Introduction to Fibrates

Fibrates are a form of ‘cholesterol lowering drug’ – that is, medications that are useful in lowering cholesterol and other lipids in the blood. Fibrates also increase the level of HDL or good cholesterol in the blood. They are often prescribed to people who are at high risk of cardiovascular problems such as atherosclerosis (hardening of arteries), heart attack and stroke. Though fibrates have been used for a number of years, there are still some doubts about whether they are more effective at reducing cardiovascular risk than other cholesterol-lowering drugs such as statins, and whether certain types of patients may be more suited to taking fibrates than others. A number of clinical trials have recently been conducted to try to answer these questions, and their findings are summarised below.

What are fibrates?

Fibrates are types of fat or lipid lowering medication. Lipids in the blood are mainly made up of cholesterol and triglycerides, and elevated levels of these have been associated with cardiovascular problems such as atherosclerosis (hardening of the arteries), heart attack and stroke. Fibrates are derivatives of fibric acid which are particularly suited to reducing triglyceride levels in the blood. Fibrates also have the effect of increasing HDL cholesterol (‘good cholesterol’). Common examples of fibrates include gemfibrozil, fenofibrate and clofibrate. See our page on fibrates for more information about how fibrates work, the different types of cholesterol, and why a fibrate might be prescribed.

Why are lipid-lowering drugs such as fibrates used?

Evidence from research studies has shown that a person’s risk of cardiovascular disease can be reduced by:

  • lowering LDL cholesterol levels in the blood; and
  • raising HDL cholesterol levels in the blood.

We also know that an increase in triglyceride levels is associated with increased risk of coronary heart disease, but it has not yet been shown that simply decreasing triglyceride levels can reduce a person’s risk. Because of this evidence, doctors may prescribe a lipid-lowering drug such as a fibrate to try to help change a patient’s blood lipid levels, and thus reduce their risk of cardiovascular disease. The treatment may be given before a patient develops clinical disease (known as ‘primary prevention’), or after they have already developed problems, such as following a heart attack (‘secondary prevention’) Drugs used for primary and secondary prevention of cardiovascular disease are given for many years, and so they have to fulfil a number of criteria to make their use worthwhile: they need to make you live longer or feel better, and they must be good enough at what they are designed to do to outweigh any possible negative effects of a taking medication for many years. It is therefore important that clinical trials are done to look at how effective they are, and that we look at the evidence these trials present carefully.

What is the evidence regarding the use of fibrates?

A number of trials have recently been undertaken worldwide to determine the effectiveness of fibrates in the prevention of cardiovascular disease. These include the Helsinki Heart Study, the Veterans Affairs High Density Lipoprotein Cholesterol Intervention Trial (VA-HIT), the Bezafibrate Infarct Prevention (BIP) trial, and the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) trial which focused on patients with diabetes and dyslipidaemia. Early results have indicated a general trend that fibrates can reduce cardiovascular events. Importantly, though, there has been no evidence that fibrates reduce mortality when compared to other lipid lowering drugs such as statins. Some studies have also suggested that fibrates may have some significant non-cardiac side effects that other drugs do not share. Some positive results have come out of the trials. Early evidence has suggested that fibrates may be particularly useful for patients with diabetes, due to their triglyceride-lowering effects. Fibrates may also be appropriate for use in patients at risk of acute pancreatitis due to high triglyceride levels.

What does this mean?

The evidence so far has shown us that although fibrates may be effective ‘on paper’ at lowering triglyceride levels, there are some factors that mean it is not an ideal first choice for medication in patients with risk factors for cardiovascular disease. This is mostly because there are other drugs that seem to be more effective at preventing cardiovascular effects, but also due to the associated side-effects of fibrates. In some cases however, a physician may choose to still use these medications either in conjunction with other medications or by themselves, according to the individual patient characteristics. You should discuss these issues fully with your doctor should you have any concerns. (Adapted from an article kindly contributed by Dr Jocelyne Benatar MBChB, Cardiovascular Research Unit, Greenlane Clinical Centre, Auckland, New Zealand.)


  1. Bruckert , Impact of lipid treatment on cardiovascular risk reduction: new therapeutic targets, Eur Heart J Suppl.2005; 7: 16-20.
  2. SM, Vega GL. Fibric acids: effects on lipids and lipoprotein metabolism. Grundy Am J Med. 1987 Nov 27;83(5B):9-20
  3. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high risk individuals: a randomised placebo-controlled trial. Lancet 2002; 360: 7-22M
  4. The Scandinavian Simvastatin Survival Study Group, Randomised Trial of Cholesterol Lowering in 4444 Patients with Coronary Heart Disease: the Scandinavian Simvastatin Survival Study (4S), Lancet 1994; 344: 1383-89
  5. The long-term intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group, Prevention of Cardiovascular Events and Death with Pravastatin in Patients with Coronary Heart Disease and a Broad Range of Initial Cholesterol Levels, N Engl J Med, Vo339:1349-1357
  6. Shepherd J., Cobbe S. M., Ford I., Isles C. G., Lorimer A. R., Macfarlane P. W., McKillop J. H., Packard C. J., The West of Scotland Coronary Prevention Study Group, Prevention of Coronary Heart Disease with Pravastatin in Men with Hypercholesterolemia. N Engl J Med, Vol333:1301-1308
  7. Sever PS, Poulter NR, Dahlof B, et al. Reduction in cardiovascular events with atorvastatin in 2,532 patients with type 2 diabetes: Anglo-Scandinavian Cardiac Outcomes Trial-lipid-lowering arm (ASCOT-LLA). Diabetes Care 2005; 28: 1151-1157.
  8. Colhoun HM, Betteridge DJ, Durrington PNfor the CARDS Group. Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): multicentre randomised placebo-controlled trial. Lancet 2004; 364: 685-696.
  9. ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial. Major outcomes in moderately hypercholesterolemic, hypertensive patients randomized to pravastatin vs usual care: the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT-LLT). JAMA 2002; 288: 2998-3007.
  10. Baigent C, Keech A, Kearney PMfor the Cholesterol Treatment Trialists’ (CTT) Collaborators. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90056 participants in 14 randomised trials of statins. Lancet 2005; 366: 1267-1278.
  11. De Backer G, Ambrosioni E, Borch-Johnsen K, et al. Executive summary. European guidelines on cardiovascular disease prevention in clinical practice: third joint task force of European and other societies on cardiovascular disease prevention in clinical practice (constituted by representatives of eight societies and by invited experts). Atherosclerosis 2004; 173: 381-391.
  12. Grundy SM, Cleeman JI, Merz CNCoordinating Committee of the National Cholesterol Education Program. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines. J Am Coll Cardiol 2004; 44: 720-732.
  13. American Diabetes Association. Standards of medical care. Diabetes Care 2005; 28: S4-S36.
  14. The FIELD study investigators, Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial, The Lancet 2005; 366:1849-1861
  15. Frick MH, Heinonen OP, Huttunen JK, Koskinen P, Manttari M, Manninen V. Efficacy of gemfibrozil in dyslipidaemic subjects with suspected heart disease: an ancillary study in the Helsinki Heart Study frame population. Ann Med 1993; 25: 41-45.
  16. Rubins HB, Robins SJ, Collins D. Diabetes, plasma insulin, and cardiovascular disease: subgroup analysis from the Department of Veterans Affairs high-density lipoprotein intervention trial (VA-HIT). Arch Intern Med 2002; 162: 2597-2604.
  17. Tenenbaum, A; Motro, M; Fisman E.Z., Tanne,D; Boyko, V; Behar S, Bezafibrate for the Secondary Prevention of Myocardial Infarction in Patients With Metabolic Syndrome, Arch Intern Med. 2005;165:1154-1160.
  18. Marco Studer et al, Effect of different antilipidemic agents and diets on mortality – A systematic review. Archives of Internal Medicine; Apr 11, 2005; 165(7): 725-730.
  19. Joseph Hung, for the Medical Issues Committee of the National Heart Foundation of Australia, Aspirin for cardiovascular disease prevention, MJA 2003; 179 (3): 147-152
  20. American Diabetes Association. Aspirin therapy in diabetes. Diabetes Care 2004; 27 (Suppl 1): S72-S73.
  21. Antiplatelet Trialists’ Collaboration. Collaborative overview of randomised trials of antiplatelet therapy – 1: Prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. BMJ 1994; 308: 81-106.
  22. Antithrombotic Trialists’ Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction and stroke in high risk patients. BMJ 2002; 324: 71-86.
  23. Hansson L, Zanchetti A, Carruthers S, et al. Effects of intensive blood-pressure lowering and low-dose aspirin in patients with hypertension: principal results of the Hypertension Optimal Treatment (HOT) randomised trial. Lancet 1998; 351: 1755-1762
  24. The Heart Outcomes Prevention Evaluation (HOPE) study investigators, Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients, N Engl J Med. 2000; 342:145-53.
  25. Lindon M.H. Wing, M.B., B.S., Christopher M. Reid, Ph.D., Philip Ryan, M.B., B.S., Lawrence J. Beilin, M.D., Mark A. Brown, M.B., B.S., M.D., Garry L.R. Jennings, M.D., Colin I. Johnston, M.B., B.S., John J. McNeil, M.B., B.S., Graham J. Macdonald, M.D., John E. Marley, M.D., M.B., Ch.B., Trefor O. Morgan, M.B., B.S., Malcolm J. West, M.B., B.S., for the Second Australian National Blood Pressure Study Group, Comparison of Outcomes with Angiotensin-Converting–Enzyme Inhibitors and Diuretics for Hypertension in the Elderly, N Engl J Med. 2003; 348:583-592
  26. PROGRESS Collaborative Group. Randomised trial of a perindopril-based blood-pressure-lowering regimen among 6105 individuals with previous stroke or transient ischaemic attack. Lancet 2001; 358: 1033-1041.
  27. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines, ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction , J Am Coll Cardiol 2004;44:671-719.
  28. The EURopean trial On reduction of cardiac events with Perindopril in stable coronary Artery disease Investigators. Efficacy of perindopril in reduction of cardiovascular events among patients with stable coronary artery disease: randomised, double-blind, placebo-controlled, multicentre trial (the EUROPA study). Lancet 2003; 362: 782-788.
  29. PROGRESS Collaborative Group. Effects of a perindopril-based blood pressure lowering regimen on cardiac outcomes among patients with cerebrovascular disease. Eur Heart J 2003; 24: 475-484..
  30. Acute Infarction Ramipril Efficacy (AIRE) Investigators. Effect of ramipril on mortality and morbidity of survivors of acute myocardial infarction with clinical evidence of heart failure. Lancet 1993; 342: 821-828.
  31. Wing L, Reid C, Ryan P, et al. A comparison of outcomes with angiotensin-converting-enzyme inhibitors and diuretics for hypertension in the elderly. N Engl J Med 2003; 348: 583-592.
  32. Lindholm L, Ibsen H, Dahlof B, et al. Cardiovascular morbidity and mortality in patients with diabetes in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol. Lancet 2002; 359: 1004-1010.
  33. Sever P, Dahlof B, Poulter N, et al. Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial–Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial. Lancet 2003; 361: 1149-1158
  34. Flack J, Neaton J, Grimm R Jr, et al. Blood pressure and mortality among men with prior myocardial infarction. Multiple Risk Factor Intervention Trial Research Group. Circulation 1995; 92: 2437-2445.
  35. Lenfant C, Chobanian A, Jones D, et al. Seventh report of the Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7): resetting the hypertension sails. Hypertension 2003; 41: 1178-1179.
  36. National Heart Foundation. Hypertension management guide for doctors 2004. Canberra: NHF, 2003. Available at:
  37. Brewer HB Jr. Increasing HDL cholesterol levels. N Engl J Med. 2004;350:1491-1494
  38. ACCORD. ACCORD purpose: protocol abstract, November 14, 2002 (accessed Dec 5, 2006).
  39. Athyros, Vassilios G. M.D.; Giouleme, Olga I. M.D.; Nikolaidis, Nikolaos L. M.D.; Vasiliadis, Themistoklis V. M.D.; Bouloukos, Vassilios I. M.D.; Kontopoulos, Athanasios G. M.D.; Eugenidis, Nikolaos. Long-term Follow-up of Patients With Acute Hypertriglyceridemia-Induced Pancreatitis. Journal of Clinical Gastroenterology. 34(4):472-475, April 2002.
  40. Stampfer MJ, Krauss RM, Ma J, Blanche PJ, Holl LG, Sacks F, et al. A prospective study of triglyceride level, low-density lipoprotein particle diameter and risk of myocardial infarction. JAMA 1996; 276: 882-888.
  41. Hokanson JE, Austin MA. Plasma triglyceride level is a risk factor for cardiovascular disease independent of high-density lipoprotein cholesterol level: a meta-analysis of population-based prospective studies. J Cardiovasc Risk 1996; 3: 213-219

(Adapted from an article kindly contributed by Dr Jocelyne Benatar MBChB, Cardiovascular Research Unit, Greenlane Clinical Centre, Auckland, New Zealand.)

All content and media on the HealthEngine Blog is created and published online for informational purposes only. It is not intended to be a substitute for professional medical advice and should not be relied on as health or personal advice. Always seek the guidance of your doctor or other qualified health professional with any questions you may have regarding your health or a medical condition. Never disregard the advice of a medical professional, or delay in seeking it because of something you have read on this Website. If you think you may have a medical emergency, call your doctor, go to the nearest hospital emergency department, or call the emergency services immediately.