Most health-conscious individuals engage in various lifestyle strategies designed to reduce the risk for certain chronic diseases, to control body composition, or improve overall health, fitness, and well-being. This of course makes sense, and often results in the achievement of individual goals by those who effectively and consistently implement targeted lifestyle strategies.
Except for 1918, during the time of the Spanish Flu, cardiovascular disease (CVD) has been the number 1 killer in the United States since 1900. This disease claims the life of more than 2,600 Americans each day – 365 days a year, with nearly the same percentage of death for male and female.
Risk factors for developing CVD include high blood pressure, high blood cholesterol, smoking, diabetes, obesity, an imbalance between free radicals and antioxidants, and a sedentary lifestyle. However, mounting evidence indicates another very important risk factor is that of the physiological responses that take place in the arteries of the body, and especially those of the heart, after consuming a meal. This is known as the postprandial period.
What is the Postprandial Period and What Physiological Responses Occur that Increase the Risk for CVD?
The postprandial period that follows consumption of a meal or significant number of calories, is associated with significant physiological responses taking place in the body related to the foods and beverages consumed. This postprandial period peaks at around the 2.0 to 2.5-hour mark after eating the meal.
“To date, researchers have found that there is just one sure way to increase biological life span – eat fewer calories” Harvard Medical School statement
Unfortunately, many of the physiological responses taking place during this time are pathophysiological or disease promoting and can cause damage to arteries and contribute to atherosclerosis, the disease that leads to the progressive narrowing and hardening of arteries due to the buildup of plaque. This is a major cause of CVD and can lead to heart attack or stroke.
The inner lining of an artery wall is composed of with a single layer of endothelial cells (EC’s). When healthy, these cells produce normal amounts of prostacyclin (PG12) and nitric oxide (NO), two very important substances that function to inhibit hyperactive blood platelets and white blood cells from sticking to the arterial wall. These substances also act on the vascular smooth muscle cells (VSMC) of the middle layer of an artery to help keep them relaxed and dilated thus maintaining normal healthy blood flow through the artery.
Following the consumption of a meal, a number of pathophysiological mechanisms are initiated, and can cause damage to the arterial wall, impede some normal functions, and set in motion the disease process of atherosclerosis.
These pathological mechanisms include:
- Damage and dysfunction of endothelial cells. A variety of known CVD risk factors can lead to the damage of endothelial cells including high blood pressure, high blood cholesterol, high blood sugar (diabetes), cigarette smoke, and a high concentration of free radicals. Some of these even occur acutely in the postprandial period, especially if the meal is high in fat, sugar, and total calories. When damaged, these cells are hindered in their ability to release NO and PG12. As a result, the arterial wall cannot as effectively repel blood platelets (specialized blood cells involved in clotting) and white blood cells (WBC) from sticking to the arterial wall and contribute to the atherosclerotic process.
- Platelet activation and vascular smooth muscle cell multiplication. While platelets are important in helping to control bleeding, they are also involved in helping to heal damaged endothelial cells via the release of platelet derived growth factors (PDGF). This is good in that as previously discussed; many of the CVD risk factors cause damage to EC’s and during the postprandial period the EC’s can be temporarily rendered dysfunctional. However, these same CVD risk factors also activate platelets, and during the postprandial period they are also triggered to be hyperactive. Hyperactive platelets are drawn to the site of damaged endothelial cells (to aid in their healing) in excessive numbers, and then release excessive amounts of platelet derived growth factors (PDGF). The PDGF works to heal the damaged endothelial cells of the inner lining of the artery, but because it has been released in excessive amounts, it diffuses through the arterial inner lining and stimulates the vascular smooth muscular cells of the middle arterial layer to divide and multiply aggressively. The result is that these cells grow in number and migrate inward into the lumen (opening) of the artery, effectively narrowing the opening. A narrowed artery will impede blood flow. This truly is an example of too much of a good thing.
- Oxidation of LDL cholesterol and an inflammatory immune response. Body cells and substances, such as LDL cholesterol, are constantly being bombarded with potentially harmful free radicals or oxidants. These unstable oxygen molecules, formed as a byproduct of our own metabolism, can “oxidize” and alter or modify LDL cholesterol molecules and damage body tissues. Fortunately, we have antioxidants in our body that can neutralize the free radicals (oxidants) before they can oxidize the LDL cholesterol or do harm to body cells. Some of our antioxidants are endogenous or manufactured by our bodies, and others we must consume in our diet. As long as we maintain a good balance between the number of free radicals and antioxidants, our cells are not damaged and LDL cholesterol is not oxidized.
We often hear of LDL cholesterol as being the “bad” cholesterol as it is the main constituent of the atherosclerotic plaque that builds up in our arteries and leads to heart disease, heart attack, or stroke. This is true. However, the LDL cholesterol circulating in our blood are an essential element in the production of adrenal steroids and sex hormones, and a vital component of the walls of all body cells.
As an essential structural component of cell walls, including those in our arteries, LDL cholesterol must pass through the inner layer to drop off the needed cholesterol for these purposes. However, if there are excessive amounts of LDL cholesterol in the blood (high blood cholesterol), and/or if we have insufficient antioxidants in our body, an imbalance is created that increases the chance that these LDL cholesterol molecules will be oxidized by free radicals.
If oxidized, the LDL cholesterol is altered chemically and then perceived by the body’s immune system as a foreign invader, similar to a pathogen (disease causing organism). These oxidized LDL molecules are detected by endothelial cells, which initiate an elaborate series of chemical reactions, that bring the body’s immune system into action. In response, white blood cells (WBC) circulating in the blood are drawn to the site of the oxidized LDL cholesterol.
As the WBC’s pass through the inner layer of endothelial cells they are converted to macrophages (MAC) and begin scavenging the oxidized LDL cholesterol molecules, similar to what they would do to invading pathogens. When they become engorged with the oxidized LDL cholesterol the MAC’s become what are known as foam cells. These foam cells accumulate in the arterial walls and contribute to the development of atherosclerotic plaque. Overtime this plaque causes a narrowing of the artery and the development of cardiovascular disease. This process can take years and decades as the plague accumulates before the problem leads to a heart attack, or a stroke if occurring in the arteries that feed the brain.
The process of atherosclerosis is known to begin as early as age 10 in some individuals and progress slowly over the next decades of life. In fact, studies have shown that fatty streaks in arteries increase rapidly in prevalence and extent during the ages of 15 to 34. As such, can we see how early identification of CVD risk factors and early intervention of modify risk factors, including those occurring during the postprandial period, the greater the potential for deferring the onset of heart disease. Therefore, primary prevention of atherosclerosis must begin in childhood or adolescence.
There are several accepted intervention strategies designed and touted to reduce the known CVD risk factors. These of course should be implemented in your life as soon and as much as possible. However, what can we do to lessen the occurrence and magnitude of these pathological mechanisms taking place during the postprandial period?
What Can You Do to Mitigate the Pathological Mechanisms of the Postprandial Response and Lower Your Risk for CVD?
The quick and short answer to this question is to include with your meals plant derived polyphenolic compounds, e.g. flavonoids.
There are over 4,000 identified flavonoids and they are found in fruits, vegetables, nuts, seeds, and plant derived beverages like wine, tea, and fruit juices. These are not vitamins, fat, carbohydrate, or protein.
They are plant derived chemicals (phytochemicals) and have extraordinary health protection properties. Many polyphenolic compounds (flavonoids) are rich in powerful antioxidants, have platelet inhibitory and anti-inflammatory properties, and have demonstrated the ability to combat the postprandial period pathological responses by enhancing positive physiological responses that offer protection to the cardiovascular system.
The Evidence for Flavonoids
These unique and beneficial properties have been demonstrated in many in vitro (test tube) studies and in vivo (living organisms – animal and human) studies.
Multiple epidemiological studies spanning decades have shown an inverse relationship between death from CVD and the dietary intake of flavonoids. The so called “French Paradox” asks the question as to why the French, despite having comparable risk factors for CVD as Americans, have 1/3 the rate of heart attacks.
What Specific Strategies Can You Implement in Your Life to Dramatically Increase the Quantity and Quality of Flavonoids Consumed with Meals to Reduce the Postprandial Period Pathological Response Mechanisms?
Because the period following consumption of a meal is associated with some of the greatest pathological insults to the cardiovascular system, the targeted and timely consumption of protective flavonoids in conjunction with your meal can blunt the detrimental effects that occur during the postprandial period.
Keep in mind that the greater the content of saturated and hydrogenated fats, refined sugars, and total calories in a meal, the greater the pathological postprandial response of disease mechanisms. The following are targeted ways to enhance the intake of cardio protective flavonoids with your meal, providing timely intervention against pathological postprandial responses when your cardiovascular system most needs the protection.
- Regardless of the breakfast you consume, include a cup of berries. It really does not matter the kind of berry as all have various flavonoids that can offer some protection against the pathological postprandial period responses.
- If you like to drink a fruit beverage in the morning, both 100% purple grape juice and 100% pomegranate juice have powerful properties shown to reduce the pathological postprandial responses.
- When dining out at a nice restaurant, whatever meal you select, be sure to include a fruit or vegetable with your order. Again, the key is to always include a source of flavonoids whenever you consume significant calories, especially if those calories come largely from fats or sugars.
- Most folks, but certainly not all, will hit a fast food restaurant as part of their weekly routine. Usually these establishments do not have options for fruits and vegetables that include flavonoids. Bringing along your own fruit can provide a source of flavonoids to help blunt the effects of the postprandial period.
- The evening meal tends to be the meal where people consume the most calories. Drinking a glass of red wine or purple grape juice or pomegranate juice with your meal has shown to provide significant cardio protective benefits against the pathological mechanisms of the postprandial response.
- For some individuals, the consumption of alcohol in any form is a risk and therefore should be avoided. The diabetic may should avoid drinks that are high in sugars as are fruit juices. The obese individual who is working hard to reduce caloric intake needs to be sensitive to high caloric sources during their weight loss efforts. And, some simply do not like the taste of red wine and purple grape juice or pomegranate juice. For these individuals, there are supplement products such as grape seed and grape skin extracts that potentially offer benefits to that of red wine and purple grape juice. As these substances are not regulated by the FDA, their potency and bioavailability are questionable. However, some have been tested and offer similar benefits to the high flavonoid concentration sources of red wine and purple grape juice. It should also be noted that as a “supplement”, these products would be effective to help “supplement” your total dietary flavonoid intake. In doing so, keep in mind that several epidemiological studies have shown an inverse relationship between death from CVD and the total intake of flavonoids.
References
Britt Burton-Freeman, et. al., Postprandial metabolic events and fruit-derived phenolics: a review of the science. Published online by Cambridge University Press: 19 Oct 2010.
Demrow HS, et al., Administration of wine (red wine but not white wine) and (purple) grape juice inhibits in vivo platelet activity and thrombosis in stenosed canine coronary arteries. Circulation 1995;91: 1182-8.
Keevil JG et.al., Grape Juice, but not orange juice or grapefruit juice, inhibits human platelet aggregation. Journal of Nutrition 2000;130: 53-6
Shanmuganayagam D, et. al., Effect of purple grape juice on platelet activity and development of atherosclerosis in hypercholesterolemic rabbits. FASEB J. 1999; 13:239A.
Stein JH, et. Al., Purple grape juice improves endothelial function and reduces the susceptibility of LDL cholesterol to oxidation in patients with coronary artery disease. Circulation 1999; 100:1050-5
About author
Lynn Perkes is a full-time faculty member at Brigham Young University-Idaho teaching courses in Kinesiology and Biomechanics, Applied Kinesiology and Assessment, Therapeutic Exercise, and Health Appraisal and Prescription. He writes part time for ProhealthcareProducts.com, who sells healthcare, therapy, and fitness products.
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