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Review
. 2011 Apr;7 Suppl 2(Suppl 2):17-26.
doi: 10.1111/j.1740-8709.2011.00299.x.

Conversion of linoleic acid and alpha-linolenic acid to long-chain polyunsaturated fatty acids (LCPUFAs), with a focus on pregnancy, lactation and the first 2 years of life

Affiliations
Review

Conversion of linoleic acid and alpha-linolenic acid to long-chain polyunsaturated fatty acids (LCPUFAs), with a focus on pregnancy, lactation and the first 2 years of life

Robert A Gibson et al. Matern Child Nutr. 2011 Apr.

Abstract

Over the past two decades, there has been a marked shift in the fatty acid composition of the diets of industrialized nations towards increased intake of the n-6 fatty acid linoleic acid (LA, 18:2n-6), largely as a result of the replacement of saturated fats with plant-based polyunsaturated fatty acid (PUFA). While health agencies internationally continue to advocate for high n-6 PUFA intake combined with increased intakes of preformed n-3 long-chain PUFAs (LCPUFA) docosahexaenoic acid (DHA, 22:6n-3) and eicosapentaenoic acid (EPA, 20:5n-3) to reduce the incidence of cardiovascular disease (CVD), there are questions as to whether this is the best approach. LA competes with alpha-linolenic acid (18:3n-3) for endogenous conversion to the LC derivatives EPA and DHA, and LA also inhibits incorporation of DHA and EPA into tissues. Thus, high-LA levels in the diet generally result in low n-3 LCPUFA status. Pregnancy and infancy are developmental periods during which the fatty acid supply is particularly critical. The importance of an adequate supply of n-3 LCPUFA for ensuring optimal development of infant brain and visual systems is well established, and there is now evidence that the supply of n-3 LCPUFA also influences a range of growth, metabolic and immune outcomes in childhood. This review will re-evaluate the health benefits of modern Western diets and pose the question of whether the introduction of similar diets to nations with emerging economies is the most prudent public health strategy for improving health in these populations.

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Conflict of interest statement

The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Diagrammatic representation of our current understanding of the synthetic pathway for n‐3 and n‐6 fatty acids. AA, arachidonic acid; ALA, alpha‐linolenic acid; DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; LA, linoleic acid.
Figure 2
Figure 2
Results of an experiment illustrating the effect of feeding chickens a range of diets varying in the LA : ALA ratio on the EPA (close circles) and AA (closed squares) content of tissues as a % of total fatty acids. AA, arachidonic acid; ALA, alpha‐linolenic acid; EPA, eicosapentaenoic acid; LA, linoleic acid.
Figure 3
Figure 3
Effect of dietary ALA levels on (A) plasma and (B) liver phospholipid fatty acid content in rats fed diets containing various levels of ALA ranging from 0.2 to 2.9%en for 3 weeks. Fatty acids include EPA (circles), DPA (open triangles), DHA (closed triangles) and AA (open squares). Reprinted from Tu et al. (2010). AA, arachidonic acid; ALA, alpha‐linolenic acid; DHA, docosahexaenoic acid; DPA, Docosapentaenoic acid; EPA, eicosapentaenoic acid; LCPUFA, long‐chain polyunsaturated fatty acids.
Figure 4
Figure 4
Histograms depicting the average (A) LA and (B) DHA content of breast milk in Australian women in 1981 and 2000 (Gibson and Kneebone, 1981; Makrides et al., 2000). DHA, docosahexaenoic acid; LA, linoleic acid.
Figure 5
Figure 5
The effect of dietary dose of DHA corrected for BMI on the percentage of DHA in human breast milk (taken from Makrides et al. 1996).

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