A venous thrombosis is a blood clot that forms within a vein. A classical venous thrombosis is in a deep vein thrombosis, usually deep in a vein in the leg. These can break off, go to the lungs, and become a life-threatening pulmonary embolism. Complications of pulmonary embolism include coughing up blood, heart failure or shock, heart palpitations, pulmonary hypertension, severe breathing difficulty, severe bleeding (usually a complication of blood thinner treatment), and sudden death.
Venous thromboembolism is a major health problem. The average annual incidence of venous embolism among Whites is about 700,000 cases per year. The incidence appears to be higher among Blacks. Pulmonary embolism is predominantly a disease of older age as rates go up steeply with age. The incidence rates are also somewhat higher in women during their childbearing years. Birth control pills are a major risk factor for blood clots. An Italian study showed pulmonary embolism peaked in December.
Does vitamin D play a role in venous thrombosis? Dr. P. Brøndum-Jacobsen and colleagues of the Copenhagen University Hospital in Denmark obtained vitamin D levels on more than 18,000 patients and then followed them for up to 30 years to find out.
Brøndum-Jacobsen P, Benn M, Tybjaerg-Hansen A, Nordestgaard BG. 25-hydroxyvitamin D concentrations and risk of venous thromboembolism in the general population with 18,791 participants. J Thromb Haemost. 2012 Dec 29.
The mean follow up time was 13 years for this cohort, which averaged 57 years of age. Nine hundred and fifty patients ended up with a blood clot; the average time to a blood clot was 13 years. When the authors split baseline vitamin D levels into tertiles (one-thirds), they found those with the lowest vitamin D levels were 37% more likely to have a blood clot. After statistical adjustment, the relative risk increased to 106% for those with the lowest levels.
The authors postulated three mechanisms by which higher vitamin D levels were protective. First, vitamin D deficiency may lead to a decrease in the gene expression of anti-blood clot proteins (antithrombin in the liver and of thrombomodulin in the aorta) leading to more blood clots.
Second, vitamin D deficiency may lead to an increase in the gene expression of a protein (tissue factor) in the liver and kidneys, which will lead to more blood clots.
Finally, in human aortic smooth muscle cells, vitamin D like drugs have been shown to reduce the production of certain blood clotting factors (plasminogen activator inhibitor-1, thrombospondin-1, and thrombomodulin) leading to an overall anti-thrombotic effect. It turns out that atherosclerotic cardiovascular disease and blood clots may not be as separate a disease, as the two diseases share some common risk factors. It may be that reduced plasma vitamin D could be an independent and common risk factor for both conditions.
The authors concluded,
“The consistent and stepwise increasing risk that we found may tempt to suggest causality; however, one cannot infer causality from the present study. Therefore, randomized intervention trials are needed to test the question of causality, and randomized trials with vitamin D supplementation are needed before implementing supplementation in the general population or in selected patient groups to reduce the risk of venous thromboembolism.”
I disagree in that the time to act is now. Treatment of vitamin D deficiency cannot wait for further science. While scientists are required to wait, physicians caring for patients are ethically required to act on what is known now; they cannot patiently wait to find out what may be discovered in the future. Physicians have always been required, both ethically and legally, to preform risk benefit assessments of treating or not treating vitamin D deficiency. We know there are potentially huge benefits and simply no significant risks of treating deficiency.