Food Lipids: Chemistry, Nutrition, and Biotechnology

The two major causes of death in the developed world are heart disease and
cancer. Both have been described as lifestyle diseases, and effects of diet fit under
that rubric. Since diet is one of the easiest lifestyle factors to investigate and possibly
change, its role has been pursued with vigor. However, dietary data are not as simple
to obtain as one might expect. Population-based data, derived from availability statistics,
do not account for individual variations. Recall may be flawed by habitual
underreporting of intake [1,2]. These methods provide useful data but their shortcomings
should be kept in mind.
II. LIPIDS AND CARDIOVASCULAR DISEASE
The major difficulty in assessment of the roles of diet and other factors is the absence
of a clear, unequivocal, antemortem diagnosis. Failing that, the data have been analyzed
to provide ‘‘risk’’ factors (called ‘‘odds’’ in Las Vegas) for indication of
susceptibility. Among the major risk factors for coronary heart disease (CHD), also
termed cardiovascular disease (CVD), are cigarette smoking, elevated cholesterol
level, elevated blood pressure, obesity, and maleness. The first of these is correctable
and the last is an unalterable fact of life, but the others may, to some extent, be
amenable to nutritional intervention. However, it is oversimplification to regard atherosclerosis
as a consequence of diet or aging or both. The molecular mechanisms
underlying the atherosclerotic process are being elucidated, and increasingly aspects
of the disease exhibit a genetic component. We are discovering new molecular and
immunological factors related to this disease. Fatal outcome is associated with plaque
rupture and thrombosis, and the notion of the disease being due to simple accretion
of cholesterol in the arteries is no longer tenable. Lusis [3] has published an elegant
description of factors involved in atherogenesis.
Although an experimental relationship between dietary cholesterol and atherosclerosis
had been adduced in 1913 when Anitschkow was able to produce aortic
lesions in rabbits [4], interest in fat in the diet and its relation to this disease began
to blossom in the 1950s. In 1950 Gofman and his colleagues [5] developed a method
for the ultracentrifugal separation of plasma lipoproteins, showed how these fractionated
particles could be related to heart disease, and implicated diet as a factor.
In 1952 Keys [6] described what was the beginning of his Seven Countries Study
and indicated atherosclerosis as a new public health problem.
The lipoproteins are lipid–protein agglomerates rather than real chemical compounds.
They are described by their hydrated densities (a physical property) but may
differ in size and composition. Thus, although the chemical analyses of low density
lipoprotein (LDL), high density lipoprotein (HDL), etc., are often published, they
represent average values and are not as precise indicators of identity as melting point
or spectrum. As research continues we continue to discover subfractions of lipoproteins
that affect CHD risk. Lipoprotein (a) [Lp(a)], which was described first by Berg
[7], is an LDL particle in which apoprotein B is linked to an apoprotein unit [apoprotein
(a)] via a disulfide bridge. Elevated Lp(a) levels have been associated with
a high risk of CHD [8–10]. Lp(a) interferes with fibrinolysis [11], and its levels in
the blood appear not to be affected by diet [12] or drugs [13].
Krauss and his co-workers [14,15] have identified subpopulations of LDL particles
that differ in size and composition (Table 1). The smaller, denser particles may
be associated more strongly with the risk of coronary disease [16–18], and their
Copyright 2002 by Marcel Dekker, Inc. All Rights Reserved.