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November 2009 | Back to Table of Contents

Clinical and Health Affairs

Weather or Not

The Importance of Vitamin D Status Monitoring and Supplementation

By Gregory A. Plotnikoff, M.D., M.T.S.

Abstract
The Centers for Disease Control and Prevention’s latest data show markedly high prevalence rates of severe vitamin D deficiency among Americans of all ages. Because of the numerous negative health consequences associated with vitamin D deficiency, we must consider all potential causes including insufficient exposure to the sun’s ultraviolet B radiation. This article presents data from the National Weather Service that documents how few days in Minnesota offer the opportunity to make vitamin D. Thus, even Minnesotans who spend a significant amount of time outdoors and consider themselves to have sufficient sun exposure may still be at risk for vitamin D deficiency. This is especially true for the elderly, those with high melanin content in their skin, and those with a higher body mass index, all of whom require significantly more sun to achieve adequate levels of vitamin D. Given the lack of sufficient ultraviolet B radiation people in Minnesota get from the sun between October and April, measurement of vitamin D status is required for rational replenishment and maintenance dosing. The goal of replenishment should be at least 32 ng/mL and, ideally, more than 50 ng/mL.


During the past 20 years, health professionals have called attention to the many consequences of vitamin D deficiency, which affects people of all ages in all parts of the world. This attention appears warranted as vitamin D status and all-cause mortality rates are correlated.1,2 Several studies demonstrate a strong inverse causal relationship: The higher the vitamin D level, the lower the all-cause mortality rate.3

Vitamin D’s role goes far beyond calcium-phosphorous homeostasis and bone health. Vitamin D also plays a role in reversing insulin resistance, regulating the renin-angiotensin system, and controlling cellular proliferation, differentiation, and apoptosis. Vitamin D deficiency is associated clinical consequences including hip fractures, metabolic syndrome, type I and type II diabetes, infectious disease, autoimmune disease, chronic pain, hypertension, and many types of cancer including the deadliest ones.4 Even with prescription supplementation, vitamin D is the single most cost-effective medical intervention in the United States today.

Multiple Causes

A number of factors promote vitamin D deficiency in Minnesota. Living in northern latitudes plays a significant role, as do cultural realities such as our emphasis on limiting sun exposure, using sunblock in order to prevent skin cancers, and working long hours indoors. Because vitamin D is fat soluble and distributes efficiently into all adipose tissue, any increase in body mass index (BMI) requires a concomitant increase in vitamin D production or ingestion. Additionally, antivitamin D agents such as prednisone, antiepileptic drugs, or antiretroviral therapy are also implicated in vitamin D deficiency.

The Centers for Disease Control and Prevention (CDC) has documented that in the summer the percentage of white adults in the United States who have achieved the very lowest acceptable level of vitamin D sufficiency (30 ng/mL) has declined from more than 55% to less than 30% since the late 1980s. For black adults, the number with levels greater than 30 ng/mL has fallen to just 5%. At the same time, the number of white adults with severely low levels (less than 10 ng/mL) more than doubled and the number of black adults with such low levels increased nearly six-fold to nearly 30%.5 Children in the United States also have significant vitamin D deficiency.6

Consuming large volumes of fortified foods cannot make up for the severe vitamin D deficiency documented by the CDC. For example, an entire gallon of milk contains less than one-tenth the amount of vitamin D that one would get by spending an afternoon at the beach. Because vitamin D’s half-life is approximately two months (shorter in persons from the Indian subcontinent), even a summer of outdoor work is not enough to maintain sufficient levels for most people in the winter.7,8

One would think that in Minnesota a summer afternoon working in the garden or playing outside would have the potential to provide one with a good dose of vitamin D. After all, we were designed to make our vitamin D from sun exposure. However, smog and weather-related factors need to be considered in the vitamin D deficiency equation.

Understanding the UV Index

To understand one’s capacity to make vitamin D and the need for safe sunning, that is exposure without burning, we must know something about the Ultra-Violet (UV) Index. The UV Index provides a formal measurement of the three types of ultraviolet radiation that come from the sun: ultraviolet A, B, and C. Of these, only UVB has the capacity to produce vitamin D. Most UVB rays are absorbed by the ozone layer, so they are less plentiful at the earth’s surface than UVA rays. Also, UVB rays do not penetrate the skin as deeply as UVA rays but are more readily absorbed by DNA. Ultraviolet C rays are very dangerous, but they are absorbed by the ozone layer and do not reach the ground. We need to protect our skin from both UVA and UVB rays.

Ultraviolet B carries the energy needed to break a double-bond in the second of the four rings of the steroid backbone for the vitamin D precursor in the skin, termed 7-deoxycholesterol. This UVB-induced break is what produces the pro-vitamin cholecalciferol, also known as D3. This is the first step in a series of events that takes place before vitamin D is activated as 1,25 dihydroxy vitamin D (calcitriol). The break in the second ring is what fundamentally differentiates vitamin D from the structurally similar cholesterol and the adrenal steroids such as cortisol, testosterone, aldosterone, and estrogen. Because of the health concerns associated with ultraviolet A and B exposure, the National Weather Service and the Environmental Protection Agency jointly created the UV Index. The UV Index predicts exposure levels on a 1 to 15 scale; higher levels indicate a higher risk of overexposure. Calculated on a next-day basis for dozens of cities across the United States, the UV Index takes into account conditions that affect the amount of UV rays that reach the ground. These include the distance between the sun and the earth, the solar zenith angle, the total amount of ozone in the atmosphere, the troposheric aerosol optical depth (smog), elevation, snow/ice reflectivity, and cloud cover.

The figure on this page shows the influence of local weather and other conditions on UV exposure in various locales. On this particular day, Bismarck, North Dakota (46° 48”), had a significantly higher UV index than Milwaukee, which is located much further to the south (43° 2”).

In Minnesota in 2008, fewer than half the days offered enough sun to make vitamin D at noon. Even if we made it a point to be outside between 10 a.m. and 3 p.m., the time of maximum exposure, chances are we would still not receive enough UVB radiation to make cholecalciferol (D3). The implications of this are particularly important for persons who need significantly more sun exposure to make a given amount of vitamin D, namely senior citizens, those with more melanin, and those with higher BMIs.

Advising Patients

The only way physicians can make sure their patients get enough vitamin D is to actually measure their patients’ serum 25-OH-vitamin D level. Supplementation with only a multivitamin (which might contain 400 IU of vitamin D) makes no sense. In my clinical experience, even persons on 2,000 IU a day can remain severely deficient even in the absence of malabsorption or any other confounding factor. Most people need at least 1,000 IU a day for maintenance and more for replenishment (Table).

For all endpoints, including such apparently unconnected phenomena as bone mineral density, lower extremity function, dental health, risk of falls, admission to a nursing home, fractures, cancer prevention, and incident hypertension, the most advantageous serum levels for 25(OH)D appear to be at least 30 ng/mL. For cancer prevention, desirable 25(OH)D levels are at least 36 to 48 ng/mL.9 In my opinion, we should aim for a serum level of greater than 50 ng/mL and a PTH level of less than 50 pcg/L. Farmers, lifeguards, and others who work outdoors typically have levels greater than 50 ng/mL. Toxicity appears to occur at levels greater than 200 ng/mL. There is no reason to supplement to levels higher than 100 ng/mL.

Testing should be done for vitamin D deficiency at least as often as it is done for TSH or B12 levels. Given the multitude of crucial genes regulated by vitamin D, a good case can be made that a low vitamin D level has a much more negative impact on health than a high cholesterol level. Forthcoming evidence will likely support the idea of physicians checking patients’ vitamin D levels as often as they check their cholesterol levels.

Ten Tips for Vitamin D Testing and Treatment

Conclusion

The bottom line is that in Minnesota, our infamous weather significantly limits our capacity to make vitamin D. Given the multitude of negative health consequences tied to vitamin D deficiency, physicians in Minnesotans, much more so than their southern colleagues, need to consider monitoring their patients’ serum vitamin D levels and supplementing appropriately. MM

Gregory Plotnikoff is medical director of the Penny George Institute for Health and Healing at Abbott Northwestern Hospital.
 
References
1. Melamed ML, Michos ED, Post W, Astor B. 25-hydroxyvitamin D levels and the risk of mortality in the general population. Arch Intern Med. 2008;168(15):1629-37.
2. Ginde AA, Scragg, R, Schwartz RS, Carmargo CA Jr. Prospective study of serum 25-hydroxyvitamin D level, cardiovascular disease mortality and all-cause mortality in older U.S. adults. J Am Geriatr Soc. 2009; Jun 22. (Epub ahead of print.)
3. Autier P, Gandini S. Vitamin D supplementation and total mortality: a meta-analysis of randomized controlled trials. Arch Intern Med. 2007;167:1730-7.
4. Holick MF. Vitamin D deficiency. N Engl J Med. 2007; 357(3):266-81.
5. Ginde AA, Liu MC, Camargo CA Jr. Demographic difference and trends of vitamin D insufficiency in the U.S. population, 1988-2004. Arch Intern Med. 2009;169(6):626-32.
6. Kumar J, Muntner P, Kaskel FJ, Hailpern SM, Melamed ML. Prevalence and Associations of 25-hydroxyvitamin D deficiency in U.S. Children: NHANES 2001-2004. Pediatrics. 2009 Aug 3. (Epub ahead of print.)
7. Jones G. Pharmacokinetics of vitamin D toxicity. Am J Clin Nutr. 2008;88(2):582S-6S.
8. Barger-Lux MJ, Heaney RP. Effects of above-average summer sun exposure on serum 25-hydroxyvitamin D and calcium absorption. J Clin Endorinol Metab. 2002;87(11):4952-6.
9. Bischoff-Ferrari HA. Optimal serum 25-hydroxyvitamin D levels for multiple health outcomes. Adv Exp Med Biol. 2008;624:55-71.

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