ATHEROSCLEROSIS

Atherosclerosis is a complex disease of the arteries; it is a form of arteriosclerosis. The passageways through the arteries become roughened and clogged with fatty deposits such that blood cannot flow freely, like clogged sink pipes (Figure 7-1). This is the form of heart disease described as ischemic. Atherosclerosis is thought to be a cause of coronary thrombosis, myocardial infarction (MI) (heart attack, or coronary), and CVA. Peripheral arterial disease (PAD) is a form of atherosclerosis and is associated with significant cardiovascular morbidity and mortality. PAD is defined as an ankle-brachial blood pressure index of less than 0.9 in either leg. As shown from the NHANES 1999 to 2004 data, PAD prevalence increases with age and is found in about 1 in 4 persons 80 years of age and older. Non-Hispanic black men and women and Mexican American women have a higher prevalence of PAD than non-Hispanic white men and women, with other risk factors being current or previous: smoking, diabetes mellitus, low kidney function, high-sensitivity C-reactive protein level greater than 3.0 mg/L, and uncontrolled hypertension, treated or not (Ostchega and colleagues, 2007).

LIPOPROTEINS

High-density–lipoprotein cholesterol (HDL-C), low-density–lipoprotein cholesterol (LDL-C), and very-low-density lipoprotein (VLDL) are all forms of cholesterol found in the blood. Lipids is the term used to describe all forms of fat found in the blood. Chylomicrons are another form of lipoprotein. VLDL is the main carrier of triglycerides (a type of blood fat) synthesized in the body. Hypercholesterolemia refers to elevated total cholesterol level but is usually a result of high serum LDL-C. Hyperlipidemia is the term generally used to describe a combination of high levels of LDL-C and triglycerides. Dyslipidemia, as discussed in Chapter 5, refers to low levels of HDL-C but usually coexists with elevated triglycerides.

What very few people know is that the total cholesterol number is based on a mathematical calculation. Total cholesterol is the sum of HDL-C plus LDL-C plus one fifth of triglycerides. The laboratory measurements are of total cholesterol, HDL-C, and triglycerides, with the difference being the calculated LDL-C level (if triglycerides are over 400 mg/dL, the calculation of LDL-C is not possible; in this case a direct laboratory measurement of LDL-C level may be performed). Therefore when a person needs to lower the total cholesterol level, he or she is really lowering the LDL-C and/or triglyceride levels. Changes made are aimed at protecting or raising the HDL-C level.

HDL-C, which has more protein than does LDL-C or VLDL, allows more cholesterol to be taken from the body’s cells, resulting in greater transport and removal of cholesterol through the liver. HDL-C is often called “good cholesterol.” In fact, research has shown that individuals with more HDL-C have less heart disease. However, one’s level of HDL-C is highly genetic, and it can be a challenge to increase it to optimal levels.

LDL-C is often referred to as “bad cholesterol.” It is well recognized that a high level of LDL-C induces atherosclerosis and is a strong risk factor for heart disease. The majority of cholesterol medications are aimed at lowering LDL-C. Diet can have a strong influence, but it can take at least 3 months for an impact to be seen. Unfortunately, not everyone responds to changes in the diet. However, because there are no adverse health outcomes with medical nutrition therapy (MNT), this is advised as the primary strategy before use of medications (Table 7-1).

It was as recently as the early 1990s that elevated triglyceride levels started being recognized as a contributor to CVD, although controversy still exists as to its role in CVD. In recent years the American Heart Association (AHA) lowered the definition of high fasting triglyceride level from 200 to 150 mg/dL. This was a result of the realization that the higher the fasting triglyceride level, the greater the rise of postprandial triglycerides. It has been shown among women that triglyceride levels, in either fasting or fed states, correlated with known cardiac risk factors and indicators of insulin resistance. However, elevated triglyceride levels measured 2 to 4 hours postprandially had the strongest association with cardiovascular events (Bansal and colleagues, 2007). Arterial stiffness has been noted in women with elevated triglyceride levels and CVD (Le and colleagues, 2005).

Nutritional habits have a significant impact on triglyceride levels and are described below. In a person whose only elevated lipid is triglycerides, the condition is referred to as hypertriglyceridemia. There are some medications that address triglycerides and are described at the end of the chapter.

GOALS FOR BLOOD CHOLESTEROL LEVELS

Total cholesterol level should be less than 200 mg/dL. The National Cholesterol Education Program (NCEP) indicates the goal for LDL-C is less than 130 mg/dL for moderately high-risk persons (two or more risk factors and a 10-year risk for CHD of 10% to 20%—see Figure 7-2). The NCEP III guidelines state that in very high-risk patients a LDL-C level of less than 70 mg/dL is a reasonable goal, regardless of age (Aronow, 2006).

Triglyceride levels are advised to be less than 150 mg/dL, and HDL greater than 40 mg/dL for men and 50 mg/dL for women, with the goal being greater than 60 mg/dL to best help prevent CVD. However, triglyceride levels greater than 100 mg/dL have been linked with high C-reactive protein (CRP) levels, suggesting that fasting triglyceride levels under 100 mg/dL may further reduce CVD risk (Ahmad and colleagues, 2005).

On the other hand, low levels of total cholesterol less than 160 mg/dL, referred to as hypocholesterolemia, can be an indicator of poor health. Lipid metabolism is known to be altered in many acute diseases. There are many potential causes of decreased serum cholesterol levels. Malabsorption is one factor, and this is likely the factor behind hypocholesterolemia with the active phase of Crohn’s disease. There may also be altered synthesis of cholesterol (Hrabovský and colleagues, 2007). In solid tumors and those of the blood, hypocholesterolemia may be due to increased use of cholesterol by cancer cells (Yavasoglu and colleagues, 2008).

Hypocholesterolemia has been implicated in genetically based violent behavior (Edgar and colleagues, 2007). Low levels of cholesterol have been found to help predict mortality in critically ill surgical patients. Promotion of higher levels of cholesterol is advised for the management of critical illness (Bonville and colleagues, 2004).

The guidelines of the NCEP now recommend that adults 20 years of age and older have their total cholesterol and HDL-C levels measured. If the total cholesterol is 200 mg/dL or more, or the HDL is less than 40 mg/dL, a complete lipoprotein profile is advised (including the LDL-C and triglyceride levels). In assessing risk for CHD it has been noted that total cholesterol level, blood pressure, and body mass index (BMI) showed average levels significantly higher during the winter months (Ulmer and colleagues, 2004). This is likely due, in part, to decreased production of vitamin D from a cholesterol-based hormone with reduced sunlight.

Goals for MNT and use of medications vary depending on the differing levels of these lipids and risk factors. There is debate on goals and treatment for the elder population, in part due to limited research verifying the benefit of cholesterol-lowering medications. Polypharmacy, with excess prescription of medications, continues to be a potential problem especially for the elder population (see Chapter 13). Before the use of lipid-lowering medications, referral to a registered dietitian is advised by the AHA, unless the individual is at very high risk for an MI or CVA.

RISK FACTORS FOR CORONARY HEART DISEASE

The 2004 guidelines to control CVD as developed by the Adult Treatment Panel III (ATP III) is an updated version of recommendations made initially in 2001 by the NCEP of the National Heart, Lung, and Blood Institute. The goals were aimed at lowering cholesterol levels. Changes in the updated 2004 ATP III report are primarily aimed at guidelines for medication use. The ATP IV guidelines are expected in 2010. Although LDL has received the most attention in regard to medical and nutritional management, there are other risk factors that can be controlled for greatest reduction in CVD risk. The following are considered risk factors for CVD:

The AHA guidelines indicate that HDL-C greater than 60 mg/dL counts as a negative risk factor; its presence removes one risk factor from the total count from the list. This is because HDL particles have the capacity to promote cholesterol transport out of the body and antagonize pathways of inflammation, thrombosis, and oxidation.

RISK FACTORS AND PREVENTION STRATEGIES FOR STROKES

There are a variety of risk factors for stroke, including hypertension, diabetes, obesity, and lack of physical activity. Research related to stroke risk and the metabolic syndrome indicates that individuals with CVD, especially women, are at high risk for ischemic stroke or TIA (Koren-Morag, Goldbourt, and Tanne, 2005).

Trans fatty acids increase risk of stroke. Protection from stroke occurs with omega-3 fatty acids and other unsaturated fats, including oleic, linolenic, and arachidonic fatty acids (see Chapter 2 for food sources—Table 2-5). The unsaturated fats appear protective in women but appear to increase risk of ischemic stroke in men (Monteiro and Vaz Almeid, 2007). Another benefit of omega-3 fats as found in fish oil includes increasing the size of LDL particles, making them more fluffy and less likely to adhere to the lining of vascular walls.

A high glycemic load along with a higher intake of fatty meats has been found to increase stroke risk. A diet low in fruits, vegetables, fish, and whole grains is associated with increased risk of stroke (Fung and colleagues, 2004). High glycemic load is related to high postprandial insulin production and, along with reduced antioxidant vitamins with low intake of high-fiber plant-based foods, likely has an enhanced risk of atherosclerosis.

Following stroke or TIA there is increased risk of future incidents. Riboflavin deficiency has been found to be common after stroke. Supplementation of vitamin B₂ may be beneficial after CVA due to reduced oxidative damage and consequent cerebral edema (Gariballa and Ullegaddi, 2007).

CHOLESTEROL INTAKE

There still remains controversy regarding cholesterol intake for heart health. Research shows conflicting outcomes. Data from free-living populations show that egg intake generally does not cause higher cholesterol levels. The most recent AHA guidelines no longer specifically advise limiting egg intake (Kritchevsky, 2004). However, the ATP III guidelines still advocate reduced cholesterol intake with a goal of less than 200 mg of cholesterol daily. This essentially limits egg, shellfish, and organ-meat intake. The yolk of a medium-sized egg is estimated to contain about 225 mg of cholesterol. Three ounces of beef liver contains over 400 mg of cholesterol. Canada does not have a specific guideline on cholesterol intake because of the evidence suggesting a closer link between saturated and trans fatty acid intake and increased endogenous production of cholesterol. For most healthy individuals, synthesis of cholesterol by the liver adjusts to the level of dietary cholesterol intake.

One study found that with a restricted carbohydrate intake an additional 640 mg of cholesterol from eggs had an antiinflammatory effect with increased HDL-C. This finding may be due to the cholesterol itself or possibly due to the antioxidant lutein content of egg yolk, which helps lower an inflammatory response (Ratliff and colleagues, 2008).

As with much of nutrition, individualized guidance should be advocated. Choline, for example, with the highest dietary sources being liver and eggs, has been shown to reduce homocysteine levels (Olthof and colleagues, 2005). Individuals who want to include whole eggs and liver in the diet because of taste preference and/or positive health associations should have their serum cholesterol levels assessed to ensure tolerance.

Research outcomes of two studies further indicate the need for individualization. The first study found that in men, consumption of two or more eggs daily was not related to total cholesterol level as compared with a lower intake of eggs; for women, there was an association. Women who limit their intake to one to two eggs weekly had significantly lower cholesterol levels than those with daily consumption (Nakamura and colleagues, 2004). Among persons with insulin resistance, a high-cholesterol diet did not promote an increase in inflammation as indicated by CRP levels or non–HDL-C levels, but it did have an adverse effect among insulin-sensitive individuals (Tannock and colleagues, 2005). Generally, if LDL-C is at the very high risk level of over 200 mg/dL, cholesterol intake should be limited to under 200 mg daily average. If LDL is at a more moderately low risk level (Table 7-2), cholesterol intake can be more moderate as per food label guidelines at 300 mg daily.

DIETARY FATS

There is strong evidence that the type of fat rather than the total amount of fat is most important in preventing CVD. Low-fat diets have been advocated because this is one simple strategy to lower intake of saturated and trans fats. However, this can be confusing to the consumer who may assume that carbohydrates may be included freely in the diet with a low-fat diet, which would have an adverse effect on individuals with the metabolic syndrome. It also has been found that a very low-fat diet with 10% fat increased fasting triglyceride level and the total cholesterol to HDL-C ratio, whereas a moderate fat intake of 35% lowered triglyceride level and the total cholesterol to HDL-C ratio. This adverse impact of a very low-fat diet was found even in healthy, endurance-trained runners (Larson-Meyer and colleagues, 2008).

As reviewed in Chapter 2, there are many forms of fatty acids. Some are beneficial to cholesterol levels and heart disease and others have adverse effects. In moderation, all may be included. Research continues on the impact of specific fatty acids. Although saturated fat is generally advised to be reduced in the prevention and management of CVD, a low intake of certain fats in butter has been found to be detrimental. This includes lauric acid from dairy products, with low intake being associated with acute MI. It is advised that recommendations on fatty acid intake should aim for both an upper and lower limit (Lopes and colleagues, 2007).

SATURATED AND TRANS FATTY ACIDS

Saturated fat has long been known to raise cholesterol levels, specifically LDL-C levels. Because risk of heart disease begins in childhood, the American Academy of Pediatrics advises low-fat or fat-free milk for children older than 2 years of age.

Although saturated fat intake should be lowered to reduce risk of CVD, food sources are not always as clear. Among the 12 major milk fatty acids, only 3 (lauric, myristic, and palmitic—see Table 2-5) have been associated with raising total serum cholesterol levels. However, their individual effects are variable regarding impact on LDL-C and HDL-C (German and Dillard, 2006). Moderate supply of myristic acid (see Table 2-5) at less than 2% of total kcalories with the recommended intake of alpha-linolenic acid from canola oil at about 1% of total kcalories contributes to improved cholesterol removal from tissues into HDL-C, dependent on enzyme activity (Vaysse-Boué and colleagues, 2007).

Although red meat is thought of as being high in saturated fat, it was found that lean red meat, trimmed of visible fat, did not increase cholesterol levels or risk of thrombosis (D Li and colleagues, 2005). A fast-food meal of a burger and fries was found to have more myristic (C14:0), palmitic (C16:0), stearic (C18:0), and trans fatty acids (C18:1) than an organic beef meal. LDL-C decreased more with the organic beef meal, which had lesser amounts of saturated and trans fatty acids, than in the fast-food beef meal (Bray and colleagues, 2007).

It is now recognized that trans fatty acids act as saturated fats do in the body and have been linked with inflammation in women (Mozaffarian and colleagues, 2004). As reviewed in Chapter 2, hydrogenated fats are referred to as trans fatty acids. In the last 10 years or so, the adverse health effect of hydrogenated fats has been recognized. One explanation for the increased CVD associated with trans fatty acids is that they decrease HDL-C level (Dyerberg and colleagues, 2004). In January 2006, listing of the estimated amount of trans fatty acids on the Nutrition Facts section of food labels became mandatory; the listing can be found under saturated fats.

As the percentage of kcalories from trans fatty acids increases, there is a linear impact on increasing LDL-C levels in relation to reducing HDL-C levels. There appears to be no safe level of intake of trans fatty acids, and they have double the adverse impact of saturated fats (Ascherio, 2006).

UNSATURATED FATS

The unsaturated fats in general are helpful for reducing LDL-C levels. In the 1970s only polyunsaturated fats (see Figure 2-4), as primarily found in seed and vegetable oils, were promoted as a means to normalize hypercholesterolemia. Although this was effective, the unintended effect was that HDL-C levels also were reduced with a high intake of polyunsaturated fats. Excess intake of the polyunsaturated type of fat found in seed oils, linoleic acid (see Table 2-5), has been shown to oxidize LDL-C and increase risk of clot formation (Khor, 2004). Further research has found monounsaturated fats lower LDL-C levels but are protective to the HDL-C levels, the desired effect.

The form of polyunsaturated fats known as the omega-3 fatty acids do have beneficial effects and generally are advised. Diets rich in eicosapentaenoic acid (EPA), an omega-3 fatty acid, are associated with decreased arterial stiffness; adding EPA to a high-fat meal results in acute changes in vascular tone, independent of changes in oxidative stress (Hall and colleagues, 2008). For vegans or others who do not consume fatty fish, it is advised to increase intake of alpha-linolenic acid and decrease linoleic acid to promote the endogenous production of these longer chain n-3 polyunsaturated fatty acids (Griffin, 2008).

Omega-3 fats are known to reduce blood levels of triglycerides and therefore are recommended in the control of CVD. These fats also reduce the inflammation process of the body and tend to reduce the clotting time of the blood. A study looking at changes in triglyceride levels with fish consumption found that triglycerides fell almost 30% with intake of fish and almost 40% with both fish consumption and weight loss. Furthermore, one form of HDL-C, HDL2, increased by about 25% (Mori and colleagues, 1999). Fish intake has been found to help prevent worsening of atherosclerosis in women (Erkkila and colleagues, 2004).

The cardioprotective effect of omega-3 fatty acids is so great that the AHA is now recommending that everyone consume fatty fish at least twice weekly. This equates to 6 oz of salmon or other fatty fish such as lake trout or one can of sardines or herring weekly. If an individual will not eat fish, it is now advised that omega-3 fatty acid supplements be taken. An alternative to which some individuals do not object is to take cod-liver oil. One teaspoon of cod-liver oil is the equivalent of eating about 2 oz of fatty fish and contains approximately 500 mg of EPA and docosahexaenoic acid (DHA)—two forms of omega-3 fats as found in fish oil supplements. One-half teaspoon of cod liver oil daily will meet the guideline set forth by the AHA to eat fatty fish twice weekly. Supplement use should be reviewed with the person’s physician to avoid excess intake because of the anticlotting aspect of omega-3 fatty acids.

Related posts:

Renal Disease The Nutrition Care Process in the Health Care Setting The Art of Nutrition in a Social Context Carbohydrates, Proteins, and Fats Obesity and Healthy Weight Management Growth and Development Issues in Promoting Good Health

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