Eicosapentaenoic acid (EPA) 20:5 n-3 in membrane
Diet n-3 decreases AA
Diet n-6 decreases EPA
Synthesis from 18:3 n-3
Synthesis from 18:3 n-3
Fig. 4.5 Influence of dietary n-3/n-6 polyunsaturated fatty acids and drugs on inflammatory eicosanoid production. NSAID: non-steroidal anti-inflammatory drugs; AO: antioxidants; +: signifies weakly inflammatory; +++: signifies strongly inflammatory.
ments for essential fatty acids are summarized in Box 4.2.
Finally, our discussion of 'conditional essentiality' has followed the generally made assumption that the body's requirements for saturated and monounsaturated fatty acids can always be met entirely by endogenous biosynthesis; in other words there is never a dietary requirement for them. There is evidence, albeit limited, that fatty acid biosynthesis is a slow process in human tissues even when people are consuming diets with a low fat content. It is worth considering, therefore, whether there may be circumstances of high demand for saturated fatty acids (for example in brain or lung development), during which even saturated fatty acids become conditionally essential. Such a concept has not been actively researched.
Box 4.2 Views on human requirements for essential fatty acids
An answer to the apparently simple question, 'What are the requirements of human beings for essential fatty acids (EFA)?' is in fact not at all simple for several reasons.
• We must first define whether we mean EFA of the n-6 or n-3 families. As discussed in the text, needs for the n-6 family seem to be much greater than those for the n-3 family.
• Within each family, we must define whether we mean the parent acids (18:2n-6 or 18:3n-3) or their long chain polyunsaturated (LCP) metabolites. When the desaturation/elongation enzymes are fully active, then there may be a strict requirement only for the parent acids; when the activity of these enzymes is limiting, a requirement for the LCP may be defined (conditional essentiality).
• We must understand how members of the n-3 and n-6 families interact to influence each other's requirements. For example, because of competition for desaturases, a large excess of dietary n-6 over n-3 acids (which is usually the case in industrialized countries) may increase the requirement for the n-3 family.
• We must be clear what the requirement is for:
- at the lowest level, there is a minimum requirement for either n-3 or n-6 acids to prevent the onset of overt deficiency signs;
- over and above this level of intake, although no deficiency signs are seen, there may be public health recommendations for intakes to, for example, maintain low plasma concentrations of LDL (n-6 acids) or VLDL (n-3 family), to stimulate anti-inflammatory eicosanoid formation or limit platelet aggregation tendency etc.;
- intermediate levels of intake may be required to optimize visual and other functions that are not necessarily easy to quantify.
Each country tends to make slightly different recommendations, based on consensus views of its own scientists. In the UK, for example, recommended intakes to avoid deficiency are not less than 1% of dietary energy of 18:2n-6 (approximately 1-2.5g day"1) and 0.2% of dietary energy for 18:3n-3 (approximately 0.4-0.5 g day-1). Some authorities may recommend intakes of up to 3% of dietary energy as n-6 polyunsaturated fatty acids during pregnancy and lactation to account for increased needs of the foetus or milk for the new-born. However, this assumes that there is no metabolic adaptation. For example stores of EFA in adipose tissues (which are very large) could be mobilized for this purpose.
Recommendations to maintain optimum blood lipid concentrations
There is clearly less precision in such recommendations because of differing views on what is 'optimal'. In the UK, the recommended intake is 6% of dietary energy as n-6 polyunsaturates, or approximately 12-15g day-1. No recommendation has been made for the n-3/n-6 ratio in this regard, although it is clearly an important issue to be resolved. Most authorities now set an upper limit for n-6 polyunsaturates intake of about 10% of dietary energy. The reasons include concern for the effects of peroxidative damage (see Box 4.3) and to avoid inhibiting pathways of n-3 polyunsaturated fatty acid metabolism.
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