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Controlling Blood Lipids. Part 1: A Practical Role for Diet and Exercise

Tedd L. Mitchell, MD; Larry W. Gibbons, MD, MPH

THE PHYSICIAN AND SPORTSMEDICINE - VOL 26 - NO. 10 - OCTOBER 2021


This is the first of two articles on controlling blood lipids. The second article, on medication, will appear in a subsequent issue.

In Brief: Dietary measures that can improve blood lipids include limiting consumption of saturated fats, trans fatty acids, simple sugars, and stearic acid and consuming adequate amounts of vitamins C and E and beta-carotene. Eating certain fish once a week may significantly lower the risk of sudden cardiac death. Aerobic exercise three times per week for 20 to 30 minutes at 60% to 80% of the age-predicted maximum heart rate may also improve lipid levels. Research indicates that modest fitness reduces overall mortality, and higher levels benefit those who have abnormally high cholesterol. Moderate alcohol consumption may influence a person's lipid profile favorably but is not recommended for nondrinkers.

The advances of the past 40 years have given us an effective armamentarium for managing coronary artery disease (CAD) and have increased our understanding of its progression. Yet CAD continues to be the No. 1 killer in the United States. This is especially ironic in that most of the major risk factors for CAD are modifiable.

In particular, decades of clinical studies have shown an association between cardiovascular disease and cholesterol abnormalities (1), and the American Heart Association (AHA) has classified cholesterol abnormalities as one of the major modifiable cardiovascular risk factors. By managing cholesterol levels, physicians and patients can reduce the threat of cardiovascular disease.

This article focuses on controlling blood lipids through diet and exercise, two important lifestyle elements that patients can control. (Also see "Alcohol and Cholesterol," below and "Triglycerides and Heart Disease," below.) Part 2, to appear in an upcoming issue, will cover the role of medication in modifying blood lipids.

Dietary Measures

The revised National Cholesterol Education Program (NCEP) guidelines (2) establish a practical, clear-cut, and useful framework for treating abnormal low-density lipoprotein cholesterol (LDL-C) levels with diet therapy (table 1). (The guidelines also present a coordinated framework for drug therapy that will be discussed in part 2 of this series.)


Table 1. Diet Therapy for Elevated Low-Density Lipoprotein Cholesterol (LDL-C) Levels: Initiation Criteria and Goals

Indications LDL-C (mg/dL)
Initiation Level
Goal

No CAD, fewer than 2 risk factors* >160 <160
No CAD, 2 or more risk factors >130 <130
CAD >100 <100


Source: National Cholesterol Education Program (2).

CAD = Coronary artery disease

*Risk factors include age (men >45 years; women >55 years or who have premature menopause and are not taking estrogen); family history of premature coronary disease (infarction or sudden death before age 55 in a male parent or sibling or before age 65 in a female parent or sibling); cigarette smoking; low high-density lipoprotein cholesterol (HDL-C) (<35md/dL); and diabetes. Subtract one risk factor for those whose HDL-C is >60 mg/dL.


Saturated fats. The dietary guidelines call for decreasing fat consumption in general and saturated fats in particular, since the latter are directly related to the development of atherosclerosis. While intake of monounsaturated fats has an inverse relationship with atherosclerosis development, saturated fats, more than any other component of the diet, raise LDL-C (3). Additionally, diets high in saturated fats tend to be high in calories and low in other nutrients.

Stearic acid is a saturated fat found in foods such as beef and chocolate. Although it may not raise LDL-C, it is contained in foods—such as cocoa butter, beef tallow, lard, butter oil, chicken fat, and to a lesser extent, palm, soybean, coconut, and cottonseed oils—that are high in other types of saturated fats. Thus, limiting foods that contain stearic acid is recommended.

Can dietary therapy alone improve cholesterol profiles? Absolutely. The NCEP Step 2 Diet is designed to reduce serum cholesterol by limiting the intake of total fat and saturated fat to 30% and 7% of total calories, respectively, and the intake of cholesterol to 200 mg/day—guidelines also supported by the AHA (4). (Another method is to limit fat intake to 30 g/1,000 calories consumed, not to exceed 50 g/day.)

For CAD patients who change from an average American diet to the NCEP Step 2 Diet, dietary equations predict a drop of 10% to 20% in LDL-C. For patients whose diets include more fat than the average American diet, greater reductions in LDL-C can be expected. However, patients who have extremely high LDL-C levels (above 190 mg/dL) usually require medical therapy to control their abnormal cholesterol profiles. Dietary therapy is also appropriate in these patients. In fact, studies have shown that medication and diet work synergistically for such patients (5).

Other fats. In addition to saturated fat, certain other types of fat can affect cholesterol profiles and cardiovascular disease risk, according to recent research.

Trans fatty acids. Trans fatty acids are partially hydrogenated fats derived from vegetable sources, such as those in margarine. Because these acids are not fully hydrogenated, they have been thought to be less atherogenic than fully hydrogenated (saturated) fats, which typically are derived from animal fats. For this reason, margarine has been widely used in cooking, particularly in foods such as cookies, pastries, breads, and french fries.

Unfortunately, trans fatty acids can negatively affect blood lipids, raising LDL-C levels and perhaps lowering high-density lipoprotein cholesterol (HDL-C). Furthermore, studies have implicated trans fatty acid intake in heart disease and myocardial infarctions (6,7). Although some smaller studies have not shown as significant a trend, it stands to reason that trans fatty acids should be limited according to the same criteria used for other fats.

Fish oils. Fats derived from fish have received attention for many years because of their potential for reducing cardiovascular disease risk. A recent report (8) suggests that healthy men who consume at least one serving of fish per week could reduce the risk of sudden cardiac death by 52% relative to those who never or rarely consume fish. This association held even after other cardiovascular risk factors were controlled.

Interestingly, subjects who consumed more than one serving of fish per week did not enjoy significantly more benefit than those who ate one serving per week, suggesting a threshold effect. The study suggests that a component of fish may have antiarrhythmic properties that reduce patients' risk of life-threatening arrhythmias during cardiac ischemia, thus decreasing sudden cardiac death.

Sugar. Another element of diet that is important in individuals who have abnormal cholesterol—and triglyceride—levels is sugar. Because of the emphasis on reducing dietary fat, many individuals have worked to decrease their fat consumption, but have actually increased their overall calorie intake because they have not paid attention to the amount of sugar they eat. This adversely affects their cholesterol profile, and the resulting calorie surplus can lead to weight gain. Patients need to know that dietary programs target fat consumption because fats are calorie dense and raise LDL-C, but low-fat diets that are high in sugar can cause problems as well.

We recommend that patients obtain 50% to 60% of their total calories from carbohydrates but limit simple carbohydrates (sugars) to 10% of total calories.

Antioxidants. In the past several years, the role of antioxidant supplements in preventing atherosclerosis and its progression has been of significant interest. Although much remains to be discovered, some effects of antioxidants are emerging.

Antioxidants do not work by lowering LDL-C or altering the cholesterol profile in general. Rather, they seem to decrease the incorporation of cholesterol particles into atherosclerotic plaque. Because oxidation of LDL-C is part of the process of generating luminal plaques, it stands to reason that substances that reduce this oxidation could favorably alter the cellular environment, decreasing the risk of plaque formation. Antioxidants are such substances because they can reduce the oxidative stress of tissues without themselves becoming pro-oxidative. Antioxidants may also play a role in decreasing the risk of plaque rupture, which leads to occlusion of the vessel and subsequent infarction.

Research regarding this role of antioxidants focuses particularly on vitamins E and C and beta-carotene. Studies are ongoing, but the preliminary data are sufficient to recommend the use of antioxidants, particularly in secondary prevention (9,10). Our standard recommendation is that patients take vitamin C, 500 mg twice daily; vitamin E, 400 IU once daily; and beta-carotene, 25,000 IU once daily. (Smokers should not take beta-carotene because current data show that it is not helpful and may be problematic (11,12). These recommendations are general guidelines and should be tailored to individual patients.

Patients should preferably receive most of their antioxidant vitamins through diet. With some attention, much of the daily vitamin C can be obtained through diet. However, taking in enough vitamin E through diet is much more difficult, since the foods that contain it also tend to be high in fats, so supplementation is typically necessary.

Although numerous other substances—such as selenium and ubiquinone—have been shown to have antioxidant properties, research on their effectiveness is limited and inconclusive.

Follow-up. In our experience, patients follow dietary guidelines well only if they have a specific, structured plan. Consequently, our nutrition staff works with each person to outline an appropriate and workable diet. Physicians who do not have nutritionists at hand should refer patients to a nutrition program in the community, especially those patients who are overweight or who have abnormal LDL-C, triglycerides, blood pressure, or blood sugar.

Further follow-up is important. We generally repeat lipid profiles after patients have followed a diet for 2 to 3 months. We use the opportunity to motivate patients who are making progress, adjust recommendations, and undertake more aggressive treatment for those whose lipids remain elevated.

Exercise

The role of exercise in reducing long-term cardiovascular risk is multifaceted. Regular aerobic exercise simultaneously improves cholesterol, blood pressure, blood sugar, and body fat percentage, so it is an important part of an ongoing preventive health program. However, patients considered to be high risk should undergo exercise test screening before beginning an exercise program.

Amount and type. Most of the data that deal with the effect of exercise on cholesterol metabolism focus on aerobic exercise. Research indicates that the volume of exercise may be more important than intensity in changing cholesterol profiles (13). More specifically, studies show that the volume of exercise—eg, miles run per week—has the most consistent effect on HDL-C levels.

A study (13) published by the Stanford Heart Disease Prevention Program suggested that reaching a threshold of running 10 miles per week for at least 9 months—or its equivalent in energy expenditure from other aerobic exercise—was necessary to produce a significant increase in the HDL-C level. Kokkinos et al(14) drew similar conclusions; they found that statistically significant increases in HDL-C occurred at distances of 7 miles or more per week and that the most important changes in HDL-C occurred in those who ran from 7 to 14 miles per week.

Though reaching an exercise threshold may significantly improve HDL-C levels, going beyond that threshold does not necessarily result in higher HDL-C levels. A 120219 study (15) from Japan evaluated runners who ran 30, 60, and 100 km/wk. It found that those who ran more than 30 km/wk did not have significantly higher HDL-C levels.

Other types of exercise, such as nonaerobic strength training, do not seem to increase HDL-C levels significantly. Furthermore, most of those doing research in this area believe that aerobic exercise, rather than anaerobic exercise, is necessary to raise HDL-C levels. Thus, physicians should emphasize the need for a foundation of aerobic exercise, even for athletes involved in strength training programs (13-15).

FIT guidelines. Predicting the effect of aerobic exercise on HDL-C in a given patient is difficult because of the many variables involved. Nevertheless, the "FIT" training principle (for frequency, intensity, and time or duration of exercise) (16) is useful for patients who are beginning an aerobic exercise program.

  • Frequency is the first consideration. Beginning with 3 days per week is appropriate for patients who are not overweight. Obese patients who want to use exercise to help control their weight may need to exercise 5 days per week.
  • Duration is the second consideration. Each session should involve at least 20 to 30 minutes of sustained aerobic exercise, such as walking, jogging, cycling, or swimming. In addition, individuals should spend 5 to 10 minutes in warm-up and cool-down exercise.
  • After frequency and duration, patients should focus on exercise intensity. This may be gauged in a variety of ways, but, in general, a heart rate between 60% and 80% of the age-predicted maximum capacity is a good goal. Too often patients exercise less frequently and more intensely (the "weekend warrior" syndrome), but studies have shown that such an exercise pattern does little to reduce mortality (17,18).

Physicians should consistently reinforce the need for a consistent, moderate aerobic exercise program as an ongoing part of patients' cholesterol treatment plan.

Fitness, Cholesterol, and Mortality

Exercise is also important in lowering the risk of mortality. Blair et al (19) have examined the relationship of physical fitness to cholesterol abnormalities and mortality. They found that patients who have low levels of fitness and abnormal cholesterol profiles are the most likely to die prematurely, while those who have high levels of fitness and normal cholesterol profiles are the least likely.

Their data include two striking scientific findings: (1) Patients who were only modestly fit had a 55% reduction in overall premature mortality compared with the rate of premature mortality in unfit individuals; and (2) highly fit patients who had high cholesterol had lower premature mortality than unfit patients who had normal cholesterol profiles. A follow-up study (20) revealed that subjects who improved their level of fitness thereby lowered their risk of early death, further supporting the theory that physical fitness affects mortality.

Back to Basics

Though sophisticated technology has been important in developing modern means for treating patients who have CAD, basics such as diet and exercise are obviously essential. Physicians and patients who focus on these two areas can work as partners to promote cardiovascular health.

Medications are also an important part of the modern armamentarium. Part 2 of this series will focus on the role of bile acid sequestrants, fibric acid derivatives, statins, and niacin in controlling blood lipids.

References

  1. LaRosa JC, Hunninghake D, Bush D, et al: The cholesterol facts: a summary of the evidence relating dietary fats, serum cholesterol, and coronary heart disease: a joint statement by the American Heart Association and the National Heart, Lung, and Blood Institute. Circulation 1990;81(5):1721-1733
  2. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults: Summary of the Second Report of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel II). JAMA 1993;269(23):3015-3023
  3. Butter or margarine? Harvard Heart Letter 1997;8(2):1-2
  4. Smith SC, Blair SN, Criqui MH, et al: Preventing heart attack and death in patients with coronary disease: consensus panel statement. Circulation 1995;92(1):2-4
  5. Pearson T: Diet alone versus diet plus lipid-lowering drugs. Presented at American Heart Association National Meeting, New Orleans, Nov 11-14, 1996
  6. Women and risk: some findings from the Nurses' Study, Harvard Heart Letter 1996;7(4):3
  7. Ascherio A, Hennekens CH, Buring JE, et al: Trans-fatty acid intake and risk of myocardial infarction. Circulation. 1994;89(1):94-101
  8. Albert CM, Hennekens CH, O'Donnell CJ, et al: Fish consumption and risk of sudden cardiac death. JAMA 192021;279(1):23-28
  9. Hodis HN, Mack WJ, LaBree L, et al: Serial coronary angiographic evidence that antioxidant vitamin intake reduces progression of coronary artery atherosclerosis. JAMA 1995;273(23):1849-1854
  10. Rapola JM, Virtamo J, Haukka JK, et al: Effect of vitamin E and beta-carotene on the incidence of angina pectoris: a randomized, double-blind, controlled trial. JAMA 1996;275(1):693-62021
  11. The effect of vitamin E and beta-carotene on the incidence of lung cancer and other cancers in male smokers. The Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group. N Engl J Med 1994;330(15):1029-1035
  12. Omenn GS, Goodman GE, Thornquist MD, et al: Risk factors for lung cancer and for intervention effects in CARET, the Beta-Carotene and Efficacy Trial. J Natl Cancer Inst 1996;88(21):1550-1559
  13. Williams PT, Wood PD, Haskell WL, et al: The effects of running mileage and duration on plasma lipoprotein levels. JAMA 120212;247(19):2674-2679
  14. Kokkinos PF, Holland JC, Narayan P, et al: Miles run per week and high-density lipoprotein cholesterol levels in healthy, middle-aged men: a dose-response relationship. Arch Intern Med 1995;155(4):415-420
  15. Higuchi M, Iwaoka K, Fuchi T, et al: Relation of running distance to plasma HDL-cholesterol level in middle-aged male runners. Clin Physiol 120219;9(2):121-130
  16. American College of Sports Medicine: The recommended quantity and quality of exercise for developing and maintaining cardiorespiratory and muscular fitness in healthy adults. Med Sci Sports Exerc 1990;22(2):265-274
  17. Norris JN, Clayton DG, Everitt MG, et al: Exercise in leisure time: coronary attack and death rates. Br Heart J 1990;63(6):325-334
  18. Linsted KD, Tonstad S, Kusma JW: Self-report of physical activity and patterns of mortality in Seventh-Day Adventist men. J Clin Epidemiol 1991;44(4-5):355-364
  19. Blair SN, Kohl HW III, Paffenbarger RS Jr, et al: Physical fitness and all-cause mortality: a prospective study of healthy men and women. JAMA 120219;262(17):2395-2401
  20. Blair SN, Kohl HW III, Barlow CE, et al: Changes in physical fitness and all-cause mortality: a prospective study of healthy and unhealthy men. JAMA 1995;273(14):1093-102021

Alcohol and Cholesterol

Increased HDL. Alcohol influences different blood lipids differently. It appears to affect low-density lipoprotein cholesterol (LDL-C) only by adding calories that can lead to increased weight, which elevates LDL-C. The major effect of alcohol on cholesterol is on the high-density lipoprotein (HDL) fraction, which alcohol consumption raises.

Decreased heart disease. The French have a relatively high-fat diet and a low incidence of coronary artery disease (CAD). Some think this is because wine raises their HDL cholesterol (HDL-C) levels, but these levels are actually not very high. Another theory suggests that antioxidants in red wine, not alcohol itself, protect against CAD. Still others have proposed that wine drinkers have less CAD because of their higher socioeconomic status, greater inclination to exercise, and greater attention to diet.

Whatever the cause, there is convincing evidence that those who consume modest amounts of alcohol have a lower risk of CAD than those who drink no alcohol (1). This is true for drinkers of beer and spirits as well as for wine drinkers, though the association appears to be stronger in the case of people who drink wine (2). However, alcohol may not increase HDL-C levels in people who are already very active.

A cautious approach. We still have much to learn about the effects of alcohol on HDL-C and CAD, so it is not wise to recommend that patients begin drinking alcohol to raise HDL-C and lower the risk of heart disease. The risks of drinking, in fact, may outweigh the benefits. Some individuals may be predisposed to alcoholism, and drinking small amounts of alcohol could be dangerous. In addition, modest amounts of alcohol may harm patients who have medical conditions such as high blood pressure.

The National Institutes of Health consensus conference on HDL-C does not recommend treating low HDL-C levels with alcohol (3). Further, the National Institute on Alcohol Abuse and Alcoholism (NIAAA) recommends (4) that the following persons avoid drinking alcoholic beverages:

  • women who are pregnant or trying to conceive;
  • people who plan to drive or perform other activities requiring unimpaired attention or muscular coordination;
  • people taking antihistamines, sedatives, or other medications that can magnify alcohol's effects;
  • recovering alcoholics; and
  • people under age 21.

The NIAAA also suggests that caution be exercised by:

  • those who have certain medical conditions, like peptic ulcers or diabetes, that may be exacerbated by alcohol;
  • persons who have a strong family history of alcoholism; and
  • individuals concerned about increasing their risk of breast and colorectal cancer, since studies suggest an association between moderate drinking and an increased risk of these diseases.

Our advice to the patient is this: If you don't drink, don't start. If you do drink, limit alcohol to two daily servings, with each serving consisting of either 12 oz of beer, 5 oz of wine, or 2.5 oz of liquor.

References

  1. Criqui MH, Ringel BL: Does diet or alcohol explain the French paradox? Lancet 1994;344:1719-1723
  2. Harvard Health Letter 1994;19(5):4
  3. Einhorn PT, Rifkind BM: The NIH Consensus Development Conference on triglyceride, high density lipoprotein, and coronary heart disease. Cardiovasc Risk Factors 1993;Sept:327-331
  4. Harvard Health Letter 1994;19(5):5


Triglycerides and Heart Disease

The relationship between triglycerides and coronary heart disease is complex. It is quite clear that not all forms of hypertriglyceridemia increase heart disease risk equally. High triglyceride levels are more dangerous for patients with certain genetic conditions, diabetes, or central obesity. High triglyceride levels may be a greater risk factor in women than in men. Triglycerides may be more important and dangerous in those who have a family history of early heart disease than in those who have none.

In addition, many forms of hypertriglyceridemia may simply reflect the presence of other risk factors, such as a low level of high-density lipoprotein cholesterol (HDL-C) or diabetes, rather than being independent risk factors. Elevated triglycerides are associated with a number of genetic disorders and may be the result of excess weight, excess alcohol consumption, hypothyroidism, liver disease, or kidney disease.

Serum level guidelines. In our clinic, we have set the ideal level of triglycerides at 125 mg/dL or less. However, there seems to be very little risk with a level of 200 mg/dL or less.

The National Cholesterol Education Program(1) classifies triglycerides as follows:

  • Borderline high: 200 to 400 mg/dL;
  • High: 400 to 1,000 mg/dL; and
  • Very high: greater than 1,000 mg/dL.

Control. Lifestyle change is the most effective way to lower triglycerides. Weight loss, regular exercise, eating a low-fat and low-sugar diet, restricting alcohol use, and stopping smoking are all helpful. Weight loss is particularly important, and exercise strongly and independently lowers triglycerides.

Drug treatment may be appropriate if a patient has a strong family history of premature heart disease, a concomitant high low-density lipoprotein cholesterol level, an extremely low HDL-C level, or certain high-risk genetic forms of hypertriglyceridemia. Nicotinic acid and fibric acid derivatives both effectively lower triglycerides. The newest statin—atorvastatin—may have more triglyceride-lowering potential than the earlier generations, which lower triglycerides modestly.

Two special treatment concerns are:

  • Patients whose triglycerides are over 1,000 mg/dL: Pancreatitis is a significant risk, and very aggressive treatment is warranted.
  • Diabetic patients, who have an increased risk of high triglyceride levels: Effective treatment of diabetes with consistent control of blood sugar helps regulate triglycerides.

Reference

  1. Report of the National Cholesterol Education Program Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults. Arch Intern Med 120218;148(1):36-39


Dr Mitchell is the medical director of the Cooper Wellness Program and Dr Gibbons the medical director of Cooper Clinic, both in Dallas. Address correspondence to Tedd L. Mitchell, MD, Cooper Clinic, 12200 Preston Rd, Dallas, TX 75230.


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