B. Recognition of a possible healthy upper limit on linoleic acid intake:

The current dietary intake of LA in most populations is higher than the 2 energy % that is adequate for health. Questions recently have been raised about the possible unhealthy effects of high intake of w6 PUFA. Because of this concern, there is a need to indicate not only what dietary LA intake is adequate, but also how much can be consumed without undue risk to health. No conclusive scientific evidence regarding the issue of a safe upper limit for w6 PUFA is presently available. Therefore, tangential information have to be relied upon to determine whether there may be a healthy upper limit for LA and, if so, what that limit is.

Some data indicate that a higher than required dietary intake of LA is beneficial. For example, epidemiological evidence indicates that higher ratios of dietary LA to saturated fat are associated with reductions in total plasma cholesterol and low density lipoprotein (LDL)-cholesterol (Bronte-Stewart, 1956; Keys, 1970; Pederesen 2003). High LA intake also increases fecal sterol excretion and leads to more efficient clearance of a dietary fat load (Spritz, 1965; Weintraub, 1988). Approximately 20 en% as PUFA promoted a significant reduction of myocardial infraction without observed side effects (Leren 1966, 1970).

On the other hand, there are potential dangers associated with high LA intake. One reason is that they reduce apolipoprotein A-I production (Shepherd, 1978). This may lower high density lipoprotein (HDL) levels and thereby decrease reverse cholesterol transport, increasing the risk of atherosclerotic cardiovascular disease. High LA intake over long periods in males also increases the risk of gallstone formation (Sturdevant, 1973). Biochemical evidence suggests that increased levels of LA in vascular cells may predispose to lipid peroxidation (Alexander-North, 1994), and there also is a risk that through competition, increased w6 PUFA may reduce the incorporation of w3 PUFA, thereby leading to unhealthy imbalances in tissue lipids (Spector, 1985).

These examples outline briefly the controversy as it stands regarding the health merits of LA intake above an adequate intake of 2 energy %. This committee recognises that some national bodies have already taken a stand and recommended a healthy upper limit for LA intake. At present, this committee could not reach consensus and has no recommendation to make on this question.

Notes on the reports forming the basis for an adequate linoleic acid intake

Collins et al (1971) reported on the effect of adding soybean oil to fat free intravenous total parenteral nutrition (TPN) given to two adult patients with short bowel syndrome. Plasma linoleic acid was very low before addition of the soybean oil. Linoleic acid increased but the ‘triene’ (20 :3w9) content of the plasma did not change after addition of soybean oil. No other outcomes (physiological or clinical) were considered. In the authors’ terms, 2.2 en% linoleic acid ‘appears’ sufficient. NOTE : these were sick patients and there were only two of them. However, this is one of a very few studies of this kind in which w3 PUFA were provided.

Combes et al (1962) reported on the effects of different levels of linoleic acid intake on weight gain in infants. The milk formulas contained 18 en% fat based on a mixture of corn oil and coconut oil providing 0.01%, 0.4% or 4.5% linoleic acid. The nursery was maintained at 100% humidity. No differences in weight gain or clinical health were noted. Higher intake of linoleic acid resulted in higher plasma linoleic acid but plasma triene levels did not differ between the groups. NOTE : Unusually high humidity was provided but, still, very low linoleic acid intakes did not cause deficiency symptoms (in infants).

Cuthbertson (1976) reviewed the impact of formulas providing different intakes of linoleic acid on infant growth and health. He noted that the linoleic acid content of breast milk varies from about 1 wt% in East Africa to more than 15 wt% in the Middle East. He noted that if linoleic acid requirement was higher than 1 en%, reports of deficiency symptoms in such infants should be more prevalent in the literature than they were at the time. The conclusion was that the linoleic acid requirement of infants was unlikely to be greater than 0.6 en%.

Goodgame et al (1978) did a prospective study in adult surgery patients receiving fat-free total parenteral nutrition. They observed that the fatty acid changes consistent with EFA deficiency occurred within four weeks of starting the fat free TPN but found that a link to the onset of clinical symptoms was unclear. They noted that ‘unfortunately, the functional definition of EFA deficiency is somewhat arbitrary and indistinct’. They reported reductions in w6 PUFA and reciprocal increases in 20 :3w9 but suggested that these ‘changes do not in themselves demand treatment’. They also said that ‘our understanding of which of the particular fatty acid moieties relates most closely to clinical symptoms is minimal’. Their (soft) conclusion was that 1 en% linoleic acid ‘seems’ sufficient.

Hansen et al (1958) provided infants with milk formula containing 1.4 en% fat and providing <0.1 en% linoleic acid. The infants had normal weight gain but also had perianal irrition, some diarrhea, and dryness and desquamation of the skin. They reported that 2 en% tripalmitin had no remedial effect and that 2 en% arachidonate was less effective than 1.3 en% LA. NOTE : The formula contained no w3 PUFA.

Hansen al (1963) evaluated the impact on infant growth and development of a milk formula containing 41 wt% fat providing 0.07, 1.3, 2.8 or 7.3 en% linoleic acid. A separate formula containing 1 wt% fat and providing 0.04 wt% linoleic acid was also evaluated. They observed that growth retardation and skin symptoms began when plasma linoleic acid (measured as dienes) fell to about 6% from the normal mean of about 12%. Their conclusion was that 1 en% LA sufficient. NOTE : This was a w3 PUFA deficient formula.

Mascioli et al (1996) showed that increasing the linoleic acid content of home TPN given to adults from 1.7 to 2.5 en% reduced the triene-tetraene ratio by 25-50%, but in none was the ratio reduced to zero. They noted that some patients on the fat free TPN had no clinical symptoms for several months but gave no specific recommendation regarding linoleic acid intake.

O’Neill et al (1977) studied the impact of fat free TPN in 28 patients ranging in age from newborn to 66 years old, all of whom required surgery. Infants needed no more than two weeks of TPN to have lower linoleic acid, but needed longer for the appearance of dermatitis. Adults needed four weeks to raise the triene-tetraene ratio over 0.4 but, even then, no patients exhibited ‘gross deficiencies’. Interestingly, topical application of safflower oil corrected the dermatitis without changing the triene-tetraene ratio.

Wene et al (1975) evaluated the effect of  intravenous or nasogastric feeding with a fat-free solution containing glucose, amino acids, vitamins and minerals (latter not indicated) for two weeks in healthy men. They observed a rapid drop in plasma linoleic acid and rise in 20:3w9, and emphasized that this effect was dependent on giving glucose to prevent fatty acid mobilization (thus preventing release of linoleic acid from adipose tissue reserves). They corrected the fatty acid changes with 2.6 en% linoleic acid and proposed that 1-2 en% linoleic acid should prevent symptoms of w6 PUFA deficiency. NOTE : the formula they used contained no w3 PUFA.