Email a Friend
Print Article
Vitamin D and Cardiovascular Disease - Part 1
Vitamin D is a topic that is rarely discussed but has been the subject of new and exciting research regarding its role in cardiovascular disease.
Vitamin D deficiency is now recognized as a pandemic. One billon people worldwide have deficiency or insufficiency. You may ask yourself why is this important and how does it relate to cardiovascular disease? The simple reason is that the evidence of the association between low levels of 25 hydroxyvitamin D [25(OH)D] and higher risk of cardiovascular disease is growing. 25(OH)D levels in the blood is the best functional measure of vitamin D status.
In a recent prospective case-controlled study, 18,225 men free of cardiovascular disease were followed for 10 years. It was shown that blood levels of [25(OH)D], vitamin D, less than 30 ng/ml are associated with an increase risk of heart attack. Men who had a level greater than or equal to 30 ng/ml had half the risk of a heart attack independent of other cardiovascular risk factors. Another recently published study from Austria and Germany looked at 3,258 patients who were going to have a coronary angiogram and followed them for 7.7 years.
Low vitamin D levels were associated with cardiovascular death. The American Heart Association has published findings online based on NHANES data which indicated a strong graded association between low vitamin D levels and peripheral vascular disease (PAD) with the incidence rising by 35% for each 10 ng/ml decline in vitamin D levels even after statistically adjusting for CVD risk factors.
Vitamin D deficiency is associated with obesity, hypertension, glucose intolerance, and metabolic syndrome (insulin resistance). It has also been associated with other chronic illnesses including colon, prostate, and breast cancer, autoimmune disorders, and polycystic ovarian disease to name a few.
We have long known the effects of vitamin D on the musculoskeletal system. Deficiencies affect muscle performance and may contribute to myalgias (muscle pain), proximal muscle weakness, loss of muscle mass, and increased risk of falling.
One study showed that 93% of persons 10-65 years of age who came to a hospital emergency room complaining of muscle aches and bone pain were deficient in vitamin D. I bring this up because some patients on statins complain of muscle and joint pain and many physicians blame the medication and stop it. Statins can reduce cardiovascular morbidity and mortality by up to 40%. Many patients, therefore, would not be on necessary drugs (statins) to reduce their cardiometabolic risk because of a presumed side effect of the medication when the person may be vitamin D deficient.
The major source of vitamin D is from the sun, diet, and dietary supplements. 25(OH)D level is the most accurate way to test for a deficiency. It should be noted that the blood concentrations varies by season so levels may need to be done again to accurately reflect one's true level.
While the optimal level of 25(OH)D is the subject of debate, most experts consider 32-50 ng/ml (or 50-80 nmol/L) to be normal. A level less than 20 ng/dl indicates deficiency and 21-29 ng/dl is considered insufficiency. Since sunlight is a major source of vitamin D, sunscreen reduces synthesis of D3 by 93-99% depending on the SPF. Synthesis also decreases with age and obesity decreases the amount available for use in the body.
Little or no D3 is produced from November to February for those residing above 35 degrees north latitude. The darker one's skin pigmentation, the more exposure to sunlight necessary to achieve the same levels as a lighter skinned person. There are numerous drugs that lower absorption or increase the destruction of vitamin D in the body. Some stains, however, have been found to increase the levels of vitamin D.
In the next part, I'll discuss treatments for Vitamin D deficiency.
Vitamin D and Cardiovascular Disease - Part 2
Related Topics:
Vitamin D deficiency is now recognized as a pandemic. One billon people worldwide have deficiency or insufficiency. You may ask yourself why is this important and how does it relate to cardiovascular disease? The simple reason is that the evidence of the association between low levels of 25 hydroxyvitamin D [25(OH)D] and higher risk of cardiovascular disease is growing. 25(OH)D levels in the blood is the best functional measure of vitamin D status.
In a recent prospective case-controlled study, 18,225 men free of cardiovascular disease were followed for 10 years. It was shown that blood levels of [25(OH)D], vitamin D, less than 30 ng/ml are associated with an increase risk of heart attack. Men who had a level greater than or equal to 30 ng/ml had half the risk of a heart attack independent of other cardiovascular risk factors. Another recently published study from Austria and Germany looked at 3,258 patients who were going to have a coronary angiogram and followed them for 7.7 years.
Low vitamin D levels were associated with cardiovascular death. The American Heart Association has published findings online based on NHANES data which indicated a strong graded association between low vitamin D levels and peripheral vascular disease (PAD) with the incidence rising by 35% for each 10 ng/ml decline in vitamin D levels even after statistically adjusting for CVD risk factors.
Vitamin D deficiency is associated with obesity, hypertension, glucose intolerance, and metabolic syndrome (insulin resistance). It has also been associated with other chronic illnesses including colon, prostate, and breast cancer, autoimmune disorders, and polycystic ovarian disease to name a few.
We have long known the effects of vitamin D on the musculoskeletal system. Deficiencies affect muscle performance and may contribute to myalgias (muscle pain), proximal muscle weakness, loss of muscle mass, and increased risk of falling.
One study showed that 93% of persons 10-65 years of age who came to a hospital emergency room complaining of muscle aches and bone pain were deficient in vitamin D. I bring this up because some patients on statins complain of muscle and joint pain and many physicians blame the medication and stop it. Statins can reduce cardiovascular morbidity and mortality by up to 40%. Many patients, therefore, would not be on necessary drugs (statins) to reduce their cardiometabolic risk because of a presumed side effect of the medication when the person may be vitamin D deficient.
The major source of vitamin D is from the sun, diet, and dietary supplements. 25(OH)D level is the most accurate way to test for a deficiency. It should be noted that the blood concentrations varies by season so levels may need to be done again to accurately reflect one's true level.
While the optimal level of 25(OH)D is the subject of debate, most experts consider 32-50 ng/ml (or 50-80 nmol/L) to be normal. A level less than 20 ng/dl indicates deficiency and 21-29 ng/dl is considered insufficiency. Since sunlight is a major source of vitamin D, sunscreen reduces synthesis of D3 by 93-99% depending on the SPF. Synthesis also decreases with age and obesity decreases the amount available for use in the body.
Little or no D3 is produced from November to February for those residing above 35 degrees north latitude. The darker one's skin pigmentation, the more exposure to sunlight necessary to achieve the same levels as a lighter skinned person. There are numerous drugs that lower absorption or increase the destruction of vitamin D in the body. Some stains, however, have been found to increase the levels of vitamin D.
In the next part, I'll discuss treatments for Vitamin D deficiency.
Vitamin D and Cardiovascular Disease - Part 2
Related Topics:
7 Comments:
Thank you so much for your excellent commentary. I had no clue that vitamin D had a role in cardiovascular disease. I look forward to reading your next piece about treatment of low levels.
I am extremely interested in the complete article on this subject. I had a sudden 100% heart blood clot blockage and immediate stent surgery 20 months ago. Prior to that I had been unaware that my D was very low until I saw a rheumatologist for pain in my calves. He prescribed the 50,000 units weekly for 3 months and the D rose to a median. I cannot now recall the dates involved but I am over a year and a half out from that heart problem and again my D went down to 22 when I asked my primary for a test. She suggested I stay on caltrate but I called my Rheumatologist and he started me again on the 50,0000 units. I am now at 37. Evidently I have a bent towards low D. I expect this needs constant attention. I wonder about the heart attack now with the D problem since I was
borderline cholesterol and CPR had read 1 most of my time before any problem. I had never had heart problems and I am now 79.
The error in this study is to measure only 25D and not 1,25 D (which is the active metabolite)
High levels of 1,25 D and low levels of 25 D are associated with TH1 inflammation, that is with high probability caused by bacterial infection of L-Form or CWD (cell wand deficient bacteria)
The low vitamin D levels are not the cause but the consequence. Supplementation of exogeneous vitamin D will not help at all, would make even the situation worse.
More information in:
http://www.marshallprotocol.com/
I have a question, does anyone know what this means. I got my Lipid Pane w/DLDL test back with all my numbers and it also stated: "TG reater than 400 mg'dl invalidated the calculated LDL. Do you know that that means.
If you have a comment about this blog post, you are in the right place. However, if you have a question for Dr. Richman, please visit him on the Cholesterol Management message board.
It is interesting that at least some studies show that statins increase circulating vitamin d levels.
MY most recent blood work showed my Vitamin D level at 27 even after taken the prescription weekly dose as well as 1100 IU daily. I also showed too much Calcium and low Iron. I take less to 100% of the daily recommended amount of Calcium. It also showed my White count to be low. What do you think. Oh by the way. I feel like a cat that just had kittens.
DCF
Post a Comment