Efficiency of conversion of α-linolenic acid to long chain n-3 fatty acids in man

Alpha-linolenic acid (18:3n-3) is the major n-3 (w3) fatty acid in the human diet. It is derived mainly from terrestrial plant consumption and it has long been thought that its major biochemical role is as the principal precursor for long chain polyunsaturated fatty acids, of which eicosapentaenoic (20:5n-3) and docosahexaenoic acid (22:6n-3) are the most prevalent. For infants,n-3 long chain polyunsaturated fatty acids are required for rapid growth of neural tissue in the perinatal period and a nutritional supply is particularly important for development of premature infants. For adults, n-3 long chain polyunsaturated fatty acid supplementation is implicated in improving a wide range of clinical pathologies involving cardiac, kidney, and neural tissues. Studies generally agree that whole body conversion of 18:3n-3 to 22:6n-3 is below 5% in humans, and depends on a concentration of n-6 fatty acids and, long chain polyunsaturated fatty acids in the diet. Complete oxidation of dietary 18:3n-3 to CO2 accounts for about 25% of 18:3n-3 in the first 24 h, reaching 60% by 7 days. Much of the remaining 18:3n-3 serves as a source of acetate for synthesis of saturates and monounsaturates, with very little stored as 18:3n-3. In term and preterm infants, studies show wide variability in the plasma kinetics of 13C n-3 long chain polyunsaturated fatty acids after 13C-18:3n-3 dosing, suggesting wide variability among human infants in the development of biosynthetic capability to convert 18:3n-3 to 22:6n-3. Tracer studies show that humans of all ages can perform the conversion of 18:3n-3 to 22:6n-3. Further studies are required to establish quantitatively the partitioning of dietary 18:3n-3 among metabolic pathways and the influence of other dietary components and of physiological states on these processes. (Author's abstract)
This review focuses on the metabolism of 18:3n-3. 18:3n-3 concentration in plasma and tissues tend to be lower than 18:2n-6 concentrations even when 18:3n-3 is rich in the diet, and 18:3n-3 storage as triglycerides in adipose is also relatively low.  The authors provide data showing that humans of all ages, including preterms and very likely fetuses, convert 18:3n-3 to 22:6n-3. Available data indicate that conversion of 18:3n-3 to 22:5n-3,22:5n-3, and 22:6n-3is a minor quantitative fact of 18:3n-3. Total oxidation and partial oxidation with carbon recycling appear to be predominant mechanisms and may be important processes per se. Conversion 18:3n-3 to n-3 LCP is progressively less efficient in the order consistent with the sequence of n-3 PUFA in the pathway leading to 22:6n-3, so that 22:6n-3 is the least efficient formed n-3 LCP in humans. Conversion efficiency also appears to decrease as infants mature, and may be less efficient in omnivorous adults where most estimates put it at around 1% or less of dietary consumption. A relatively high dietary n-6/n-3 ratio characteristic of modern diets is expected to reduce efficiency yet further. (Editor's comments)