Meat quality describes the attractiveness of meat to consumers. The present paper focuses on two major aspects of meat quality, tenderness and flavour. Both aspects of quality can be influenced by nutrition, principally through its effects on the amount and type of fat in meat. In several countries, high levels of intramuscular fat (marbling fat), i.e. above 30 g/kg muscle weight in longissimus, are deemed necessary for optimum tenderness, although poor relationships between fat content and tenderness have generally been found in European studies, where fat levels are often very low, e.g. below 10 g/kg in UK pigs. Muscle lipid may be a marker for red oxidative (type 1) muscle fibres which are found at higher concentrations in tender muscles and carcasses. Nutritional treatment can be used to manipulate the fatty acid content of muscle to improve nutritional balance, i.e. increase the polyunsaturated (PUFA) : saturated fatty acid value and reduce the n−6 : n−3 PUFA value. Increasing PUFA levels may also change flavour because of their greater susceptibility to oxidative breakdown and the generation of abnormal volatile compounds during cooking. This situation particularly applies to the n−3 PUFA which are the most unsaturated meat lipids. In pigs, a concentration of 3 mg α-linolenic acid (18 : 3)/100 mg in muscle and fat tissue fatty acids can easily be achieved by including whole linseed in the diet. This level has led to abnormal odours and flavours in some studies, but not in others. In cattle and sheep, feeding whole linseed raised 18 : 3 concentrations in muscle fatty acids from about 0.7 mg/100 mg to > 1 mg/100 mg. As with pigs, this diet also increased levels of long-chain n−3 PUFA formed from 18 : 3, including eicosapentaenoic acid (20 : 5). Although this increase led to greater oxidative breakdown of lipids during storage and the generation of large quantities of lipid-derived volatile compounds during cooking, there were no deleterious effects on odour or flavour. When 18 : 3 levels are raised in lamb and beef because of grass feeding, the intensity of the flavours increases in comparison with grain-fed animals which consume and deposit relatively more linoleic acid (18 : 2). In ruminants, very high levels of 18 : 2 produced by feeding protected oil supplements cause the cooked beef to be described as oily, bland or pork-like.

Developing countries have very diverse food consumption patterns and agricultural production systems. The proportion of meat in national diets varies from negligible in some countries in central Africa to 30–40% in some countries in Latin America and Mongolia. However, the demand for meat in developing countries is increasing rapidly (53%/year from 1982 to 1993), as the result of population growth and the trend for people to move to the cities. Growth rates in consumption are greatest in Asia, with China dominating the statistics, in view of the size of its population. Theoretically, livestock production can be increased to meet this demand, but the multiple roles of livestock in developing countries must be recognized if this is to be achieved in a sustainable manner. Resource-poor farmers who keep livestock may value more highly their contribution to livelihoods and to crop production, through provision of draught power and improvements in soil fertility through the recycling of manure, than the production of more meat. Recognition of the goals of the farmer and the wishes of the consumer regarding meat quality need to be reflected in the way in which opportunities for increasing meat production are identified and communicated to farmers. The impact of the global economy on cereal prices, for example, will also influence which interventions will be economically viable. Interpretation of information in an integral manner, using geographical information systems, mathematical models and/or simple spreadsheet models will be an important ingredient in turning scientific knowledge into increased meat production in developing countries.

The projected stagnation in the catch from global fisheries and the continuing expansion of aquaculture is considered against the background that fishmeal and fish oil are major feed stocks for farmed salmon and trout, and also for marine fish. The dietary requirement of these farmed fish for high-quality protein, rich in essential amino acids, can be met by sources other than fishmeal. However, the highly-polyunsaturated fatty acids eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3) present in high concentrations in fish oil are essential dietary constituents for marine fish and highly-desirable dietary constituents for salmonids. Currently, there is no feasible alternative source to fish oil for these nutrients in fish feeds. Vegetable oils rich in linoleic acid (18:2n-6) can partially substitute for 20:5n-3 and 22:6n-3 in salmonid and marinefish feeds. However, this is nutritionally undesirable for human nutrition because the healthpromoting effects of fish-derived 20:5n-3 and 22:6n-3 reflect a very high intake of 18:2n-6 relative to linolenic acid (18:3n-3) in Western diets. If partial replacement of fish oils in fish feeds with vegetable oils becomes necessary in future, it is argued that 18:3n-3-rich oils, such as linseed oil, are the oils of choice because they are much more acceptable lrom a human nutritional perspective, especially given the innate ability of freshwater fish, including salmonids, to convert dietary 18:3n-3 to 20:5n-3 and 22:6n-3. In the meantime, a more judicious use of increasinglyexpensive fish oil in aquaculture is recommended. High priorities in the future development of aquaculture are considered to be genetic improvement of farmed fish stocks with enhanced abilities to convert C18 to C20 and C22n-3 polyunsaturated fatty acids, enhanced development of primary production of 20:5n-3 and 22:6n-3 by single-cell marine organisms, and continuing development of new species.

A public-health approach considers the relevance of nutritional research in the prevention and management of obesity. Well-defined and internationally-agreed definitions based on BMI allow an assessment of the worldwide prevalence of overweight and obesity. There are about 250 million obese adults in the world, and many more overweight. Obesity is emerging in the Third World, first in urban middle-aged women. With economic developments, obesity then occurs in men and younger women. In the West childhood obesity is rapidly emerging, with concern that early-onset obesity is especially hazardous. In Asians the risks of excess visceral fat occur at lower body weights than in Caucasians. The propensity to visceral obesity in Asians may relate to malnourished mothers and low birth weight. The International Obesity Task Force is considering many issues, including the health economics of obesity. It has developed a strategy to define childhood obesity, which in children over 6 years is likely to predict long-term weight and health problems. While the search for genetic markers of obesity continues, with particular interest in the leptin gene, it is clear that societal change, with the decline in physical activity and the passive overconsumption of high-fat diets are major contributors to the global increase in obesity. The public-health aspects of obesity research are therefore challenging.

There is good scientific evidence that dietary fatty acid composition is involved in the aetiology of many diseases. Increasing the supply of n−3 polyunsaturated fatty acids (PUFA) may reduce the risk of CHD. Several scientific organizations (for example, see Department of Health, 1991, 1994; British Nutrition Foundation, 1992; Scientific Committee for Food, 1993; Food and Agriculture Organization/World Health Organization, 1998) have made recommendations for n−3 PUFA; however, there is a high degree of variation both in terms of the type and amount of n−3 PUFA (up to 7-fold). This variation reflects the different scientific axioms which underlie the different recommendations. Optimal nutrition may be defined in terms of the level of a nutrient required to avoid deficiency, or the amount required to have an effect on biomarkers and functional indicators of nutrient intake, or the level of a nutrient which prevents disease. Functional biomarkers of n−3 PUFA include plasma, platelet and erythrocyte phospholipid-n−3 PUFA levels. Plasma triacylglycerol concentrations represent a functional indicator of n−3 PUFA because n−3 PUFA exert a consistent hypotriacylglycerolaemic effect which is dose-dependent and persistent. In terms of disease status, epidemiological studies have demonstrated that the incidence of CHD is inversely associated with consumption of n−3 PUFA. Despite the health benefits of n−3 PUFA, the mean daily intake falls far short of most of the recommendations. Increasing fish intake is the most obvious way to increase n−3 PUFA intake. However, a large percentage (up to 65) of the population do not eat fish. Thus, there is a need for alternative sources of n−3 PUFA, such as functional foods, whose unique fatty acid composition could fortify staple foods thereby promoting optimal levels of n−3 PUFA intake.

For protein, progress is slow in defining quantifiable indicators of adequacy other than balance and growth. As far as current requirements are concerned, only in the case of infants and children is there any case for revision, and this change is to lower values. Such intakes would appear to be safe when consumed as milk formula. In pregnancy, notwithstanding the concern that deficiency may influence programming of disease in later life, there is little evidence of any increased need, and some evidence that increased intakes would pose a risk. For the elderly there is no evidence of an increased requirement or of benefit from increased intakes, except possibly for bone health. For adults, while we now know much more about metabolic adaptation to varying intakes, there would appear to be no case for a change in current recommendations. As far as risks and benefits of high intakes are concerned, there is now only a weak case for risk for renal function. For bone health the established views of risk of high protein intakes are not supported by newly emerging data, with benefit indicated in the elderly. There is also circumstantial evidence for benefit on blood pressure and stroke mortality. With athletes there is little evidence of benefit of increased intakes in terms of performance, with older literature suggesting an adverse influence. Thus, given that a safe upper limit is currently defined as twice the reference nutrient intake, and that for individuals with high energy requirements this value (1.5 g/kg per d) is easily exceeded, there is a case for revising the definition of a safe upper limit.

There is currently intense research interest in secondary plant metabolites because of their potential preventative effects on the chronic diseases of Western societies, especially cardiovascular disease and cancer. To date most of the research has focused on the identification of plant-derived substances and their potential protective effects against specific chronic diseases. The important issue of determining the optimal intake of those substances, such that the beneficial effects are maximized without manifestation of adverse effects, has yet to be addressed in most cases. Furthermore, there are no specific functional markers that can be used to assess optimal intake, although it may be possible to use biomarkers such as serum cholesterol if the rest of the diet is strictly controlled. The present review discusses a wide range of substances associated with plants, including dietary fibre, resistant starch, oligosaccharides, phyto-oestrogens, phytosterols, flavonoids, terpenes and isothiocyanates, and attempts where possible to indicate optimal intakes and to suggest functional markers.

There is at present a justifiable debate as to the optimum level of total dietary fat which will reduce the risk of obesity without an elevation of plasma triacylglycerol or a depression of plasma HDL-cholesterol. Total plasma cholesterol and LDL-cholesterol levels are lowered and risk of fatal myocardial infarction is lowered when either saturated or trans-unsaturated fatty acids are replaced isoenergetically by either monounsaturated or polyunsaturated fatty acids. The triacylglycerol-raising and HDL-lowering effects of low-fat high-carbohydrate diets can be over-come with low intakes of n−3 polyunsaturated fatty acids and moderate exercise. Whilst a reduction in dietary fat is being attained in many countries, the reduction is uniform across all fatty acids, leaving dietary fat composition unchanged. The ability of low-fat diets to reduce cholesterol and cause a fall in body weight is not influenced by the carbohydrate ratio starch: sugars in the diet. However, weight-gain susceptibility to high intakes of dietary fat and the plasma cholesterol responsiveness to diet are considerably influenced by common genetic polymorphisms.

The metabolism of glucose is deranged in thiamin deficiency, but once any deficiency has been corrected there is no further effect of increased thiamin intake on the ability to metabolize glucose through either pyruvate dehydrogenase (EC 1.2.4.1) and the citric acid cycle, or the pentose phosphate pathway, in which transketolase (EC 2.2.1.1) is the thiamin-dependent step. It has been suggested that the Wernicke-Korsakoff syndrome is associated with a genetic variant of transketolase which requires a higher than normal concentration of thiamin diphosphate for activity. This finding would suggest that there may be a group of the population who have a higher than average requirement for thiamin, but the evidence is not convincing. There are no estimates of biotin requirements, but either coenzyme saturation of erythrocyte pyruvate carboxylase, or the excretion of 3-hydroxy-isovalerate (perhaps after a test dose of leucine) could be used to assess requirements in depletion–repletion studies. Biotin deficiency leads to impaired glucose tolerance, but it is unlikely that glucose tolerance could be used to assess optimum biotin status, since other more common factors affect glucose tolerance to a greater extent. Plasma triacylglycerol and non-esterified fatty acids are moderately elevated in pantothenic acid deficiency. However, this is unlikely to be useful in assessing pantothenate status, since again, other more common factors affect plasma lipids. To date there are no biochemical indices of adequate pantothenate nutrition, and no estimates of requirements.

The term ‘optimum nutrition’ has evolved from a perceived need to base recommendations for nutrient intakes firmly in the context of function. It follows that ‘optimum nutritional status’ for individual nutrients should be defined in terms of biochemical or physiological markers having some functional value but also showing an appropriate relationship to nutrient intake. The present short review considers the current position regarding such markers for riboflavin, pyridoxine and niacin. It is concluded that whilst there are several biochemical measures which respond to changes in intake of each of these vitamins, no single measure is wholly satisfactory as a marker of optimum status.

The folates are made up of a pterdine ring attached to a p-aminobenzoate and a polyglutamyl chain. The active form is tetrahydrofolate which can have C1 units enzymically attached. These C1 units (as a formyl group) are passed on to enzymes in the purine pathway that insert the C−2 and C−8 into the purine ring. A methylene group (−CH2−) attached to tetrahydrofolate is used to convert the uracil-type pyrimidine base found in RNA into the thymine base found in DNA. A further folate cofactor, i.e. 5-methyltetrahydrofolate, is involved in the remethylation of the homocysteine produced in the methylation cycle back to methionine. After activation to S-adenosylmethionine this acts as a methyl donor for the dozens of different methyltransferases present in all cells. Folate deficiency results in reduction of purine and pyrimidine biosynthesis and consequently DNA biosynthesis and cell division. This process is most easily seen in a reduction of erythrocytes causing anaemia. Reduction in the methylation cycle has multiple effects less easy to identify. One such effect is certainly on the nerve cells, because interruption of the methylation cycle causing neuropathy can also happen in vitamin B12 deficiency due to reduced activity of the vitamin B12-dependent enzyme methionine synthase (EC 2.1.1.13). In vitamin B12 deficiency, blocking of the methylation cycle causes the folate cofactors in the cell to become trapped as 5-methyltetrahydrofolate. This process in turn produces a pseudo folate deficiency in such cells, preventing cell division and giving rise to an anaemia identical to that seen in folate deficiency.

There are two major dietary sources of vitamin A: easily absorbed retinyl palmitate in foods of animal origin, and poorly bioavailable carotenoids from plant foods. Plasma retinol is tightly controlled, probably by regulation of retinol-binding protein (RBP) formation in the liver, and only hormonal factors (e.g. oral contraceptives) and infection will alter the homeostasis. Delivery of retinol to the tissues is facilitated by the RBP-retinol complex; however, there is evidence that this mechanism can be bypassed when very high doses of vitamin A are given. Some retinyl ester may be released to tissues from chylomicrons when the latter bind to tissue lipoprotein receptors during their passage from the gut to the liver following a meal. High-dose vitamin A therapy is a means of rapidly improving vitamin A status in persons with sub-optimal vitamin A nutrition but there are dangers of toxic symptoms (e.g. teratogenicity) from excess vitamin A usage. Evidence is presented to suggest that the plasma retinol : RBP may be a guide to optimal vitamin A status, since values less than one frequently occur in less-developed countries and during infection. In contrast to plasma retinol, plasma carotenoids reflect the dietary intake of plant foods. However, absorption is limited by poor bioavailability and a saturable uptake mechanism in competition with other phytochemicals. Recent work on bioavailability suggests that the calculation of plant food vitamin A activity should be re-examined. Illness has little influence on plasma levels except by suppressing appetite. Carotenoids are generally regarded as non-toxic yet intervention studies with β-carotene in smokers have been associated with increased lung cancer and heart disease. Some carotenoids are important as vitamin A precursors, but the physiological importance of their antioxidant properties is not known and consequently the amount needed for optimal nutrition is uncertain.

Interest in the role of vitamin E in disease prevention has encouraged the search for reliable indices of vitamin E status. Most studies in human subjects make use of static markers, usually a-tocopherol concentrations in plasma or serum. Plasma or serum α-tocopherol concentrations of < 11.6, 11.6–16.2, and > 16.2 mmol/l are normally regarded as indicating deficient, low and acceptable vitamin E status respectively, although more recently it has been suggested that the optimal plasma α-tocopherol concentration for protection against cardiovascular disease and cancer is > 30 μmol/l at common plasma lipid concentrations in combination with plasma vitamin C concentrations of > 50 μmol/l and > 0.4 mmol β-carotene/l. Assessment of vitamin E status has also been based on α-tocopherol concentrations in erythrocytes, lymphocytes, platelets, lipoproteins, adipose tissue, buccal mucosal cells and LDL, and on α- tocopherol: γ-tocopherol in serum or plasma. Erythrocyte susceptibility to haemolysis or lipid oxidation, breath hydrocarbon exhalation, oxidative resistance of LDL, and α-tocopheryl quinone concentrations in cerebrospinal fluid have been used as functional markers of vitamin E status. However, many of these tests tend to be non-specific and poorly standardized. The recognition that vitamin E has important roles in platelet, vascular and immune function in addition to its antioxidant properties may lead to the identification of more specific biomarkers of vitamin E status.

Most species of plants and animals synthesize ascorbic acid, but human subjects cannot, making vitamin C an essential component of our diet. Relationships between vitamin C intake and status, and between status and health are not yet clear. There is evidence, however, that higher intake of vitamin C is associated with lower risk of disease, supporting the concept that optimal intake is needed for optimal vitamin C status, and that both factors are required for optimal health. Vitamin C has low toxicity in healthy subjects, but a clear definition of optimal status and the dietary intake required to meet and maintain this status is needed before a change in the current recommended intake can be considered. Available evidence suggests that intake of 200 mg vitamin C/d saturates tissues and maintains fasting plasma levels above the proposed threshold (50 μmol/l) for minimum risk of CHD. However, the issue of whether or not these levels produce ‘optimal vitamin C status’ awaits the clear and accepted definition of the term. This definition in turn awaits the development of reliable functional markers capable of assessing the effects of varying levels of vitamin C nutriture. In the present paper the relationship between intake and body stores of vitamin C and the role of vitamin C in human health are reviewed briefly. The requirements of a reliable functional marker of human vitamin C status are defined, three classes of functional markers (molecular, biochemical and physiological) are described, and possible candidate markers are examined.

In the past, a major challenge for nutrition research was in defining indicators of nutritional adequacy. More recently, the research base related to the role of nutrition in chronic disease has expanded sufficiently to permit moving beyond deficiency indicators to other indicators with broader functional significance. Thus, nutrition research is faced with the new challenge of defining ‘optimal nutrition’. One definition of optimal nutrition with respect to any particular nutrient could be when a functional marker reaches an ‘optimal value’ or plateau beyond which it is no longer affected by intake or stores of the nutrient. A functional marker of nutrient status could be defined as a physiological or biochemical factor which (1) is related to function or effect of the nutrient in target tissue(s) and (2) is affected by dietary intake or stores of the nutrient (which may include markers of disease risk). Examples of such indicators or markers are those related to risk of chronic diseases such as osteoporosis, CHD, or hypertension. The present review focuses on the concept of optimal nutrition with respect to three nutrients, Ca, Mg and P. However, for P and Mg there are as yet no functional indicators which respond to dietary intake, and in such cases nutrient requirements are established using more traditional approaches, e.g. balance data. For Ca, there has been interest in using maximal Ca retention, which is based on balance data, bone mass measurements and biomarkers of bone turnover as useful functional indicators of the adequacy of Ca intake.

The major liabilities of Fe lack include defects in psychomotor development in infants, impaired educational performance in schoolchildren, increased perinatal morbidity, and impaired work capacity. Few if any of the relevant investigations have demonstrated these abnormalities in the absence of anaemia. Consequently, adequate Fe nutrition can be defined as a normal haemoglobin concentration. On the other hand, optimal Fe nutrition should be regarded as sufficient body Fe to avoid any limitation in tissue Fe supply, termed Fe-deficient erythropoiesis. A variety of laboratory measurements have been used to identify this milder form of Fe deficiency, including serum ferritin, transferrin saturation, erythrocyte protoporphyrin, mean corpuscular volume, and more recently the concentration of the soluble fragment of transferrin receptor in serum. Recent studies indicate that the serum transferrin receptor is the preferred measurement, because enhanced synthesis of the transferrin receptor represent the initial cellular response to a declining Fe supply. Moreover, unlike other methods, it is not affected by chronic inflammation or infection which are often confused with Fe deficiency. In an otherwise normal healthy population the transferrin receptor: ferritin value provides a useful quantitative index of body Fe over a wide spectrum of Fe status, ranging from Fe repletion to Fe-deficiency anaemia. It is concluded that optimal Fe nutrition is best defined as a normal haemoglobin, serum ferritin and transferrin receptor concentration.

Defining optimal dietary intakes of Cu and Zn throughout the life cycle continues to present a considerable challenge for nutrition scientists. Although the daily intake of these micronutrients is below that currently recommended for many groups, traditional biochemical indicators of nutritional status for these trace metals largely remain within the normal range. Thus, it is unclear whether the recommended daily intakes may be unnecessarily high, or if the commonly-used markers simply lack the necessary sensitivity and specificity that are required for accurately assessing Cu and Zn status. The increasing number of reports that daily supplements with these trace metals enhance the activities of selective metalloenzymes and specific cellular and organ processes further points out the need to differentiate between meeting the requirement and providing optimal nutriture. Results from recent studies suggesting that alternative molecular and functional markers possess sufficient sensitivity to better assess Cu and Zn status are discussed. Likewise, recent studies evaluating the impact of very low and excessive levels of dietary Mn and Mo on selective biochemical and metabolic indicators are reviewed.