Vitamin D

[techlogik]

So if you just go out into the Sun for 15 minutes a day and expose your arms/face/legs...you will get more vitamin D than any supplement you waste money on. And it is all natural.

Ever notice after going out to the beach with sunblock for a few hours how you feel great later in the day/evening? The sunblock still allows UV rays and you still get get plenty of Vit D. But you have to stay out awhile and know how long so you don't get burned.

 

[Michael Scally MD]

Vitamin D Status and Cause-Specific Mortality

An inverse association between vitamin D status and all-cause mortality has been established in prospective studies. A meta-analysis of vitamin D supplementation reported a decrease in mortality, whereas a recent one found a reduced mortality with vitamin D and calcium supplementation in the elderly but no effect of vitamin D supplementation alone. The specific causes of death underlying the association with mortality lack clarity.

Vitamin D deficiency is in observational studies associated with an increased risk of cancers such as colorectal cancer, lung cancer, and breast cancer; cardiovascular disease (CVD); endocrine and metabolic diseases such as diabetes mellitus, obesity, and metabolic syndrome; respiratory disease such as chronic obstructive pulmonary disease (COPD), and respiratory infections; diseases of the digestive system such as liver disease, inflammatory bowel disease, and celiac disease; and mental disorders such as dementia, and depression.

No studies have investigated the association of vitamin D status and different specific causes of death in the same study population.

Skaaby T, Husemoen LLN, Pisinger C, et al. Vitamin D Status and Cause-Specific Mortality: A General Population Study. PLoS ONE 2012;7(12):e52423. PLOS ONE: Vitamin D Status and Cause-Specific Mortality: A General Population Study

Background - Vitamin D deficiency is associated with an increased risk of all-cause mortality in observational studies. The specific causes of death underlying this association lack clarity. We investigated the association between vitamin D status and cause-specific mortality.

Methods - We included a total of 9,146 individuals from the two population-based studies, Monica10 and Inter99, conducted in 1993–94 and 1999–2001, respectively. Vitamin D status was assessed as serum 25-hydroxyvitamin D. Information on causes of death was obtained from The Danish Register of Causes of Death until 31 December 2009. There were a total of 832 deaths (median follow-up 10.3 years).

Results - Multivariable Cox regression analyses with age as underlying time axis and vitamin D quartiles showed significant associations between vitamin D status and death caused by diseases of the respiratory system, the digestive system, and endocrine, nutritional and metabolic diseases with hazard ratios (HRs) 0.26 (ptrend = 0.0042), 0.28 (ptrend = 0.0040), and 0.21 (ptrend = 0.035), respectively, for the fourth vitamin D quartile compared to the first. We found non-significantly lower HRs for death caused by mental and behavioural diseases and diseases of the nervous system, but no association between vitamin D status and death caused by neoplasms or diseases of the circulatory system.

Conclusion - The associations of vitamin D status and cause-specific mortality suggest that we also look elsewhere (than to cardiovascular disease and cancer) to explain the inverse association between vitamin D status and mortality.

 

[Michael Scally MD]

Turner C, Dalton N, Inaoui R, Fogelman I, Fraser WD, Hampson G. Effect of a 300 000-IU Loading Dose of Ergocalciferol (Vitamin D2) on Circulating 1,25(OH)2-Vitamin D and Fibroblast Growth Factor-23 (FGF-23) in Vitamin D Insufficiency. Journal of Clinical Endocrinology & Metabolism. Effect of a 300 000-IU Loading Dose of Ergocalciferol (Vitamin D2) on Circulating 1,25(OH)2-Vitamin D and Fibroblast Growth Factor-23 (FGF-23) in Vitamin D Insufficiency

Context: Several trials have reported an increased risk of fractures and falls after intermittent high-dose vitamin D. Treatment with loading doses of vitamin D may increase 1,25(OH)2 vitamin D catabolism through changes in calcium/phosphate homeostasis and fibroblast growth factor-23 (FGF-23).

Objective: The aim was to determine the effects of high-dose vitamin D on circulating concentrations of 1,25(OH)2 vitamin D and FGF-23 in patients with osteoporosis and vitamin D insufficiency.

Design, Setting, Patients, and Intervention: We carried out a prospective study of 45 subjects with vitamin D deficiency/insufficiency treated with a bolus dose of 300 000 IU of vitamin D2 im. Blood samples were obtained at baseline and 1, 2, and 3 months after treatment.

Outcome Measures: Changes in 1,25(OH)2-vitamin D and FGF-23 were measured.

Results: Loading dose of vitamin D2 increased 1,25(OH)2-vitamin D2 at 3 months, with a mean [SD] of 41 [56] pmol/L at baseline and 162.3 [137.8] pmol/L at 3 months (P < .001). FGF-23 increased significantly at all time points with a peak at 3 months, with percent change from baseline (mean [SEM]) of 50% [48%] at 3 months (P < .01). There was a positive correlation between FGF-23 and serum phosphate (r = 0.36, P = .024) and calcium (r = 0.532, P < .001) and a negative correlation between total 1,25(OH)2-vitamin D and FGF-23 (r = ?0.32, P = .036) at 3 months.

Conclusions: High-dose vitamin D increases 1,25(OH)2-vitamin D and FGF-23 concentration. Further studies are required to determine whether adjusting vitamin D dose and frequency to minimize increases in FGF-23 may prevent the adverse outcomes associated with high-dose intermittent vitamin D supplementation.

 

[mikejamesjhm]

Well, Michael the information would suffice, the importance of Vitamin D is so much essential for maintaining health, this deficiency can really lead to such major problems. Its better to take the precautions before time and make our life secured from Arthritis.

 

[MarkHolland]

Hi,
This is a admirable post. Thanks for everything.

Mark Holland

 

[Michael Scally MD]

Causal Relationship between Obesity and Vitamin D Status

These findings suggest that a higher BMI leads to a lower vitamin D status whereas any effects of low vitamin D status on BMI are likely to be small. That is, these findings provide evidence for obesity as a causal factor in the development of vitamin D deficiency but not for vitamin D deficiency as a causal factor in the development of obesity. These findings suggest that population-level interventions to reduce obesity should lead to a reduction in the prevalence of vitamin D deficiency and highlight the importance of monitoring and treating vitamin D deficiency as a means of alleviating the adverse influences of obesity on health.


Vimaleswaran KS, Berry DJ, Lu C, et al. Causal Relationship between Obesity and Vitamin D Status: Bi-Directional Mendelian Randomization Analysis of Multiple Cohorts. PLoS Med 2013;10(2):e1001383. PLOS Medicine: Causal Relationship between Obesity and Vitamin D Status: Bi-Directional Mendelian Randomization Analysis of Multiple Cohorts

Background - Obesity is associated with vitamin D deficiency, and both are areas of active public health concern. We explored the causality and direction of the relationship between body mass index (BMI) and 25-hydroxyvitamin D [25(OH)D] using genetic markers as instrumental variables (IVs) in bi-directional Mendelian randomization (MR) analysis.

Methods and Findings - We used information from 21 adult cohorts (up to 42,024 participants) with 12 BMI-related SNPs (combined in an allelic score) to produce an instrument for BMI and four SNPs associated with 25(OH)D (combined in two allelic scores, separately for genes encoding its synthesis or metabolism) as an instrument for vitamin D. Regression estimates for the IVs (allele scores) were generated within-study and pooled by meta-analysis to generate summary effects.

Associations between vitamin D scores and BMI were confirmed in the Genetic Investigation of Anthropometric Traits (GIANT) consortium (n = 123,864). Each 1 kg/m2 higher BMI was associated with 1.15% lower 25(OH)D (p = 6.52×10?27). The BMI allele score was associated both with BMI (p = 6.30×10?62) and 25(OH)D (?0.06% [95% CI ?0.10 to ?0.02], p = 0.004) in the cohorts that underwent meta-analysis. The two vitamin D allele scores were strongly associated with 25(OH)D (p?8.07×10?57 for both scores) but not with BMI (synthesis score, p = 0.88; metabolism score, p = 0.08) in the meta-analysis. A 10% higher genetically instrumented BMI was associated with 4.2% lower 25(OH)D concentrations (IV ratio: ?4.2 [95% CI ?7.1 to ?1.3], p= 0.005). No association was seen for genetically instrumented 25(OH)D with BMI, a finding that was confirmed using data from the GIANT consortium (p?0.57 for both vitamin D scores).

Conclusions - On the basis of a bi-directional genetic approach that limits confounding, our study suggests that a higher BMI leads to lower 25(OH)D, while any effects of lower 25(OH)D increasing BMI are likely to be small. Population level interventions to reduce BMI are expected to decrease the prevalence of vitamin D deficiency.

 

[Michael Scally MD]

Dietary and Supplemental Calcium Intake and Cardiovascular Disease Mortality

Xiao Q, Murphy RA, Houston DK, Harris TB, Chow W, Park Y. Dietary and Supplemental Calcium Intake and Cardiovascular Disease Mortality: The National Institutes of Health–AARP Diet and Health Study. JAMA Intern Med. 2013:1-8. JAMA Network | JAMA Internal Medicine | Dietary and Supplemental Calcium Intake and Cardiovascular Disease MortalityThe National Institutes of Health–AARP Diet and Health StudyCalcium Intake and CVD Mortality

Importance - Calcium intake has been promoted because of its proposed benefit on bone health, particularly among the older population. However, concerns have been raised about the potential adverse effect of high calcium intake on cardiovascular health.

Objective - To investigate whether intake of dietary and supplemental calcium is associated with mortality from total cardiovascular disease (CVD), heart disease, and cerebrovascular diseases.

Design and Setting - Prospective study from 1995 through 1996 in California, Florida, Louisiana, New Jersey, North Carolina, and Pennsylvania and the 2 metropolitan areas of Atlanta, Georgia, and Detroit, Michigan.

Participants - A total of 388 229 men and women aged 50 to 71 years from the National Institutes of Health–AARP Diet and Health Study.

Main Outcome Measures - Dietary and supplemental calcium intake was assessed at baseline (1995-1996). Supplemental calcium intake included calcium from multivitamins and individual calcium supplements. Cardiovascular disease deaths were ascertained using the National Death Index. Multivariate Cox proportional hazards regression models adjusted for demographic, lifestyle, and dietary variables were used to estimate relative risks (RRs) and 95% CIs.

Results - During a mean of 12 years of follow-up, 7904 and 3874 CVD deaths in men and women, respectively, were identified. Supplements containing calcium were used by 51% of men and 70% of women. In men, supplemental calcium intake was associated with an elevated risk of CVD death (RR>1000 vs 0 mg/d, 1.20; 95% CI, 1.05-1.36), more specifically with heart disease death (RR, 1.19; 95% CI, 1.03-1.37) but not significantly with cerebrovascular disease death (RR, 1.14; 95% CI, 0.81-1.61). In women, supplemental calcium intake was not associated with CVD death (RR, 1.06; 95% CI, 0.96-1.18), heart disease death (1.05; 0.93-1.18), or cerebrovascular disease death (1.08; 0.87-1.33). Dietary calcium intake was unrelated to CVD death in either men or women.

Conclusions and Relevance - Our findings suggest that high intake of supplemental calcium is associated with an excess risk of CVD death in men but not in women. Additional studies are needed to investigate the effect of supplemental calcium use beyond bone health.

Available data are suggestive of adverse cardiovascular effects with an excessive intake of supplemental calcium. More large studies are needed to further assess the potential health risks or benefits of calcium supplement use on CVD morbidity and mortality. Meanwhile, a safe alternative to calcium supplements is to consume calcium-rich foods, such as low-fat dairy foods, beans, and green leafy vegetables, which contain not only calcium but also a cocktail of essential minerals and vitamins. These nondairy food sources of calcium have the added health benefits and have recently been reported to improve glycemic control in persons with diabetes. The paradigm “the more the better” is invalid for calcium supplementation.

Larsson SC. Are Calcium Supplements Harmful to Cardiovascular Disease?: Comment on “ Dietary and Supplemental Calcium Intake and Cardiovascular Diseases Mortality: The National Institutes of Health–AARP Diet and Health Study”. JAMA Intern Med. 2013:1-2. JAMA Network | JAMA Internal Medicine | Are Calcium Supplements Harmful to Cardiovascular Disease?Comment on “ Dietary and Supplemental Calcium Intake and Cardiovascular Diseases Mortality: The National Institutes of Health–AARP Diet and Health Study

 

[Michael Scally MD]

Prevalence Of Vitamin D Deficiency In Australian

Boyages S, Bilinski K. Seasonal reduction in vitamin D level persists into spring in NSW Australia: implications for monitoring and replacement therapy. Clinical Endocrinology 2012;77(4):515-23. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2265.2012.04398.x/abstract

Context Seasonal variation in 25-hydroxyvitamin D [25OHD] status and its relationship to gender, age, socioeconomic and geographic determinants in Australians has not been described in large biomedical sampling cohorts.

Objectives To analyse 25OHD levels in all primary tests undertaken consecutively in a 2-year period to determine the prevalence of 25OHD deficiency and its relation to patient setting, gender, age, season, urban or rural residency, socioeconomic status, latitude and longitude.

Design We assessed 24 819 ambulatory and inpatient samples taken from the largest reference laboratory in NSW, Australia between 01 July 2008 and 30 July 2010.

Main outcome measures Serum 25OHD was measured using chemiluminescent immunoassay. Vitamin D deficiency was defined as 25OHD <50 nm.

Results Median 25OHD was 54 nm ranging from 63 nm in summer to 44 nm in spring and was lowest in inpatient women (49 nm) and highest in ambulatory men (64 nm). Mean 25OHD peaked in January (67 nm) and reached a nadir in August/September (39 nm). During summer, 36% subjects overall had a level below 50 nm, increasing to 58% in spring. The highest prevalence of deficiency occurred in female inpatients (42% in summer and 62% in spring). Factors associated with lower 25OHD included being tested in spring, an inpatient, female, aged 20–39 or >79 years, socioeconomically disadvantaged and from a major city.

Conclusion This cross-sectional study demonstrates the extent and duration of 25OHD deficiency is greater than expected, and particular individuals are at higher risk. Our findings imply that supplementation guidelines need to be modified and strengthened.


Daly RM, Gagnon C, Lu ZX, et al. Prevalence of vitamin D deficiency and its determinants in Australian adults aged 25 years and older: a national, population-based study. Clin Endocrinol (Oxf) 2012;77(1):26-35. Prevalence of vitamin D deficiency and its determinants in Australian adults aged 25

OBJECTIVE: Vitamin D deficiency is recognized as a global public health problem, but the population-based prevalence of deficiency and its determinants in Australian adults is not known. This study evaluated the vitamin D status of Australian adults aged >/=25 years and risk factors associated with vitamin D deficiency in this population.

DESIGN and PATIENTS: We studied a national sample of 11,247 Australian adults enrolled in the 1999/2000 Australian Diabetes, Obesity and Lifestyle (AusDiab) study drawn from 42 randomly selected districts throughout Australia.

MEASUREMENTS: Serum concentrations of 25-hydroxyvitamin D [25(OH)D] were measured by immunoassay. Vitamin D deficiency was defined as a concentration <50 nmol/l. Information on demographic and lifestyle factors was derived from interview-administered questionnaires.

RESULTS: The mean serum 25(OH)D concentration was 63 nmol/l (95% CI: 59-67 nmol/l). Only 4% of the population had a level <25 nmol/l, but the prevalence of vitamin D deficiency (<50 nmol/l) was 31% (22% men; 39% women); 73% had levels <75 nmol/l. The prevalence of vitamin D deficiency increased significantly with age, was greater in women, in those of non-Europid origin, in the obese and those who were physically inactive and with a higher level of education. Deficiency was also more common during winter and in people residing in southern Australia (latitude >35 degrees S); 42% of women and 27% of men were deficient during summer-autumn, which increased to 58% and 35%, respectively, during winter-spring.

CONCLUSION: Vitamin D deficiency is common in Australia affecting nearly one-third of adults aged >/=25 years. This indicates that strategies are needed at the population level to improve vitamin D status of Australians.

 

[Michael Scally MD]

Ryan KJp, Daniel ZCtr, Craggs LJl, Parr T, Brameld JM. Dose-dependent effects of Vitamin D on transdifferentiation of muscle to adipose cells. Journal of Endocrinology. http://joe.endocrinology-journals.org/content/early/2013/01/17/JOE-12-0234.abstract

Fat infiltration within muscle is one of a number of features of vitamin D deficiency which leads to a decline in muscle functionality. The origin of this fat is unclear but one possibility is that it forms from myogenic precursor cells present in the muscle, which transdifferentiate into mature adipocytes. The current study examined the effect of the active form of vitamin D3, 1,25 dihydroxyvitamin D3 (1,25(OH)2D3), on the capacity of the C2C12 muscle cell line to differentiate towards the myogenic and adipogenic lineages. Cells were cultured in myogenic or adipogenic differentiation media containing increasing concentrations (0, 10-13, 10-11, 10-9, 10-7 or 10-5M) of 1,25(OH)2D3 for up to 6 days and markers of muscle and fat development measured.

Mature myofibres were formed in both adipogenic and myogenic media, but fat droplets were only observed in adipogenic media. Relative to controls, low physiological concentrations (10-13 and 10-11M) of 1,25(OH)2D3 increased fat droplet accumulation, whereas high physiological (10-9M) and supraphysiological concentrations (?10-7M) inhibited fat accumulation. This increased accumulation of fat with low physiological concentrations (10-13 and 10-11M) was associated with a sequential up-regulation of PPAR?2 and FABP4 mRNA, indicating formation of adipocytes, whereas higher concentrations (?10-9M) reduced all these effects, and the highest concentration (10-5M) appeared to have toxic effects.

This is the first study to demonstrate dose-dependent effects of 1,25(OH)2D3 on the transdifferentiation of muscle cells into adipose cells. Low physiological concentrations (possibly mimicking a deficient state) induced adipogenesis, whereas higher (physiological and supraphysiological) concentrations attenuated this effect.

 

[Michael Scally MD]

Gallagher JC. Vitamin D Deficiency and Muscle Strength: Are They Related? Journal of Clinical Endocrinology & Metabolism 2012;97(12):4366-9. Vitamin D Deficiency and Muscle Strength: Are They Related?

 

[bcfromfl]

"Plasma zinc levels have been found to be dependent upon vitamins A and D. This suggests that a Vitamin A or D deficiency could cause a secondary zinc deficiency and that for treatment of zinc deficiency one should ensure adequate vitamin A and D intake."

Of special interest to those on this board:

"Zinc is required by men to produce testosterone. Thus, Zinc deficiency can lead to less testosterone production in men and hence show up with the symptoms associated with low testosterone."

From: [ame=http://en.wikipedia.org/wiki/Zinc_deficiency]Zinc deficiency - Wikipedia, the free encyclopedia[/ame]

Also:Zinc &mdash; Health Professional Fact Sheet

Keep in mind that adequate intake of vitamins and minerals may not result in proper serum levels, due to malabsorption, either by way of poor bioavailability or gastrointestinal/autoimmune disease. Unfortunately, serum and cellular zinc levels are difficult to determine accurately.

Men with low T must consider malabsorption of D as a contributing factor! The damage to the small intestine from food intolerance/sensitivity is a leading cause of malabsorption.

 

[Michael Scally MD]

Sanders KM, Nicholson GC, Ebeling PR. Is high dose vitamin D harmful? Calcif Tissue Int 2013;92(2):191-206. Is High Dose Vitamin D Harmful? - Springer

With the potential to minimize the risk of many chronic diseases and the apparent biochemical safety of ingesting doses of oral vitamin D several-fold higher than the current recommended intakes, recent research has focussed on supplementing individuals with intermittent, high-dose vitamin D. However, two recent randomized controlled trials (RCTs) both using annual high-dose vitamin D reported an increase, rather than a decrease, in the primary outcome of fractures. This review summarises the results from studies that have used intermittent, high doses of vitamin D, with particular attention to those finding evidence of adverse effects. Results from observational, population-based studies with evidence of a U- or J-shaped curve are also presented as these findings suggest an increased risk in those with the highest serum 25D levels. Speculative mechanisms are discussed and biochemical results from studies using high-dose vitamin D are also presented. Emerging evidence from both observational studies and RCTs suggests there should be a degree of caution about recommending high serum 25D concentrations for the entire population. Furthermore, benefit of the higher doses commonly used in clinical practice on falls risk reduction needs to be demonstrated. The safety of loading doses of vitamin D should be demonstrated before these regimens become recommended as routine clinical practice. The current dilemma of defining vitamin D insufficiency and identifying safe and efficacious repletion regimens needs to be resolved.

 

[Michael Scally MD]

Jones ML, Martoni CJ, Prakash S. Oral supplementation with probiotic L. reuteri NCIMB 30242 increases mean circulating 25-hydroxyvitamin D: a post-hoc analysis of a randomized controlled trial. Journal of Clinical Endocrinology & Metabolism. Oral supplementation with probiotic L. reuteri NCIMB 30242 increases mean circulating 25-hydroxyvitamin D: a post-hoc analysis of a randomized controlled trial

Context: Low serum 25-hydroxyvitamin D is a risk factor for osteoporosis, cardiovascular disease, diabetes and cancer. Disruption of non-cholesterol sterol absorption due to cholesterol lowering therapies may result in reduced fat soluble vitamin absorption.

Objective: We have previously reported on the cholesterol lowering efficacy and reduced sterol absorption of probiotic bile salt hydrolase active L. reuteri NCIMB 30242; however, the effects on fat soluble vitamins was previously unknown and the objective of the present study.

Design, Settings, Patients and Intervention: The study was double-blind, placebo-controlled, randomized, parallel-arm, multi-center lasting 13 weeks. 127 otherwise healthy hypercholesterolemic adults with LDL-cholesterol >3.4 mmol/l, triglycerides <4.0 mmol/l and body mass index of 22-32 kg/m2were included. Subjects were recruited from 6 private practices in Prague, CZ and randomized to consume L. reuteri NCIMB 30242 or placebo capsules over a 9-week intervention period.

Outcome measures: The primary outcome measure was the change in serum LDL-cholesterol over the 9-week intervention. Analysis of fat soluble vitamins at Weeks 0 and 9 were performed post-hoc.

Results: There were no significant differences between L. reuteri NCIMB 30242 and placebo capsule groups in serum vitamin A, vitamin E, ?-carotene or dietary intake over the intervention period (P>0.05). L. reuteri NCIMB 30242 increased serum 25-hydroxyvitamin D by 14.9 nmol/l or 25.5% over the intervention period, which was a significant mean change relative to placebo of 17.1 nmol/l or 22.4% respectively (P=0.003).

Conclusions: To our knowledge this is the first report of increased circulating 25-hydroxyvitamin D in response to oral probiotic supplementation.

 

[akiravp82]

ive been taking 20,000 iu vitamin D daily for a year now with my levels not going past 32 wtf is wrong with me ? ive even tried bio forte liquid emulsion at 20,000 iu a day for months and for some reason im always stuck at the number 32 im starting to get really fed up with this , how can i raise it ? should i do 50,000 iu a day for months i dont get it ? and it is D3 i am taking....

 

[Michael Scally MD]

Dror Y, Giveon S, Hoshen M, Feldhamer I, Balicer R, Feldman B. Vitamin D Levels for Preventing Acute Coronary Syndrome and Mortality: Evidence of a Non-Linear Association. Journal of Clinical Endocrinology & Metabolism. Vitamin D Levels for Preventing Acute Coronary Syndrome and Mortality: Evidence of a Non-Linear Association

Context: Low serum calcidiol has been associated with multiple co-morbidities and mortality but no “safe” range has been found for the upper concentration.

Objective: To establish the upper threshold of serum calcidiol, beyond which there is an increased risk for acute coronary syndrome and/or mortality.

Design, Setting, and Participants: We extracted data for 1,282,822 Clalit Health Services members aged > 45 between July 2007 and December 2011. Records of mortality or acute coronary syndrome were extracted during the follow-up period. Kaplan Meier analysis calculated time to episode and Cox regression models generated adjusted hazard ratios for episode by calcidiol group (< 10, 10.1–20, 20.1–36 and > 36.1 ng/mL).

Outcome Measures: Acute coronary syndrome subsuming all-cause mortality.

Results: During the 54-month study period, 422,822 Clalit Health Services members were tested for calcidiol of which 12,280 died of any cause (905 with acute coronary syndrome) and 3,933 were diagnosed with acute coronary syndrome. Compared to those with 20–36 ng/ml, the adjusted hazard ratios among those with levels of < 10, 10–20 and > 36 ng/ml were 1.88 [CI: 1.80–1.96], 1.25 [CI:1.21–1.30] and 1.13 [CI:1.04–1.22], (P < 0.05) respectively.

Limitations: The study cohort comprised only 30% of the population, those tested for vitamin D. The small sample size of those with calcidiol > 36 ng/mL prevented further analysis of this group.

Conclusions: Vitamin D in the 20–36 ng/ml range was associated with the lowest risk for mortality and morbidity. The hazard ratio below and above this range increases significantly.


Evidence for a U-shaped vitamin D level-mortality or acute coronary syndrome relation is not convincing
Replies to Vitamin D Levels for Preventing Acute Coronary Syndrome and Mortality: Evidence of a Non-Linear Association

 

[Michael Scally MD]

Jorde R, Grimnes G, Hutchinson MS, Kjaergaard M, Kamycheva E, Svartberg J. Supplementation with Vitamin D Does not Increase Serum Testosterone Levels in Healthy Males. Horm Metab Res. https://www.thieme-connect.de/ejournals/abstract/10.1055/s-0033-1345139

Cross-sectional studies indicate a positive relation between serum 25-hydroxyvitamin D [25(OH)D] and testosterone. It is not known if this relation is causal, which in theory could be in both directions. A cross-sectional population based study was designed with pooled data from 3 vitamin D randomized clinical trials (RCTs) performed in Tromso with weight reduction, insulin sensitivity, and depression scores as endpoints, and one testosterone RCT in subjects with low serum testosterone (<11.0 nmol/l) and with body composition as endpoint. Serum 25(OH)D and androgens were measured in 893 males in the cross-sectional part, at baseline and after 6-12 months of supplementation with vitamin D 20 000 IU-40 000 IU per week vs. placebo in the vitamin D RCTs (n=282), and at baseline and after one year treatment with testosterone undecanoate 1 000 mg or placebo injections (at baseline and after 6, 16, 28, and 40 weeks) in the testosterone RCT (n=37). In the cross-sectional study, serum 25(OH)D was found to be a significant and positive predictor of serum testosterone. In the vitamin D RCTs, no significant effect on serum total or free testosterone levels was seen, and in the testosterone RCT no significant effect on serum 25(OH)D was seen. This was unchanged in sub-analyses in subjects with low serum 25(OH)D (or testosterone) levels. In conclusion, in subjects without significant vitamin D deficiency, there is no increase in serum testosterone after high dose vitamin D supplementation. Similarly, in subjects with moderately low serum testosterone levels, substitution with testosterone does not increase serum 25(OH)D.

 

[Michael Scally MD]

Pinzone MR, Di Rosa M, Malaguarnera M, et al. Vitamin D deficiency in HIV infection: an underestimated and undertreated epidemic. Eur Rev Med Pharmacol Sci 2013;17(9):1218-32. Vitamin D deficiency in HIV infection: an underestimated and undertreated epidemic

Hypovitaminosis D is a very common disorder, regarding both Western and developing countries. A growing amount of data over the last years have shown vitamin D deficiency to be high prevalent among HIV-positive subjects. In addition to "classic" risk factors, such as female sex, low dietary intake, dark skin pigmentation and low sun exposure, HIV-related factors, including immune activation and antiretroviral adverse effects, may affect vitamin D status. Even if both protease inhibitors and non-nucleoside reverse transcriptase inhibitors have been associated with low vitamin D levels, available evidences have failed to univocally associate hypovitaminosis D with specific antiretroviral class effects.

Low vitamin D is known to have a negative impact not only on bone health, but also on neurocognitive, metabolic, cardiovascular and immune functions. Similarly to the general population, several studies conducted on HIV-infected subjects have associated hypovitaminosis D with a greater risk of developing osteopenia/osteoporosis and fragility fractures. Analogously, vitamin D deficiency has been described as an independent risk factor for cardiovascular disease and metabolic disorders, such as insulin resistance and type 2 diabetes mellitus.

Last EACS guidelines suggest to screen for hypovitaminosis D every HIV-positive subject having a history of bone disease, chronic kidney disease or other known risk factors for vitamin D deficiency. Vitamin D repletion is recommended when 25-hydroxyvitamin D levels are below 10 ng/ml. Furthermore, it may be indicated in presence of 25OHD values between 10 and 30 ng/ml, if associated with osteoporosis, osteomalacia or increased parathyroid hormone levels. The optimal repletion and maintenance dosing regimens remain to be established, as well as the impact of vitamin D supplementation in preventing comorbidities.

 

[Superman4hire]

For those living in the Northern US or Canada cod liver oil is a great source of vitD.

 

[adleylab]

If you shun the sun, suffer from milk allergies, or adhere to a strict vegetarian diet, you may be at risk for vitamin D deficiency. Known as the sunshine vitamin, vitamin D is produced by the body in response to sunlight. It is also occurs naturally in a few foods -- including some fish, fish liver oils, and egg yolks -- and in fortified dairy and grain products.

Vitamin D is essential for strong bones because it helps the body use calcium from the diet. Traditionally, vitamin D deficiency has been associated with rickets, a disease in which the bone tissue doesn't properly mineralization, leading to soft bones and skeletal deformities. But increasingly, research is revealing the importance of vitamin D in protecting against a host of health problems.

 

[johndenny]

How are we going to get mine up. It's been around 46 for months now. I upped my dose to 20000iu's, but was told to cut back to 16000.

Vitamin D deficiency causes osteomalacia (called rickets when it occurs in children). Beyond that, low serum vitamin D levels have been associated with falls, and low bone mineral density. Vitamin D is necessary for strong bones as it assists the body use calcium from the diet.