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Vitamin D Improves Bone Health/Reduces Fracture Risk-Bone Loss: IOM, Endocrine Society - How Much Vit D Supp?/Calcium
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Institute of Medicine Report on Vit D concludes: "available scientific evidence supports a key role of calcium and vitamin D in skeletal health, consistent with a cause-and-effect relationship and providing a sound basis for determination of intake requirements"......"calcium and vitamin D supplementation was associated with a 12% risk reduction in all fractures......calcium and vitamin D treatment was associated with reduced rates of bone loss.....Thus, whereas calcium and vitamin D do have beneficial effects on fracture risk and rates of bone loss, the magnitude of this effect is much smaller than that of standard pharmacological therapy.....calcium and vitamin D treatment was associated with reduced rates of bone loss at the hip of 0.54% and spine of 1.19% . To put this in context for patients, the commonly used drug for osteoporosis, oral alendronate, reduces hip fracture risk by 51% and increases hip and spine bone mineral density over 3 yr by 4.7 and 6.1%, respectively, compared with placebo......Anti-fracture efficacy started at 25(OH)D levels of at least 30 ng/ml......The higher received dose (treatment dose/adherence) of 482-770 IU/d vitamin D reduced nonvertebral fractures in community-dwelling (- 29%) and institutionalized (- 15%) older individuals, and its effect was independent of additional calcium supplementation.....Muscle weakness is a prominent feature of the clinical syndrome of severe vitamin D deficiency. Clinical findings in vitamin D-deficiency myopathy include proximal muscle weakness, diffuse muscle pain, and gait impairments such as a waddling way of walking"
"The available scientific evidence supports a key role for calcium and vitamin D in skeletal health"
"The 2011 DRIs (dietary recommended intakes) for vitamin D specify RDAs, with levels of 400 IU/d for infants, 600 IU/d for children and adults through age 70, and 800 IU/d for ages 71 and older. However, the 2011 DRIs for vitamin D are nonetheless lower than those proposed by some in the current literature based on higher 25OHD levels that the Committee did not find justified by the evidence.....calcium and vitamin D treatment was associated with reduced rates of bone loss at the hip of 0.54% and spine of 1.19% . To put this in context for patients, the commonly used drug for osteoporosis, oral alendronate, reduces hip fracture risk by 51% and increases hip and spine bone mineral density over 3 yr by 4.7 and 6.1%, respectively, compared with placebo......Anti-fracture efficacy started at 25(OH)D levels of at least 30 ng/ml......The available scientific evidence supports a key role for calcium and vitamin D in skeletal health, providing a sound basis for DRIs. The evidence, however, is not yet compelling that either nutrient confers benefits for, or is causally related to, extraskeletal health outcomes. Moreover, existing evidence suggests that nearly all individuals meet their needs at intake levels (RDAs) provided in this report and, for vitamin D, at 25OHD levels of at least 20 ng/ml (50 nmol/liter) even under conditions of minimal sun exposure. Furthermore, higher levels have not been shown consistently to confer greater benefits, challenging the concept that "more is better." The Committee finds that the prevalence of vitamin D inadequacy in the North American population has been overestimated by some groups due to the use of inappropriate cut-points that greatly exceed the levels identified in this report. Serum concentrations of 25OHD above 30 ng/ml (75 nmol/liter) are not consistently associated with increased benefit, and risks have been identified for some outcomes at 25OHD levels above 50 ng/ml (125 nmol/liter). Additional research, including large-scale, randomized clinical trials, is needed. In the meantime, however, we believe that there is an urgent clinical and public health need for consensus cut-points for serum 25OHD inadequacy to avoid problems of both undertreatment and overtreatment."
The 2011 Report on Dietary Reference Intakes for Calcium ... - NATAP
www.natap.org/2010/HIV/120210_01.htm
The 2011 Report on Dietary Reference Intakes for Calcium and Vitamin D from the Institute of Medicine: What Clinicians Need to Know - publication pdf attached
This article summarizes the new 2011 report on dietary requirements for calcium and vitamin D from the Institute of Medicine (IOM). An IOM Committee charged with determining the population needs for these nutrients in North America conducted a comprehensive review of the evidence for both skeletal and extraskeletal outcomes. The Committee concluded that available scientific evidence supports a key role of calcium and vitamin D in skeletal health, consistent with a cause-and-effect relationship and providing a sound basis for determination of intake requirements. For extraskeletal outcomes, including cancer, cardiovascular disease, diabetes, and autoimmune disorders, the evidence was inconsistent, inconclusive as to causality, and insufficient to inform nutritional requirements. Randomized clinical trial evidence for extraskeletal outcomes was limited and generally uninformative. Based on bone health, Recommended Dietary Allowances (RDAs; covering requirements of 97.5% of the population) for calcium range from 700 to 1300 mg/d for life-stage groups at least 1 yr of age. For vitamin D, RDAs of 600 IU/d for ages 1-70 yr and 800 IU/d for ages 71 yr and older, corresponding to a serum 25-hydroxyvitamin D level of at least 20 ng/ml (50 nmol/liter), meet the requirements of at least 97.5% of the population.
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What Do We Tell Our Patients about Calcium and Vitamin D - NATAP
www.natap.org/2011/HIV/012711_02.htm
The Journal of Clinical Endocrinology & Metabolism Jan 2011 ... A case in point is the previously simple issue of calcium and vitamin D ... It is in this context that the 2010 Institute of Medicine (IOM) report on dietary reference intakes for vitamin D and calcium is of particular importance (1). ... As summarized by Ross et al
patients are likely to ask how much of an effect calcium and vitamin D supplementation, as recommended above, is likely to have on reducing the risk of fracture. Perhaps the best estimates of this come from several meta-analyses (6, 7); for example, Tang et al. (7) combined results from 17 trials (n = 52,625) that reported fracture as an outcome and found that calcium and vitamin D supplementation was associated with a 12% risk reduction in all fractures [risk ratio, 0.88; 95% confidence interval (CI), 0.83-0.75]. In trials that reported bone mineral density as an outcome (23 trials, n = 41,419), calcium and vitamin D treatment was associated with reduced rates of bone loss (relative to placebo) at the hip of 0.54% (95% CI, 0.35-0.73) and spine of 1.19% (95% CI, 0.76-1.61). To put this in context for patients, the commonly used drug for osteoporosis, oral alendronate, reduces hip fracture risk by 51% and increases hip and spine bone mineral density over 3 yr by 4.7 and 6.1%, respectively, compared with placebo (8). Thus, whereas calcium and vitamin D do have beneficial effects on fracture risk and rates of bone loss, the magnitude of this effect is much smaller than that of standard pharmacological therapy. However, given the low cost and minimal side effects of calcium and vitamin D supplementation, this should be part of the regimen for the prevention or treatment of osteoporosis in virtually all patients (unless there are specific contraindications, such as a history of nephrolithiasis or known hypercalciuria).
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Evaluation, Treatment, and Prevention of Vitamin D Deficiency: an Endocrine Society Clinical Practice Guideline
[PDF] Evaluation, Treatment, and Prevention of Vitamin D Deficiency: an ...
www.natap.org/2011/HIV/jc20110385full.pdf
by MF Holick - 2011
Jun 6, 2011 - vention of vitamin D deficiency with an emphasis on the care of patients ... contain vitamin D, the Task Force recommended supplementation
(Vitamin D Guidelines) Evaluation, Treatment, and Prevention of ...
www.natap.org/2011/HIV/060911_02.htm
Jun 6, 2011 - "Increased use of clothing and sunscreen over sun-exposed areas and de- creased consumption of vitamin D-fortified milk increases the risk
Many studies have evaluated the influence of dietary vitamin D supplementation on serum 25(OH)D, PTH, and bone health as measured by BMD and fracture risks in older men and women. Several randomized, double-blind clinical trials of senior men and women who had an intake of 400 IU/d showed insufficient 25(OH)D levels (25, 55, 80, 109-112). When men and women received supplements of 400-1000 IU/d, they had a significant reduction in bone resorption. In a randomized, placebo- controlled trial of elderly French women, those given calcium and 800 IU/d of vitamin D had significantly fewer vertebral and nonvertebral fractures (113). A similar observation was made in free-living men and women aged 65 yr and older who received 500 mg of calcium and 700 IU/d of vitamin D (114).
A threshold for optimal 25(OH)D and hip BMD has been addressed among 13,432 individuals studied in the NHANES III, including both younger (20-49 yr) and older (50 yr) individuals with different ethnic and racial backgrounds (98). In the regression plots, higher hip BMD was associated with higher serum 25(OH)D levels throughout the reference range of 9-37 ng/ml in all subgroups.
A 2005 meta-analysis of high-quality primary prevention RCT of vitamin D and fracture risk consistently found that antifracture efficacy of vitamin D increases with a higher achieved level of 25(OH)D (Fig. 1) (51). Anti-fracture efficacy started at 25(OH)D levels of at least 30 ng/ml. This level was reached only in trials that gave 700-800 IU/d vitamin D3 (high-quality trials with oral vitamin D2 were not available at the time).
The most up-to-date meta-analysis focused on antifracture efficacy from high-quality double-blind RCT (55). The higher received dose (treatment dose/adherence) of 482-770 IU/d vitamin D reduced nonvertebral fractures in community-dwelling (- 29%) and institutionalized (- 15%) older individuals, and its effect was independent of additional calcium supplementation (- 21% with additional calcium supplementation; - 21% for the main effect of vitamin D). As with the 2005 meta-analysis, anti-fracture efficacy started at 25(OH)D levels of at least 30 ng/ml (75 nmol/liter).
Muscle weakness is a prominent feature of the clinical syndrome of severe vitamin D deficiency. Clinical findings in vitamin D-deficiency myopathy include proximal muscle weakness, diffuse muscle pain, and gait impairments such as a waddling way of walking (115, 116). Double-blind RCT demonstrated that 800 IU/d vitamin D3 resulted in a 4-11% gain in lower extremity strength or function (80, 117), an up to 2 8% improvement in body sway (117, 118), and an up to 72% reduction in the rate of falling (119) in adults older than 65 yr after 5 months of treatment.
Several systematic reviews and meta-analyses have demonstrated a reduction in falls associated with interventions to raise 25(OH)D levels. Murad et al. (120) demonstrated that such interventions were associated with statistically significant reduction in the risk of falls [odds ratio (OR) 0.84; 95% confidence interval (CI), 0.76-0.93; inconsistency (I2 )61%; 23 studies). This effect was more prominent in patients who were vitamin D deficient at baseline. Results of other reviews were consistent. Ameta-analysis of only five high-quality double-blind RCT (n =1237) found that vitamin D reduced the falling risk by 22% (pooled corrected OR 0.78; 95% CI, 0.64-0.92) compared with calcium or placebo (116). For two trials with a total of 259 subjects using 800 IU/d of vitamin D3 over 2 to 3 months (117, 121), the corrected pooled OR was 0.65 (95% CI, 0.40- 1.00) (116), whereas 400 IU/d was insufficient to reduce falls (122). The importance of dose of supplemental vitamin D in minimizing risk of falls was confirmed by a multidose double-blind RCT among 124 nursing home residents receiving 200, 400, 600, or 800 IU/d vitamin D or placebo over 5 months (119) and by a 2009 meta-analysis (52). Participants receiving 800 IU/d had a 72% lower rate of falls than those taking placebo or a lower dose of vitamin D (rate ratio 0.28; 95% CI, 0.11-0.75).
Without vitamin D, only 10 to 15% of dietary calcium and about 60% of phosphorus are absorbed. Vitamin D sufficiency enhances calcium and phosphorus absorption by 30-40%and 80%, respectively (3, 10). 1,25(OH)2D interacts with its vitamin D receptor in the osteoblast to stimulate the expression of receptor activator of nuclear factor B ligand; this, in turn, interacts with receptor activator of nuclear factor B to induce immature monocytes to become mature osteoclasts, which dissolve the matrix and mobilize calcium and other minerals from the skeleton. In the kidney, 1,25(OH)2D stimulates calcium reabsorption from the glomerular filtrate (3, 11).
Consequences of Vitamin D Deficiency
Vitamin D deficiency results in abnormalities in calcium, phosphorus, and bone metabolism. Specifically, vitamin D deficiency causes a decrease in the efficiency of intestinal calcium and phosphorus absorption of dietary calcium and phosphorus, resulting in an increase in PTH levels (3,10, 22, 23). Secondary hyperparathyroidism maintains serum calcium in the normal range at the expense of mobilizing calcium from the skeleton and increasing phosphorus wasting in the kidneys. The PTH-mediated increase in osteoclastic activity creates local foci of bone weakness and causes a generalized decrease in bone mineral density (BMD), resulting in osteopenia and osteoporosis. Phosphaturia caused by secondary hyperparathyroidism results in a low normal or low serum phosphorus level. This results in an inadequate calcium phosphorus product, causing a mineralization defect in the skeleton (3, 46).
A major source of vitamin D for most humans comes from exposure of the skin to sunlight typically between 1000 h and 1500 h in the spring, summer, and fall (3-5, 7). Vitamin D produced in the skin may last at least twice as long in the blood compared with ingested vitamin D (53). When an adult wearing a bathing suit is exposed to one minimal erythemal dose of UV radiation (a slight pinkness to the skin 24 h after exposure), the amount of vitamin D produced is equivalent to ingesting between 10,000 and 25,000 IU (5). Avariety of factors reduce the skin's production of vitamin D3, including increased skin pigmentation, aging, and the topical application of a sunscreen (3, 39, 40). Analteration in the zenith angle of the sun caused by a change in latitude, season of the year, or time of day dramatically influences the skin's production of vitamin D3 (3, 5). Above and below latitudes of approximately 33°, vitamin D3 synthesis in the skin is very low or absent during most of the winter.
Few foods naturally contain vitamin D2 or vitamin D3 (Table 1).
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