Wednesday, January 18, 2017
Wisdom Wednesday: Coronary Risk Assessment
Most PCP (primary care physicians) and too many cardiologists prescribe statin drugs based on the total cholesterol and LDL levels. However, there are a couple of additional lab tests that can really define your cardiac risk factors. Three of these tests, the CRP, fibrinogen activity and homocysteine are included in my routine testing. The fourth, the L(p)a I run when I suspect that my patient’s elevated cholesterol is genetic (familial hypercholesterinemia).
The high-sensitivity C-reactive protein (CRP) measures inflammatory proteins in the blood. It is fairly specific for artery inflammation but dental issues and other vascular inflammatory conditions can also elevate the test. As I have reviewed in many previous blogs, artery inflammation is the real trigger for cardiovascular disease.
The normal range for CRP is 0.0 – 3.0, but levels less than 1.0 indicate low future risk of a cardiovascular event. Statin drugs actually do lower CRP and, in fact, that is why they do reduce the risk of CVA slightly. However, I believe there are better ways to lower CRP without the potential side effects associated with statin drugs.
Nattokinase, a protein extract from Japanese fermented soy, is excellent at reducing the CRP. It was discovered in 1980 by Dr. Sumi who looked at 173 different foods that seemed to reduce clots in the circulatory system. Generally, two capsules per day for three months will bring the CRP within medical norms.
Fibrinogen is a protein necessary for clot formation. The fibrinogen activity test is most commonly run to evaluate bleeding disorders. The normal range is 193-507 mg/dL. It’s levels below 193 that are associated with delayed clotting. However, levels above 507 are associated with cardiovascular disease. There is no known medical treatment to lower fibrinogen but my clinical experience has been that treating the other factors often results in a drop in the fibrinogen activity as well.
Homocysteine is in intermediate metabolite in the sulfur amino acid pathway. The normal levels are 0-15 umol/L. However, healthy levels are below 8. Homocysteine attaches to the LDL particle under the influence of fibrinogen, forming plaque against an inflamed artery wall when CRP is elevated. So medically, homocysteine is used to assess cardiovascular risk.
Proper conversion of homocysteine back to methionine is dependent on the active forms of folic acid and vitamin B12, so it is also used to evaluate potential folic acid and/or B12 deficiency. Conversion to cysteine is dependent on the active form of vitamin B6 yet the test is rarely considered an indication of B6 deficiency.
This whole sulfur amino acid pathway yields SAM-e which has a calming effect on the brain and free sulfur. Free sulfur in needed for five of the ten pathways of phase II liver detoxification. It is also needed to form glucosamine sulfate and chondroitin sulfate for connective tissue repair and finally, to control candida in the gut.
I run the homocysteine test for all of these reasons.
The L(p)a is another lipoprotein much like LDL or HDL. However, it correlates much more closely to increased cardiovascular risk when elevated than any other serum lipid test. The normal range is less than 75 nmol/L, but I prefer levels below 35. L(p)a is considered a genetic factor and there are no drugs on the market to lower these lipoproteins. That’s probably why the test is run so infrequently.
I run the L(p)a when I suspect a patient has familial hyperlipidemia. This is the least common cause of high cholesterol and typically, the doctor will say, “well, it runs in your family.”
Gingko leak extract and niacin both lower the L(p)a extremely well. Most patients prefer the Gingko as you have to take enough niacin to cause a “flush” for it to be effective. Personally, I find the “niacin flush” a minor inconvenience and it dropped my L(p)a by 50%.
The Bottom Line:
I recommend the CRP, fibrinogen activity, and homocysteine be performed yearly. The L(p)a should be run as a baseline test if you have a family history and personal history of high cholesterol.