Printer Friendly

Cholesterol: be aware of your ratio!

Even with a "safe" level of total cholesterol, there are still several ways that your risk of coronary artery disease may be too high.

Assume you're sitting in on a conversation in a doctor's office about the results of a thorough blood examination. The first question many patients ask in such a situation is, "What's my cholesterol level?"

If the doctor responds that the level is in the low 200s or below--and if the patient knows just a little bit about cholesterol--you'll probably hear a big sigh or relief.

But this sinse of well-being may be a bit premature--especially if any of the compronents of the person's cholesterol are out of balance. In fact, 40 percent of patients with coronary artery disease have normal total cholesterol levels, says Dr. Gerald Berenson, the director of the Bogalusa Heart Study and the head of Louisiana State University's Specialized Center of Research on Atherosclerosis.

Even with a "safe" level of total cholesterol, there are still several ways that your risk of coronary artery disease may be too high. One major set of problems may involve some of the possible "heroes" in your cholesterol scenario-namely, the highdensity lipoproteins, or HDLs.

There are two factors we need to consider in evaluating the role of the HDLs. First, the level of HDLs in your blood is an important factor all by itself. If the HDL level is unusually low, your risk of cardiovascular disease may increase dramatically. On the other hand, if your HDLs are relatively high, you can expect to have some degree of protection against atherosclerosis.

Second, the HDLs are important as they relate to the total cholesterol levels. Specifically, it's important for the ratio of your total cholesterol to your HDL cholesterol to be below certain levels. The higher your ratio is, the greater your risk of having a cardiovascular problem. In short, as far as your ratio is concerned, the lower, the better!

For example, in men, it's important to keep this ratio below 4.6. So, suppose you are a man and your total cholesterol count is 200 mg/dl-not a bad level according to many longitudinal studies. But if your HDLs are 40 mg/dl, that means your ratio will be 200/40 or 5.0--a figure that's perhaps a little too high to give you adequate protection against cardiovascular disease. To drop you rate, you'll have to take steps to lower your total cholesterol, raise the HDL level, or rely on the combination of both.

Paying attention to your ratio becomes even more important if you already have been diagnosed as having coronary-artery disease. In the Leiden Intervention lTrial conducted in the Netherlands, a study of 39 patients with stable angina reported in the New England Journal of Medicine, March 28, 1985, each patient had at least one coronary artery more than 50 percent obstructed. All were placed on a strict vegetarian diet, with fewer than 100 mg of cholesterol per day, and then they were followed for two years.

During that time, their body weights decreased, their cholesterol levels dropped, and their total cholesterol/HDL ratios all decreased. Twenty-four months later, the researchers once again examined all 39 patients, using computer-assisted coronary angiography.

In 21 of the 39 patients, there was progression of the disease, whereas in 18 of the patients, lesions associated with the disease failed to grow. Furthermore, changes in the coronary lesions didn't correlate with changes in blood pressure, smoking habits, alcohol intake, weight loss, or drug therapy. But there was a correlation between coronary artery disease and the ratio.

Specifically, disease progression occurred in those patients who had cholesterol/HDL ratios above 6.9 throughout the 24 months. And the researchers observed no coronary lesion growth in patients who had a cholesterol/HDL ratio less than 6.9. Likewise, there was no progression of disease in those who initially had values above 6.9 but then were able to significantly lower them by dietary intervention.

The moral of this story is that if you already have been diagnosed as having coronary artery disease, you must resort to whatever means are necessary to lower your cholesterol/HDL ratio to less than 6.9. One way this can be accomplished is by increasing your HDL cholesterol level, and an excellent approach is through exercise. (See "How to Control Your Cholesterol," SEP April '88.) But first, it's important to understand a little more about HDLs and also about the ratio.

The exact way that the HDLs work in your blood is not clear. They may act independently as a kind of "hero" or "garbage-removal agent," which cleans the excess, plaqueforming LDLs and Apolipoprotein Bs, or Apo Bs, out of the blood. Somehow, according to this view, the HDLs may take the LDLs and Apo Bs back to the liver for final disposal before they can do any damage to the blood vessels.

On the other hand, a second theory says the HDLs may not be particularly active at all. Their presence may simply signal the fact that the LDLs and other fatty remnants in the blood are being cleaned out through some other means.

Whatever their particular role, the HDLs and the total cholesterol/HDL cholesterol ratio arevery important indicators of your risk of cardiovascular disease. To help us in this discussion, here is that portion of the Cardiovascular Disease Risk Chart showing the risk ranges for these two lipid factors.

Now let's consider this HDL issue with a practical example.

A patient whom I will call Mike came to our clinic in 1979, when he was 47 years of age. For his age, he seemed in relatively good physical condition. His 213-pound frame consisted of 18.24 percent body fat--a level we regard as well within normal limits, particularly considering his weight. His total cholesterol level wasn't bad either-192 mg/dI. We checked him out with both a resting and a stress electrocardiogram, and they came out normal.

But then potential problems began to emerge as we focused on his laboratory results. His HDL level was 30 and his total cholesterol/HDL cholesterol ratio was 6.4-both figures in the "high risk" categories.

Even though Mike felt fine and had no signs or symptoms of heart disease, he was still worried because there was a strong history of heart disease in his family. His father had suffered his first heart attack at age 53 and had died at age 56, following a second heart attack.

In light of his family background, I agreed with Mike that we should take some precautionary measures. And caution seemed appropriate in view of his below-normal HDL level and the elevated ratio. So I put him on a special diet and increased his exercise in an effort to get his cholesterol in better balance. I also suggested that the use of certain drugs might help him.

In many ways, Mike was the "perfect" patient, in that he adhered exactly to the program I prescribed for him-with one exception: he preferred not to try any drugs to control his cholesterol. In fact, when he returned one year later, his weight had dropped 15 pounds, and his body fat was down to 15 percent. But his cholesterol situation was getting worse. His total cholesterol went up from 192 to 213, and his HDL cholesterol went down to 28, to give him a ratio of 7.6.

Still, he wasn't displaying any symptoms of cardiovascular disease, and his resting and exercise electrocardiograms continued to be normal. So, despite our advice, he still resisted using drugs at this point. Instead, he restricted his low-fat, low-cholesterol diet even more.

When Mike returned a year later, at age 49, he had managed to maintain his weight, and his total cholesterol had dropped back to a more acceptable 197 mg/dl. His HDL cholesterol level had come up slightly to 32 mg/dl, to give him a better ratio of 6.2-although this ratio was still higher than we wanted. Overall, Mike's exercise program was putting him in even better physical condition.

At this point, we were beginning to think that Mike might be one of those people with genetically low HDLs, which don't respond to a lifestylechanging program. Normally, if a person is on a regular aerobic exercise program, such activity tends to elevate the HDL levels. In fact, exercise is probably the most effective thing available to elevate the HDL cholesterol levels. But despite Mike's exercise regimen and his obvious improvement in conditioning-as evidenced by his outstanding performance on the treadmill stress test-his HDL cholesterol level remained relatively low.

Unfortunately, the advice we had given him about the need for drugs turned out to be correct. Mike suffered a major heart attack just a few months after his third physical exam. At the time, he was only 50 years of age. About a month later, he underwent a coronary arteriogram. The pictures taken of his heart and coronary arteries showed that one coronary artery was completely obstructed, and two others were 30 to 40 percent obstructed.

When Mike returned to the clinic a couple of months after his heart attack, we started him on a slowly progressive cardiac rehabilitation program. As a result, his weight dropped even lower, to 192 pounds. In addition, this time he was placed on the lipid-lowering drug Lopid. Soon his total cholesterol level had dropped to 156 mg/dl. But unfortunately, his HDLs went down as well, to 23 mg/dI. This gave him a ratio of 6.78, again a figure that continued to trouble us. So he became even more aggressive with his diet and lifestyle program.

When Mike was tested eight months later, at age 51, he had responded well. His weight had gone down again, to 186 pounds, and his body fat was now at 12 percent. Even a well-conditioned athlete would have been pleased with these results. But his total cholesterol level was again up to 198 mg/dl, and with an HDL level of 27, his ratio was 7.3.

Soon after this, I took him off Lopid and placed him on a combination of the cholesterol-lowering drug colestipol hydrochloride (Colestid) and niacin. This change seemed to help. His total cholesterol/HDL cholesterol ratio is too high. But at least he's showing some progress in getting his cholesterol in better balance. If he does eventually enjoy a long life, at least two things will have done a great deal to help him accomplish this goal: his willingness to work closely with his physicians to correct a troublesome cholesterol problem, and the availability of certain modern drugs. When the problem is one of genetics, as indicated in Mike's case, drugs are nearly always required.

What other lessons can we learn from Mike's situation?

The National Institutes of Health, and also a number of the major longitudinal studies, indicate that a total cholesterol of less than 200 mg/dl should provide significant protection against cardiovascular disease. But Mike's experience demonstrates that it's also absolutely essential to look at all parts of the cholesterol picture-including the very important ratio.

It has been said that "heart attacks do not occur in people who have total cholesterol levels under 150 mg/dl." But let me give you an example that questions the accuracy of that statement. I had followed one man at our clinic for more than five years. His cholesterol ranged from 140 to 185 mg/dl, and at the time of a massive heart attack at age 61, his total cholesterol was 147 mg/dl. Only a sixvessel bypass procedure saved his life.

When you look beyond the total cholesterol level, you begin to see this man's real problem. His HDLs had been extremely low, ranging from 20 to 22 mg/dl. As a result, his total cholesterol/HDL cholesterol ratio stayed above 7.0. In this executive's case, as in Mike's, the most dangerous, life-threatening factor seemed to be the HDL level and the ratio, not the total cholesterol level.

Clearly, then, high-density lipoproteins play a major role in our arteriosclerosis/heart disease scenario. But even as we resent these examples, I should add that there's still a great deal that we don't know about HDLs and the various proteins and lipids which are associated with them. Even now, research is under way on several fronts to expand our knowledge in these areas. It's important that you understand something about these efforts so that you can know what to expect in the future.

For example, research in recent years has shown that there may be better indicators of protection against cardiovascular disease in the blood than the level of the HDL cholesterol.

One line of investigation has focused on what's called the "subftactions" of the HDL, including a component labeled HDL-2. This component is rather difficult to measure, and at present evaluations are limited to research laboratories. Still, the HDL-2 has become one of the front runners for the title of "hero" in preventing clogging of the arteries.

Studies have shown that HDL-2 levels are low in the presence of cardiovascular disease. This subfraction tends to be significantly higher in the blood of women. Interestingly, HDL2 is the component in HDL that increases significantly in the blood of runners and others involved in aerobic exercise.

The HDL-2 subfraction of the HDL seems to perform a special beneficial role that other subfractions don't perform. For example, another subfraction, HDL-3, may or may not be related to cardiovascular disease. And, interestingly, this HDL-3 subfraction shows no clear relationship to aerobic exercise. But the HDL-3 level tends to increase with the consumption of alcoholic beverages.

So what should we conclude about these subfractions of the HDL?

The jury is still out on this issue. But I feel that the total HDL cholesterol is probably a better predictor of cardiovascular disease and atherosclerosis than either of the HDL subfractions.

An even more promising risk indicator of cardiovascular disease may be apolipoprotein A-I, or Apo A-I. A number of studies, including one reported in the August 18, 1983, issue of the New England Journal of Medicine, have concluded that Apo A-I is "by itself . . . more useful than HDL cholesterol for identifying patients with coronary-artery disease."

How does Apo A-I work? It attaches itself to the HDL, much as the Apo B does with the LDL. But the Apo A-I is definitely a "hero," in contrast to the Apo B, which is one of our major "villains." The Apo B contributes to the buildup of lifethreatening plaque in our blood vessels. This Apo A-I, on the other hand, apparently takes used cholesterol out of the body's cells and blood. Then it wraps up the cholesterol and transports it back to the liver for final disposal. There's still considerable discussion over exactly how the Apo A-I works, and any final word on this topic must await further research.

The measurement of the blood level of the enzyme HGM-CoA-Reductase is another promising field of research. Since the level of this enzyme is the best indicator of the amount of cholesterol being produced in the body, its measurement may be invaluable in controlling arteriosclerosis.

So stay tuned! In the next few years, the information on apolipoproteins, the subfractions of HDL, and the enzyme HMG-CoA-Reductase will almost certainly increase dramatically, as will our ability to routinely test for their presence in our blood.
COPYRIGHT 1988 Saturday Evening Post Society
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 1988 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Title Annotation:high-density lipoproteins in relation to total cholesterol count
Author:Cooper, Kenneth H.
Publication:Saturday Evening Post
Date:May 1, 1988
Previous Article:Get your own blood back.
Next Article:Roberta Baskin's radon gas attack.

Related Articles
Low levels of good cholesterol a bad sign.
Do you know your HDL? The 'good cholesterol' proves a strong predictor of coronary risk - and a potent provoker of controversy.
'Good' lipoprotein shows its bad side.
Soy protein intake.
Nuts reduce cholesterol via monounsaturated fatty acids.
Development of a homogeneous assay to measure remnant lipoprotein cholesterol.
Fractional esterification rate of cholesterol and ratio of triglycerides to HDL-cholesterol are powerful predictors of positive findings on coronary...
Quantification of lipoprotein subclasses by proton nuclear magnetic resonance--based partial least-squares regression models.
In search of the ideal measure of high-density lipoprotein.

Terms of use | Copyright © 2018 Farlex, Inc. | Feedback | For webmasters