Vitamin D and Health: Do We Need More Than the Current DRI?: Part 2 : ACSM's Health & Fitness Journal

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Vitamin D and Health: Do We Need More Than the Current DRI?

Part 2

Volpe, Stella Lucia Ph.D., R.D., L.D.N., FACSM

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ACSM's Health & Fitness Journal 13(1):p 33-34, January 2009. | DOI: 10.1249/FIT.0b013e3181916ed4
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In Brief

At ACSM's Health & Fitness Summit & Exposition in Long Beach, CA, last spring, I was asked to give a presentation on Vitamin D and Health. I thought it would be appropriate to write a two-part series on this topic for ACSM's Health & Fitness Journal® because vitamin D has been a hot topic in the scientific and lay communities. In Part I, I provided background information for vitamin D, and in Part II, I will discuss vitamin D's role in disease prevention and health.


Although it may seem that our bones are stagnant organs, they are constantly remodeling. That is, bone builds with bone cells called osteoblasts and resorbs (break down) with bone cells called osteoclasts. Osteomalacia (literally defined as "softening of the bones" and called rickets in children), is a disease caused by vitamin D deficiency. It results in decreased calcification of bone tissue, bowed legs, and severe muscle weakness. Osteomalacia was practically eliminated in the United States after fortification of vitamin D in dairy products occurred in the 1930s.

In 2007, Bischoff-Ferrari and Dawson-Hughes (2) published a "meta-analysis of primary prevention high-quality trials published in 2005." In brief, a meta-analysis entails that the authors conduct an intense statistical analyses of the trials they have accepted for their manuscript, to evaluate the cumulative effect of the trials (in this case, on vitamin D and bone density). Bischoff-Ferrari and Dawson-Hughes (2) reported that supplementation with vitamin D3 (cholecalciferol) at 700 to 800 international units (IU) per day, or occasionally with 100,000 IU every 4 months, with or without calcium, should facilitate a reduction in both hip and nonvertebral fractures. They also reported that those trials where 400 IU of vitamin D supplementation were used did not have a positive effect on fracture reduction. Additionally, they found a significant inverse correlation between higher blood concentrations of 25-hydroxyvitamin D levels and risk of fractures. The minimum concentration of vitamin D in the blood and reduced risk of fractures was 74 nM of 25-hydroxyvitamin D. Furthermore, the authors stated that the use of vitamin D2 does not reduce fractures in older adults. More recently, Blum et al. (4) reported that body size needs to be taken into account when approximating the amount of vitamin D supplementation needed to increase blood concentrations of 25-hydroxyvitamin D.

In addition, Dawson-Hughes (5) published an article that evaluated vitamin D's effects on bone mass, decreased rates of bone loss, improved muscle performance, decreased risk of falls, and decreased fracture occurrence. She stated that the elderly need to maintain an average blood level of 65 nM or greater of 25-hydroxyvitamin D to improve muscle performance and decrease fall risk; however, a blood concentration of 75 nM or greater of 25-hydroxyvitamin D is required to decrease fracture risk. Because much of the elderly in the United States have blood 25-hydroxyvitamin D levels below the recommendations, supplementation with vitamin D3 (cholecalciferol) could greatly benefit health and decrease health care costs in the elderly (5).


Although most of the research on vitamin D has been focused on bone and muscle health, as well as prevention of falls, other research is emerging on the possible role of vitamin D in other diseases. For example, Grant (8) reported that periodontal disease and tooth loss are correlated with different types of cancer. He suggests that vitamin D status could be the underlying cause of periodontal disease. Grant (8) states that cancers that have been significantly correlated with periodontal disease or tooth loss (e.g., bladder, gastric, hemopoietic, kidney, lung, esophageal, oral, and pancreatic), also are linked to low solar ultraviolet B and blood 25-hydroxyvitamin D concentrations. Other cancers linked to low blood vitamin D concentrations in the blood are breast and colorectal.

Garland and colleagues (7) stated that a 50% reduction in colon cancer prevalence would necessitate a widespread intake of 2,000 IU per day of vitamin D3. A comparable decrease in breast cancer occurrence would necessitate 3,500 IU per day of vitamin D3. This dose surpasses the tolerable upper intake level (UL) for vitamin D of 2,000 IU per day (6) and may help prevent cancer by maintaining healthy cells with normal life spans, discouraging out-of-control cell reproduction, and deterring the synthesis of new blood vessels for tumor proliferation (7). In addition, they suggest that obtaining from 3 to 15 minutes of sun exposure on sunny days, with 40% of the skin exposed without sunscreen, can help prevent breast and colon cancers.


Low concentrations of 25-hydroxyvitamin D in the blood also have been linked with multiple sclerosis (MS). Ascherio and Munger (1) state that, although the genetic susceptibility can account for MS within families, these genetics cannot entirely elucidate the changes in risk due to geographic alterations in MS frequency and the changes in risk with people moving from one area to another. Ashcerio and Munger (1) reported that vitamin D status, Epstein-Barr virus infection, and cigarette smoking are materializing as the most consistent predictors of MS.


Bischoff-Ferrari et al. (3) summarized support from studies that evaluated thresholds for blood 25-hydroxyvitamin D levels with respect to bone mineral density, risk of falls, risk of fractures, lower-extremity function, dental health, and risk of colorectal cancer. They reported that the most beneficial blood concentrations of 25-hydroxyvitamin D begin at 75 nM (similar to Dawson-Hughes'[5] recommendations) and are optimal between 90 and 100 nM [3]).


Based on the previous review of research on vitamin D, it seems that the concentrations that are optimal for health cannot be achieved with the current Dietary Reference Intake (DRI) of 200 and 600 IU per day for younger and older adults, respectively (3). Bischoff-Ferrari et al. (3) state that an increase in the DRI for vitamin D is required. They suggest that an intake of 1,000 IU per day of vitamin D3 (cholecalciferol) is required to increase 25-hydroxyvitamin D blood levels up to 75 nM in at least 50% of the population. They also suggest that higher doses need to be researched for the entire adult population.

Lee and Jiang (9) agree with these recommendations. They report that "hypovitaminosis D" (below normal levels of 25-hydroxyvitamin D in the blood) has become widespread, regardless of latitude, and state that "hypovitaminosis D is a multifactorial condition related to vitamin D scarcity in foods, latitude, solar irradiation, atmospheric pollution, skin pigmentation, clothing, sunscreen use, and indoor activities, etc" (9). They also emphasize that the combined supplementation of vitamin D with calcium has been found "superior" to vitamin D supplementation alone to increase bone mass in younger and older individuals. Lee and Jiang (9) emphasize the need to redefine the UL for vitamin D and to standardize laboratory methods of vitamin D assessment.


Vitamin D is a required nutrient that is important to maintain bone health and may stave off other serious diseases such as cancer and MS. Although no nutrient is a panacea for being a cure-all, it has been well recognized in the scientific and clinical communities that the DRI for vitamin D needs to be seriously reconsidered and increased (10). Three ways that individuals can increase their serum levels of vitamin D to the more optimal range are by increased sunlight exposure, increased consumption of vitamin D-rich foods, and supplementation with vitamin D (Table).

Three Ways to Obtain Vitamin D


1. Ascherio A, Munger K. Epidemiology of multiple sclerosis: from risk factors to prevention. Semin Neurol. 2008;28(1):17-28.
2. Bischoff-Ferrari HA, Dawson-Hughes B. Where do we stand on vitamin D? Bone. 2007;41(1 suppl 1):S13-9. Epub 2007 Mar 24.
3. Bischoff-Ferrari HA, Giovannucci E, Willett WC, Dietrich T, Dawson-Hughes B. Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr. 2006;84(1):18-28.
4. Blum M, Dallal GE, Dawson-Hughes B. Body size and serum 25 hydroxy vitamin D response to oral supplements in healthy older adults. J Am Coll Nutr. 2008;27(2):274-79.
5. Dawson-Hughes B. Serum 25-hydroxyvitamin D and functional outcomes in the elderly. Am J Clin Nutr. 2008;88(2):537S-40S.
6. Food and Nutrition Board of the Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Washington (DC): National Academy Press; 1997.
7. Garland CF, Grant WB, Mohr SB, Gorham ED, Garland FC. What is the dose-response relationship between vitamin D and cancer risk? Nutr Rev. 2007;65(8 Pt 2):S91-5.
8. Grant WB. Vitamin D, periodontal disease, tooth loss, and cancer risk. Lancet Oncol. 2008;9(7):612-3.
9. Lee WT, Jiang J. The resurgence of the importance of vitamin D in bone health. Asia Pac J Clin Nutr. 2008;17(suppl 1):138-42.
10. Vieth R, Bischoff-Ferrari H, Boucher BJ, et al. The urgent need to recommend an intake of vitamin D that is effective. Am J Clin Nutr. 2007;85(3):649-50.
© 2009 American College of Sports Medicine