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plasma triacylglycerol and the ratio of total to HDL cholesterol.
These Inuit had higher n3 fatty acid (EPA+DHA) concentrations
in their plasma phospholipids proportional to the intakes
of typical Eskimo marine foods. However, plasma total and
LDL-cholesterol concentrations correlated positively with n3
fatty acid concentrations. The divergent effects of n3 fatty
acids to reduce plasma triacylglycerol and elevate LDL may be
explained by a dietary background high in cholesterol and saturated
fat as well as in n3 fatty acids. The 2 situations are completely
compatible. In a feeding experiment by Nordoy et al
(15), a diet high in n3 fatty acids but also high in cholesterol
and saturated fat decreased plasma triacylglycerol and VLDL
and at the same time increased plasma LDL. The optimal diet
would be one high in n3 fatty acids and low in cholesterol and
saturated fat, thus reducing both triacylglycerol and LDL concentrations
in the plasma.
This pronounced effect of fish oil on hyperlipidemia is especially
well documented by precise dietary studies in which a diet
rich in salmon oil was fed and contrasted with a vegetable oil
diet and a diet high in saturated fat (16). Fish oil lowers plasma
triacylglycerol concentrations by inhibiting the synthesis of triacylglycerol
and VLDL in the liver. Apolipoprotein B production
is lower after consumption of fish oil than after consumption of
vegetable oils such as safflower or olive oil. This mechanism of
action is further substantiated by cultures of rabbit and rat hepatocytes
in which EPA, for example, in contrast with oleic acid,
inhibited triacylglycerol synthesis and stimulated the synthesis
of membrane phospholipid.
Pronounced postprandial lipemia occurs after the absoprtion
of fat from diets with high fat contents. Postprandial lipoproteins
are known to be atherogenic. They are also thrombogenic
because postprandial lipemia increases activated factor VII, a
procoagulant. Pretreatment with fish oil greatly lessens postprandial
lipemia (17), and this effect should be considered both
anti-atherogenic and anti-thrombotic.
The emphasis on fish and fish oil for coronary prevention does
not mean that vegetarians could not benefit from the consumption
of n3 fatty acids. The precursor to EPA and DHA in the
n3 fatty acid synthetic pathway is -linolenic acid (18:3n3),
which is especially rich in certain vegetable oils such as canola,
soy, flaxseed, and walnut oils. In the Lyon Heart Study, which
emphasized linolenic acid consumption from canola margarine,
blood EPA concentrations increased and the death rate from
coronary artery disease was reduced by 70% with a concomitant
reduction in sudden death (18). A vegetarian diet, then, can still
benefit from an increased n3 fatty acid content.
In summary, n3 fatty acids from fish and fish oil are natural
food substances that prevent coronary artery disease and sudden
death. Physicians should become acquainted with the powerful
therapeutic potential of these fatty acids. n3 Fatty acids have
immense public health significance for the control of the current
coronary epidemic.
REFERENCES
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Greenlandic Eskimos. Acta Med Scand 1973;200:69–73.
2. Dyerberg J, Bang HO, Hjorne N. Fatty acid composition of the plasma
lipids in Greenland Eskimos. Am J Clin Nutr 1975;28:958–66.
3. Dyerberg J, Bang HO. Haemostatic function and platelet polyunsaturated
fatty acids in Eskimos. Lancet 1979;2:433–5.
4. Dewailly E, Blanchet C, Lemieux S, et al. n3 Fatty acids and cardiovascular
disease risk factors among the Inuit of Nunavik. Am J
Clin Nutr 2001;74:464–73.
5. Connor WE. n3 Fatty acids and heart disease. In: Kritchevsky D,
Carroll KK, eds. Nutrition and disease update: heart disease. Champaign,
IL: American Oil Chemist’s Society, 1994:7–42.
6. Siscovick DS, Raghunathan TE, King I, et al. Dietary intake and
cell membrane levels of long-chain n3 polyunsaturated fatty acids
and the risk of primary cardiac arrest. JAMA 1995;274:1363–7.
7. Albert CM, Hennekens CH, O’Donnell CJ, et al. Fish consumption
and risk of sudden cardiac death. JAMA 1998;279:23–8.
8. Kromhout D, Bosschieter EB, Coulander C. The inverse relation
between fish consumption and 20-year mortality from coronary
heart disease. N Engl J Med 1985;312:1205–9.
9. Burr ML, Fehily AM, Gilbert JF, et al. Effects of changes in fat, fish,
and fibre intakes on death and myocardial reinfarction: diet and
reinfarction trial (DART). Lancet 1989;2:757–61.
10. GISSI Prevenzione Investigators. Dietary supplementation with n3
polyunsaturated fatty acids and vitamin E after myocardial infarction:
results of the GISSI-Prevenzione Trial. Lancet 1999;354:447–55.
11. Kang JX, Leaf A. Antiarrhythmic effects of polyunsaturated fatty
acids. Circulation 1996;94:1774–80.
12. Goodnight SH Jr, Harris WS, Connor WE. The effects of dietary
omega-3 fatty acids upon platelet composition and function in man:
a prospective, controlled study. Blood 1981;58:880–5.
13. Harker LA, Kelly AB, Hanson SR, et al. Interruption of vascular
thrombus formation and vascular lesion formation by dietary n3
fatty acids in fish oil in non human primates. Circulation 1993;87:
1017–29.
14. Davis HR, Bridenstine RT, Vesselinovitch D, Wissler RW. Fish oil
inhibits development of athersclerosis in rhesus monkeys. Arteriosclerosis
1987;7:441–9.
15. Nordoy A, Hatcher LF, Ullmann DL, Connor WE. Individual effects
of dietary saturated fatty acids and fish oil on plasma lipids and
lipoproteins in normal men. Am J Clin Nutr 1993;57:634–9.
16. Phillipson BE, Rothrock DW, Connor WE, Harris WS, Illingworth DR.
Reduction of plasma lipids, lipoproteins, and apoproteins by dietary
fish oils in patients with hypertriglyceridemia. N Engl J Med 1985;
312:1210–6.
17. Harris WS, Connor WE, Alam N, Illingworth DR. The reduction of
postprandial triglyceridemia in humans by dietary n3 fatty acids.
J Lipid Res 1988;29:1451–60.
18. De Lorgeril M, Renaud S, Mamelle N, et al. Mediterranean alphalinolenic
acid-rich diet in secondary prevention of coronary heart
disease. Lancet 1994;343:1454–9.
416 EDITORIAL
TABLE 1
Actions of n3 fatty acids to prevent coronary heart disease and sudden
death
1) Prevent cardiac arrhythmias (ventricular tachycardia and fibrillation)
2) Act as antithrombotic agents
3) Inhibit the growth of atherosclerotic plaques
4) Act as antiinflammatory agent (inhibit synthesis of cytokines and
mitogens)
5) Stimulate endothelial-derived nitric oxide
6) Lower plasma concentration of triacylglycerol and VLDL cholesterol
and increase plasma concentrations of HDL cholesterol
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