Susan A. New, BA, MSc, PhD


October 09, 2003


How important is sunlight exposure to activate vitamin D? Is it even necessary to "activate" vitamin D taken as a supplement?

Response from Susan A. New, BA, MSc, PhD

Vitamin D synthesis from sunlight exposure is an intriguing and complex area, and considerable debate continues about the definition of thresholds for vitamin D insufficiency and its subsequent consequences for bone health.

In the aging population (65 years and older), and in particular in those populations living in a northern latitude, vitamin D requirements are unlikely to be met sufficiently by exposure to sunlight. This is for 2 principle reasons: (1) skin pigmentation deteriorates with age, and thus the conversion of the UV light on the skin is much less efficient; (2) less surface skin is exposed to sunlight, as the elderly do not spend as much time out of doors and are often covered up so that sunlight cannot penetrate the skin sufficiently.[1]

From the data currently available, it would appear that in the aging population, sunlight exposure is not required to "activate" vitamin D and that vitamin D supplements (with Ca) are sufficient. The level of supplementation that is beneficial with respect to fracture reduction is somewhat controversial, but it seems that 1200 mg of Ca and 800 IU (20 micrograms [mcg]) of cholecalciferol is effective in fracture reduction.[2]

Vitamin D and Ca supplementation studies have been shown to significantly reduce fracture rates in both institutionalized[3] and free-living elderly populations.[4] However, intriguing is the finding that vitamin D supplementation alone is not effective[5]; the most recent study found that cod liver oil containing 10 mcg (400 IU) of vitamin D did not prevent fracture in 1144 nursing home residents.[6] A point of note is the difference between vitamin D supplementation levels used in the various studies. In the studies by Chapuy[3] and Dawson-Hughes,[4] 20 mcg/d and 17.5 mcg/d of vitamin D were supplemented, respectively, whereas in the studies by Lips[5] and Meyer,[6] only 10 mcg/d was used, without additional Ca.

Less information is available concerning the requirement of vitamin D in the younger population. A 4% difference in the adjusted 3-year bone mineral density (BMD) accumulation from baseline between young girls who had a normal vitamin D status (> 37.5 nmol/L) and those who had severe hypovitaminosis (< 20 nmol/L) (actual values were 16.7% vs 12.7%) have been reported.[7] Furthermore, in girls of advanced sexual maturation, the adjusted 3-year change of BMD at the lumbar spine was 27% greater in the highest vitamin D intake tertile than in the lowest tertile. These and other data clearly suggest that pubertal adolescent females with hypovitaminosis D are at a significant risk of not reaching maximum peak bone mass, particularly at the lumbar spine. This is certainly an area that requires further investigation.


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