The news is troubling: Humans are, today, absolutely deficient in vitamin D, and evidence is accumulating that this deficiency is damaging the health of our patients and their children. How did we arrive at such a state?
Sources are numerous but lifestyle and miscalculation confound intake
We have several main sources of vitamin D:
- fatty fish (e.g., salmon, which contains 500 IU in 3 oz)
- eggs (25 IU in one yolk)
- vitamin D-enriched milk products (cow’s milk, 100 IU in every 8 oz)
- vitamin D supplements
- exposure to sunlight.
On the whole, we’ve markedly reduced our exposure to sunlight as we’ve changed from living outdoors in rural agrarian communities to an indoor urban lifestyle. Dermatologists have long crusaded against exposure to sunlight as a way to reduce our risk of skin cancer. And milk intake has dropped significantly over the past decade.
To those shifts, add the fact that the US government and its advisory councils have, historically, recommended an intake of vitamin D—200 IU/d for children and 400 IU/d for adults—that is too low to prevent vitamin D deficiency.
In short, our low exposure to sunlight and our low intake of vitamin D have caused an epidemic of vitamin D deficiency. Here is a look at key facets of the problem; the benefits of maintaining adequate stores of vitamin D; and recommendations for ending the epidemic.
Pregnant women are vitamin D deficient, most studies show
Measurement of circulating 25-hydroxyvitamin D (25OH vitamin D) is an accepted method of assessing vitamin D physiologic status. Many authorities believe that 1) a 25OH vitamin D concentration >30 ng/mL indicates adequate vitamin D stores and that 2) a level <20 ng/mL clearly represents vitamin D deficiency. In a recent study of pregnant women from Finland, more than 70% of subjects were vitamin D deficient.1
In turn, many of the newborns of subjects in the Finnish study were also vitamin D deficient.1
Preventing preeclampsia. Does vitamin D supplementation in pregnant women reduce their risk of preeclampsia? We don’t know—no randomized clinical trial has demonstrated such an effect. But investigators in several observational studies have reported that a low maternal serum concentration of 25OH vitamin D is associated with an increased risk of preeclampsia.2,3
In one such study, an imputed total vitamin D intake of 600 to 800 IU/d was associated with a 24% reduction in the risk of preeclampsia from what was seen when total vitamin D intake was 200 IU/d.4
Many infants are vitamin D deficient
Bone mass is reduced in children who are vitamin D deficient.1 Historically, the American Academy of Pediatrics (AAP) has asserted that vitamin D intake of 200 IU/d was adequate for infants,5 but the Academy recently changed its recommendation to daily supplementation with 400 IU/d for infants, beginning soon after birth.6
A recent survey showed that the majority of children do not receive adequate vitamin D supplementation.7
Lactation and vitamin D deficiency. The concentration of 25OH vitamin D in breast milk correlates with maternal vitamin D stores. Because most pregnant women are vitamin D deficient, their infants are, when breast-fed, also at higher risk of vitamin D deficiency.8,9
Authorities recommend that all infants who are being breast-fed receive vitamin D supplementation with 400 IU/d.
Vitamin D supplements and toxicity
The two commonly available forms of supplemental vitamin D are ergocalciferol (D2) and cholecalciferol (D3). Both are effective supplements,1 although some authorities contend that cholecalciferol may be slightly better absorbed.2
Commercial laboratories typically measure and report 1) total 25OH vitamin D as a single value, or 2) two values, one for 25OH vitamin D2 and one for 25OH vitamin D3. If two values are reported, you should add them together to assess the total concentration of 25OH vitamin D. Most authorities believe that a 25OH vitamin D level >30 ng/mL is normal and a value <20 ng/mL is clearly abnormally low.
For nonpregnant women who have a 25OH vitamin D level <20 ng/mL, some authorities recommend a weekly dosage of 50,000 IU of vitamin D for 8 weeks followed by a repeat measurement of 25OH vitamin D. If the post-treatment 25OH vitamin D level is >30 ng/mL, a daily dosage of 800 IU is initiated. If the vitamin D level is still very low, the 8-week course of high-dose vitamin D may be repeated.
For pregnant women, some authorities recommend a daily dose of 2,000 IU of vitamin D. This can be achieved by taking a prenatal vitamin (vitamin D, 400 IU) and two capsules of vitamin D, 800 IU per capsule, daily. Toxicity is poorly understood. The dose of vitamin D that is toxic is not well defined. In 1997, the Institute of Medicine of the National Academy of Sciences concluded that the “tolerable upper intake level” for vitamin D was 2,000 IU daily.3 Recent data suggest that dosages as high as 10,000 IU/d taken for as long as 5 months are not toxic.4,5
Excessive vitamin D intake, especially when combined with calcium supplementation, may be associated with hypercalcemia, hypercalciuria, and kidney stones.
1. Holick MF, Biancuzzo RM, Chen TC, et al. Vitamin D2 is as effective as vitamin D3 in maintaining circulating concentrations of 25-hydroxyvtiamn D. J Clin Endocrinol Metab. 2008;93(3):677-681.
2. Armas LA, Hollis BW, Heaney RP. Vitamin D2 is much less effective than vitamin D3 in humans. J Clin Endocrinol Metab. 2004;89(11):5387-5391.
3. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Dietary Reference intakes for calcium phosphorus, magnesium, vitamin D and fluoride. National Academy Press, Washington DC 1997.
4. Heaney RP, Davies KM, Chen TC, Holick MF, Barger-Lux MJ. Human serum 25-hydroxycholecalciferol response to extended oral dosing with cholecalciferol. Am J Clin Nutr. 2003;77(1):204-210.
5. Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266-281.