Anatomy of a portion of the cardiovascular system, showing the heart, aorta, and prominent arteries of the upper torso. An arteriole (small branch of an artery) is shown in cross-section.
If you’ve seen a loved one suffer and die from cardiovascular disease, knowing that your own cholesterol is normal can be a relief. Unfortunately, standard cholesterol panels based on fasting blood samples may overlook a hidden, potentially deadly cause of cardiovascular disease: dysfunctional lipid (fat) metabolism patterns known as postprandial disorders.
Postprandial (after-meal) disorders are characterized by abnormally persistent lipid (fat) remnants that persist in the bloodstream for up to 24 hours after eating. Hours after dinner, and even during sleep, these abnormal fat particles can inflict serious damage to your arteries. In fact, postprandial disorders are among the most potent—yet widely ignored—causes of heart disease, stroke, and aneurysm.
In this article, we examine lipid remnants that lurk in the blood between meals, how you can detect the presence of these deadly compounds, and nutritional strategies that can help you reduce and eliminate them.
As you eat a meal of, say, steak, buttered rolls, salad dressing on your lettuce, and cream in your coffee, food passes through your digestive tract. The fats contained within this food are first broken down by enzymes, and then absorbed into veins passing through the liver. From there, they go into the body’s circulatory system.
Four to six hours later, the remnants of your meal should be history. Digestion and clearance from the blood should be quick and efficient. After six hours, these remnants should no longer be detectable in the bloodstream.
In some people, however, meal remnants persist in the blood even 10, 12, or 24 hours later. The longer they stick around, the more opportunity they have to trigger the growth of atherosclerotic plaque in arteries. Clinical studies show that these postprandial lipoproteins (lipids that are transported by protein carriers known as “lipo-proteins”) are powerful instigators of coronary plaque, carotid plaque, and aneurysms of the aorta.
| |Cut-away view of the primary parts of the digestive system
. After processing in the stomach, food passes to the duodenum (the first portion of the small intestine). Here, it is combined with bile (fat-digesting juices made in the liver and stored in the gall bladder), pancreatic juices and enzymes (made by the pancreas), and intestinal enzymes for further digestion.
These post-meal lipid remnants lurk in the blood from the moment you begin eating, but usually dissipate by the time your “fasting” blood is drawn to assess your risk for vascular disease. Postprandial disorders are therefore almost always overlooked or ignored, and rarely enter into a doctor’s assessment and treatment of vascular risk and disease. Although their presence may not be apparent from a fasting blood sample, postprandial lipoproteins can still be a critically important instigator of vascular disease.
Postprandial Patterns: Potent Causes of Vascular Disease
When postprandial lipoproteins linger for many hours after eating, they are afforded ample opportunity to exert damaging effects on vascular structures. Postprandial lipoprotein particles insert themselves into atherosclerotic plaque, fueling its growth.1 They contribute to atherosclerosis through other paths as well:
- Postprandial lipoproteins block the natural artery-relaxing agent known as nitric oxide, while increasing the artery constrictor called endothelin. This induces endothelial dysfunction (an impaired ability of the arterial walls to dilate),2,3 which in turn contributes to the formation of atherosclerotic plaque.4
- Postprandial lipoproteins increase blood levels of cellular adhesion molecules, allowing inflammatory white blood cells to more readily adhere and gain entry to the arterial wall, which also leads to atherosclerotic plaque formation.5
- Postprandial lipoproteins activate blood clotting by increasing factors that both promote blood clotting and inhibit clot breakdown.6
- Postprandial lipoproteins trigger the formation of a cascade of other abnormal lipoprotein particles that contribute to heart and vascular disease, such as small low-density lipoprotein (small LDL) particles.7
Carotid ultrasound studies show that people who have elevated postprandial lipoproteins have more carotid plaque than people who do not, independent of their cholesterol values.8,9 Postprandial lipoproteins also predict a greater likelihood of coronary atherosclerotic plaque, and people with excessive postprandial abnormalities experience more rapid plaque growth.8-11
Triglycerides: Building Block of Postprandial Lipoproteins
Because triglycerides are a principal component of postprandial lipoproteins, elevated fasting triglycerides—which can be readily measured using a standard lipid or cholesterol test panel—can serve as an indirect index of increased postprandial lipoproteins.
If triglycerides are high, postprandial lipoproteins are likely to be present. What constitutes “high” is arguable, though fasting triglycerides equal to or greater than 100 mg/dL are clearly associated with greater postprandial lipoproteins. This issue is essentially ignored in the national guidelines for cholesterol and lipid management (the National Cholesterol Education Program Adult Treatment Panel III),12 which specify that triglyceride levels of 150 mg/dL or higher are associated with an increased likelihood of postprandial lipoprotein elevation.13,14 It has long been the position of the Life Extension Foundation that aggressive steps (such as using fish oil supplements) should be taken to reduce triglycerides over 100 mg/dL.
Simply put, the higher your triglycerides, the more likely postprandial lipoproteins are also present, potentially putting you at risk for atherosclerotic disease. However, fasting triglycerides are not foolproof, and an excess of postprandial lipoproteins can still occur even with triglyceride levels of less than 100 mg/dL.1
Metabolic Syndrome Promotes Postprandial Lipoproteins
Metabolic syndrome is a frighteningly common precursor to diabetes that can create an excess of postprandial lipoprotein abnormalities.
Metabolic syndrome—the cluster of metabolic abnormalities that include high triglycerides, high blood pressure, high blood sugar, excess abdominal fat, and low HDL—is rampant throughout America, with one in four adults now showing established degrees of this condition.15 The more features of metabolic syndrome present, the more likely postprandial lipoproteins are elevated—even if fasting triglycerides are normal. In the presence of metabolic syndrome, postprandial lipoproteins are not only present at higher levels, but may persist longer in the bloodstream.16 Full-blown metabolic syndrome is not required for a person to exhibit excessive postprandial lipoproteins. Having hypertension alone, for example, suggests the presence of greater postprandial lipoprotein levels.16,17 People with metabolic syndrome exhibit higher blood sugar after meals (usually 140 mg/dL or more), since sugar is unable to enter into the body’s tissues. Now deprived of sugar, these tissues (particularly muscle) turn to burning fat for energy, which causes the release of free fatty acids in the blood. This cascades into an increase of postprandial triglycerides and other abnormal particles.18
Increased blood insulin levels associated with metabolic syndrome trigger the liver to overproduce very-low-density lipoprotein (VLDL) particles, a principal postprandial lipoprotein particle. Postprandial lipoproteins, including VLDL, are ineffectively cleared from blood, permitting their accumulation and raising blood levels of VLDL as much as several-fold.19,20
Postprandial lipoproteins such as VLDL spark formation of potentially harmful small LDL particles, a leading cause of coronary plaque. The abundant triglycerides in postprandial lipoproteins are inserted into LDL particles by an enzyme known as cholesteryl-ester transfer protein, which is the crucial first step in creating small LDL particles.21 Thus, persistent postprandial lipoproteins not only cause atherosclerosis, but also set in motion a “domino effect” of other particles that likewise contribute to atherosclerotic disease.22
While the elevated insulin levels associated with metabolic syndrome cause postprandial lipoproteins to persist in the blood, the reverse also occurs: postprandial lipoproteins block the body’s response to insulin, aggravating pre-diabetes.23 Thus begins a vicious cycle that accelerates toward full-blown diabetes.
Although metabolic syndrome is an important indicator of increased and persistent postprandial particles, increased postprandial lipoproteins commonly occur without metabolic syndrome and when fasting triglycerides are at desirable levels. This has led doctors and scientists to wonder whether a better indicator of persistent and elevated postprandial particles exists.
Critical Role of Intermediate-Density Lipoprotein (IDL)
Beyond fasting triglycerides and VLDL, there is a measure of postprandial lipoproteins that is reliable and readily available: intermediate-density lipoprotein (IDL).
After being released into the blood by the liver, VLDL particles are processed in the blood over several hours, yielding IDL. IDL persists longer than VLDL and signals the persistence of postprandial particles.
A normal amount of IDL is none—that is, no IDL whatsoever should be detected in fasting blood. If present, IDL triggers atherosclerotic plaque growth.24,25 It may also be a potent risk factor for abdominal and thoracic aneurysms of the aorta (a bulging of part of the wall of the body’s largest artery). The presence of IDL also heightens the likelihood of pure soft plaque in carotid arteries, the kind that easily fragments, releases debris, and causes strokes.26,27
IDL can be measured using the Vertical Auto Profile lipoprotein test (VAP™ test). For lipoprotein testing, blood is usually drawn after an 8- to 12-hour fast. IDL particles can persist up to 24 hours after a meal and thus may remain elevated even during the “fasting” period. If IDL particles are present in a fasting blood sample, a substantial postprandial abnormality is clearly present, which can play a major role in causing atherosclerotic disease.