Introduction
The pathophysiology of atherosclerosis involves a series of complex events that can be likened to that of a chronic inflammatory process, which results in the development of an atherosclerotic plaque. The first step in the process involves injury to the endothelial cells of the artery that results in endothelial cell dysfunction. The activated endothelial cells attract vascular smooth muscle cells (VSMC) and leukocytes, which proliferate and accumulate in the walls of the artery (Seidman, Mitchell, & Stone, 2014). These cellular components lead to the formation of a large amount of connective tissue matrix. This is the ultimate end point in the development of a mature fibrosis plaque. The occurrence of symptoms is as a result of advanced lesions being complicated by thrombosis, plaque rupture, hemorrhage into the plaque and emboli (Seidman et al., 2014).
The prevalence of atherosclerosis currently stands at 17 per 1000, with a prevalence rate of 1.70% or 4.6 million people in the US (Mozaffarian et al., 2014). The death toll from atherosclerotic cardiovascular disease (CDV) stood at 71.926. The death rate extrapolation for the US is 1 per hour, 41 per day, 288 per week, 1,248 per month and 14,979 per year (Mozaffarian et al., 2014). The 14,979 deaths are as a result of atherosclerosis contributing to other causes rather than it causing death directly. The total number of cases of hospitalization stood at 20,000 with 8,000 for atherosclerotic CVD and 12,000 for atherosclerosis (Mozaffarian et al., 2014).
Atherosclerosis is idiopathic, but there are certain habits, conditions or traits that raise the risk of one getting the condition. One of the risk factors includes unhealthy blood cholesterol levels whereby a person has high low-density lipoproteins (LDL cholesterol) and low high-density lipoproteins (HDL cholesterol). High blood pressure is also considered a risk factor (above 140/90 mmHg over time) for atherosclerosis. Smoking usually tightens and damages blood vessels, raise blood pressure and raise cholesterol levels thus qualifying it as a risk factor for atherosclerosis (Seidman et al., 2014). Being overweight or obese (as determined by the body mass index) and lack of physical activity form part of the list of risk factors. Lastly, an unhealthy diet consisting of foods that are rich in saturated and trans fats, sugar, sodium (salt) and cholesterol worsen other risk factors for atherosclerosis.
Role of Nutrition
Diets rich in low-density lipoproteins (LDLs) play a direct role in the development and progression of atherosclerosis. In a healthy state, the endothelium through the release of molecules such as nitric oxide (NO), regulates the recruitment of inflammatory cells onto the vascular wall, maintains the balance between fibrinolysis and thrombosis and controls the vascular tone (Martins e Silva & Saldanha, 2007). However, the exposure to high LDLs has been shown to reduce NO bioavailability either by enhancing NO degradation or by reducing the activation of NO synthetase. The endothelial dysfunction that is characterized by a decrease in NO availability is the preceding step to LDL entry into the arterial intima hence leading to the progression and development of atherosclerosis (Martins e Silva & Saldanha, 2007).
Diet rich in high-density lipoprotein (HDL) is known to play a significant role in the prevention and treatment of atherosclerosis. HDLs directly oppose atherosclerosis by inhibiting the oxidation of LDLs, by limiting the inflammatory process underlying atherosclerosis and removing cholesterol from foam cells. HDLs have been shown to reduce the expression of adhesion molecules thus leading to a decreased binding of inflammatory cells (Martins e Silva & Saldanha, 2007). This is consistent with functional inhibition of atherosclerosis. HDLs also have antithrombotic properties. Hence, HDL-cholesterol interrupts the entire process of atherogenesis at several key stages.
Intervention
1. Begin exercising three days per week for 1 hour within 30 days.
2. Reduce intake of foods with high saturated fat such as pizza and regular cheese within four months
3. Eat three additional servings of fresh vegetables and fruits daily.
4. Reduce the number of cigarettes one smokes from five to two per day for two months.
Mediterranean diet
There is no fixed “Mediterranean” diet that is supposed to be followed. There are many variations depending on one’s dietary goals. However, the diet has certain basic characteristics including high consumptions of bread, vegetable, fruits and other cereals, seeds, nuts, beans, and potatoes. It also incorporates poultry, fish and dairy products which are consumed in low to moderate amounts. Replacing butter with healthy fats, including olive oil and using spices and herbs in the place of salt when flavoring foods. This type of diet also emphasizes on limiting the amount of red meat to just a few times in a month as well as well as drinking wine in moderation although this is optional. It also recognizes the significances of being physically active as well as well as enjoying meals with friends and family.
Mediterranean diet is recommended by many medical practitioners as it has less saturated fat as compared to the American diet. More than half of the fat found in a Mediterranean diet are sourced from monounsaturated fats (mainly from olive oil). This type of fat does not raise the blood cholesterol levels as compared to saturated fat. Statistics have even revealed that the incidences of cardiovascular disease in Mediterranean countries is lower than in the United States.
The Mediterranean dietary pattern is of great benefit in the management of atherosclerosis as it increases the activity of serum paraoxonase (PON 1), which is an enzyme that is transported on HDL in the blood. This enzyme inhibits macrophage foam cell formation and protects cholesterol from oxidation, which are the two initiating steps when it comes to the development of atherosclerosis. The Mediterranean diet also increases the levels of carotenoids by a whopping 74% (Seidman et al., 2014). Carotenoids function as protective antioxidants. In combination to these defensive benefits, this type of diet causes a drop in the levels of inflammatory C-reactive protein. Such benefits have not been seen from those taking western-type of meals.
A Two-day Menu of a Mediterranean Meal Plan
Day 1
Breakfast
1/2 English muffin with 1 teaspoon light margarine.
Smoothie: Blend 1/2 banana, 8 ounces fat-free milk, and 1 cup frozen berries.
Lunch
6 ounces light yogurt
15 grapes
1 veggie burger with lettuce and salsa
1 cup vegetarian vegetable soup
Dinner
1/2 cup vegetarian baked beans
BBQ chicken: Brush 4 ounces skinless, boneless breast with barbecue sauce and grill.
2 small boiled white potatoes
Day 2
Breakfast
8 ounces fat-free milk
1 toasted frozen waffle topped with 1/2 sliced banana
Lunch
Tuna pita: 1 mini whole wheat pita, 2 ounces water-packed light tuna, cucumber and onion slices.
6 ounces light yogurt together with 1/2 banana
10 baby carrots
Dinner
Jambalaya: Combine 3/4 cup cooked brown rice; 1/2 cup corn; 1/4 cup canned kidney beans; and 1/3 cup salsa. Heat through.
1 medium apple
3 cups spinach, steamed
Evaluation
The Body Mass Index (BMI) which is a measure of body fat based on weight and height is one of the values that will enable one to gauge the effectiveness of one’s interventions. According to the values obtained one can either be classified as underweight (less than 18.5), overweight (25-29.9), normal weight (18.5-24.9), or obese (equal or greater than 30). The BMI will enable one to evaluate how much fat they have lost thus reducing their risk of getting atherosclerosis. A lipid profile should also be done to check for the triglycerides, HDL cholesterol, LDL cholesterol and total cholesterol in the blood. The desirable value of total cholesterol is less than 200 (Seidman et al., 2014). As for the LDL cholesterol values greater than 100 increase the risk of atherosclerosis as it deposits inside the vessels to form a plaque. HDL less than 40 in men and less than 50 in women is a risk factor for atherosclerosis. On the other hand, the value of the triglycerides should be less than 150. These values will help in the evaluation of the goals set earlier since proper dieting, reduced smoking and increased physical activity should reflect accordingly on those values.
References
Martins e Silva, J., & Saldanha, C. (2007). Diet, atherosclerosis and atherothrombotic events. Revista Portuguesa de Cardiologia : Orgão Oficial Da Sociedade Portuguesa de Cardiologia = Portuguese Journal of Cardiology : An Official Journal of the Portuguese Society of Cardiology, 26(3), 277–94.
Mozaffarian, D., Benjamin, E. J., Go, A. S., Arnett, D. K., Blaha, M. J., Cushman, M., Turner, M. B. (2014). Heart Disease and Stroke Statistics-2015 Update: A Report From the American Heart Association. Circulation, 131(4), e29–322.
Seidman, M. A., Mitchell, R. N., & Stone, J. R. (2014). Pathophysiology of Atherosclerosis. In Cellular and Molecular Pathobiology of Cardiovascular Disease (pp. 221–237).
