The relationship of physiological and behavioral functions to dietary levels of ra3 and ra6 essential nutrients are now being investigated intensely, whereas talk of such relationships was almost heresy a few years ago. The climate was similar 70 years ago, for the community of nutritional scientists did not immediately accept the concept of essential fatty acids when George and Mildred Burr proposed it in 1930. They had found that elimination of fat in the diet induced a dermatitis in rats, and that dietary linoleic and linolenic acids could prevent or correct the dermatitis. Arild Hansen, who had done his thesis with George Burr at the University of Minnesota, pursued the possibility of the essentiality in human infants, and put his findings into the medical literature in the 1930s through the 1950s. Both linoleic acid and linolenic acid were effective suppressants of dermatitis, and thus came to be considered equivalent. At Texas A & M in the 1950s, my student Carl Widmer and I were the first to show that linoleic acid is the precursor of arachidonic acid, and that linolenic acid is the precursor of eicosapentaenoic and docosahexaenoic acids in the rat. Now, 70 years later, we are treating neurological diseases with ra3 essential fatty acids. We have come a long way.

Because linolenic acid is much more subject to autoxidation than is linoleic acid, nutritionists and industrial laboratories attempted to eliminate linolenic acid from food formulations to minimize rancidity during storage. Autoxidation was the great enemy for designers of stable foods, and a lifetime of effort was required to breed linolenic acid out of soybeans sufficiently to make soybean oil a more stable and convenient component of industrial products intended for human consumption.

In the 1950s and 1960s, worldwide studies concluded that linoleate-rich dietary oils, such as corn oil and cottonseed oil, lowered the cholesterol level of human plasma, and therefore were advocated as preferred sources of polyunsaturated fatty acids. Hence, in the food industry, polyunsaturated began to mean two double bonds per molecule. More than two double bonds per molecule was associated with rapid unwanted rancidity. In the effort to minimize plasma cholesterol, food oils for humans became richer in linoleic acid (18:2w6) and lower in linolenic acid (18:3w3), but were also becoming deficient in essential ra3 polyunsaturates normally found in high levels in brain and nerve lipids.

Our studies in the 1960s revealed that with a constant dietary level of 18:3ra3, increasing dietary 18:2ra6 suppressed the metabolism of the 18:3ra3 to its more highly unsat-urated products. Our later studies of EFA profiles in human health and in disease, revealed that in immune-deficiency diseases, and in diseases with neurological manifestations, low levels of ra3 polyunsaturated acids were found in plasma phospholipids. Our studies of several human populations revealed that Americans had the lowest levels of ra3 polyunsaturated acids in their plasmas. We have come to believe that low ra3 status is a feature of many diseases, and that the American public is chronically deficient in ra3, in comparison with other national populations.

We now realize that deficiencies of ra3 essential fatty acids are pandemic, especially in modern industrialized societies, and that this is an underlying cause of many burgeoning neurological diseases. The United States of America probably is the current leader in ra3 deficiencies. How can we reverse the trend? Our entire agricultural industry is currently dedicated to the production of crops and products low in ra3 and high ra6

essential fatty acids. Most of our food animals are fed in feed lots, largely on corn, which contains little ra3 fatty acids, but is rich in linoleic acid, a competitor for enzyme sites. Therefore, our major national sources of animal protein are now relatively ra3-deficient. We cannot cure our ra3 deficiency by eating ra3-deficient meat. However, we can replace mammalian meat by fish and enhance our intake of ra3 fatty acids. Present supplies of fish may not be sufficient to meet future demand. Current fish-farming practices must be modified to enhance the ra3 content of the fish, for we cannot cure our ra3 deficiencies with present-day corn-fed ra3-deficient fish.

Perhaps part of the solution to this national and worldwide problem, could be the insertion of genes for ra3 synthesis into corn, rather than trying to shift to new crop species for farmers and their animals. This one effort to enhance the ratio of the ra3/ra6 in corn could solve the problems related to many of our farm animals. Another solution could be to revive the soybean strains that we had 50 years ago. At this stage of the game, one cannot predict what the solution will be, but a solution must be found to eliminate our current pandemic ra3 deficiency.

Ralph T. Holman, PhD

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