by Paul D. Tortland, D.O.
Awareness of the role vitamin D plays in health and disease has grown exponentially, and many researchers and clinicians are now concerned about the possibility of an epidemic of vitamin D deficiency. Whether this is due truly to decreasing levels of vitamin D or greater awareness of, and screening for, D deficiency remains to be seen.
Activated vitamin D (calcitriol) is not actually a vitamin in the traditional sense. Vitamins are either co-factors in enzymatic processes or antioxidants. Vitamin D, on the other hand, is a prohormone, a secosteroid.
Like all steroids, vitamin D acts as a molecular switch to trigger gene transcription. Vitamin D targets or affects over 1000 human genes, and affects organs including the heart, lungs, adrenal medulla, neurons, muscle, pituitary, bone and brain.
The principle source of vitamin D is cutaneous production from skin exposure to ultraviolet B (UVB) sun radiation, not from dietary sources. Due to concerns over skin cancer risk, people increasingly are shielding themselves from excess UVB exposure, including use of sunscreens and protective clothing. It might seem ironic that populations found to be particularly low in vitamin D stores include Saudi Arabians and residents of Miami. Persons living in northern latitudes are also at risk, due to decreased sun exposure during winter months.
A surprising number of athletes have been found to be D deficient. 77% of German gymnasts were found to have 25(OH)D levels below 35 ng/mL, and 37% had levels below 10 ng/mL. A study of Finnish female athletes found 67% with levels below 15 ng/mL during the winter months.
Vitamin D affects de novo protein synthesis in muscle, acting directly to increase protein synthesis. Studies involving humans, including biopsies of muscle fibers, found that vitamin D administration enhanced cros–sectional hypertrophy of Type II muscle fibers and resulted increased strength.
Several randomized controlled trials in older adults found that vitamin D administration improves neuromuscular functioning, including balance, muscle strength, and reaction time.
In addition, numerous studies have found an association between seasonal vitamin D level variations and athletic performance, with peak performance and trainability occurring during the warmer months when D levels are the highest, with a sharp autumn decline and nadirs in the winter.
Of course, the largest improvements in performance will be seen in those who have the lowest levels of vitamin D, for instance when raising the level from, say, 15 ng/mL to 30 ng/mL.
Although a level above 50 ng/mL is now considered by many to be optimal, we still do not know what is actually an ideal level, either for general health or for athletic performance, or whether higher levels might actually impair performance.
Few athletes live and train in sun–rich environments. And those that do may be negating the exposure effects as noted above. Therefore, dietary sources of vitamin D must supplant cutaneous production.
The metabolically active form of vitamin D is D3 (milk typically is fortified with D2). Target ranges for therapeutically significant vitamin D blood levels are greater than 50 ng/mL. Over the counter D3 capsules are available in various doses, and prescription strengths are available in strengths up to 50,000 IU.
Baseline fasting blood levels of D3 should be obtained before initiating treatment. I typically start with 2000 IU or 5000 IU D3 capsules daily, depending on blood levels. In patients with severely low levels I will often use prescription–strength 50,000 IU once a week for 8 weeks, then titrate down to 5000 IU. Levels should be rechecked roughly at 8 week intervals until stable.