Epidemiological evidence has shown a beneficial association between PUFA (specifically the n-6 PUFA linoleic acid) intake and CHD morbidity and mortality. Clinical studies have shown that n-6 PUFA have the most potent cholesterol-lowering effects of the individual fatty acid classes. More recently, researchers have started to examine the possible role of n-3 PUFA in reducing the risk of CHD. The most important dietary n-3 dietary PUFA are α-linolenic acid (18:3n-3; ALA), EPA (20:5n-3) and DHA (22:6n-3). ALA is an essential fatty acid and is present in rapeseed oil, soyabean oil, linseed oil, walnuts and some seeds (see Fig. 2). EPA and DHA, which are often grouped together and referred to as very-long-chain PUFA, occur in oily fish and other marine animals. Furthermore, a small amount can be derived by conversion of dietary ALA (typically, only 1–10% of the ALA in the diet is converted to EPA and DHA); however, there is large variation between individuals, and conversion rates can be influenced by the dietary intake of linoleic acid and ALA (Goyens et al. 2005).
Diets high in ALA have been demonstrated to reduce the risk of CHD in several large cohort studies (Dolecek, 1992; Ascherio et al. 1996; Hu et al. 1997; Pietinen et al. 1997). Furthermore, a recent cross-sectional study in >1500 participants has found that higher intakes of ALA are inversely correlated with the occurrence of coronary artery disease (Djousse et al. 2003). Data from secondary intervention studies using ALA-rich mustard seed oil and Mediterranean-type diets enriched with ALA further support a beneficial effect on CVD (de Lorgeril et al. 1999).
Evidence from prospective secondary prevention studies suggests that EPA and DHA intakes ranging from 0·5 to 1·8 g/d markedly reduce CHD mortality (Burr et al. 1989) and non-fatal myocardial infarction (Singh et al. 1997; Marchioli et al. 2002). Furthermore, a recent meta-analysis of eleven randomised controlled intervention trials with >7900 patients in the intervention groups has reported a reduction in overall mortality, mortality associated with myocardial infarction and sudden death in patients with CHD (Bucher et al. 2002). However, the evidence relating to the dose of EPA and DHA and the EPA:DHA that is protective for CHD is less clear, particularly in relation to primary prevention (Kris-Etherton et al. 2003; Hooper et al. 2004).
n-3 and n-6 PUFA may protect against CVD in different ways. Substituting PUFA for SFA or MUFA appears to protect against arrhythmia, thrombosis, haemostasis and inflammation, but the greatest effect is seen with n-3 long-chain PUFA (EPA and DHA). In addition, high doses (>3·5 g/d) of n-3 long-chain PUFA have been reported to reduce blood pressure and TG and increase HDL-cholesterol but they do not lower LDL-cholesterol (Kris-Etherton et al. 2003).
Current dietary guidelines make specific recommendations about the composition of PUFA that should be included in a healthy diet (see Table 1). It is recommended that total PUFA should contribute 4–10% energy and linoleic acid between 4 and 8% energy. Recently, dietary guidelines have also included specific recommendations for n-3 PUFA such as ALA (2 g/d) and EPA and DHA (0·2–0·5 g/d). Data from the TRANSFAIR study indicates that the current intake of n-3 PUFA (especially ALA) may be inadequate for a substantial proportion of the population (Hulshof et al. 1999). Thus, the composition of a good ‘heart health’ spread should contain appropriate amounts of linoleic acid and ALA.
However, when the level of ALA is increased at the expense of linoleic acid, the oil blend becomes more sensitive to oxidation; as the number of double bonds in the oil blend increases, it becomes more susceptible to oxidation. The technical challenge is to control oxidation during processing and storage. Auto-oxidation is a natural process that takes place between molecules of O2 and unsaturated fatty acids, and is initiated by light, metals and/or pro-oxidants (Frankel, 1998). The risk of oxidative reactions taking place during spread manufacture and storage is high, as they occur at the many interfaces between phases, e.g. water and oil, oil and fat crystals and at the air surface. To combat the oxidation risk, manufacturers use several techniques during formulation and processing. Antioxidants are added to protect the unsaturated fatty acids, and location of the antioxidant to the site where oxidation is occurring is important and primarily determined by the polarity of the antioxidant. Polar antioxidants are more effective in the bulk lipids whereas non-polar antioxidants are more effective in the dispersed lipids (Frankel, 1998). By selecting a range of antioxidants the lipids in the different phases can be protected. Iron, copper and other transition metals catalyse peroxidation of unsaturated fatty acids, but it is impossible to remove these metals from the manufacturing process as they are in many of the ingredients (e.g. oils, starch, milk proteins) and are usually present in water, as well as the equipment. In addition, oxidative reactions are influenced by temperature. Thus, by developing tight raw material specifications and strictly adhering to good manufacturing processes it is possible to keep oxidation to a minimum.
Another challenge to achieving a good balance between n-3 and n-6 fatty acids has been to find an oil that is sufficiently high in ALA. Nature only provides a limited range of oils. Rapeseed oil and linseed oil are the oils with the highest level of ALA (100 and 530 g/kg respectively), but linseed oil is the only suitable oil to achieve the required ALA level in the product. However, linseed oil is not commonly used in the food industry, so it has been a challenge to set up a reliable supply chain. Furthermore, food authorities in some countries, being unfamiliar with this oil, have questioned its use in spreads and have had to be convinced of the safety and quality of linseed oil in this application.
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