The ineffectiveness of a commonly recommended lipid-lowering diet in significantly lowering the serum total and low-density lipoprotein cholesterol levels

FROM THE EDITOR

The Ineffectiveness of a Commonly Recommended Lipid-Lowering Diet in Significantly Lowering the Serum Total and low-Density lipoprotein Cholesterol levels

I

t has long been recognized that long-term excessive intake of salt often leads to elevation of the systemic arterial pressure.’Adults in the USA consumean averageof about 10g of salt daily and an estimated60 million adults in the USA have systemic arterial pressures >140/90 mm Hg. If the salt intake is decreasedby 50% to 5 g daily, there is an insignificant change in the systemic arterial pressure.’If, however, the salt intake is decreased to 240 mg/dl (>6.2 mmol/l iter).s,h The former translates into nearly 40% of total calories being derived from fat. A reduction in the percentageof calories from fat from near 40% to 30% with saturated fat ~7% and cholesterol ~200 mg/day (The National Cholesterol Education Program Step 2 diet7s) results in an averagereduction in both the serum total and low-density lipoprotein (LDL) cholesterol levels of only 5% (e.g., 2404228 mg/dl [6.2+5.9 mmol/liter])!” Although a reduction in the calories from fat from 40% to 20% (The American Heart Association phase III diet) decreasesthe total and LDL cholesterol levels by an average of 20% (e.g., 24OW192 mg/dl [6.2+5.0 mmol/liter]),tO most adults in the USA are unwilling to reduce to this level their percentageof calories from fat. (The average percentageof calories from fat for the averageadult in Japan is now 23%, although historically it has been about IO%.) A reduction to 10% of calories from fat, a level achieved for practical purposesonly by a vegetarian-fruit diet, can lower the serum total cholesterol level to near 150mg/dl(3.9 mmol/liter), a level where atherosclerotic plaques do not form, and where those present shrink in size. Fortunately, for those of us unwilling to reduce our percentageof calories from fat to more desirable levels, the addition of a single 20 mg tablet daily of lovastatin (and probably also of simvastatin [lo mg] and pravastatin [20 mg]) will reduce both the serum total and LDL cholesterol levels by an averageof 27% (e.g., 240+175 mg/dl [6.2+4.5 mmol/liter]) even if the percentageof calories from fat remains at nearly 40%!” If the perThe Editor in Chief and his family have no stocks in any pharmaceutical company, and the Editor in Chief is not a consultant to any pharmaceutical company.

centageof calories from fat is reduced from 40% to 30% and at the sametime a 20 mg tablet of lovastatin is administered, both the serum total and LDL cholesterol levels are reduced an additional 5% on the averagefor a total 32% reduction (e.g., 240-163 mg/dl[6.2+4.2 mmoljhter]). And the side effectsof a once-daily 20 mg tablet of lovastatin are the sameas a similar dose of placebo.’ ‘,I2 How should this heretofore mentioned information be usedclinically? It should be applied now, in my view, to virtually all patients who already have had an atherosclerotic event (secondary prevention). Several studies, 5 published in 1990,have indicated that further luminal narrowing by atherosclerotic plaques can be delayed or even prevented, and that the frequency of subsequent atherosclerotic events can be decreasedin patients who have had atherosclerotic events if their total and LDL cholesterol levels are substantially lowered indefinitely.‘jm’s If the serum total cholesterol is lowered to about 150 mg/dl (3.9 mmol/hter), the atherosclerotic plaques will shrink with a resulting increase in luminal size and new plaques will not form. Furthermore, the vasoconstrictor substances released by platelets and other cells may lose their effect when the serum cholesterol levels are substantially lowered. In other words, atherosclerotic arteries that lose the fatty componentsof their plaques may revert physiologically to behave like normal arteries. Additionally, the frequency of plaque disruption may be decreased.ty The Expert Panel of the National Cholesterol Education Program issuedguidelines for adults with hypercholesterolemiain 1987.7,8This group of experts recommendedas the first step a diet low in saturatedfat and cholesterol to be followed later, if needed,by lipid-lowering drug therapy. Although its effectivenessin some patients may be impressive, particularly when the serum triglyceride level is >300 mg/dl (3.4 mmol/hter), the 30%-of-calories-from-fat and 200 mg cholesterol diet used by Hunninghake and associates”on the average lowered the serum total and LDL cholesterol levels by only 5%, and there is no evidence that such a small reduction would either halt plaque progression or initiate plaque regression.In actuality, this 25% reduction in percentage of calories from fat simply leads to false hope on the part of both patient and physician and, indeed, to the frustration of each. The person who has had an atherosclerotic event needsto lower the serum total and FROMTHE EDITOR 623

LDL cholesterol levels (and raise the serum high-density lipoprotein cholesterol) as much and as rapidly as possible to reducethe chanceof a subsequentatherosclerotic event. Therefore, lipid-lowering drug therapy,in my view, should be initiated immediately after an atherosclerotic event, irrespective of the level of the serum total or LDL cholesterol, becausewhatevertheselevels are, they are too high for that particular patient.20At the same time, the change to a lower fat-lower cholesterol diet can begin, but unlessthe fat-cholesterol reduction is dramatic (about a 50% reduction in calories from fat), meaningful serum LDL cholesterol reductions will not be achieved in most patients. Diet, in other words, after an atherosclerotic event should be viewed as secondary rather than asprimary lipid-lowering therapy,the reverse of what has been recommendedby the Expert Panel of the National Cholesterol Education Program.In contrast, before an atherosclerotic event, a low fat-low cholesterol diet should be the primary lipid-lowering therapy, and lipid-lowering drug therapy should be viewed as secondary and only necessary when the reduced fat and cholesterol intake do not achieve meaningful reductions in the serum total and LDL cholesterol levels.

Gordon DJ, Burt VL, Brown CD, Lippel K, Cleeman II. Declining serum total cholesterol levels among US adults. The National Health and Nutrition Examination Surveys. ./AMA 1993;269:3002-3008. 6. Sempos CT, Cleeman JI, Carroll MD, Johnson CL, Bachorik PS, Gordon DJ, Burt VL, Briefel RR, Brown CD, Lippel K, Rifitind BM. Prevalence of high blood cholesterol among US adults. An update based on guidelines from the second report of the National Cholesterol Education Program Adult Treatment Panels. JAMA 1993;269:300%3013. 7. Report of the National Cholesterol Education Program Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults. Arch lntrrn Med 1988; 148:36-69. 6. 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;

269:3015-3023. 6. Hunninghake DB, Stein EA, Dujovne

CA, Harris WS, Feldman EB, Miller VT, Tolbert JA, Laskarzewski PM, Quiter E, Held J, Taylor AM, Hopper S, Leonard SB, Brewer BK. The efficacy of intensive dietary therapy alone or combined with lovastatin in outpatients with hypercholesterolemia. N .&I J Med 1993;328: 12 I31219. 10. Gmndy SM. NIX D, Whelan MF. Franklin L. Comparison of three cholesteroll-2355. lowering diets in normolipidemic men. JAMA 1986;256:235 il. Bradford RH, Shear CL, Chremos AN, Dujovne C, Franklin FA, Hesney M, Higgins J, Langend6rfer A, Pool JL, Schnaper H, Stephenson WP. Expanded clinical evaluation of lovastatin (EXCEL) study: design and patient characteristics of a double-blind, placebo-controlled study in patients with moderate hypercholesterolemia. Am .I Curdiol 1990;66:4JB-55B. 12. Bradford RH, Shear CL, Chremos AN, Dujovne C, Downton M, Franklin FA, Gould AL, Hesney M, Higgins J, Hurley DP, Langenddrfer A, Nash DT, Pool JL, Schnaper H. Expanded Clinical Evaluation of Lovastatin (EXCEL) study results. 1. Efficacy in modifying plasma lipoproteins and adverse event profile in 8245 patients with moderate hypercholesterolemia. Arch Intern Med 1991:151:43-49. 13. LaRosa JC, Cleeman JI. Cholesterol lowering as a treatment for established coronary heart disease. Circularion 199285: 1229.1235. 14. Watts GF, Lewis B, Brunt JNH, Lewis ES, Coltart DJ, Smith LDR, Mann Jl, Swan AV. Effects on coronary artery disease of lipid-lowering diet, or diet plus cholestyramine, in the St. Thomas’ Atherosclerosis Regression Study (STARS). 1992339563.569. 15. Schuler G, Hambrecht R, Schlierf G, Niebauer J, Hauer K, Neumann J, Hoberg E, Drinkmann A, Bather F, Grunze M, Kubler W. Regular physical exercise and low-fat diet. Effects on progression of coronary artery disease. Ciruhtion 1992;86: l-l I. 16. The Pravastatin Multinational Study Group for Cardiac Risk Patients. Effects of Pravaatatin in patients with serum total cholesterol levels from 5.2 to 7.8 mmol/liter (200 to 300 mg/dl) plus two additional atherosclerotic tisk factors. Am J Curdiol 1993;72: 103 l- 1037. 17. Blankenhom DH, Azen SP, Kramsch DM, Mack WJ, Cashin-Hemphill L, Hodis HN. DeBoer LWV, Mahrer PR, Mastelier MJ, Vailas LI, Alaupovic P, Hirsh LJ, and the MARS Research Group. Coronary angiographic changes with lovastatin therapy. The Monitored Atherosclerosis Regression Study (MARS). Ann Intern Med 1993; I 19~969.976. 18. Haskell WL, Alderman EL, Fair JM, Maron DJ, Mackey SF, Superko HR. Williams PT, Johnstone IM, Champagne MA, Krauss RM, Farquhar JW. The effects of intensive multiple risk factor reduction on coronary atherosclerosis and clinical cardiac events in men and women with coronary artery disease: The Stanford Coronary Risk Intervention Project (SCRIP). Cimdution 1994$9:ooOOoo (due March or April 1994). 19. Brown BG, Xue-Qiao X, Sacco DE, Albers JJ. Lipid lowering and plaque regression. New insights into prevention of plaque disruption and clinical events in coronary disease. Circulufion 1993;87: 178 l-1791. 20. Roberts WC. Lipid-lowering therapy after an atherosclerotic event. Am J Cmdidiol 1989;64:693-695.

Lmrrt

William Clifford Baylor University

1. Freir

ED.

Salt,

volume

and the prevention

Roberts, MD Editor in Chief Medical Center Dallas, Texas

of hypertension.

Circulurion

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FT, Gutman AB. Effects of diet in essential hypertension. II. Results of unmodified Kempner rice diet in fifty hospitalized patients. Am J Med 1950;9:44 I-450. 3. Roberts WC. Factors linking cholesterol to atherosclerotic plaques. Am

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Issues, American Heart Association chaired by LaRosa JC. The Cholesterol Facts. A summary of the evidence relating dietary fats, serum cholesterol, and coronary heart disease. A joint statement of the American Heart Association and the National Heart, Lung, and Blood Institute. Ciwdotion 1990: 8 I : 172 I 1733. 5. Johnson CL, Rifkind BM, Sempos CT, Carroll MD, Bachorik PS, Briefel RR,

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THE AMERICANJOURNALOF CARDIOLOGY VOLUME73

MARCH15,1994