I reference the fallacy of treating high cholesterol with statin drugs frequently. Maybe too frequently. However, for those of you taking a statin (soon to be 50% of the population over the age of 45) I would like to give some background information to discuss with your PCP.
These are the most common causes of high cholesterol:
- The most common cause is a diet high in saturated fat or trans-fats. Saturated fats are found mostly in animal products and recent research indicates that in moderation, saturated fats are safe. Trans-fats are rare in nature but rather are the result of modifying fats to increase shelf life. The trans- bond is very difficult for the body to break. The half-life of a trans-fat in the body is 59 days and it takes five half-lives to eliminate a substance from the body. So the trans-fat oils in those French fries stay in your body for nine months.
- The second most common cause is an underactive thyroid. Hypothyroidism is epidemic in the U.S., especially in women after menopause. Although almost immune to heart attack prior to menopause, the rate of heart attack in women exceeds that of men within five years of menopause. This and insulin resistance are major factors in metabolic syndrome. Laboratory testing for the thyroid begins with a TSH (thyroid stimulating hormone). Although the lab normal range runs from 0.4 to 4.5, the ideal range is 1-2. Running a T3 and T4 gives a better perspective of hormone production and the TPO (thyroid peroxidase) and thyroid auto-antibodies can reveal autoimmune disease of the thyroid (Hashimoto’s thyroiditis).
- In third is dysbiosis. If the microbiome of the digestive tract is disturbed, harmful bacteria can liberate spent estrogen being discarded from the liver. They also produce estrogen analogs. These products are then resorbed in the lining of the large intestine and stimulate cholesterol production in the liver. A history of IBS (irritable bowel syndrome), GERD, acid-reflux or food sensitivities is usually evident but complete digestive stool analysis can identify offending organisms and evaluate the immune status of the gut.
- Last and the least common is genetic, inherited over production of cholesterol in the liver. The lab test for this issue is an L(p)a, a portion of the LDL cholesterol. It is seldom run because there are no drugs currently available to lower the L(p)a. However, both niacin and Gingko leaf extract can often reduce the L(p)a by 50% in three months.
The bigger issue is artery inflammation. This is the ultimate cause of atherosclerosis. When an artery wall becomes inflamed. The inflammation triggers homocysteine to attract LDL cholesterol and attach it to the inflamed artery wall. On a small scale, this protects the inflamed wall. When excessive coronary artery disease is the result.
Statin drugs work because they reduce inflammation, not because they reduce cholesterol. However, there are safer, more effective ways to lower inflammation. So if your cholesterol is elevated, the real question is are you inflamed?
The answer can be found with simple laboratory testing. You need to have a CRP (high sensitivity C-reactive protein), homocysteine, and L(p)a run. That will truly measure your risk factors. If you cannot normalize these values with diet and nutrition, then perhaps, you should consider a statin drug.
The Bottom Line:
If you have not measured the CRP, homocysteine, L(p)a, and TSH as a minimum, you should not be on a statin drug no matter how high your total cholesterol and LDL levels run.