D. Research questions. This study will be guided by the following three research questions:
1. Can high cholesterol levels be genetically related?
2. Can high cholesterol levels be anatomically induced?
3. Do high cholesterol levels always result from poor eating choices?
E. Assumptions and Limitations. For the purposes of this study, it will be assumed that a chi-square analysis represents a superior methodology for the investigation of the above-stated general hypothesis.
F. Definition of terms.
1. Coronary heart disease (CHD).
1. High-density lipoprotein (HDL). This is the so-called "good" cholesterol (Griffith & Wood, 1997).
2. Hypercholesterolemia.
This term refers to an elevation of cholesterol in blood plasma (Albertine, 2001).
3. Low-density lipoprotein (LDL). This is the so-called "bad" cholesterol; these are the particles that contribute to atherosclerosis (e.g., the hardening and narrowing of the arteries) (Ulrich, 2002).
Chapter 2: Review of the Literature
Overview. As noted above, there are two types of lipoproteins in the blood; their relative quantities in the blood are main factors in heart disease risk (Henkel, 1999).
1. Low-density lipoprotein (LDL). This is the so-called "bad" cholesterol; LDLs are the form in which cholesterol is communicated into the blood and represent the primary cause of harmful fatty buildup in arteries. Henkel notes that the higher the LDL cholesterol level in the blood, the higher the risk of contracting heart disease.
2. High-density lipoprotein (HDL). By contrast, HDLs are the so-called "good" form of cholesterol, HDLs carry blood cholesterol back to the liver, where it can be eliminated. According to Henkel, HDL serves to prevent cholesterol accumulations in blood vessels; therefore, low HDL levels tend to increase the associated risk of heart disease.
One of the basic ways LDL cholesterol levels can reach dangerous levels is through eating too much of two nutrients: 1) saturated fat (commonly found mostly in animal products, and 2) cholesterol (found only in animal products); saturated fat increases LDL levels more than anything else in the diet. A wide range of other factors, though, also affect blood cholesterol levels including:
1. Genetic. According to Henkel, high cholesterol levels can frequently be found in families. "Even though specific genetic causes have been identified in only a minority of cases, genes still play a role in influencing blood cholesterol levels," he says (p. 23).
2. Overweight and Obesity. The author reports that excess weight tends to increase blood cholesterol levels; therefore, reducing weight may help to lower levels (Henkel, 1999).
3. Sedentary or Active Lifestyles. Henkel points out that regular physical activity may not only lower LDL cholesterol, but it may increase the levels of desirable HDL.
4. Age and Gender. Prior to experiencing menopause, Henkel points out that women tend to have total cholesterol levels that are lower than men of the same age; however, as shown in Figure 1 below, cholesterol levels naturally increase as both men and women age. According to Henkel, menopause has been associated with increases in LDL cholesterol in women in a number of studies.
5. Stress. Finally, although clinical studies have not demonstrated any direct connection between cholesterol levels and stress, clinicians advise that because people sometimes eat fatty foods to console themselves when under stress, this can result in higher blood cholesterol (Henkel, 1999).
While high total and LDL cholesterol levels, together with low HDL cholesterol, can tend to increase heart disease risk, these are just some of a wider range of other risk factors that include cigarette smoking, high blood pressure, diabetes, obesity, and physical inactivity. "If any of these is present in addition to high blood cholesterol, the risk of heart disease is even greater" (Henkel, p. 23).
Etiology. Total serum cholesterol levels gradually rise from childhood through adulthood. Cross-sectional studies indicate that cholesterol tends to peak in both sexes at around age 60 years; in fact, after a certain age, cholesterol levels tend to decline (see Figure 1 below) (Baum et al., 2000). According to Baum and his colleagues, "Prospective data corroborate these age and gender patterns, and the data further reveal that body mass index changes in parallel with cholesterol levels. Therefore, the rise in cholesterol during adulthood and the fall after age 60 may be attributable, in part, to weight change" (p. 227). While there is some evidence that the incidence of hypocholesterolemia (cholesterol < mg/dl) tends to increase in prevalence between the ages of 65 and 85 years, Baum et al. point out that other evidence suggests that individuals who manage to reach age 80 years in otherwise good health tend to enjoy "normal" cholesterol levels, without an overrepresentation of either hypo- or hypercholesterolemia (Baum et al., 2000).
Figure 1. Mean serum cholesterol levels by
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