Clinical Review

How much vitamin D should you recommend to your nonpregnant patients?

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Two experts explain what’s known about vitamin D, review the guidance offered to clinicians by the Institute of Medicine, and offer concrete recommendations for vitamin D intake and supplementation



No question: Vitamin D plays a vital role in bone health. In recent years, the possibility that it plays a role in other aspects of health has prompted considerable speculation, fueled by both widespread media coverage and dissemination of conflicting information about the potential nonskeletal benefits of high-dose vitamin D supplementation. Controversy has emerged about:

  • the appropriate criteria for defining vitamin D deficiency
  • the extent to which vitamin D influences nonskeletal health conditions
  • the optimal level of vitamin D supplementation.

In 2010, the Institute of Medicine (IOM) released a report that provided recommendations for vitamin D intake, which were also summarized in a recent article for clinicians.1,2 The IOM report provided much-needed clinical guidance, but it has also fueled additional questions.

This article describes the IOM recommendations, explains what we know now about the effect of vitamin D on various health outcomes, and offers concrete recommendations on vitamin D measurement, intake, and supplementation.

How the Institute of Medicine formulated its recommendations

The Institute of Medicine (IOM) committee conducted a comprehensive review of the literature to date on the relationship between vitamin D (and calcium) intake and several health outcomes. In terms of skeletal health, the IOM committee concluded that a 25OHD level of at least 20 ng/mL is sufficient to meet the needs of at least 97.5% of the population. The vitamin D intake thought to be necessary to achieve this 25OHD level for at least 97.5% of the population was provided for different age groups (TABLE 2).

The Recommended Dietary Allowance (RDA) of vitamin D is 600 IU daily for all adults up to age 70 years, and 800 IU daily for adults older than 70 years. These values were based on an assumption of minimal sun exposure, due to wide variability in vitamin D synthesis from ultraviolet light, as well as the risk of skin cancer. The IOM concluded that there is no compelling evidence that a 25OHD level above 20 ng/mL or a vitamin D intake greater than 600 IU (800Â IU for adults over 70) affords greater skeletal or nonskeletal benefits.

The IOM recommendations were based on the integration of bone health outcomes. The evidence supporting causal relationships between vitamin D insufficiency and nonskeletal outcomes such as cancer, cardiovascular disease, diabetes, impaired physical performance, autoimmune disorders, and other chronic diseases was found to be inconsistent and inconclusive.

The IOM report also noted the emergence of a “U”-shaped curve in regard to vitamin D and several health outcomes, which has fueled concern about attainment of a 25OHD level above 50 ng/mL. The IOM committee designated 4,000 IU daily as the tolerable upper intake but emphasized that research into long-term outcomes and safety at intakes above the RDA is limited. Therefore, this upper limit should not be interpreted as a target intake level.

How is vitamin D metabolized?

Vitamin D is produced endogenously in the skin in the form of vitamin D3 (cholecalciferol). It also can be ingested exogenously in the form of vitamin D3 or vitamin D2 (ergocalciferol). Cutaneous synthesis of vitamin D is stimulated by solar ultraviolet radiation.

Vitamin D2 and D3 are hydroxylated in the liver to form 25-hydroxyvitamin D (25OHD). Measurement of the serum 25OHD level is thought to be the most reliable indicator of vitamin D exposure.3 25OHD is hydroxylated again, primarily in the kidneys, to the most active form of vitamin D (1,25-dihydroxyvitamin D).

The adverse skeletal effects of severe vitamin D deficiency are well established; those effects include calcium malabsorption, secondary hyperparathyroidism, bone loss, and increased risk of fracture. In this setting, secondary hyperparathyroidism results from both decreased gastrointestinal calcium absorption and decreased suppression of parathyroid hormone (PTH) production by the parathyroid glands from vitamin D metabolites. Secondary hyperparathyroidism leads to increased bone resorption and bone loss. Rickets, osteomalacia, hypocalcemia, hypophosphatemia, muscle weakness, and bone pain are less common effects that can occur with severe vitamin D deficiency.

It is worth noting that women of color are at increased risk of vitamin D deficiency as a result of greater skin pigmentation.3 Obesity is also a risk factor for vitamin D deficiency.3 Additional risk factors for vitamin D insufficiency are listed in TABLE 1.


Risk factors for vitamin D insufficiency

Dark skin pigmentation
Decreased sun exposure
  • Lack of outdoor activity
  • Institutionalization
  • Wearing of protective clothing
  • Regular, conscientious use of sunscreen
Low dietary intake of vitamin D
Malabsorption of ingested vitamin D
Increased hepatic degradation of 25-hydroxyvitamin D
  • Use of anticonvulsant medications
  • Antituberculous therapy
Decreased hepatic hydroxylation of vitamin D (occurs only with severe hepatic disease)
Impaired renal hydroxylation of vitamin D (renal insufficiency)
Osteoporosis or osteopenia


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