|September 2002 Vol. 1 No. 9|
Cholesterol – When and How to Treat
Elevated cholesterol is the most common concern I face in my live-in clinic in Santa Rosa, California, and it is one of the most common health worries among people of Western cultures. One reason for this heightened awareness is the sale of a class of powerful and expensive cholesterol lowering agents, known as HMG-CoA reductase inhibitors and commonly called “statins.” Pharmaceutical companies want you to know about this risk factor for heart disease in order to enhance the market. Even so, elevated cholesterol is a real crystal ball to your future and should not be ignored.
What is Normal Cholesterol?
Normal cholesterol was once based upon what was common for Americans. Their average cholesterol is 210 to 220 mg/dl. So this was considered the desirable range until someone noticed that the average American was sick. The average American has a 50% chance of dying prematurely of heart disease or stroke. “Average” you don’t want to be. So about 15 years ago recommendations for “desirable” cholesterol levels began to be used in laboratories and medical practices. Unfortunately, to date, there are few official recommendations for “ideal” cholesterol – a cholesterol level associated with the best possible health, and more specifically, the lowest risk of dying of heart disease.
Ideal Cholesterol is Below 150 mg/dl:
Worldwide and nationwide heart disease is very rare when people have blood cholesterol levels below 150 mg/dl.1,2 This is why I have set this value for your laboratory results as “a great big A+” on the report card. This level can be attained by almost everyone by following a strict low-fat, no cholesterol diet, such as I recommend, and judicious use of medications.
Should Get Medication?
The most recent guidelines of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults considered that an ideal LDL cholesterol level is below 100 mg/dl and recommended that persons with coronary heart disease or similar high risk should be considered for drug therapy when LDL is equal to or greater than 130 mg/dl.3 However, some doctors are even more aggressive and recommend medication when LDL cholesterol of less than 100 mg/dl cannot be obtained with diet and lifestyle changes alone.3
My goal is to have all my patients achieve total cholesterol below 150 mg/dl (and LDL cholesterol below 90 mg/dl) with diet alone. So what do I recommend for those who cannot accomplish this with diet alone?
I have little hesitation recommending they take relatively safe “natural” cholesterol-lowering medications like garlic, oat bran (oatmeal cereal), vitamin C and E, and/or gugulipid for those who have tried without success.
Use of Prescription Medications:
decision to use prescription medications is much more difficult. Some of my
thoughts when I am trying to help a patient make the right decision are:
2) People with a high risk of heart disease because of a previous history of heart attack, an alarmingly positive heart test (an angiogram or ultra-fast CT scan), angioplasty, bypass surgery or angina (chest pains), I tend to treat very conscientiously with medications – my goal is to get their cholesterol levels below 150 mg/dl and out of risk for future problems. Other issues such as age, diabetes, hypertension, obesity, family history, and especially, the patient’s own feelings and fears heavily influence my recommendations.
3) Occasionally, someone has a very alarming history with maybe heart attacks and heart surgery, along with diabetes, and/or obesity; and yet still has low cholesterol (say 140 to 170 mg/dl). In these difficult cases, I will still treat them with medications to lower their cholesterol even further. Obviously, the low level they had at the time of their problem was too high for them.4
4) An Ultrafast CT (Heart) Scan will sometimes help me make the decision to recommend treatment. This test looks at the amount of calcium in the heart arteries. Calcium is a reflection of previous inflammation from years of atherosclerosis and does not accurately predict who is going to have a heart attack, but simply indicates a history of previous damage. If someone has a concerning cholesterol level and a “clean” heart scan, then I will tend to avoid recommending medication. If the calcium count was mild to moderately elevated, then I will tend to recommend no drug therapy for now, but a follow-up scan in two years to assess the benefits of any treatments, like diet, exercise and “natural” medication. If the initial scan showed a high calcium count and indicated very serious inflammation in the past, then I will tend to start drug therapy without waiting for a follow-up test.
There are two general approaches to prescription medications:
1) Cholesterol binding agents, called bile acid sequestrants, and/or niacin (nicotinic acid). These binding agents are found as powders or pills. They bind cholesterol and bile acids (which form cholesterol) in their intestine and they prevent the absorption into the body; causing them to be eliminated in the stool. Niacin’s actions are not fully understood, but it decreases cholesterol production in the liver, and may remove fats from the lipids (cholesterol-fat particles) in a variety of ways. Niacin is difficult to take because of a flushing reaction. Reductions in lipids with 2000 mg of niacin can be as much as: total cholesterol 12%, LDL 17% and triglycerides 35%, while HDL can rise 26%. Binding agents (like Colestid) can lower total cholesterol by 25% and LDL by 31%, but triglycerides often rise. Their main side effect is constipation.
2) HMG-CoA reductase inhibitors (“statins”) are very powerful medications that inhibit cholesterol production in the liver. They are easy to take in pill form and have few side effects. The most common problems are an elevation of liver enzymes due to liver damage (about 2% of users) and a rare, but serious form of muscle damage. Total cholesterol levels are typically reduced by 13 to 32% and LDL by 21 to 40%. Triglycerides are reduced by 12 to 24%.
Both approaches have been shown to reduce the progression of atherosclerosis almost immediately, and actually cause regression of disease after two to four years of treatment.5
Recently, I have been prescribing pravastatin (Pravachol) because of evidence that it is the most effective drug for lowering the risk of heart attacks and death.6 The action of Pravachol is different from other “statins” in that it does not enter the cells of the body easily and therefore avoids some of the effects within the cells that may cause an increase in risk of atherosclerosis and heart attacks.
Everyone should be on a low-fat, no-cholesterol, diet based on unrefined starches with the addition of vegetables and fruits. People with elevated triglycerides should further limit simple sugars, even fruit and juices, because they raise triglyceride levels and may cause rises in total cholesterol levels.7-9 All people with elevated cholesterol and/or triglyceride levels should consider the “natural” cholesterol-lowering agents. People with a higher risk of complications of atherosclerosis should consider prescription medications. One of our goals for our patients at the Santa Rosa live-in clinic is a level below 150 mg/dl for both cholesterol and triglyceride levels. You should check your blood levels every 3 to 6 weeks when making changes in your diet or medication therapy to assess the results. When everything is stable (and hopefully ideal) then you should check your blood levels every six to 12 months or less.
Don’t forget other important health issues, such as habits (smoking, coffee, and alcohol), body fatness, and daily exercise. You have control over your future health – even if you are already in trouble – and by making the right decisions you can solve your problems and enjoy excellent health.
1) Roberts W. Atherosclerotic risk factors--are there ten or is there only one? Am J Cardiol. 1989 Sep 1;64(8):552-4.
2) Kannel W. Is Is the serum total cholesterol an anachronism? Lancet. 1979 Nov 3;2(8149):950-1.
3) Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA. 2001 May 16;285(19):2486-97.
4) Roberts W. Lipid-lowering therapy after an atherosclerotic event. Am J Cardiol. 1989 Sep 15;64(10):693-5.
5) Mack WJ. Efficacy of two lipid-lowering treatments on quantitative coronary angiographic endpoints. Cardiovasc Drugs Ther. 2000 Aug;14(4):411-8.
6) Ichihara K. Disparity between angiographic regression and clinical event rates with hydrophobic statins. Lancet. 2002 Jun 22;359(9324):2195-8.
7) Hollenbeck C. Dietary fructose effects on lipoprotein metabolism and risk for coronary artery disease. Am J Clin Nutr. 1993 Nov;58(5 Suppl):800S-809S.
8) Hallfrisch J. Metabolic effects of dietary fructose. FASEB J. 1990 Jun;4(9):2652-60.
9) Swanson J. Metabolic effects of dietary fructose in healthy subjects. Am J Clin Nutr. 1992 Apr;55(4):851-6.
John McDougall All Rights Reserved