrast, the increment in 25OHD was significantly positively associated with total daily monounsaturated fatty acids (MUFA) intake and inversely associated with total polyunsaturated fatty acids (PUFA) intake.


Niramitmahapanya S, Harris SS, Dawson-Hughes B. Type of Dietary Fat Is Associated with the 25-Hydroxyvitamin D3 Increment in Response to Vitamin D Supplementation. Journal of Clinical Endocrinology & Metabolism. http://jcem.endojournals.org/content/early/2011/07/28/jc.2011-1518.abstract (Type of Dietary Fat Is Associated with the 25-Hydroxyvitamin D3 Increment in Response to Vitamin D Supplementation)

Context: Mono- and polyunsaturated fats may have opposing effects on vitamin D absorption.
Objective: The purpose of this study was to determine whether intakes of different dietary fats are associated with the increase in serum 25-hydroxyvitamin D (25OHD) after supplementation with vitamin D3.

Design, Setting, and Participants: This analysis was conducted in the active treatment arm of a randomized, double-blind, placebo-controlled trial of vitamin D and calcium supplementation to prevent bone loss and fracture. Subjects included 152 healthy men and women age 65 and older who were assigned to 700 IU/d vitamin D3 and 500 mg/d calcium. Intakes of monounsaturated fatty acids (MUFA), polyunsaturated fatty acids (PUFA), and saturated fatty acids (SFA) were estimated by food frequency questionnaire.

Main Outcome Measure: The change in plasma 25OHD during 2 yr vitamin D and calcium supplementation was assessed.

Results: The change in plasma 25OHD (nanograms per milliliter) during vitamin D supplementation was positively associated with MUFA, (? = 0.94; P = 0.016), negatively associated with PUFA, (? = ?0.93; P = 0.038), and positively associated with the MUFA/PUFA ratio (? = 6.46; P = 0.014).

Conclusion: The fat composition of the diet may influence the 25OHD response to supplemental vitamin D3. Diets rich in MUFA may improve and those rich in PUFA may reduce the effectiveness of vitamin D3 supplements in healthy older adults. More studies are needed to confirm these findings.

 

[KTMguy]

I went ahead and tested my Vitamin D at my last draw. I don't have my results in front of me but Quest put my level at 31 and there was a note that it was considered semi-deficient.

I was a bit surprised due to my fortified milk consumption, my oily fish consumption,, and significant Sun exposure.

Anyways, I have begun supplementing Vit D.

Thanks for the heads up Dr. Scally as I would have never thought to have it checked. My doctors sure never mentioned it as part of a routine health screening.

 

[Michael Scally MD]

Vitamin D Intoxication with Severe Hypercalcemia due to Manufacturing and Labeling Errors of Dietary Supplements Made in the USA

Researchers present two cases of manufacturing and labeling errors of dietary supplements that caused vitamin D toxicity. The patients admitted to taking multiple dietary supplements. One of the supplements (Gary Null’s Ultimate Power Meal; Triarco Industries, Wayne, NJ) was purported to contain 1000 IU of vitamin D3 per daily dose. Analysis of this product by UV spectrophotometry followed by HPLC revealed a manufacturing error in which the daily recommended dose of two scoops actually contained 970,000 IU of vitamin D3. Similarly, as in case 1, this manufacturing error resulted in a vitamin D content 1,000 times more than the label claimed.


Araki T, Holick MF, Alfonso BD, et al. Vitamin D Intoxication with Severe Hypercalcemia due to Manufacturing and Labeling Errors of Two Dietary Supplements Made in the United States. Journal of Clinical Endocrinology & Metabolism. http://jcem.endojournals.org/content/early/2011/09/08/jc.2011-1443.abstract (Vitamin D Intoxication with Severe Hypercalcemia due to Manufacturing and Labeling Errors of Two Dietary Supplements Made in the United States)

Context: More than 50% of Americans use dietary supplements, and 60-70% fail to report this use to their physicians. Intoxication from vitamin D supplements has been rarely reported but may now occur more frequently. This may be attributable to an increase in vitamin D supplement intake due to the findings that deficiency is common and has been associated with a number of disease states.

Objective: We report two cases of vitamin D intoxication with dietary supplements made in the United States caused by manufacturing and labeling errors.

Methods: Case histories were obtained, and serial laboratory data (calcium and vitamin D metabolites) were measured. Each dietary supplement was analyzed by UV spectrophotometry followed by HPLC.

Results: In both cases, repetitive inquiries were required to elicit the use of dietary supplements. Because of significant manufacturer errors and a labeling error, patients had been consuming more than 1000 times the recommended daily dose of vitamin D3. Hypercalcemia is directly proportional to serum 25-hydroxyvitamin D [25(OH)D] but not 1,25-dihydroxyvitamin D levels. It took approximately 1 yr to normalize 25(OH)D levels. However, once 25(OH)D levels decreased below 400 ng/ml, both patients became normocalcemic and asymptomatic without long-term sequelae.

Conclusions: Although rare, vitamin D intoxication should be considered in the differential diagnosis of hypercalcemia. Patients should be asked whether they are using dietary supplements, and serial questioning may be required because patients may not consider these supplements to be potential health risks. Errors in the manufacturing and labeling of dietary supplements made in the United States may place individuals at increased risks for side effects.

 

[CubbieBlue]

Vitamin D Intoxication with Severe Hypercalcemia due to Manufacturing and Labeling Errors of Dietary Supplements Made in the USA

Researchers present two cases of manufacturing and labeling errors of dietary supplements that caused vitamin D toxicity. The patients admitted to taking multiple dietary supplements. One of the supplements (Gary Null’s Ultimate Power Meal; Triarco Industries, Wayne, NJ) was purported to contain 1000 IU of vitamin D3 per daily dose. Analysis of this product by UV spectrophotometry followed by HPLC revealed a manufacturing error in which the daily recommended dose of two scoops actually contained 970,000 IU of vitamin D3. Similarly, as in case 1, this manufacturing error resulted in a vitamin D content 1,000 times more than the label claimed.


Araki T, Holick MF, Alfonso BD, et al. Vitamin D Intoxication with Severe Hypercalcemia due to Manufacturing and Labeling Errors of Two Dietary Supplements Made in the United States. Journal of Clinical Endocrinology & Metabolism. http://jcem.endojournals.org/content/early/2011/09/08/jc.2011-1443.abstract (Vitamin D Intoxication with Severe Hypercalcemia due to Manufacturing and Labeling Errors of Two Dietary Supplements Made in the United States)

Context: More than 50% of Americans use dietary supplements, and 60-70% fail to report this use to their physicians. Intoxication from vitamin D supplements has been rarely reported but may now occur more frequently. This may be attributable to an increase in vitamin D supplement intake due to the findings that deficiency is common and has been associated with a number of disease states.

Objective: We report two cases of vitamin D intoxication with dietary supplements made in the United States caused by manufacturing and labeling errors.

Methods: Case histories were obtained, and serial laboratory data (calcium and vitamin D metabolites) were measured. Each dietary supplement was analyzed by UV spectrophotometry followed by HPLC.

Results: In both cases, repetitive inquiries were required to elicit the use of dietary supplements. Because of significant manufacturer errors and a labeling error, patients had been consuming more than 1000 times the recommended daily dose of vitamin D3. Hypercalcemia is directly proportional to serum 25-hydroxyvitamin D [25(OH)D] but not 1,25-dihydroxyvitamin D levels. It took approximately 1 yr to normalize 25(OH)D levels. However, once 25(OH)D levels decreased below 400 ng/ml, both patients became normocalcemic and asymptomatic without long-term sequelae.

Conclusions: Although rare, vitamin D intoxication should be considered in the differential diagnosis of hypercalcemia. Patients should be asked whether they are using dietary supplements, and serial questioning may be required because patients may not consider these supplements to be potential health risks. Errors in the manufacturing and labeling of dietary supplements made in the United States may place individuals at increased risks for side effects.

Wow! Be careful with your supplements guys!

 

[Michael Scally MD]

Lee DM, Tajar A, Pye SR, et al. Association of hypogonadism with vitamin D status: the European Male Ageing Study. European Journal of Endocrinology. http://www.eje-online.org/content/early/2011/10/27/EJE-11-0743.abstract (Association of hypogonadism with vitamin D status: the European Male Ageing Study)

Objective: Interrelationships between hormones of the hypothalamic-pituitary-testicular (HPT) axis, hypogonadism, vitamin D and seasonality remain poorly defined. We investigated whether HPT axis hormones and hypogonadism are associated with serum levels of 25-hydroxyvitamin D (25(OH)D) in men.

Design and methods: Cross-sectional survey of 3,369 community-dwelling men aged 40-79 in eight European centres. Testosterone (T), oestradiol (E2) and dihydrotestosterone (DHT) were measured by gas chromatography-mass spectrometry; luteinising hormone (LH), follicle-stimulating hormone (FSH), sex-hormone binding globulin (SHBG), 25(OH)D and parathyroid hormone (PTH) by immunoassay. Free T was calculated from T, SHBG and albumin. Gonadal status was categorised as eugonadal (normal T/LH), secondary (low T, low/normal LH), primary (low T, elevated LH) and compensated (normal T, elevated LH) hypogonadism. Associations of HPT axis hormones with 25(OH)D were examined using linear regression, and hypogonadism with vitamin D using multinomial logistic regression.

Results: In univariate analyses free T levels were lower (P=0.02) and E2 and LH higher (P<0.05) in men with deficient vitamin D (25(OH)D<50nmol/L). 25(OH)D was positively associated with total and free T, and negatively with E2 and LH in age and centre adjusted linear regressions. After adjusting for health and lifestyle factors no significant associations were observed between 25(OH)D and individual hormones of the HPT axis. However, deficient vitamin D was significantly associated with compensated [relative risk ratio (RRR)=1.52, P=0.03] and secondary hypogonadism (RRR=1.16, P=0.05). Seasonal variation was only observed for 25(OH)D (P<0.001).

Conclusions: Secondary and compensated hypogonadism were associated with vitamin D deficiency and the clinical significance of this relationship warrants further investigation.

 

[LW64]

I remember telling my GP that low T and low D are related...and the blank stare/silence I got in return...

 

[TRTman]

A couple years back , I tested very deficient (12, with the range being 30 - 75). I began supplementing with the liquid drops. Got my level to 60, then it dropped to 30 and has stayed between 30 and 40 even thought I am taking 8 - 10000 per day. Any ideas what could be going on? Can levels lower if you take too much?

 

[bodybuilding0841]

Yes I checked it every 5 to 6 weeks for monitoring