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LE Magazine March 2007
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Uncovering a Hidden Source of Cardiovascular Disease Risk


By William Davis, MD

Strategies for Reducing Postprandial Lipoproteins

Saturated fats, like those found in butter, shortening, and fried foods, are especially potent inducers of excess postprandial lipoproteins. Because postprandial disorders cause fats to linger longer, avoiding unhealthy fats is doubly important. Minimizing these fats is advisable for other reasons, such as reducing LDL, blood pressure, inflammation, and cancer risk. While avoiding saturated fats will not eliminate postprandial lipoproteins, it will help reduce them.29 A polyunsaturated omega-6 fatty acid—linoleic acid derived from safflower oil—also raises postprandial lipoprotein levels, just as saturated fats do.3

Although the immediate cause of persistent and increased postprandial lipoproteins is an unhealthy fat-containing meal, two varieties of fat reduce postprandial lipoproteins:

• Monounsaturated oils, like olive oil, modestly reduce postprandial lipoproteins. Monounsaturated oils may thus be a preferable form of oil for cooking and everyday use.3,30

• Polyunsaturated omega-3 fatty acids reduce postprandial lipoproteins dramatically. It is not uncommon to see omega-3 supplementation eliminate abnormal postprandial patterns entirely. Sources of omega-3 fatty acids include fish oil, flaxseed oil, and walnuts.

If undesirable saturated fats lead to increased postprandial lipoprotein particles, does a low-fat diet reduce postprandial lipoproteins? Paradoxically, it does not. All too often, low-fat diets can evolve into diets rich in processed carbohydrates, which cause postprandial lipoprotein particles to multiply out of control.31 Diets that are rich in monounsaturated fats, omega-3 fats, fiber, and lean proteins, and low in saturated fats and processed carbohydrates, are effective tools in reducing postprandial lipoproteins.32

The following strategies can reduce triglycerides dramatically, and help reduce or eliminate IDL and postprandial lipoproteins:

• Weight loss can greatly reduce triglycerides and postprandial lipoproteins, particularly with a diet that is low in carbohydrates and high in protein and monounsaturated fats. Cutting out processed carbohydrates (such as breads, crackers, breakfast cereals, bagels, and pretzels) alone can yield a 30% reduction in postprandial lipoproteins.33,34 Increasing your intake of yogurt, cottage cheese, and other low-fat dairy products, raw almonds and walnuts, and fish, chicken, turkey, and other sources of lean protein will also yield substantial reductions in postprandial lipoprotein particles. Weight loss restores the insulin responsiveness lost in metabolic syndrome, which also reduces postprandial lipoproteins.31

Illustration of the structure of a low-density lipoprotein (LDL) particle, a form of cholesterol found in the blood.

• Omega-3 fatty acids in fish oil exert powerful effects in reducing postprandial lipoproteins. Ingesting just 1200 mg of EPA/ DHA from fish oil can easily lower IDL by 50%, and higher doses can produce even greater reductions. When fasting triglycerides are higher than 200 mg/dL, or when IDL is increased, higher doses of fish oil may be indicated to fight excess postprandial lipoproteins. Omega-3 fatty acids decrease liver production of VLDL by 30% or more, and lower IDL by 70% or more.35,36 Omega-3s also activate the enzyme known as lipoprotein lipase, which accelerates clearance of postprandial lipoproteins from the blood.37 Fish oil can safely augment the cholesterol-lowering effects of statin drugs such as Lipitor®, yielding dramatic improvement in triglycerides, VLDL, and postprandial lipoproteins.38

• Soy protein (20 grams per day) from tofu, soy milk, soy protein powder, and other sources can lower LDL by 10-20 mg/dL and reduce postprandial lipoproteins by 10%.39

• Green tea contains catechins (flavonoids) that can decrease postprandial lipoproteins by up to 30%. Approximately 600-700 mg of green tea catechins are required to achieve this effect, the equivalent of 6-12 servings of brewed tea. Nutritional supplements also provide green tea catechins at this dose.40 Green tea’s effectiveness in accelerating weight loss may augment its ability to reduce postprandial lipoproteins.

• White bean extract blocks the sugar-digesting enzyme known as alpha-amylase, thereby reducing the absorption of sugars. A recent study showed that participants who took 1500 mg of white bean extract twice a day for eight weeks lost an average of four pounds and lowered their triglycerides by an average of 26 mg/dL.41

• Vigorous exercise can reduce postprandial lipoproteins by 30%.42

• Diabetes treatment (with insulin or oral hypoglycemic drugs, for example) significantly reduces postprandial lipoprotein levels.43,44 The thiazolidinedione drug Actos® may be especially effective for its postprandial lipid-suppressing effects; a similar agent, Avandia®, may be modestly effective.45,46 The agent metformin also reduces fasting and postprandial triglycerides by 25%.47 (Caution: Like other thiazolidinediones, Actos® and Avandia® can cause fluid retention, which may lead to or exacerbate heart failure. Actos® and Avandia® should be discontinued if any deterioration in cardiac status occurs.)

• Statin drugs such as Zocor®, Crestor®, and Lipitor® not only lower cholesterol, but can reduce postprandial lipoproteins by 30-80%.48

• Fibrates (cholesterol-lowering drugs such as Lopid® and Lofibra®) can reduce postprandial lipoproteins by 70%. They can be a useful second-line strategy if fish oil, weight loss, and nutritional efforts fail to do the job.49

Clearly, choosing the right foods and fish oil supplements should be your first choice in controlling a postprandial disorder. Fish oil is safe, inexpensive, and easy to take, yet it provides an extraordinary array of benefits, including reduced risk of sudden cardiac death, stroke, and depression.50 Weight loss, exercise, soy protein, and green tea can all increase your likelihood of success. Because of their possible side effects, prescription drugs should always be your last choice for correcting postprandial patterns and other disorders.

Why Fasting Is Necessary for Blood Work

When you have blood drawn to measure cholesterol and other markers, you are instructed to fast for 8-12 hours beforehand. If postprandial disorders (such as IDL or an exaggerated increase in triglycerides) become apparent only after eating, why not have blood drawn after a meal?

Doctors instruct their patients to fast for cholesterol tests because triglycerides rise after a meal, and triglycerides are used to calculate LDL. Because LDL is usually the sole focus of the conventional approach to heart disease prevention, the fact that triglycerides are elevated, postprandial or fasting, is simply ignored. Thus, over the years, doctors have failed to recognize elevated triglycerides in the after-meal period as a powerful, independent indicator of risk.

In the future, there will be growing recognition of our over-reliance on LDL as the only important value for gauging the risk of atherosclerotic disease, and measures of postprandial triglycerides and other postprandial lipoproteins will gain increased recognition. Rather than fasting for your blood work, it may be obtained in the first few hours after a meal. Right now, however, there are insufficient data to justify this practice on a broad scale, though we occasionally do such testing on certain patients in our clinical practice.

Improvements over conventionally calculated LDL that requires fasting will also allow blood to be drawn in a non-fasting state. Measures that are superior to calculated LDL—such as directly measured LDL, VLDL, and LDL particle number and size (all available through VAP™ lipoprotein testing)—can eliminate the need for fasting while providing more clinically useful information.

As experience grows, standard meals (that is, specific preparations of known fat, protein, carbohydrate, nutrient, and fiber composition) will be used to develop standards to better diagnose postprandial disorders. This way, people and populations can be compared based on their response to a standardized meal. Because the meals you choose yourself can vary tremendously in composition, postprandial blood obtained for analysis can likewise vary, whether or not you have a postprandial disorder.

Until then, we are left with reasonably good insight into postprandial patterns provided by fasting triglycerides, VLDL, and IDL levels. Mindful attention to these critical blood markers can greatly enhance and preserve your vascular health.

Dr. William Davis is an author and cardiologist practicing in Milwaukee, Wisconsin. He is author of the book, Track Your Plaque: The only heart disease prevention program that shows you how to use the new heart scans to detect, track, and control coronary plaque. He can be contacted through www.trackyourplaque.com.

References

1. Twickler TB, linga-Thie GM, Cohn JS, Chapman MJ. Elevated remnant-like particle cholesterol concentration: a characteristic feature of the atherogenic lipoprotein phenotype. Circulation. 2004 Apr 27;109(16):1918-25.

2. Ceriello A, Taboga C, Tonutti L, et al. Evidence for an independent and cumulative effect of postprandial hypertriglyceridemia and hyperglycemia on endothelial dysfunction and oxidative stress generation: effects of short- and long-term simvastatin treatment. Circulation. 2002 Sep 3;106(10):1211-8.

3. Jagla A, Schrezenmeir J. Postprandial triglycerides and endothelial function. Exp Clin Endocrinol Diabetes. 2001;109(4):S533-47.

4. Maggi FM, Raselli S, Grigore L, et al. Lipoprotein remnants and endothelial dysfunction in the postprandial phase. J Clin Endocrinol Metab. 2004 Jun;89(6):2946-50.

5. Ceriello A, Quagliaro L, Piconi L, et al. Effect of postprandial hypertriglyceridemia and hyperglycemia on circulating adhesion molecules and oxidative stress generation and the possible role of simvastatin treatment. Diabetes. 2004 Mar;53(3):701-10.

6. Silveira A. Postprandial triglycerides and blood coagulation. Exp Clin Endocrinol Diabetes. 2001;109(4):S527-32.

7. Ebenbichler CF, Kirchmair R, Egger C, Patsch JR. Postprandial state and atherosclerosis. Curr Opin Lipidol. 1995 Oct;6(5):286-90.

8. Teno S, Uto Y, Nagashima H, et al. Association of postprandial hypertriglyceridemia and carotid intima-media thickness in patients with type 2 diabetes. Diabetes Care. 2000 Sep;23(9):1401-6.

9. Mori Y, Itoh Y, Komiya H, Tajima N. Association between postprandial remnant-like particle triglyceride (RLP-TG) levels and carotid intima-media thickness (IMT) in Japanese patients with type 2 diabetes: assessment by meal tolerance tests (MTT). Endocrine. 2005 Nov;28(2):157-63.

10. Hyson D, Rutledge JC, Berglund L. Postprandial lipemia and cardiovascular disease. Curr Atheroscler Rep. 2003 Nov;5(6):437-44.

11. Karpe F, Steiner G, Uffelman K, Olivecrona T, Hamsten A. Postprandial lipoproteins and progression of coronary atherosclerosis. Atherosclerosis. 1994 Mar;106(1):83-97.

12. Grundy SM, Cleeman JI, Merz CN, et al. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines. J Am Coll Cardiol. 2004 Aug 4;44(3):720-32.

13. Miller M, Zhan M, Georgopoulos A. Effect of desirable fasting triglycerides on the postprandial response to dietary fat. J Investig Med. 2003 Feb;51(1):50-5.

14. Johanson EH, Jansson PA, Gustafson B, et al. Early alterations in the postprandial VLDL1 apoB-100 and apoB-48 metabolism in men with strong heredity for type 2 diabetes. J Intern Med. 2004 Feb;255(2):273-9.

15. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. JAMA. 2002 Jan 16;287(3):356-9.

16. Kolovou GD, Anagnostopoulou KK, Pavlidis AN, et al. Postprandial lipemia in men with metabolic syndrome, hypertensives and healthy subjects. Lipids Health Dis. 2005;421.

17. van Oostrom AJ, Castro CM, Ribalta J, et al. Diurnal triglyceride profiles in healthy normolipidemic male subjects are associated to insulin sensitivity, body composition and diet. Eur J Clin Invest. 2000 Nov;30(11):964-71.

18. Tenenbaum A, Fisman EZ, Motro M, Adler Y. Atherogenic dyslipidemia in metabolic syndrome and type 2 diabetes: therapeutic options beyond statins. Cardiovasc Diabetol. 2006;5:20.

19. Duez H, Lamarche B, Uffelman KD,, et al. Hyperinsulinemia is associated with increased production rate of intestinal apolipoprotein B-48-containing lipoproteins in humans. Arterioscler Thromb Vasc Biol. 2006 Jun;26(6):1357-63.

20. Annuzzi G, De NC, Iovine C, et al. Insulin resistance is independently associated with postprandial alterations of triglyceride-rich lipoproteins in type 2 diabetes mellitus. Arterioscler Thromb Vasc Biol. 2004 Dec;24(12):2397-402.

21. Tsunoda F, Koba S, Hirano T, et al. Association between small dense low-density lipoprotein and postprandial accumulation of triglyceride-rich remnant-like particles in normotriglyceridemic patients with myocardial infarction. Circ J. 2004 Dec;68(12):1165-72.

22. Karpe F, Hamsten A. Postprandial lipoprotein metabolism and atherosclerosis. Curr Opin Lipidol. 1995 Jun;6(3):123-9.

23. Pedrini MT, Niederwanger A, Kranebitter M, et al. Postprandial lipaemia induces an acute decrease of insulin sensitivity in healthy men independently of plasma NEFA levels. Diabetologia. 2006 Jul;49(7):1612-8.

24. Krauss RM. Atherogenicity of triglyceride-rich lipoproteins. Am J Cardiol. 1998 Feb 26;81(4A):13B-7B.

25. Sutherland WH, Restieaux NJ, Nye ER, et al. IDL composition and angiographically determined progression of atherosclerotic lesions during simvastatin therapy. Arterioscler Thromb Vasc Biol. 1998 Apr;18(4):577-83.

26. Lyons TJ, Jenkins AJ, Zheng D, et al. Nuclear magnetic resonance-determined lipoprotein subclass profile in the DCCT/EDIC cohort: associations with carotid intima-media thickness. Diabet Med. 2006 Sep;23(9):955-66.

27. Batista MC, Welty FK, Diffenderfer MR, et al. Apolipoprotein A-I, B-100, and B-48 metabolism in subjects with chronic kidney disease, obesity, and the metabolic syndrome. Metabolism. 2004 Oct;53(10):1255-61.

28. Schrezenmeir J, Keppler I, Fenselau S, et al. The phenomenon of a high triglyceride response to an oral lipid load in healthy subjects and its link to the metabolic syndrome. Ann NY Acad Sci. 1993 Jun 14;683:302-14.

29. Bergeron N, Havel RJ. Influence of diets rich in saturated and omega-6 polyunsaturated fatty acids on the postprandial responses of apolipoproteins B-48, B-100, E, and lipids in triglyceride-rich lipoproteins. Arterioscler Thromb Vasc Biol. 1995 Dec;15(12):2111-21.

30. Thomsen C, Storm H, Holst JJ, Hermansen K. Differential effects of saturated and monounsaturated fats on postprandial lipemia and glucagon-like peptide 1 responses in patients with type 2 diabetes. Am J Clin Nutr. 2003 Mar;77(3):605-11.

31. Sharman MJ, Gomez AL, Kraemer WJ, Volek JS. Very low-carbohydrate and low-fat diets affect fasting lipids and postprandial lipemia differently in overweight men. J Nutr. 2004 Apr;134(4):880-5.

32. Volek JS, Gomez AL, Kraemer WJ. Fasting lipoprotein and postprandial triacylglycerol responses to a low-carbohydrate diet supplemented with n-3 fatty acids. J Am Coll Nutr. 2000 Jun;19(3):383-91.

33. Sharman MJ, Kraemer WJ, Love DM, et al. A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men. J Nutr. 2002 Jul;132(7):1879-85.

34. Volek JS, Sharman MJ, Forsythe CE. Modification of lipoproteins by very low-carbohydrate diets. J Nutr. 2005 Jun;135(6):1339-42.

35. Chan DC, Watts GF, Mori TA, et al. Randomized controlled trial of the effect of n-3 fatty acid supplementation on the metabolism of apolipoprotein B-100 and chylomicron remnants in men with visceral obesity. Am J Clin Nutr. 2003 Feb;77(2):300-7.

36. Westphal S, Orth M, Ambrosch A, Osmundsen K, Luley C. Postprandial chylomicrons and VLDLs in severe hypertriacylglycerolemia are lowered more effectively than are chylomicron remnants after treatment with n-3 fatty acids. Am J Clin Nutr. 2000 Apr;71(4):914-20.

37. Park Y, Harris WS. Omega-3 fatty acid supplementation accelerates chylomicron triglyceride clearance. J Lipid Res. 2003 Mar;44(3):455-63.

38. Nordoy A, Hansen JB, Brox J, Svensson B. Effects of atorvastatin and omega-3 fatty acids on LDL subfractions and postprandial hyperlipemia in patients with combined hyperlipemia. Nutr Metab Cardiovasc Dis. 2001 Feb;11(1):7-16.

39. Westphal S, Taneva E, Kastner S, et al. Endothelial dysfunction induced by postprandial lipemia is neutralized by addition of proteins to the fatty meal. Atherosclerosis. 2006 Apr;185(2):313-9.

40. Unno T, Tago M, Suzuki Y, et al. Effect of tea catechins on postprandial plasma lipid responses in human subjects. Br J Nutr. 2005 Apr;93(4):543-7.

41. Udani J, Hardy M, Madsen DC. Blocking carbohydrate absorption and weight loss: a clinical trial using Phase 2 brand proprietary fractionated white bean extract. Altern Med Rev. 2004 Mar;9(1):63-9.

42. Katsanos CS. Prescribing aerobic exercise for the regulation of postprandial lipid metabolism: current research and recommendations. Sports Med. 2006;36(7):547-60.

43. van Wijk JP, de Koning EJ, Castro Cabezas M, Rabelink TJ. Rosiglitazone improves postprandial triglyceride and free fatty acid metabolism in type 2 diabetes. Diabetes Care. 2005 Apr;28(4):844-9.

44. Caixas A, Perez A, Payes A, et al. Effects of a short-acting insulin analog (Insulin Lispro) versus regular insulin on lipid metabolism in insulin-dependent diabetes mellitus. Metabolism. 1998 Apr;47(4):371-6.

45. Al Majali K, Cooper MB, Staels B, Luc G, Taskinen MR, Betteridge DJ. The effect of sensitisation to insulin with pioglitazone on fasting and postprandial lipid metabolism, lipoprotein modification by lipases, and lipid transfer activities in type 2 diabetic patients. Diabetologia. 2006 Mar;49(3):527-37.

46. Tan GD, Fielding BA, Currie JM, et al. The effects of rosiglitazone on fatty acid and triglyceride metabolism in type 2 diabetes. Diabetologia. 2005 Jan;48(1):83-95.

47. Emral R, Koseoglulari O, Tonyukuk V, Uysal AR, Kamel N, Corapcioglu D. The effect of short-term glycemic regulation with gliclazide and metformin on postprandial lipemia. Exp Clin Endocrinol Diabetes. 2005 Feb;113(2):80-4.

48. Schaefer EJ, McNamara JR, Tayler T, et al. Comparisons of effects of statins (atorvastatin, fluvastatin, lovastatin, pravastatin, and simvastatin) on fasting and postprandial lipoproteins in patients with coronary heart disease versus control subjects. Am J Cardiol. 2004 Jan 1;93(1):31-9.

49. Ooi TC, Cousins M, Ooi DS, Nakajima K, Edwards AL. Effect of fibrates on postprandial remnant-like particles in patients with combined hyperlipidemia. Atherosclerosis. 2004 Feb;172(2):375-82.

50. Li D. Omega-3 fatty acids and non-communicable diseases. Chin Med J (Engl). 2003 Mar;116(3):453-8.