Food Lipids: Chemistry, Nutrition, and Biotechnology

Table 1 Classification of LDL Particles
Class
Subfraction density
(g/mL)
Particle diameter
(nm)
LDL I 1.025–1.035 26–27
LDL II 1.032–1.038 25.5–26
LDL IIIA 1.038–1.050 24.7–25.6
LDL IIIB 24.2–24.6
LDL IVA 1.048–1.065 23.3–24.2
LDL IVB 21.8–23.2
Note LDL receptor activity and antioxidant content highest in LDL I and
II. Triglyceride content increases with decreasing size.
Source: From Ref. 15.
levels may be determined genetically [19]. Animal studies had shown earlier that
large lipoprotein molecules do not enter the arterial wall [20,21].
Cholesterol has assumed a central role in experimental and human atherosclerosis,
and the public is being exhorted to know its ‘‘cholesterol number.’’ However,
cholesterol levels tend to vary diurnally and with season [22–24], and single
measurements may not be an accurate indicator of risk. This is especially true if the
single determined value is near one of the accepted cut points [25]. Low levels of
cholesterol may lead to increased risk of noncardiovascular death [26–28].
Low cholesterol may become a problem at levels below 160 mg/dL [28] or 180
mg/dL [26].
Since ingested cholesterol has been shown to be atherogenic in some animal
species, since elevated levels of cholesterol are a risk factor, and since it is relatively
easy to measure, cholesterol has borne the brunt of the attack on CHD. The effect
of dietary cholesterol on levels of blood cholesterol appears to be small. In 1950
Gertler et al. [29] isolated from a large study of coronary disease 4 groups of 10
men each. They were the men with lowest or highest serum cholesterol and those
who ingested the most or the least dietary cholesterol. They were compared with
similar groups selected from the control subjects. In every group the men with coronary
disease exhibited significantly higher cholesterol levels than the controls but
in no case was any relation to cholesterol intake seen. Early in the Framingham
Study it was found that plasma cholesterol levels were unrelated to diet [30], a
finding also reported from the Tecumseh Study [31]. Several groups have reported
that addition of eggs to the diet of free-living subjects did not affect their cholesterol
level [32–34]. Gordon et al. [35] analyzed and compared the diets of men who did
or did not have coronary disease in three large prospective coronary disease studies
—Framingham, Puerto Rico, and Honolulu. Men who had coronary disease ingested
fewer total calories, less carbohydrate, and less alcohol. Intakes of cholesterol and
the P/S ratio of their dietary fat were similar for men who did or did not have
coronary disease. McNamara [36] reviewed data from 68 clinical studies relating to
effect of dietary cholesterol on plasma cholesterol. He concluded that there was a
mean rise of 2.3 � 0.2 mg/dL of plasma cholesterol for every 100 mg of ingested
cholesterol. Hopkins [37] described the complexity of the association between cholesterol
intake and plasma cholesterol. He found that the magnitude of the change
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