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Treatment of Hypertriglyceridemia

National Institutes of Health
Consensus Development Conference Statement
September 27-29, 1983

Conference artwork, showing a valentines style red heard with red and blue ribbons on a darker blue background.

This statement is more than five years old and is provided solely for historical purposes. Due to the cumulative nature of medical research, new knowledge has inevitably accumulated in this subject area in the time since the statement was initially prepared. Thus some of the material is likely to be out of date, and at worst simply wrong. For reliable, current information on this and other health topics, we recommend consulting the National Institutes of Health's MedlinePlus

This statement was originally published as: Treatment of Hypertriglyceridemia. NIH Consens Statement 1983 Sep 27-29;4(8):1-5.

For making bibliographic reference to the statement in the electronic form displayed here, it is recommended that the following format be used: Treatment of Hypertriglyceridemia. NIH Consens Statement Online 1983 Sep 27-29 [cited year month day];4(8):1-5.

Introduction and Conclusions


Major advances in the understanding and definition of the hyperlipidemias have occurred during the past 15 years. Treatment of the common forms of hyperlipidemia, including hypertriglyceridemia, is often undertaken to prevent atherosclerotic cardiovascular disease, although current data do not definitively demonstrate that such therapy achieves its objectives. It is possible to normalize or substantially reduce elevated triglyceride levels in the majority of persons using dietary intervention and/or medications. The frequency with which hypertriglyceridemia is diagnosed in the population, the controversy concerning the association of plasma triglyceride levels and cardiovascular disease, and the potential need for life long therapy have made consideration of this topic timely.

To resolve some of these questions, the National Institutes of Health, Bethesda, Maryland, convened a
Consensus Development Conference on the treatment of hypertriglyceridemia on September 27 to 29, 1983. After a day and a half of expert presentation of the available data, a consensus panel consisting of lipidologists, cardiologists, primary care physicians, epidemiologists, and experts in exercise considered the evidence and agreed on answers to the following questions:

  1. What is hypertriglyceridemia?
  2. What is the evidence that plasma triglycerides are associated with disease?
  3. What patients with hypertriglyceridemia are candidates for therapy?
  4. What can be achieved with dietary and other therapies?
  5. What should be guidelines for dietary and drug therapy?
  6. What should be the direction for future research?



Careful evaluation of existing data indicates that in the presence of normal cholesterol levels, mild elevations of plasma triglyceride levels do not necessarily increase the risk for cardiovascular disease. When triglyceride levels are less than 250 mg/dL, risk generally does not exceed that of other Americans, and changes in life-style are unnecessary beyond those recommended for the general public. The same can be said for many normocholesterolemic persons with borderline hypertriglyceridemia who have no risk factors for or family history of cardiovascular disease. However, triglyceride levels in the range of 250 to 500 mg/dL can be a marker for secondary disorders for a subset of patients with genetic forms of hyperlipoproteinemia who are at increased risk and who need specific therapy. Dietary intervention is the primary approach to therapy in these patients, but drugs have a role in selected persons not responding to dietary management. Finally, the danger of pancreatitis is present in frank hypertriglyceridemia (triglyceride level > 500 mg/dL), and the lowering of triglyceride levels by diet and, if necessary, by drugs is indicated.  

What Is Hypertriglyceridemia?

Triglycerides are lipid molecules derived from dietary fat or endogenous synthesis. They are transported from the intestine and liver within plasma lipoproteins to tissues for use as fuel or to adipose tissue for storage. After an overnight fast, they are normally found predominantly as part of triglyceride-rich very-low-density lipoproteins (VLDLs).

Fasting levels of plasma or serum triglycerides are distributed across a broad range in apparently healthy populations. Median and 95th percentile levels tend to be higher and to increase with age in Western industrialized societies compared to other cultures, a difference that parallels obesity patterns. Because triglyceride levels have a continuous distribution, the distinction between "normal" and "abnormal" is arbitrary. The levels suggested herein are based on their ability either to act as a marker for an existing metabolic abnormality or to predict a substantial excess risk of subsequent disease, rather than on some reference level above the mean or median value in the population. The following levels are suggested to guide physician management only and do not imply that disease will inevitably follow or that intervention will necessarily prevent disease.

Fasting plasma triglyceride levels above 1,000 mg/dL carry a substantial risk of pancreatitis. Based on this risk and coupled with the large intraindividual variation in repeated triglyceride measurements, a triglyceride level greater than 500 mg/dL is considered to be abnormal and warrants the label "hypertriglyceridemia."

There is little evidence that triglyceride levels below 250 mg/dL, in the presence of normal cholesterol levels, predict an increased risk of any disease. These levels can be considered normal, although it is recognized that some persons with thus-defined normal triglyceride levels may have other notable lipoprotein or apoprotein abnormalities.

Persons with fasting plasma triglyceride levels between 250 and 500 mg/dL represent a different problem, because in the aggregate such levels are associated with an approximate twofold excess risk of cardiovascular disease. In a patient, these triglyceride levels may be normal or a marker for increased risk. If these borderline levels are confirmed by repeated measurement, they warrant further investigation in a patient who has a family history of premature cardiovascular disease (such as myocardial infarction in a first-degree relative before age 55 years), other heart disease risk factors such as high cholesterol levels, hypertension, cigarette smoking, or obesity, or a secondary cause for elevated triglyceride levels, as listed in a subsequent section of this statement. Some of these persons will be found to have a dyslipoproteinemia, and others will ultimately be considered normal.  

What Is the Evidence That Plasma Triglycerides Are Associated With Disease?

The link between triglyceride levels and disease is most clear for severe hypertriglyceridemia associated with chylomicronemia and eruptive xanthomata, abdominal pain, and/or pancreatitis; the latter, although uncommon, can be fatal. This relationship is believed to be direct and the disease consequences preventable by triglyceridemia reduction.

The relationship between triglyceride and cardiovascular disease is more controversial but potentially of greater relevance to public health and to clinical practice. Although triglyceride levels are positively associated with an increased risk of cardiovascular disease in most prospective population studies, much of the recent controversy about their importance stems from the finding that they are not independently predictive after statistically adjusting for closely associated attributes such as obesity, total cholesterol, high-density lipoprotein (HDL) cholesterol, hypertension, and cigarette smoking. These data suggest that triglyceride, rather than contributing directly to the risk of cardiovascular disease, is a marker for other life-style or metabolic characteristics or genetic lipoprotein disorders. Other observations that support a lack of a causal association between triglyceride and cardiovascular disease include the absence of premature cardiovascular disease in some persons with familial hypertriglyceridemia or with chylomicronemia.

On the other hand, almost all case-control studies of survivors of myocardial infarction have shown higher triglyceride levels in the affected patients. Similarly, many diseases associated with high triglyceride levels, such as diabetes mellitus, chronic renal disease, and certain primary hyperlipidemias, are associated with an increase in risk for cardiovascular disease. Moreover, plasma triglyceride levels between 250-500 mg/dL may be a marker for lipoprotein abnormalities that are more directly associated with atherosclerosis, such as low HDL cholesterol levels, low apoprotein AI levels, and high apoprotein B levels. Alternatively, these triglyceride levels may reflect the presence of the triglyceride-rich lipoprotein particles and/or their metabolic products that may be directly involved in processes associated with enhanced atherogenesis.

Whether or not triglycerides are directly involved in the atherogenic process, elevated levels sometimes can be helpful for identification of persons with increased risk of cardiovascular disease.  

What Patients With Hypertriglyceridemia Are Candidates for Therapy?

Candidates for treatment of hypertriglyceridemia include those patients with primary and secondary hyperlipoproteinemia.

Secondary Hyperlipoproteinemia

Much of the hypertriglyceridemia seen in clinical practice is secondary to a variety of exogenous factors or clinical disorders. This category is defined as secondary hyperlipoproteinemia. The most common secondary factor raising triglyceride levels is obesity. It is probably the major cause of mild elevations of plasma triglyceride levels, which frequently normalize after restoration of desirable weight. Other conditions raising the plasma triglyceride levels include excessive alcohol intake, and the use of a variety of drugs, including thiazide diuretics, oral contraceptives and other estrogens, and some beta-adrenergic blocking drugs. Clinical conditions associated with high plasma triglyceride levels include diabetes mellitus, hypothyroidism, renal disease (uremia, nephrotic syndrome, maintenance dialysis, and renal transplantation), liver disease, dysproteinemias, and occasionally other metabolic and endocrine diseases. Acute stress states such as burns, trauma, myocardial infarction, and sepsis may also induce hypertriglyceridemia. If hypertriglyceridemia persists despite treatment of the underlying condition, consideration must be given to the possibility that the patient has a primary form of hyperlipoproteinemia, such as familial hypertriglyceridemia.

Primary Hyperlipoproteinemia

It is convenient to classify primary hyperlipoproteinemias that are associated with plasma triglyceride elevations into two categories, depending on the concentration of serum triglycerides. These are distinct hypertriglyceridemia (triglyceride level > 500 mg/dL) and borderline hypertriglyceridemia (triglyceride level 250 to 500 mg/dL).


Patients with triglyceride levels between 500 and 1,500 mg/dL (type IV or mild type V hyperlipoproteinemia) sometimes accumulate chylomicrons and pancreatitis can develop. Probably fewer than 1 in 1,000 persons have triglyceride levels of more than 500 mg/dL. Opinion is divided as to whether such levels are associated with increased risk for cardiovascular disease in the absence of other risk factors, but triglyceride levels should be reduced in any event to prevent pancreatitis.

Marked elevation of serum triglyceride levels (> 1,500 mg/dL) occurs in two forms. In both, the risk of acute pancreatitis is high and immediate attention must be given to lowering the triglyceride levels. The first form (type I hyperlipoproteinemia) is a rare condition characterized by an increase in chylomicrons alone. It is caused by a deficiency of lipoprotein lipase and is manifest in childhood. The second form is severe (Type V hyperlipoproteinemia), characterized by an increase in chylomicrons and VLDL; it is relatively uncommon and occurs most often in adults. In many cases diabetes mellitus is present, although there is usually an underlying primary disorder of triglyceride metabolism.

Borderline Hypertriglyceridemia

The triglyceride levels in this category range between 250 and 500 mg/dL. Five to 10 percent of adult Americans have triglyceride levels in this range. In the absence of elevated serum cholesterol levels (in the individual or family members), other risk factors for heart disease, or premature cardiovascular disease in other family members, there is no evidence for increased cardiovascular risk; specific triglyceride-lowering therapy seems unnecessary. If the person has other major risk factors, such as hypertension, smoking, or obesity, vigorous attempts to modify these factors should be undertaken.

One genetic form of hyperlipidemia in which triglyceride levels can be mildly elevated is familial combined lipidemia. Affected persons of one family can have various lipoprotein phenotypes--Type IV (increased VLDL), Type IIA (increased low-density lipoproteins [LDLs]), or Type IIB (increased VLDL and LDL). One person can demonstrate different phenotypes at different times, and risk for cardiovascular disease is increased regardless of the lipoprotein pattern. Patients with familial combined hyperlipidemia deserve attempts at lipid lowering, with diet first and, if necessary, with drugs. Any patient with borderline hypertriglyceridemia who already has clinical manifestations of premature cardiovascular disease can be treated as if he or she has familial combined hyperlipidemia.

Another group of patients with increased risk of cardiovascular disease has the relatively rare entity familial dysbetalipoproteinemia (Type III hyperlipoproteinemia). This condition is an inherited disorder characterized by the accumulation of catabolic remnants of VLDL and chylomicrons. Consequently, plasma levels of both triglycerides and cholesterol are increased, and occasionally, triglyceride concentrations may exceed 500 mg/dL. Dietary and/or pharmacologic intervention as well as treatment of any concomitant clinical disorder should be instituted.  

What Can Be Achieved With Dietary and Other Therapies?

Changes in life-style--weight control, increased physical activity, alcohol restriction, and fat restriction--are primary therapy for reducing elevated triglyceride levels.

Weight Control

In overweight persons with elevated triglyceride levels, the primary goal of therapy is achieving and maintaining desirable weight. Weight loss and maintenance of desirable weight will decrease plasma VLDL and triglyceride levels, often to normal, and at the same time they increase HDL cholesterol. Lower triglyceride levels generally are maintained in the steady state at reduced levels. Treatment by caloric restriction should emphasize decreased intakes of fats, especially saturated fats. A reduction in dietary saturated fats not only facilitates weight loss but also promotes the lowering of cholesterol levels.

Increased Physical Activity

In most training studies, short-term and long-term increases in aerobic exercise cause a substantial decrease in plasma triglyceride levels, except in persons who already have low-normal levels. Adoption of a prescribed exercise program is usually accompanied by other advantageous changes: an increase in HDL cholesterol levels, a rise in apolipoprotein AI levels, and an increase in activity of lipoprotein lipase. Most persons who adopt and maintain a program of progressive aerobic exercise also lose and then stabilize body weight.

Alcohol Restriction

In some persons, triglyceride levels are particularly sensitive to alcohol. In these persons alcohol intake should be restricted.

Fat Restriction

If achieving desirable weight, alcohol reduction, and exercise do not produce a satisfactory lowering of lipid levels, further alteration of diet must be considered. The next step is to reduce saturated fat and cholesterol intake progressively. For the person already at desirable weight, a decreased intake of saturated fats requires replacement by other calories. Substitution by carbohydrates generally is favored; although increasing the carbohydrates in the diet may raise triglyceride levels, the response usually is transient and triglyceride levels later decline.  

What Should Be the Guidelines for Dietary and Drug Therapy?

Dietary therapy is the primary approach to treatment of hypertriglyceridemia. The combination of weight control, exercise, alcohol restriction, and reduction of fat intake should be used to the fullest extent possible before considering drug therapy. In patients who do not respond satisfactorily to physician guidance, the assistance of a trained dietitian can be helpful. Since people may require a considerable period of time to adjust to diet modification, a precipitous decision to use drugs should not be made. Except in cases of severe chylomicronemia in which danger of pancreatitis is high, several months to a year may be taken to allow for the full benefits of diet before resorting to drugs. Even if the response to diet is considered inadequate, drug therapy should be employed only under certain circumstances. Persistence of hyperlipidemia first must be documented in multiple measurements (usually three) before starting drug therapy. Without question, use of drugs can be helpful in some patients to prevent pancreatitis from developing. However, drugs should be employed for prevention of atherosclerotic disease only if a favorable response can be demonstrated in the plasma lipids--at the minimum a substantial lowering of plasma total cholesterol as well as triglyceride levels. Therefore, the therapeutic response must be monitored, and drug therapy should be discontinued if the response is inadequate.

Diet in Specific Disorders


In the presence of severe chylomicronemia, very-low-fat diets (10 to 20 percent of total calories) may be required to prevent pancreatitis. Dietary therapy is the only available treatment for Type I hyperlipoproteinemia. In other forms of chylomicronemia (Type V hyperlipoproteinemia, e.g., severe Type V), fat restriction often is successful in lowering triglyceride levels to a safe range. The need to maintain a very-low-fat intake at all times must be emphasized. Some patients are extremely sensitive to dietary fat, and acute pancreatitis may develop with a single high-fat meal. In some patients, repeated bouts of pancreatitis occur despite all attempts at dietary control. In such patients, or in others who persistently have severe chylomicronemia, a trial with drug therapy is justified.

Borderline Hypertriglyceridemia.

With familial combined hyperlipidemia, hypertriglyceridemia often is accentuated by obesity, and weight control therefore is the first goal of therapy. Furthermore, the composition of the diet should be modified to restrict fat intake to 30 percent of calories, saturated fats to less than 10 percent, and cholesterol to 300 mg/day. If these changes do not normalize the plasma lipid levels, further restriction of dietary fat may be needed. An alternative to severe fat restriction is use of drugs, as will be discussed below.

In familial dysbetalipoproteinemia, the same approach can be used as with familial combined hyperlipidemia. Dietary therapy often is successful in lowering triglyceride levels in patients with dysbetalipoproteinemia, but again, drugs may be required.

Secondary Hyperlipidemia.

In most secondary hyperlipoproteinemias, the first step is to treat the underlying disorder. In some instances, the lowering of lipid levels may be facilitated by modification of the diet. This will usually involve weight reduction and alcohol restriction. Again, it should be emphasized that obesity is the most common cause of borderline hypertriglyceridemia, and triglyceride levels often can be normalized completely by weight reduction.

Drugs in Specific Disorders

As indicated previously, drug therapy in hypertriglyceridemia should take a second place to modification of the diet. Drugs nevertheless may be required to avoid abdominal pain and pancreatitis in the presence of chylomicronemia. They also can be used for regression of xanthomata in patients of this kind or in those with familial dysbetalipoproteinemia. Drugs also may be employed in the attempt to retard atherogenesis in patients with genetic hyperlipidemias, such as familial combined hyperlipidemia or familial dysbetalipoproteinemia, or in those with established cardiovascular disease; it must be emphasized, however, that a definitive clinical trial has never been carried out to determine whether drug therapy will cause a decrease in the morbidity and mortality from cardiovascular disease in any form of hypertriglyceridemia.

The three currently approved drugs, which are generally recognized as being effective in lowering triglyceride levels, are clofibrate, gemfibrozil, and niacin. Experts do not agree on the drug of choice.

The rational choice of drugs requires knowledge of their pharmacokinetic properties and their adverse effects or toxicity. Clofibrate administration is associated with few overt side effects, but cholethiasis, myalgias, and, in rare instances, ventricular arrhythmias have been reported. In a large clinical trial to assess the efficacy of clofibrate in persons with hypercholesterolemia, an increase in drug-associated mortality was reported that offset the beneficial response to cholesterol lowering; therefore, the potential dangers of this drug must be kept in mind when prescribing it for patients with hypertriglyceridemia. Also, a lowering of triglyceride levels by clofibrate often is associated with an increase in LDL levels, a response that has caused many to question whether any net gain is achieved in overall lipoprotein metabolism.

There is limited clinical experience with a related drug, gemfibrozil, which has many of the actions of clofibrate. Again, reduction of triglyceride levels can result in a rise in LDL levels. The side effects of gemfibrozil resemble those of clofibrate, although effects on overall mortality in a large population have not been defined.

Flushing and pruritus are important early side effects of niacin administration, but a tolerance develops in most people. A variety of other skin changes have been noted. More severe side effects of niacin are hyperuricemia, hyperglycemia, and hepatic function abnormalities, but these are more frequent with higher doses. Gastrointestinal complaints are also common.


Drug therapy is of no benefit in familial lipoprotein lipase deficiency in children. When drugs are employed for Type V hyperlipoproteinemia, clofibrate or gemfibrozil generally is used first, followed by niacin if one of these is ineffective. Drug therapy is frequently ineffective if secondary causes of hypertriglyceridemia are not controlled.

Borderline Hypertriglyceridemia.

In familial combined hyperlipidemia, niacin would seem to be the preferred drug if there are no contraindications and if the drug can be tolerated. These patients are more likely to have an increased LDL concentration, and niacin is usually more effective in lowering LDL levels than clofibrate or gemfibrozil. Combination therapy is occasionally indicated; the combination of a bile-acid sequestering agent (cholestyramine resin or colestipol hydrochloride) with niacin probably would normalize both cholesterol and triglyceride levels in most patients. The bile-acid sequestering agents may substantially increase plasma levels of triglycerides when they are not used with a triglyceride-lowering agent.

In familial dysbetalipoproteinemia, the predominant experience has been with clofibrate, which is generally very effective. Limited experience with gemfibrozil and niacin suggests that they too are effective.

Secondary Hyperlipoproteinemia.

Lipid-lowering drugs have occasionally been used in patients with chronic renal disease or diabetes mellitus. Route of elimination, serum albumin concentrations, and likelihood of producing hyperglycemia or hyperuricemia are special considerations in choice of drug and dosage.  

What Should Be the Direction for Future Research?

Certain changes in concentrations, composition, or structure of plasma lipoproteins are reflected as increased plasma triglyceride concentrations and seem to be associated with increased risk for cardiovascular disease. There is need to intensify research in several areas to understand better the pathophysiological mechanisms responsible for increased atherogenesis in these conditions. Also among the areas of needed research are determination of the epidemiologic implications of elevated triglyceride concentrations, laboratory approaches to the evaluation of hypertriglyceridemic conditions in patients, the pathogenetic mechanisms by which triglyceride-rich lipoprotein particles may influence atherogenesis, and approaches to the treatment of metabolic disorders resulting in hypertriglyceridemia.

Epidemiologic Considerations

There are three major areas of needed epidemiologic research. The first concerns the need to investigate reasons for the relatively high plasma triglyceride concentrations and the age-related increases observed in the United States compared with some other countries. For example, it would seem important to determine the degree to which age-related increases in plasma triglyceride levels are a function of obesity. The second need is to evaluate the impact of commonly used drugs (such as antihypertensives) on plasma lipid and lipoprotein distribution in population studies. The third need is for improved study design for estimating risk for cardiovascular disease from elevated triglyceride levels, particularly in subjects characterized by repeated triglyceride measurements. Subgroups of particular interest are those with genetic abnormalities of lipoprotein metabolism. Such studies should clarify the specific risks and perhaps resolve the current conflict between epidemiologic and clinical observations.

Laboratory Evaluations

The extent to which hypertriglyceridemia is a risk factor for cardiovascular disease seems to depend, among other things, on other characteristics of the plasma lipoproteins. Particular attention should be given to the linkage between hypertriglyceridemia and subclasses of LDL and HDL and specific apoproteins (e.g., apoproteins AI and B). More research is needed to identify better which of these measurements best classifies the cardiovascular disease risk associated with hypertriglyceridemia. More methodological research is called for to simplify the measurements of lipoprotein subclasses and apoproteins and thus make them more readily available to the clinician.

Pathogenetic Mechanisms of Atherogenesis

The pathogenetic mechanisms by which triglyceride-rich lipoproteins may influence atherogenesis have received little research attention in the past and research efforts should be intensified in the future. A few of the important research directions include:

  • Does the process of VLDL degradation at the level of the artery wall generate products that contribute to atherogenesis (cholesterol, free fatty acids, lysophospholipids)?
  • What is the importance of abnormal lipoprotein levels in the pathogenesis of human atherosclerosis?
  • Do the heterogeneous properties of VLDL particles (reactivity with cell-surface receptors, apolipoprotein content, or distribution) determine their atherogenicity?
  • Using appropriate animal models, what interactions can be found among the characteristics of the triglyceride-rich lipoproteins, smoking, and the development of atherosclerosis in the coronary and peripheral arteries? Attempts to establish interactions between smoking and diet-induced hyperbetalipoproteinemia proved inconclusive when using experimental animals have been negative. Clinical evidence suggests that the association between smoking and increased concentrations of the triglyceride-rich lipoproteins may be stronger.
  • There is need to develop colonies of experimental animals with hypertriglyceridemia.

Therapeutic Approaches

Nutritional approaches to the treatment of hypertriglyceridemia have not been studied sufficiently. The promising initial finding of lowering effects for VLDL and LDL levels by fish-oil-containing diets needs additional research to understand better the mechanisms, the clinical potential, and the long-term safety of such diets.

New quantitative noninvasive and invasive techniques for measuring arterial flow and atherosclerotic lesion size (and luminal impingement) should be employed to determine more directly the effects of hygienic and pharmacologic interventions. Coronary artery bypass grafts offer a promising opportunity to examine the effect of the lowering of triglyceride levels on graft occlusion.

While there are several drugs available that affect triglyceride metabolism, there is a continuing need for drugs with greater potency, minimal or no adverse effects on LDL and HDL levels, and fewer side effects.  

Consensus Development Panel

Scott M. Grundy, M.D., Ph.D. (Panel Chairman)
Professor, Internal Medicine and Biochemistry
Director, Center for Human Nutrition
University of Texas Health Science Center
Dallas, Texas
Elizabeth Barrett-Connor, M.D., Dr. P.H.
Professor, Department of Community and Family Medicine
University of California, San Diego
La Jolla, California
Edwin L. Bierman, M.D.
Professor of Medicine
Head, Division of Metabolism, Endocrinology, and Nutrition
University of Washington
Seattle, Washington
Thomas B. Clarkson, D.V.M.
Professor of Comparative Medicine
Director, Arteriosclerosis Research Center
Bowman Gray School of Medicine
Winston-Salem, North Carolina
William R. Harlan, M.D.
Professor of Internal Medicine
University of Michigan School of Medicine
Ann Arbor, Michigan
William R. Hazzard, M.D.
Associate Director
Department of Medicine
Johns Hopkins Medical School
Johns Hopkins Hospital
Baltimore, Maryland
Donald B. Hunninghake, M.D.
Associate Professor of Pharmacology and Medicine
Co-Director Lipid Research Clinic
Department of Medicine
University of Minnesota
Dean T. Mason, M.D.
Director, Cardiac Center
Cedars Medical Center
Miami, Florida
Gregory O'Keefe, M.D.
Islands Community Medical Center
Vinal Haven, Maine
Harold Rifkin, M.D.
Clinical Professor of Medicine
Albert Einstein College of Medicine
New York, New York
Arthur A. Spector, M.D.
Professor of Biochemistry
Department of Biochemistry
University of Iowa
Iowa City, Iowa
Mary Winston, Ed.D.
Science Administrator, Medical Programs
American Heart Association
Dallas, Texas
Peter D. Wood, D.Sc., Ph.D.
Professor of Medicine (Research)
Deputy Director, Stanford Heart Disease Prevention Program
Palo Alto, California


David W. Bilheimer, M.D.
"Management of Type 3 Hyperlipidemia, Phenotypic Type 2b Hyperlipidemia, and Selected Forms of Secondary Hypertriglyceridemia"
Chief Division of Lipid Metabolism
University of Texas Health Science Center
Dallas, Texas
W. Virgil Brown, M.D.
"Classification of Hypertriglyceridemia"
Professor of Medicine
Mt. Sinai School of Medicine
New York, New York
John D. Brunzell, M.D.
"Management of Moderate Hypertriglyceridemia"
Professor of Medicine
Division of Metabolism and Nutrition
University of Washington
Seattle, Washington
William E. Connor, M.D.
"Diet and Exercise in the Treatment of Hypertriglylceridemia"
Section of Clinical Nutrition and Lipid Metabolism
Oregon Health Sciences University
Portland, Oregon
Michael H. Criqui, M.D., M.P.H.
"Environmental Correlates of Hypertriglyceridemia"
Associate Professor Division of Epidemiology
Department of Community and Family Medicine
University of California, San Diego
La Jolla, California
Howard A. Eder, M.D., M.P.H.
"Management of Hypertriglyceridemia in Treated Diabetes and in Patients with Chronic Renal Failure"
Professor of Medicine
Albert Einstein College of Medicine
Bronx, New York
Leonard H. Epstein, Ph.D.
"Effects of Weight Reduction on Triglycerides in Obese Children"
Associate Professor of Psychiatry, Epidemiology and Psychology
University of Pittsburgh School of Medicine
Pittsburgh, Pennsylvania
Charles J. Glueck, M.D.
"Hypertriglyceridemia and Cardiovascular Disease: Clinical Evidence"
Professor of Medicine and Pediatrics
University of Cincinnati College of Medicine
University Hospital
Cincinnati, Ohio
DeWitt S. Goodman, M.D.
"Current Practice Presentation"
Professor of Medicine
Columbia University College of Physicians and Surgeons
New York, New York
Richard J. Havel, M.D.
"Management of Hypertriglyceridemia: Type 4, Mild Type 5"
Director Cardiovascular Research Institute
Professor of Medicine
University of California, San Francisco School of Medicine
San Francisco, California
Gerardo Heiss, M.D., Ph.D.
"Serum/Plasma Triglyceride and Ischemic Heart Disease: A Review of the Epidemiologic Evidence"
Research Associate Professor, Epidemiology
Department of Epidemiology
University of North Carolina
Chapel Hill, North Carolina
Stephen B. Hulley, M.D., M.P.H.
"Implications of Epidemiological Studies for the Clinical Management of Hypertriglyceridemia"
Professor of Epidemiology
University of California, San Francisco
San Francisco, California
Ronald M. Krauss, M.D.
"Hypertriglyceridemia and Atherogenic Particles"
Staff Medical Scientist
Lawrence Berkeley Laboratory
Donner Laboratory University of California, Berkeley
Berkeley, California
Peter O. Kwiterovich, Jr., M.D.
"Distribution of Triglyceride Levels in Populations and Clinical Implications"
Associate Professor of Pediatrics and Medicine
Johns Hopkins University
Baltimore, Maryland
Lewis H. Kuller, M.D., Dr. P.H.
"Relationship of Hypertriglyceridemia to Drugs"
Professor and Chairman Department of Epidemiology
Graduate School of Public Health
University of Pittsburgh
Pittsburgh, Pennsylvania
Robert S. Lees, M.D.
"Triglyceride-Lowering Drugs-II"
Director of Medical Research New England Deaconess Hospital
Professor of Cardiovascular Disease
Department of Nutrition and Food Sciences
Massachusetts Institute of Technology
Boston, Massachusetts
Robert I. Levy, M.D.
"Potential Risks and Limitations of Long-Term Drug Therapy"
Vice President for Health Sciences
Professor of Medicine Columbia University
College of Physicians and Surgeons
New York, New York
Paul J. Nestel, M.D.
"Triglyceride-Lowering Drugs-I"
Head Cardiovascular Metabolism and Nutrition
Research Unit
Baker Medical Research Institute
Commercial Road
Prahran, Melbourne AUSTRALIA
Esko A. Nikkila, M.D.
"Clinical Significance and Treatment of Hyperchylomicronemia"
Professor of Medicine Third Department of Medicine
University of Helsinki
Helsinki FINLAND
Basil M. Rifkind, M.D., F.R.C.P.
"Intervention Trials in Hypertriglyceridemia: Needs and Problems"
Chief, Lipid Metabolism-Atherogenesis Branch
Division of Heart and Vascular Diseases
National Heart, Lung, and Blood Institute
National Institutes of Health
Bethesda, Maryland
Daniel Steinberg, M.D., Ph.D.
"Hypertriglyceridemia and Atherogenic Particles"
Professor of Medicine University of California,
San Diego School of Medicine
La Jolla, California
Gloria Troendle, M.D.
"Lipid Altering Drugs: The FDA Perspective"
Medical Officer Food and Drug Administration
Rockville, Maryland

Planning Committee

Basil M. Rifkind, M.D, F.R.C.P. (Chairman)
Chief, Lipid Metabolism-Atherogenesis Branch
Division of Heart and Vascular Diseases
National Heart, Lung, and Blood Institute
National Institutes of Health
Bethesda, Maryland
H. Bryan Brewer, Jr., M.D.
Chief, Molecular Disease Branch
National Heart, Lung, and Blood Institute
National Institutes of Health
Bethesda, Maryland
John D. Brunzell, M.D.
Professor of Medicine
Division of Metabolism, Endocrinology, and Nutrition
University of Washington
Seattle, Washington
Scott M. Grundy, M.D., Ph.D.
Professor, Internal Medicine and Biochemistry
Director, Center for Human Nutrition
University of Texas Health Science Center
Dallas, Texas
Lewis H. Kuller, M.D., Dr. P.H.
Professor and Chairperson
Department of Epidemiology
Graduate School of Public Health
University of Pittsburgh
Pittsburgh, Pennsylvania
Fitzhugh Mullan, M.D.
Chief Medical Officer
Office of Medical Applications of Research
National Institutes of Health
Bethesda, Maryland
Gary Nelson, Ph.D.
Health Scientist Administrator
Lipid Metabolism-Atherogenesis Branch
Division of Heart and Vascular Diseases
National Heart, Lung, and Blood Institute
National Institutes of Health
Bethesda, Maryland
Pesach Segal, M.D.
Lipid Metabolism-Atherogenesis Branch
Division of Heart and Vascular Diseases
National Heart, Lung, and Blood Institute
National Institutes of Health
Bethesda, Maryland

Conference Sponsors

National Heart, Lung, and Blood Institute
Claude Lenfant, M.D.
Office of Medical Applications of Research
J. Richard Crout, M.D.

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