Triglycerides: Mother of Meddlesome Particles - Davis

Triglycerides: Mother of Meddlesome Particles



Triglycerides are a crucial risk factor for coronary plaque growth, even at levels previously thought to be normal. Dr. Davis discusses why and how this oft-neglected factor can be harnessed to strengthen your program.

While the world obsesses over cholesterol, a potent stimulator of plaque growth is frequently ignored—triglycerides. A subject of controversy in past, the data are now clear: triglycerides spawn unwanted lipoprotein particles that trigger plaque growth. Track Your Plaque members are advised that control of triglycerides is essential to everyone’s plaque control program.

Triglyceride control is crucial if you are interested in gaining control over coronary plaque. Triglycerides should be brought under control at the start of your program. If you are experiencing plaque growth (increasing heart scan scores), seriously reining in triglycerides should be considered.

How important are triglycerides?

 

For years, the relationship between coronary heart disease and triglycerides remained muddled by the confounding effects of low HDL. In other words, increased triglycerides tend to occur alongside low HDL. This caused many to dismiss the importance of triglycerides. To make matters even murkier, high triglycerides in some situations generated high risk for heart disease, while in others it appeared unrelated to heart disease, even when markedly elevated (in the thousands!).

Thanks to the evolving science of lipoproteins, the issues are crystallizing. One important fact has emerged: triglycerides are a critical risk factor for coronary plaque growth, even at levels previously thought to be normal. Yes, high triglycerides frequently occur with low HDL, but they also behave independently. High triglycerides are a common cause of heart disease, even in people with low or normal cholesterol values. It is crucial that you (and your doctor) pay close attention to triglycerides if you are to succeed in controlling your plaque. We urge Members to make triglyceride control a priority in their program.

 

Where do triglycerides come from?

 

The liver produces a particle called “very low-density lipoprotein”, or VLDL, packed full of triglycerides. The higher your triglycerides, the more VLDL you will have. Sometimes triglycerides are increased due to genetic factors. More commonly, triglycerides are high due to excess weight, indulging in processed carbohydrates, and resistance to insulin (metabolic syndrome).

VLDL is like that bad kid on the block you want your kids to avoid. VLDL particles in the blood come into contact with LDL and HDL particles and they’re never quite the same. When a LDL or HDL particle meet VLDL, the triglycerides of VLDL are passed on. The result: LDL and HDL become bloated with triglycerides. Triglyceride-loaded LDL and HDL are a ready target for a set of enzymes in the blood and liver that reconfigure these particles into smaller versions, small LDL and small HDL. Recall that both small LDL and HDL are highly undesirable particles that stimulate plaque growth.

Although “official” (ATP-III) guidelines suggest that triglycerides over 150 mg are undesirable, we regard any value over 60 mg as high. An ideal level for an intensive Track Your Plaque approach is <45 font="font" mg.="mg.">

 

How will I know if I have this pattern?

 

On a conventional cholesterol panel, increased triglycerides and low HDL are tip-offs that excess VLDL are available to contribute to coronary plaque growth. At what triglyceride level does this cascade begin to take effect and create this collection of particles? Levels of 45 mg/dl or greater. In the Track Your Plaque program, we aim for zero plaque growth or reduction, and so we target triglyceride levels of 60 mg/dl or less.

You’ll notice that low HDL and increased triglycerides are also patterns that characterize the metabolic syndrome. In our experience, over 50% of adults show at least some of the characteristics of the metabolic syndrome. In our society of inactive, sedentary lifestyles and packaged, processed foods, metabolic syndrome is rampant. That means increased triglycerides from VLDL are also running rampant. The result: a 3 to 7-fold increase in risk for heart attack. Eliminating the metabolic syndrome is another battle we need to fight to conquer plaque. (See Shutting Off the Metabolic Syndrome.)

 

How can triglycerides be reduced?

 

Our triglyceride target of 60 mg or less dramatically reduces triglyceride availability. Without triglycerides, LDL and HDL can’t be processed into undesirable small particles. Among the strategies we use to reach our triglyceride target of 60 mg or less:

• Fish oil—The omega-3 fatty acids in fish oil are our number one choice for substantially reducing triglycerides. Fish oil, 4000 mg per day, is a good starting dose (providing 1200 mg EPA+DHA); higher doses should be discussed with your physician, though we commonly use 6000–10,000 mg per day without ill-effect. Flaxseed oil, while beneficial for health, does not correct lipoprotein patterns. Consider a concentrated fish oil preparation (e.g., Omacor™, a prescription preparation, or “pharmaceutical grade” preparations from the health food store) if you and your doctor decide a high dose is necessary.
• Weight loss to ideal weight or ideal BMI (25). If achieved with a reduction in processed carbohydrates, the effect will be especially significant. Exercise will compound the benefits of weight loss, triggering an even larger drop in triglycerides.
• Reduction in processed carbohydrates—especially snacks; wheat-flour containing foods like breads, pasta, pretzels, chips, bagels, and breakfast cereals; white and brown rice; white potatoes. The reduction of high- and moderate-glycemic index foods is the factor that reduces triglycerides. High triglycerides are therefore a pattern that develops when someone follows a low-fat diet. For this reason, we do not advocate low-fat diets like the Ornish program. Reducing your exposure to wheat-containing snacks and processed foods is an especially useful and easy-to-remember strategy that dramatically reduces triglycerides.
• Elimination of high-fructose corn syrup—This ubiquitous sweetener is found in everything from beer to bread. High-fructose corn syrup causes triglycerides to skyrocket 30% or more.
• Niacin in doses of 500–1500 mg is an effective method of reducing triglycerides. Niacin also raises HDL, increases large HDL, reduces the number of small LDL particles, reduces VLDL, and modestly reduces total LDL. The preferred forms are over-the-counter Slo-Niacin® and prescription Niaspan®, the safest and best tolerated. Immediate-release niacin (just called niacin or nicotinic acid on the label) can also be taken safely, provided it is taken no more frequently than twice per day. Total daily doses of >500 mg should only be taken under medical supervision. Avoid nicotinamide and “no-flush niacin” (inositol hexaniacinate), neither of which have any effect whatsoever.
• Green tea—The catechins (flavonoids) in green tea can reduce triglycerides by 20%. Approximately 600–700 mg of green tea catechins are required for this effect, the equivalent of 6–12 servings of brewed tea. (Tea varies widely in catechin content.) Nutritional supplements are also available that provide green tea catechins at this dose. The weight loss accelerating effect of green tea may add to its triglyceride-reducing power.
• The thiazolidinediones (Actos®, or pioglitazone, and Avandia®, or rosiglitazone), usually prescribed for pre-diabetes or diabetes, can reduce triglycerides by 30%; Actos may be more effective than Avandia in this regard. However, these agents are accompanied by weight gain.
• The fibrate class of prescription drugs (fenofibrate, or Tricor®, and gemfibrozil®, or Lopid) reduce triglycerides 30–40%, i.e., almost as effectively as fish oil.

The evil influences of VLDL and triglycerides are therefore erased from your risk profile by achieving the Track Your Plaque target of triglycerides 60 mg/dl or less. One or more of these strategies are usually required to bring your triglycerides to target. 

        William Davis, MD


Selected references:

Packard CJ. Understanding coronary heart disease as a consequence of defective regulation of apolipoprotein B metabolism. Curr Opin Lipidol 1999; 10:237–244.

Otvos J. Measurement of triglyceride-rich lipoproteins by nuclear magnetic resonance spectroscopy Clin Cardiol 1999;22 (Suppl II) II-21–II-27.

Grundy SM. Hypertriglyceridemia, atherogenic dyslipidemia, and the metabolic syndrome. Am J Cardiol 1998;81(4A):18B–25B.

Zilversmit DB. Atherogenic nature of triglycerides, postprandial lipidemia, and triglyceride-rich remnant lipoproteins. Clin Chem 1995;41(1):153–158.