This review examines the data pertaining to an important and often underrated EFA, alpha-linolenic acid (ALA). It examines its sources, metabolism, and biological effects in various population studies, in vitro, animal, and human intervention studies. The main role of ALA was assumed to be as a precursor to the longer-chain n-3 PUFA, EPA and DHA, and particularly for supplying DHA for neural tissue. This paper reveals that the major metabolic route of ALA metabolism is beta-oxidation. Furthermore, ALA accumulates in specific sites in the body of mammals (carcass, adipose, and skin), and only a small proportion of the fed ALA is converted to DHA. There is some evidence that ALA may be involved with skin and fur function. There is continuing debate regarding whether ALA has actions of its own in relation to the cardiovascular system and neural function. Cardiovascular disease and cancer are two of the major burdens of disease in the 21st century, and emerging evidence suggests that diets containing ALA are associated with reductions in total deaths and sudden cardiac death. There may be aspects of the action and, more importantly, the metabolism of ALA that need to be elucidated, and these will help us understand the biological effects of this compound better. Additionally, we must not forget that ALA is part of the whole diet and should be seen in this context, not in isolation.

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A recent study on the metabolism of 1‐14C‐α‐linolenic acid in the guinea pig revealed that the fur had the highest specific activity of all tissues examined, 48 h after dosing. The present study investigated the pattern of tissue lipid labeling following an oral dose of 1‐14C‐linoleic acid after the animals had been dosed for the same time as above. Guinea pigs were fed one of two diets with a constant linoleic acid content (18% total fatty acids) and a different content of α‐linolenic acid (0.3 or 17.3%) from weaning for 3 wk and 1‐14C‐linoleic acid was given orally to each animal for 48 h prior to sacrifice. The most highly labeled tissues (dpm/mg of linoleic acid) were liver, followed by brain, lung and spleen, heart, kidney and adrenal and intestines, in both diet groups. The liver had almost a three‐fold higher specific activity than skin and fur which was more extensively labeled than the adipose and carcass. Approximately two‐thirds of the label in skin plus fur was found in the fur which, because of a low lipid mass, would indicate that the fur was highly labeled. All tissues derived from animals on the diet with the low α‐linolenic acid level were significantly more labeled than the tissues from the animals on the high α‐linolenic acid diet, by a factor of 1.5 to 3. The phospholipid fraction was the most highly labeled fraction in the liver, free fatty acids were the most labeled fraction in skin & fur, while triacyglycerols were the most labeled in the carcass and adipose tissue. In these tissues, more than 90% of the radioactivity was found in fatty acids with 2‐double bonds in the tissue lipids. These data indicate that the majority of label found in guinea pig tissues 48 h after dosing was still associated with a fatty acid fraction with 2‐double bonds, which suggests there was little metabolism of linoleic acid to more highly unsaturated fatty acids in this time frame. In this study, the labeling of guinea pig tissues with linoleic acid, 48 h after dosing, was quite different from the labeling with α‐linolenic acid reported previously. The retention of the administered radioactivity from 14C‐linoleic acid in the whole body lipids was 1.6 times higher in the group fed the low α‐linolenic acid diet (diet contained a total of 1.8 g PUFA/100 g diet)compared with the group fed the high α‐linolenic acid diet (diet contained 3.6 g PUFA/100 g diet). The lack of retention of 14C‐labeled lipids in the whole body would be consistent with an increased rate of β‐oxidation of the labeled fatty acid on the diet rich in PUFA, a result supported by other studies using direct measurement of labeled carbon dioxide.

More research is needed in this area before it can be concluded that there is an association between alpha-linolenic acid and prostate cancer.

It is widely reported that an association exists between dietary fat intake and the incidence of prostate cancer in humans. To study this association, there is a need for an animal model where prostate carcinogenesis occurs spontaneously. The canine prostate is considered a suitable experimental model for prostate cancer in humans since it is morphologically similar to the human prostate and both humans and dogs have a predisposition to benign and malignant prostate disease. In this study, the FA and lipids profiles of the normal canine prostate tissue from nine dogs were examined. The total lipid content of the canine prostate tissue was 1.7 +/- 0.5% (wet weight). The lipid composition analysis using TLC-FID showed that the two major lipid classes were phospholipids and TAG. Total FA, phospholipid, and TAG FA analysis showed that the major FA were palmitic acid (16:0), stearic acid (18:0), oleic acid (18:1), linoleic acid (18:2n-6), and arachidonic acid (20:4n-6). The n-3 FA were present at <3% of total FA and included alpha-linolenic acid (18:3n-3) (in total and TAG tissue FA), EPA (20:5n-3) (not in TAG), and DHA (22:6n-3) (not in TAG). The n-3/n-6 ratio was 1:11, 1:13, and 1:8 in total, phospholipid, and TAG FA, respectively. This study shows the canine prostate has a low level of n-3 FA and a low n-3/n-6 ratio. This is perhaps due to low n-3 content of the diet of the dogs. FA analysis of dogfoods available in Australia showed that the n-3 content in both supermarket and premium brand dogfoods was <3% (wet weight), and the n-3/n-6 ratio was low.

Sir:Although the role of individual FA in cancer has been poorly investigated (1), a number of recent prospective epidemiological and case-control studies have shown a positive relationship between α-linolenic acid (ALA) in diet or blood and prostate cancer (2-8). In contrast, other epidemiological studies have found no significant relationship between ALA in diet, blood, or adipose tissue and prostate cancer (9-15). The

Sir:We refer to the letter published in the August 2003 issue of Lipids by Lauritzen and Hansen (1). The letter raises important issues discussed by many in this field, but we believe the scope of the letter goes beyond EFA. We can see the merits in their definition of an essential nutrient ("A food component that directly, or via conversion, serves an essential biological function and which is not produced endogenously or in large enough amounts to cover the requirements"). Lauritzen and Hansen suggest that "the essentiality of n-3 PUFA seems to be due to a specific function of 22:6n-3 in membranes and neuronal tissue" (1).We would like to raise the issue of whether 22:6n-3 is the only n-3 PUFA that has biological functions in mammals. We recognize that the literature on the role of 22:6n-3 in various neural functions is abundant (for a review, see Ref. 2) and that few studies address specific roles of the other n-3 PUFA. However, readers' attention should be drawn to several papers that show that 18:4n-3, 20:4n-3, 20:5n-3, and 22:5n-3 can influence eicosanoid synthesis (3,4), endothelial cell

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