Advances in knowledge of ruminant nutrition and metabolism during the second half of the twentieth century have been reviewed. Part I is concerned with metabolism in the rumen: Part II discusses utilization of nutrients absorbed from the rumen and lower tract to support growth and reproduction. The time frame was prompted by the crucial advances in ruminant physiology which arose from the work of Sir Jospeh Barcroft and his colleagues at Cambridge in the 1940s and 50s, and by the brilliant studies of Robert Hungate on rumen microbiology at much the same time.

In reviewing the growth of knowledge of the role of bacteria, protozoa, fungi and bacteriophages in the rumen, outstanding developments have included the identification and characterization of fungi and the recognition that the utilization of polysaccharides in the rumen is accomplished by the sequential activities of consortia of rumen microorganisms. The role of protozoa is discussed in relation to the long standing debate on whether or not the removal of protozoa (defaunation) improves the efficiency of ruminant production. In relation to nitrogen (N) metabolism, the predation of bacteria by protozoa increases protein turnover in the rumen and reduces the efficiency of microbial protein production. This may account for the beneficial effects of defaunation where dietary N intakes are low and possibly rate limiting for growth and production.

Current approaches to the measurement of rates of production of short chain fatty acids (SCFA) in the rumen based on the mathematical modelling of isotope dilution data are outlined. The absorption of SCFA from the rumen and hindgut is primarily a passive permeation process.

The role of microorganisms in N metabolism in the rumen has been discussed in relation to ammonia and urea interrelationships and to current inadequacies in the measurement of both protein degradation in the rumen and microbial protein synthesis. The growth of knowledge of digestion and absorption of dietary lipids has been reviewed with emphasis on the antimicrobial activity of lipids and the biohydrogenation of unsaturated fatty acids. The protection of unsaturated dietary fats from ruminal biohydrogenation is an approach to the manipulation of the fatty acid composition of meat and dairy products.

Discussion of the production of toxins in the rumen and the role of microorganisms in detoxification has focused on the metabolism of oxalate, nitrate, mycotoxins, saponins and the amino acid mimosine. Mimosine occurs in the tropical shrub leucaena, which is toxic to cattle in Australia but not in Hawaii. Tolerance to leucaena stems from the presence of a bacterium found in the rumen of Hawaiian cattle, which when transferred to Australian cattle survives and confers protection from mimosine. The genetic modification of rumen microorganisms to improve their capacity to ultilize nutrients or to detoxify antinutritive factors is an attractive strategy which has been pursued with outstanding success in the case of fluoroacetate. A common rumen bacterium has been genetically modified to express the enzyme fluoroacetate dehalogenase. The modified organism has been shown to survive in the rumen at metabolically significant levels and to confer substantial protection from fluoroacetate poisoning.

A herbivore faces challenges while foraging—ongoing changes in its physiological condition along with variation in the nutrient and toxin concentrations of foods, spatially and temporally—that make selecting a nutritious diet a vital affair. Foraging behaviours arise from simple rules that operate across levels of resolution from cells and organs to individuals and their interactions with social and physical environments. At all these levels, behaviour is a function of its consequences: a behaviour operating on the environment to induce changes is itself changed by those events. Thus, behaviour emerges from its own functioning—behaviour self-organizes-not from that of its surroundings. This ostensible autonomy notwith-standing, no self-organizing system (cell, organ, or individual) is independent of its environs because existence consists of an ongoing exchange of energy and matter. According to this view, the notion of cause and effect is replaced with functional relationships between behaviours and environmental consequences. Changes in physical environments alter the distribution, abundance, nutritional, and toxicological characteristics of plants, which affect food preference. Social interactions early in life influence behaviour in various ways: animals prefer familiar foods and environments, and they prefer to be with companions. Animals in unfamiliar environments often walk farther, ingest less food, and suffer more from malnutrition and toxicity than animals in familiar environments. An individual's food preferences—and its ability to discriminate familiar from novel foods—arise from the functional integration of sensory (smell, taste, texture) and postingestive (effects of nutrients and toxins on chemo-, osmo-, and mechano-receptors) effects. The ability to discriminate among foods is critical for survival: all problems with poisonous plants are due to an inability to discriminate or a lack of alternatives. Animals eat a variety of foods as a result of nearing or exceeding tolerance limits for sensory and postingestive effects unique to each food. After eating any food too frequently or excessively, the likelihood increases that animals will eat alternative foods owing to exceeding sensory-, nutrient-, and toxin-specific tolerance limits. Cyclic patterns of intake of a variety of foods reflect seemingly chaotic interactions among flavours, nutrients, and toxins interacting along continua.

In this paper we respond to the criticisms of Provenza et al. (1998) that our framework of learning and feeding motivation (Day et al. 1998) resorts to higher order goals, which cannot be falsified by experimentation. We assert that in order to be able to predict the feeding behaviour of animals we first need to understand what they are trying to achieve (i.e. invoke teleonomy). We then detail our framework in such terms that one could envisage experiments that could quantitatively test its predictions. We contend that the framework of ‘the self-organization of behaviour’ proposed by Provenza et al. (1998) cannot lead to such quantitative predictions, since it is invoked to describe feeding behaviour of animals a posteriori. It is our own desire, by contrast, to assess feeding behaviour a priori, which leads us to propose and defend our framework of learning and feeding motivation.

Under-reporting of food intake is one of the fundamental obstacles preventing the collection of accurate habitual dietary intake data. The prevalence of under-reporting in large nutritional surveys ranges from 18 to 54% of the whole sample, but can be as high as 70% in particular subgroups. This wide variation between studies is partly due to different criteria used to identify under-reporters and also to non-uniformity of under-reporting across populations. The most consistent differences found are between men and women and between groups differing in body mass index. Women are more likely to under-report than men, and under-reporting is more common among overweight and obese individuals. Other associated characteristics, for which there is less consistent evidence, include age, smoking habits, level of education, social class, physical activity and dietary restraint.

Determining whether under-reporting is specific to macronutrients or food isproblematic, as most methods identify only low energy intakes. Studies that haveattempted to measure under-reporting specific to macronutrients express nutrients as percentage of energy and have tended to find carbohydrate under-reported and protein over-reported. However, care must be taken when interpreting these results, especially when data are expressed as percentages. A logical conclusion is that food items with a negative health image (e.g. cakes, sweets, confectionery) are more likely to be under-reported, whereas those with a positive health image are more likely to be over-reported (e.g. fruits and vegetables). This also suggests that dietary fat is likely to be under-reported.

However, it is necessary to distinguish between under-reporting and genuine under-eating for the duration of data collection. The key to understanding this problem, but one that has been widely neglected, concerns the processes that cause people to under-report their food intakes. The little work that has been done has simply confirmed the complexity of this issue. The importance of obtaining accurate estimates of habitual dietary intakes so as to assess health correlates of food consumption can be contrasted with the poor quality of data collected. This phenomenon should be considered a priority research area. Moreover, misreporting is not simply a nutritionist's problem, but requires a multidisciplinary approach (including psychology, sociology and physiology) to advance the understanding of under-reporting in dietary intake studies.

The ultimate goal in the design of infant formula is to achieve the outcome seen in breast fed infants. This review of lipids in infant formulas for term infants begins by referring to the lipid composition of human milk, and relates that to differences in lipid digestion and metabolism which exist between breast fed and formula fed infants and which may significantly influence fatty acid bioavailability.

Recommendations are made for the lipid content and fatty acid composition of term infant formulas (especially for lauric, linoleic, α-linolenic, long chain 20 and 22C n-3 and n-6 polyunsaturated fatty acids and the trans fatty acids).

Further research is required to define more clearly the long term nutritional, growth and developmental effects of structured lipids in formulas for term infants. More information is required on the differential handling of LCPUFA and other fatty acids at the organ and cellular level. There is a need for large (multi-centre) randomized studies to determine the short and long term functional effects of LCPUFA supplementation. Further research and development is required to determine a commercial source of LCPUFA which is safe, effective and economic. Further information is required on the short and long term effects of cholesterol intake during infancy, and in particular its relationship to LCPUFA metabolism. Long term studies should be initiated to determine the relationship of infant diet (especially saturated fatty acid and cholesterol intake) to the development of cardiovascular disease.

Irritable bowel syndrome (IBS) is a frequently occurring, benign functional gastrointestinal disorder with a complex poorly understood pathology which appears to be multifactorial in nature. There is no association with structural or biochemical abnormalities in the gastrointestinal tract. Functional variations in myoelectrical activity, visceral hypersensitivity and illness behaviours have all been observed in patients experimentally. In conjunction with environmental, psychological and alimentary factors, these mechanisms have been proposed as the major determinants of symptom genesis. Certainly, dietary factors are frequently perceived by sufferers as powerful symptom triggers, with many reporting multiple food intolerance. Physicians, however, remain divided upon the relevance of food to the disorder, with many eschewing a nutritional connection. This is unsurprising as, despite much experimental work to determine the clinical relevance of food intolerance and allergy to the aetiology of the disorder, the vast range of foodstuffs available for testing, inherent procedural problems with test foods, methodological insufficiencies and the continually evolving knowledge of the disorder, particularly the subgrouping of sufferers, have restricted the scientific validity of current findings. At the present time, it is difficult to make informed judgement upon the importance of food in IBS, and rigorously designed, large scale trials devised in the light of recent knowledge are required before conclusions can be drawn.

The objectives were firstly to assess the evidence that homocysteine is a significant and independent risk factor for vascular disease with special reference to cardiovascular disease, and secondly to evaluate the evidence that a food staple fortified with folic acid will reduce this problem on a population basis.

The structure of plasma homocysteine (tHcy) is described. Homocysteine, a highly reactive compound, is synthesized from the amino acid, methionine, and is metabolized by two pathways, the catabolic transsulphuration route via cystathionine β-synthase (EC 4.2.1.22) and the remethylation path using 5-methyltetrahy-drofolate polyglutamate, the product of 5,10-methylenetetrahydrofolate reductase (MTHFR; EC 1.1.1.171), via the cobalamin dependent enzyme, methionine synthase (MS; EC 2.1.1.13).

The mechanisms whereby hyper-tHcy is produced include both increased rates of synthesis and decreased metabolism. The latter may occur owing to nutritional deficiency of the vitamin cofactors which are necessary for the normal function of the metabolic enzymes. In particular, folate is required for methylene reductase, pyridoxal phosphate for cystathionine synthase and cobalamin for methionine synthase. When these vitamins are deficient hyper-tHcy is induced and this occurs especially in the elderly. Alternatively, a variant form of methylene reductase has recently been described which occurs in nearly 10% of the normal population. This variant is associated with hyper-tHcy, especially in situations associated with a low folate nutritional status.

Meta-analysis of both retrospective case-control studies, nested prospective case-control surveys and a secondary trial of mortality in postmyocardial infarct patients have shown that the association of hyper-tHcy with vascular disease is beyond doubt. This has been further supported by direct assessments of the degree of vascular disease in the carotid brachial and aortic arteries in relation to tHcy levels. Furthermore, treatment with a cocktail of the vitamin cofactors has produced lowering of tHcy levels and regression of the vascular disease in the carotid arteries of affected individuals.

Suggested pathogenic mechanisms in vascular disease induced by hyper-tHcy include vascular endothelial cell dysfunction, smooth muscle proliferation and derangements of normal intravascular regulation mechanisms. A variety of clinical conditions are known to be associated with a high incidence of thromboembolic complications. Some of these are associated with hyper-tHcy.

Low physiological doses of folic acid, as well as pharmocological doses, lower tHcy. However, because of the poor bioavailability of food folate (50%) and the considerable chemical instability of the naturally occurring reduced forms of folate, in most people it would require unacceptably high consumption of green vegetables to accomplish the necessary increase in intracellular folate and reduction in tHcy. Accordingly, folic acid, the nonreduced synthetic form of the vitamin, which is 100% bioavailable and chemically extremely stable, should be added to a food staple such as flour to ensure maximum protection for most of the population.