How much and which kind of fat? This has remained a surprisingly divisive issue. Surprising because the Australian population has gradually reduced fat consumption from over 40% of energy in the middle of the last century to a little over 30% by the end. This has coincided with a substantial reduction in heart attack prevalence. However, the evidence that the quantity of fat is linked to coronary heart disease (CHD) is weak — it is the quality of the dietary fatty acids that matters.1 After all, CHD prevalence remains low in southern Europe, despite high intakes of lipid, mostly as vegetable oils. Prospective cohort studies and intervention trials, both primary and secondary, point that way. The positive link between dietary saturated fat and CHD is strong, as is the evidence that substituting polyunsaturated fatty acids (PUFAs, linoleic acid) for saturates lowers CHD risk. Whereas PUFAs are part of the eating pattern associated with least CHD in prospective trials, the opposite holds for saturates.2,3

The push for even less consumption of fat has abated with recognition that a clear benefit for this is lacking. Atherogenic lipoproteins are reduced and coronary atherosclerosis itself is lessened when mononunsaturates and PUFAs displace saturates.1 On the other hand, diets very low in fat and therefore high in carbohydrates may raise the atherogenic profile of lipoproteins. (The amounts of essential PUFA required for health are relatively small: 1%–2% of energy as linoleate and only 0.5% of energy as linolenate, but the present discussion relates to reducing CHD.) Saturated fatty acids may also have other undesirable, proatherogenic properties, but the evidence for this is equivocal.4 The concerns that PUFAs may predispose to cancer and cause other harm to health have not been substantiated.5

Apart from saturates, and especially dairy fats, for which the association with CHD is possibly the strongest, trans fatty acid consumption has also been linked with excess CHD.1,4 These fatty acids appear to behave like saturates, although they are mostly isomers of oleic acid that are formed from hydrogenation during hardening of oils or by microorganisms in the rumen of cattle. Since trans fatty acids have been largely removed from Australian manufactured spreads, the remaining amounts in dairy and meat fats are of minimal health concern.

One interesting isomer of linoleic acid, conjugated linoleic acid, that is also formed in the rumen of cattle may hold possible health benefits for both cardiovascular and non-CHD disorders.6

There are two major classes of PUFA — linoleic acid, with two double-bonds (so-called omega-6) and the omega-3 (also known as n-3) fatty acids, with up to six double-bonds. The omega-3 fatty acid α-linolenic acid (three double-bonds) is widely present in plants, and the longer omega-3 fatty acids (eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]) are found in fish. Much has been made of the need to balance the omega-6 and omega-3 fatty acids, as each gives rise to different classes of eicosanoids, such as thromboxane, prostaglandins and leukotrienes, that may have opposing effects on inflammation and vascular functions. A balanced dietary mix of omega-6 and omega-3 fatty acids is probably achieved with current intake of linoleic acid (about 6% of energy) and increased consumption of omega-3. This is achievable through eating more fish and α-linolenic-rich oils such as canola.

Fish eaters experience fewer CHD events than those who seldom eat fish.7 The strongest epidemiological association between any fatty acid and CHD protection is for the long-chain omega-3 fatty acids of fish. Supplemental fish oil fatty acids tested in a large randomised, placebo-controlled trial (the GISSI trial) achieved significantly reduced cardiovascular mortality, re-infarction and sudden cardiac death.8 The findings refocused attention on the anti-arrhythmic properties of omega-3 fatty acids, clearly established in animal experimentation and also observed in case–control comparisons of sudden deaths.9 The fish oil fatty acids possess other protective characteristics: arterial function (vasodilatation) is improved, thrombogenic and inflammatory processes in the arterial wall are reduced, plasma triglycerides are lowered and HDL raised, and blood pressure may be lowered.10

Similarly strong evidence for the plant omega-3 fatty acid is lacking, although one secondary prevention trial, the Lyon Heart Study,11 provides encouragement for increased consumption of α-linolenic acid from oils such as canola, flax and soy. Several prospective cohort trials also indicate that the consumption of α-linolenic acid is linked to less CHD.1 In humans, the conversion of α-linolenic acid into the long-chain EPA and DHA is not efficient, and the fish oil fatty acids need to be also eaten in larger quantities, probably as two fish meals weekly.

Oils and fats contain mainly triglycerides (three fatty acids on a glycerol backbone), but also fat-soluble vitamins and other fat-soluble substances, so that much of the daily intake of vitamin E derives from eating oils and spreads. Vegetable oils contain no cholesterol, but their fatty acid profile greatly varies. Some, such as palm oil and coconut oil, are rich in saturated fatty acids. Olive oil is rich in the monounsaturated fatty acid oleic; safflower, sunflower and corn oils are rich in linoleic acid, while canola provides the most diversity (very low in saturates, high in oleic acid and containing valuable amounts of linoleic and α-linolenic acids). There is little doubt that most saturated fatty acids raise plasma cholesterol levels, especially low-density lipoprotein (LDL) cholesterol.1,4 The fat profile of dairy fat (butter fat) is the most potent in raising LDL levels. Palm oil (rich in the saturated fatty acid palmitic acid) raises LDL levels, but less so than butterfat. Oleic acid lowers the level of LDL modestly, whereas linoleic acid (omega-6 PUFA) reduces the LDL cholesterol level most. Occasionally, in genetically predisposed people, linoleic acid may lower the high-density lipoprotein (HDL) cholesterol level slightly. In general, saturated fats raise LDL levels most in people who are already hypercholesterolaemic, more in men than in women, and mostly after middle age as capacity for fat clearance diminishes. Although some of the response is genetically linked, this is unlikely to become clinically useful.

By contrast, the omega-3 fatty acids, although more unsaturated than linoleic acid, have little cholesterol-lowering effect. α-Linolenic acid has almost no influence on plasma lipids, whereas fish oils lower triglyceride levels potently at intakes of less than 1 g daily, and tend to raise HDL levels.