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When what you eat sticks around: Postprandial lipid disorders and their impact on your plaque-control program
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Like annoying visitors to your home who don’t know when to leave, there are a set of cholesterol-related abnormalities called “postprandial disorders”, the abnormal persistence of fatty digestive by-products that stick around for up to 24 hours after eating. They are among the most potent causes of heart disease, stroke, and aneurysm known.

Here’s the Track Your Plaque guide to what you need to know

Judy, a 53-year old nurse, prided herself on her healthy lifestyle. Her husband and two teenage kids frequently took long bicycle rides together, camped, hiked, and canoed. Though she gained nearly 20 lbs. passing through menopause, she still weighed only 144 lbs, substantially less than nearly all her friends and coworkers.

Once a year, Judy’s doctor performed a standard cholesterol panel. Year after year, her doctor pronounced that her numbers were “outstanding”. The last panel, however, showed a subtle change: the triglyceride level, previously ranging between 80–150 mg/dl (“normal” <150 mg/dl by conventional standards), was now 167 mg/dl.

When Judy pointed this out to her doctor, he just suggested that she cut back on the glass or two of wine that she indulged in with her husband most nights. Unsatisfied with this answer, Judy got a heart scan. Her score: 177, in the 90th percentile (worst 10%).

Now very concerned, Judy finagled a lipoprotein panel out of her now-confused doctor. Several new patterns emerged: small LDL (approximately 85% of all LDL particles) and intermediate-density lipoprotein (IDL). These abnormalities were present despite an HDL of 63 mg/dl and LDL of 84 mg/dl.

As you eat a fatty meal of, say, steak, buttered rolls, salad dressing on your iceberg lettuce, and cream in your coffee, food passes through your digestive tract. Fats are broken down by various enzymes, then absorbed into the veins that pass through the liver. From there, they go to the general circulation.

After 4 to 6 hours, the fatty by-products of your meal should be history. Digestion and clearance from the blood should be quick and efficient: After 6 hours, they should no longer be detectable in your blood stream.

However, in some people, 10, 12, even 24 hours later, these fatty by-products of your meal are still hanging around in your blood. The longer they persist in the blood, the more opportunity they have to cause plaque growth. Clinical studies suggest that these postprandial lipoproteins (PPL) are powerful causes of coronary plaque, carotid plaque, and aneurysms of the aorta. People with greater elevations of PPLs have more plaque with PPLs buried inside their structures.

Up to 20% of people with coronary plaque will have some degree of increased PPLs. In some cases like Judy (above), PPLs (as IDL) can be a trigger for atherosclerotic plaque even with few other abnormalities to accompany it.

Metabolic syndrome and PPLs

People with the so-called metabolic syndrome (low HDL, high triglycerides, high blood pressure, blood sugar 110–125 mg/dl, high blood pressure, increased inflammation, excess abdominal fat) are especially prone to PPL abnormalities. In this condition, both the liver and intestinal tract run at high levels, producing excessive PPLs for release into the blood. Just having hypertension alone, in fact, may serve as an indicator of greater PPL levels.

A number of abnormalities account for the persistence of fatty by-products. One prominent effect is that, when blood insulin levels are increased, the liver over-produces VLDL particles, a particle that provides triglycerides to other particles. PPLs also are cleared ineffectively from the blood, permitting their accumulation (though the reason for this is unclear). Levels can be increased several-fold.

Not only do persistent PPLs in the blood enter and trigger plaque growth, they also help create undesirable small LDL particles, another potent cause for coronary plaque. The abundant triglycerides in PPLs are inserted into LDL (by the enzyme cholesteryl-ester transfer protein). This is the first crucial step in creating small LDL particles.

Insulin therefore triggers more PPLs to persist in the blood, but more PPLs also increase the body’s unresponsiveness to insulin. Thus starts a vicious cycle that snowballs towards full-blown diabetes.

Triglycerides—Evil friends of PPLs

Because triglycerides are a principal ingredient in PPLs, elevated fasting triglycerides can serve as a very important indirect index of increased PPLs.

If your triglycerides are high (by Track Your Plaque criteria, this means ≥60 mg/dl), PPLs are more likely to be present. Certainly, triglyceride levels of >100 mg/dl predict that PPLs are increased, contrary to the national guidelines (NCEP) which advise 150 mg/dl as the cut-point, a level associated with much increased likelihood of PPL elevation.

The more features of the metabolic syndrome you have, such as low HDL, borderline high blood sugar (≥110 mg/dl), high blood pressure, etc.), the more likely you will have PPLs, even if your fasting triglycerides are normal. PPLs are not only at higher levels, but they will also persist longer.

Though metabolic syndrome is an important indicator of probable increased and persistent postprandial particles, you can still have increased PPLs without the metabolic syndrome. Judy (above) did not have metabolic syndrome features yet still had increased PPLs. Judy’s fasting triglyceride level of 167 mg/dl was a strong hint that excessive postprandial particles were present.

Intermediate-density lipoprotein (IDL)

Actual measurement of PPLs is presently available only in clinical research settings. In practice, they are simply not measured. In several years, specific measurement of PPLs will likely become available, as experience and expanding recognition of their importance forces it out of the research setting.

You already know that fasting triglycerides can be a useful index of postprandial particles. But there is a measure of PPLs that is quite reliable and available to most of us: Intermediate-density lipoprotein (IDL). IDL is obtainable through lipoprotein testing using NMR (Liposcience) and VAP (Atherotech). (Both are obtained as part of the routine panel and do not require specific effort.) The blood sample for lipoprotein testing is generally drawn after an 8–12 hour fast, not after eating, but it nonetheless serves as a pretty good index of PPLs, even better than fasting triglycerides in many cases.

Judy (above) had elevated IDL and so definitely had persistent postprandial lipoproteins as a principal cause for her high heart scan score. Not only is increased IDL a trigger for coronary plaque growth, but it is an especially potent cause behind abdominal and thoracic aneurysms of the aorta. IDL has also been shown to heighten the likelihood of pure soft plaque in carotid arteries, the sort that easily fragment, release debris, and thereby cause strokes.

The many ways to reduce PPLs

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Copyright 2006, Track Your Plaque, LLC

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