1. The oxidation rates of lauric, myristic, palmitic, stearic, oleic, a-linolenic, linoleic, y-linolenic, dihomoy-linolenic and arachidonic acids were studied by use of a radioisotope tracer technique in weanling rats at rest in a metabolism chamber over 24 h.2. Of the saturated fatty acids, lauric acid (12:O) was the most efficient energy substrate: the longer the chain length of the saturated fatty acids, the slower the rate of oxidation.3. Oleic acid (18: 1) was oxidized at a remarkably fast rate, similar to that of lauric acid. 4.Of the w6 essential fatty acids studied, linoleic acid (18:2w6) was oxidized at a faster rate than any of its 5.The rate of oxidation of y-linolenic acid (18: 3w3) was almost as fast as that of lauric and oleic acids. metabolites, with arachidonic acid (20: 4w6) being oxidized at the slowest rate.Triglycerides serve as a major component of energy intake in the human diet in western countries (Rizek et al. 1983). However, the composition of the triglyceride fatty acids vary considerably depending on the nature of foods eaten. Studies of the comparative metabolism of fatty acids in a whole-body system indicated that the cellular uptake and oxidation of long-chain fatty acids varied with the degree of unsaturation (Mead et al. 1956;Coots, 1964;Cenedella & Allen, 1969). Ockner et al. (1972) showed that there were differences in the intestinal absorption of saturated and unsaturated fatty acids and differences were also noted in their level of incorporation into chylomicrons (McDonald et al. 1980). These findings contradict a common assumption that dietary fats are all oxidized at the same rate. Whole-body oxidation rates in animals given radiolabelled fatty acids have yielded inconsistent findings, since laboratories have used different models and procedures and have studied different fatty acids. The present study was therefore carried out to investigate the difference in rates of whole-body oxidation of medium-chain fatty acids and essential polyunsaturated fatty acids in one model system. Using radioactively labelled substrates, the oxidation rates of lauric, myristic, palmitic, stearic, oleic, linoleic, y-linolenic, dihomoy-linolenic, arachidonic and a-linolenic acids were determined in weaned rats by measuring the extent of labelling in expired 14C0, over 24 h. M E T H O D S A N D MATERIALS AnimalsFor the early part of the experiment, Sprague-Dawley female rats of the CFY strain were bred in the Nuffield Laboratory and, after weaning at 21 d, were used for the metabolism experiment. However, at a later date weanling rats of the same genetic strain as those bred in the Laboratory were obtained from Benton and Kingmon (Yorkshire), since it proved to be more convenient.The rats were kept under controlled conditions with a 12 h light-12 h dark cycle (06.00-18.00 hours light), a temperature range of 19-23' and relative humidity of about 55%. All rats were allowed free access to food (Special Dietary Services, London) and tap water at all times. Rats used for the metabolism experiments ...

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The African savanna ecosystem of the large mammals and primates was associated with a dramatic decline in relative brain capacity associated with little docosahexaenoic acid (DHA), which is required for brain structures and growth. The biochemistry implies that the expansion of the human brain required a plentiful source of preformed DHA. The richest source of DHA is the marine food chain, while the savanna environment offers very little of it. Consequently Homo sapiens could not have evolved on the savannas. Recent fossil evidence indicates that the lacustrine and marine food chain was being extensively exploited at the time cerebral expansion took place and suggests the alternative that the transition from the archaic to modern humans took place at the land/water interface. Contemporary data on tropical lakeshore dwellers reaffirm the above view with nutritional support for the vascular system, the development of which would have been a prerequisite for cerebral expansion. Both arachidonic acid and DHA would have been freely available from such habitats providing the double stimulus of preformed acyl components for the developing blood vessels and brain. The n-3 docosapentaenoic acid precursor (n-3 DPA) was the major n-3-metabolite in the savanna mammals. Despite this abundance, neither it nor the corresponding n-6 DPA was used for the photoreceptor nor the synapse. A substantial difference between DHA and other fatty acids is required to explain this high specificity. Studies on fluidity and other mechanical features of cell membranes did not reveal a difference of such magnitude between even alpha-linolenic acid and DHA sufficient to explain the exclusive use of DHA. We suggest that the evolution of the large human brain depended on a rich source of DHA from the land/water interface. We review a number of proposals for the possible influence of DHA on physical properties of the brain that are essential for its function.

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Docosahexaenoate (DHA) has been increasingly recognized as an important fatty acid for neural and visual development during the first 6 mon of life. One important point of controversy that remains is the degree to which adequate levels of DHA can be acquired from endogenous synthesis in infants vs. what should be provided as dietary DHA. We have approached this problem by a retrospective analysis of published body composition data to estimate the actual accumulation of DHA in the human infant brain, liver, adipose tissue, remaining lean tissue, and whole body. Estimating whether infants can synthesize sufficient DHA required comparison to and extrapolation from animal data. Over the first 6 mon of life, DHA accumulates at about 10 mg/d in the whole body of breast-fed infants, with 48% of that amount appearing in the brain. To achieve that rate of accumulation, breast-fed infants need to consume a minimum of 20 mg DHA/d. Virtually all breast milk provides a DHA intake of at least 60 mg/d. Despite a store of about 1,050 mg of DHA in body fat at term birth and an intake of about 390 mg/d alpha-linolenate (alpha-LnA), the brain of formula-fed infants not consuming DHA accumulates half the DHA of the brain of breast-fed infants while the rest of the body actually loses DHA over the first 6 mon of life. No experimental data indicate that formula-fed infants not consuming DHA are able to convert the necessary 5.2% of alpha-LnA intake to DHA to match the DHA accumulation of breast-fed infants. We conclude that dietary DHA should likely be provided during at least the first 6 mon of life.

An abundant, balanced dietary intake of long-chain polyunsaturated fatty acids is an absolute requirement for sustaining the very rapid expansion of the hominid cerebral cortex during the last one to two million years. The brain contains 600 g lipid/kg, with a long-chain polyunsaturated fatty acid profile containing approximately equal proportions of arachidonic acid and docosahexaenoic acid. Long-chain polyunsaturated fatty acid deficiency at any stage of fetal and/or infant development can result in irreversible failure to accomplish specific components of brain growth. For the past fifteen million years, the East African Rift Valley has been a unique geological environment which contains many enormous freshwater lakes. Paleoanthropological evidence clearly indicates that hominids evolved in East Africa, and that early Homo inhabited the Rift Valley lake shores. Although earlier hominid species migrated to Eurasia, modem Homo supiens is believed to have originated in Africa between 100 and 200 thousand years ago, and subsequently migrated throughout the world. A shift in the hominid resource base towards more high-quality foods occurred approximately two million years ago; this was accompanied by an increase in relative brain size and a shift towards modem patterns of fetal and infant development. There is evidence for both meat and fish scavenging, although sophisticated tool industries and organized hunting had not yet developed. The earliest occurrences of modem H. supiens and sophisticated tool technology are associated with aquatic resource bases. Tropical freshwater fish and shellfish have long-chain polyunsaturated lipid ratios more similar to that of the human brain than any other food source known. Consistent consumption of lacustrine foods could have provided a means of initiating and sustaining cerebral cortex growth without an attendant increase in body mass. A modest intake of fish and shellfish (6-12 % total dietary energy intake) can provide more arachidonic acid and especially more docosahexaenoic acid than most diets contain today. Hence, 'brain-specific' nutrition had and still has significant potential to affect hominid brain evolution. Fish: Brain-specific nutrition: Long-chain PUFA: East Africa Rift Valley LakesMarked expansion of the hominid cerebral cortex took place only in the last one to two million years. During this small evolutionary window, genus Australopithecus became extinct while Homo greatly expanded. Sophisticated tool manufacture, organized hunting, culture, and speech followed rapidly. We hypothesize that the unique geological and ecological environment of the East African Rift Valley provided an equally unique nutritional resource base for the enlargement of the Homo brain, culminating in Homo sapiens. How in this remarkably short stretch of evolutionary history did our intelligence arise? While many physical (i.e. development of bipedalism, speech), ecoloAbbreviations: AA, arachidonic acid; CNS, central nervous system; DHA, docosahexaenoic acid; EPA, eicosapentaenoic aci...

We review evidence suggesting that pre- or postnatal deficits of arachidonic acid (AA) and docosahexaenoic acid (DHA) together with underdeveloped antioxidant protection contribute to neurovisual developmental disorders and other complications of premature birth. These two synergistic deficits occur at a time when 70% of energy is focused on brain development and when the brain and blood vessels are growing at high speed. The types of essential fatty acids fed to preterm babies bear no relation to what the infant would have received had it remained a fetus. This failure to meet essential fatty acid requirements exacerbates the AA and DHA deficits seen at birth; furthermore, the immature superoxide defenses remain depressed until the expected date of delivery. Deficits of these systems, which are required for cell membranes, the endothelium, and neural tissue, could provide the biochemical prerequisite for the membrane disorders to which these babies are at high risk: intraventricular hemorrhage, periventricular leucomalacia, retinopathy of prematurity, and bronchopulmonary dysplasia. Although poor vascular development during fetal and neonatal life may be repaired, the structural and antioxidant deficits identified in preterm babies may impair blood vessel development with long-term consequences. The conclusion drawn from this review is that present parenteral and enteral lipid nutrition for preterm babies is flawed and could be pathogenic. Full-term milk composition is the basis for the design of preterm infant foods, but full-term milk is different from the placental product that is rich in AA and DHA. Preterm lipid nutrition should be revised to be more in line with placental lipid transfer to the fetus.