Stephen C. Cunnane, Univ of Sherbrooke, Research Center on Aging and Dept of Medicine and Physiology and Biophysics, Sherbrooke, QC 000 000, Canada and Philippe Guesnet, INRA, Unit of Lipid Nutrition and Brain Function, Jouy-en-Josas, France.
There are no well-controlled studies that come close to definitively establishing the minimum required intake of Omega 6 PUFA or linoleic acid (LA) in healthy adult humans. This perhaps surprising claim arises from the fact that of the nine published papers directly addressing LA requirements in humans, all are confounded by at least one of the following three significant confounders: [1] Infants were the subject of study in four of the nine reports; [2] In eight of the nine studies (adult and infant), a dietary source of Omega 3 PUFA was not included; [3] In four of the five studies done in adults, the subjects were about to undergo surgery for gastrointestinal disease. In general, a lack of clinical symptoms analogous to those in EFA deficient animals impeded estimating LA requirement. Several authors specifically noted the difficulty in drawing conclusions about LA requirement from measuring plasma fatty acid profiles alone. Putting the methodological issues and lack of clear clinical symptoms of LA deficiency aside, the infant studies suggested that 1.0 energy % LA was sufficient for healthy human development. In the adult studies, it was generally concluded that LA intakes of 1.0-2.5 energy % would meet requirements. There is an important flaw in drawing any conclusion about LA requirements from these studies because an intake of about 0.5 energy % a-linolenic acid (ALA, 18:3w3) reduces the requirement for LA in animals (Greenberg et al 1955, Bourre et al 1990, Cunnane 2003). Competition between the w3 and w6 PUFA has long been a central tenet in the field but low intakes of ALA actually protect against LA depletion.