Food Lipids: Chemistry, Nutrition, and Biotechnology

cholesterolemic effects of trans fats seen to be related to the ratio of dietary trans
fat to linoleic acid, the cholesterol levels rising as the ratio falls. Several studies
have shown that the tissue levels of trans-fatty acids are no higher in subjects with
coronary disease than in controls [68,69]. Houtsmüller [70] suggested in 1978 that
trans fat be regarded as a quasi-saturated fat.
In 1985 the Life Sciences Research Office of the Federation of American
Societies of Experimental Biology published a report which concluded that there
was little reason for health concerns at the reported intake level of trans fat (8 g/
person/day) [71]. Two years later the British Nutrition Foundation published a report
with the same conclusion [72]. A decade later reports sponsored by the International
Life Sciences Institute [73] and the British Nutrition Foundation [74] have found no
reasons to alter their previous conclusions. All the reports contained the safe suggestion
that more research was needed. Two reviews of trans fat effects have appeared
recently [75,76]. The findings that trans fats may elevate plasma LDL cholesterol
levels, thus increasing risk, suggest that it might be prudent to replace them
when possible. It should also be noted that between 1960 and 1985, levels of trans
fats in the American diet were fairly constant (7.63 � 0.08 g/person/day) [77],
whereas total age-adjusted mortality and deaths from heart disease and strokes fell
by 28%, 37%, and 59%, respectively [78].
Several new players have appeared on the heart disease stage and they may
ultimately affect our views of fat and cholesterol as major players in the CHD arena.
Over 30 years McCully [79] suggested that homocysteinemia could be a major risk
for coronary disease, and this is being recognized today [80–82]. Studies comparing
lipid levels in European countries show little relation of these levels to CHD mortality.
Ischemic heart disease mortality is four times higher in Belfast, Ireland than
in Toulouse, France despite general similarities in their diets (the French ingest significantly
more cholesterol and alcohol) and in their risk factor profiles [83]. Similarly,
mortality from heart disease in 50- to 54-year-old men is four times higher in
Vilnius, Lithuania than it is in Linköping, Sweden despite the fact that differences
in traditional risk factors are small [84]. In the years 1985–1987 age-specific mortality
from ischemic heart disease for men aged 45–54 years was 237/100,000 in
Belfast and 56/100,000 in Toulouse. In men aged 55–64 the rates per 100,000 were
761 in Belfast and 175 in Toulouse. In the younger age group total cholesterol levels
were significantly lower in the French (230 � 41 mg/dL vs. 240 � 41 mg/dL) and
HDL cholesterol levels were higher (54 � 15 mg/dL vs. 47 � 12 mg/dL). There
were no differences in the older men. Energy intake was virtually the same in the
two groups. The French ingested significantly more protein and cholesterol and significantly
less carbohydrate while fat intake was similar. In 1977 the CHD mortality
per 100,000 men aged 50–54 was 300 in Lithuania and 220 in Sweden. In 1994
mortality was 445 in Lithuania (102% increase) and 110 in Sweden (a 50% decrease).
Data from the Russian Lipid Research Clinics show an appreciable number of deaths
in men with low levels of LDL and high levels of HDL [85].
The isolation of Chlamydia pneumoniae from atherosclerotic, but not normal,
arteries [86,87] and the finding of cytomegalovirus in diseased arteries [88] may
shed light on mechanisms underlying the onset of the disease.
The role of conjugated linoleic acid (CLA) in atherogenesis is under study.
The CLA present in the diet (in diary products and meat of ruminant animals) is
primarily octadeca-c9,t11-dienoic acid, but the commercial product used in most
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