Our interest in vitamin D follows the sun -- or rather, the lack thereof. Though many factors affect vitamin D metabolism, in general moderate sun exposure, at least 20 to 30 minutes per day, can assure adequate vitamin D status for most people.
The discovery early in this century of the role vitamin D played in rickets in children and osteomalacia in adults led to fortification of certain foods, particularly milk, to make up for inadequate sun exposure or insufficient intake of foods naturally rich in vitamin D, such as fatty fish, eggs and cheese.
Interest in vitamin D has peaked again, and this time it's gone beyond sun exposure and healthy bones. Epidemiological evidence notably from two major studies, The Nurse's Health Study and Health Professional's Follow up Study, suggest increased vitamin D status was associated with reduced incidence of colorectal cancer. There is evidence increased vitamin D intake may be protective against a variety of cancers, including prostrate, pancreatic and breast cancer, according to a recent article in the Journal of the American Dietetic Association.
However, these results are not consistent. In fact, some studies show just the opposite with increased risk of these same cancers with the highest intakes of vitamin D. All of which means more work needs to be done.
Most of us up until a few years ago stopped thinking of vitamin D because adequate seemed automatic. We didn't see rickets except as a historical reference and weren't generally aware of any other health effects of vitamin D deficiency. We thought more about calcium and weight bearing exercise as the keys to a healthy skeleton.
Attention to vitamin D first resurfaced subsequent to evidence that excessive exposure to ultraviolet light (UV) from sunbathing and tanning booths could pose a risk for skin cancer. Health professionals became concerned about a re-emergence of a vitamin D deficiency in a significant portion of the population that had begun to cover up, stay out of the sun or slather on increasingly more potent sunscreens when we did venture out. Coincidentally, milk consumption, the other key D source, decreased due to concerns over cholesterol and heart disease.
But we began to fortify the "milks" we were substituting, soy, rice, and almond along with yogurts and some margarines. Calcium and vitamin D supplements became popular, and that seemed to calm our interest in vitamin D.
Vitamin D actually is a set of compounds with properties of both a fat-soluble vitamin and a hormone. It's essential for dietary calcium absorption and for bone formation and remodeling. We can make our own vitamin D, but often not enough. That is to say we make the precursor to vitamin D called 7-dehydrocholesterol from cholesterol, the stuff that has the bad reputation for clogging our arteries.
The vitamin D precursor hangs out in the skin until UV light, the stuff that has the bad reputation for placing us at risk for skin cancer, causes it to change its shape and become vitamin D3 or cholecalciforal. Supplemental vitamin D, the kind with which we fortify foods, often is ergocalciferol, vitamin D2, which is believed to be less active.
Present recommendations for daily intake of vitamin D are 200 international units (IU) or 5 micrograms (mcg) per day for persons 1-50 years of age, 400 IU for persons 51 to 70, and 600 IU for persons over 70. Of equal interest is the tolerable upper limit of vitamin D: It's set at 2,000 IU or 50mcg for ages 14 and above.
Vitamin D deficiency has been associated with increased risk for cardiovascular disease. A review published in the American Journal of Cardiology titled, The Role of Vitamin D in Cardiovascular Health considers a variety of conditions associated with vitamin D deficiency. These include hypertension and peripheral artery disease. The incidence of PAD was 80 percent higher in participants with the lowest vitamin D levels in a study of nearly 5,000 subjects from National Health and Nutrition Examination Survey.
Increase in insulin resistance and diabetes also are associated with vitamin D deficiency. So are coronary artery disease and heart failure, along with cardiac arrhythmias. There are a number of proposed mechanisms for each of these conditions, but nothing conclusive is known.
There also is some evidence to suggest dietary vitamin D, carried by lipoproteins, may enter the cells of the artery wall, and then into the atherosclerotic plaque to be converted to its active form by monocytes drawn to this area as part of the response to injury view of plaque formation. If this is true, questions arise regarding the effects of vitamin D intake on atherosclerotic calcification and cardiovascular disease risk. Is there an increased risk with very high intakes of the vitamin?
Some have been calling for increases in both the recommended daily intake and the upper tolerable limit of vitamin D, based on much promising evidence. And this may be perfectly justified, but it's easy to think that more is better when evidence is promising. Still, researchers speculate there is a J- or U-shaped curve associated with vitamin D intake, which means more is not necessarily better or more protective, even if it is less than what are considered toxic levels.
