Omega-3 fats from plants

There have been 4 large prospective studies which have looked at the relationship between intake of linolenic acid and coronary heart disease (CHD). They consistently found strong inverse associations – about 40-50% lower risk of fatal CHD with higher intakes. In the Lyon Diet Heart study there was a 60- 70% reduction in all cause mortality, including heart attack, angina and even cancer in study subjects consuming a Mediterranean diet. This diet was high in linolenic acid compared with men on a prudent diet containing more linoleic acid but less omega 3 linolenic acid (De Lorgeril et al. Arch Inter Med 1998; 158: 1181-7).

Animal models have also shown that n-3 fats result in diminished tumour development and n-6 fats enhance tumour development (Cave. FASEB J 1991; 5: 2160-6). Human in vivo studies have shown n-3 fats to down-regulate gene expression of potent carcinogenic growth factors (Kaminski et al., Blood 1993; 81: 1871-7).

Omega 3 fats, especially linolenic, have an antiarrhythmic effect in humans and may markedly reduce the incidence of lethal arrhythmias (Burr et al. Lancet 1989; 334: 757-61; Riemersma & Sargent. J Int Med 1989; 225:111-16). This was confirmed in a study of 40,000 health professionals with high intakes of linolenic acid (Ascherio et al.BMJ 1996; 313: 84).

In the Nurses Health Study the intake of linolenic acid protected against fatal ischaemic heart disease and this protection probably resulted from an antiarrhythmic effect of linolenic acid. However, the protective effect did not extend to nonfatal myocardial infarction (Hu et al. AJCN 1999; 69: 890-7).

The multiple risk factor intervention trial (MRFIT) revealed an inverse correlation between linolenic acid and development of CHD and strokes. An inverse correlation between adipose linolenic and blood pressure has also been reported and linolenic acid may also reduce platelet aggregation. In people eating n-3 linolenic acid rich plant foods, arterial compliance or elasticity (index of blood vessel health) was better than people who were not.

Although there may be a direct effect on cardiac arrhythmias from linolenic, it is likely that its effect is mediated, in part, through the syntheses of eicosapentaenoic acid ( EPA) and docosahexaenoic acid ( DHA). An impressive array of data indicate a direct antiarrhythmic effect of EPA.

The consensus from research is that linolenic acid is equally effective in decreasing LDL cholesterol (Chan et al. AJCN 1991; 53: 1230-34) and exerts an effect on cholesterol metabolism independent of its conversion to the longer chain n-3 fats. This is why the effect of feeding marine n-3 fats differ from those of feeding plant n-3 fats. It also has triglyceride lowering properties which may be exerted via linolenic itself or an effect of the EPA produced, which is known to decrease hepatic production and secretion of triglycerides (Rustan et al J Biol Chem 1988; 29: 1417-26).

Flax (linseed) seed oil.

Tissue concentrations of EPA increase when the diet is supplemented with flaxseed oil. This oil is 54% linolenic and has been postulated to protect against CHD on the basis of it's high content of this fatty acid.Increased cellular concentrations of EPA may be of benefit in the protection against CHD and hypertension (Simopoulos et al. AJCN 1991; 54: 438-63). Fish oil is the most efficient way of increasing tissue concentrations of EPA. EPA is converted into a range of eicosanoids, some of which have anticogulant effects. The evidence that flaxseed oil may protect against CHD and hypertension is not strong enough to recommend its regular use – more research is needed. Furthermore, this oil is very prone to oxidation and some studies have shown that consuming oxidised oil may facilitate the oxidation of LDL cholesterol in the blood. Consuming flaxseed oil with antioxidant/vitamin E rich foods would minimise this possibility.

Theory into Practice.

On average, Australians are consuming only 0.3% of their energy intake as linolenic acid (ideally should be 1%). The intake of n-3 linolenic acid in Dutch elderly men in 1992 was reported to be 1.2 g/day or 0.5% of energy intake. Major sources included margarine (25%), meat (11%), bread (10%) and vegetables (8%). The researchers commented that intakes could be further increased through greater use of canola and soy bean oils and margarines (Voskin et al. Eur J Clin Nutr. 1996; 50: 784-4).

If you have a high intake of fish (100g/day) then there is no need to increase plant sources of n-3 fats, but for the majority of people who do not (especially vegetarians), increasing dietary linolenic is another mechanism of increasing tissue EPA.

Consuming about HALF A TABLESPOON of CANOLA OIL daily provides the recommended 2g of linolenic acid, because it is high in this fatty acid (10% n-3 linolenic, 20% n-6 linoleic, 60% n-9 oleic).

Many CANOLA MARGARINES are only 40% canola oil so about ONE TABLESPOON/day will provide 2g linolenic. Some ‘Light/whipped’ canola margarines do not have any linolenic acid. Consuming more dark green leafy vegetables and nuts, especially walnuts, can help increase your intake.

Soybean oil is also high in n-3 linolenic, but it is also high in n-6 linoleic (8% linolenic, 54% n-6 linoleic, 23% n-9 oleic) which may compete metabolically with n-3 linolenic and reduce its conversion to the favourable omega 3 fats EPA and DHA.

Olive oil is low in n-6 linoleic (10%) and high in n-9 oleic acid (76%) but it is low in n-3 linolenic (0.3%), but in contrast to canola oil, it is high in antioxidant phytochemicals.

 

Last Updated: March 28, 2001