Disturbances in pathways of lipolysis and fatty acid handling are of importance in the aetiology of obesity and type 2 diabetes mellitus. There is evidence that a lowered catecholamine-mediated lipolytic response may play a role in the development and maintenance of increased adipose tissue stores. Increased adipose tissue stores, a disturbed insulin-mediated regulation of lipolysis and subnormal skeletal muscle non-esterified fatty acid (NEFA) uptake under conditions of high lipolytic rate may increase circulating NEFA concentrations, which may promote insulin resistance and cardiovascular complications. In addition, a disturbance of NEFA uptake by adipose tissue postprandially is also a critical determinant of plasma NEFA concentration. Furthermore, evidence is increasing that insulin-resistant muscle is characterised by a lowered ability to oxidise fatty acids. A dysbalance between fatty acid uptake and fatty acid oxidation may in turn be a factor promoting accumulation of lipid intermediates and triacylglycerols within skeletal muscle, which is strongly associated with skeletal muscle insulin resistance. The present review describes the reported disturbances in pathways of lipolysis and skeletal muscle fatty acid handling, and discusses underlying mechanisms and metabolic consequences of these disturbances.

Enteral feeding in primary care has increased markedly over the last decade. It allows patients to be discharged to home or residential care who previously would have remained in hospital. Difficulties do arise for patients, their carers and health professionals, as care of these patients and support for health professionals is often patchy or non-existent. Dietitians are uniquely placed to participate in the management of tube feeding in primary care, provide support and education to patients and their carers, evaluate treatment and promote better outcomes for patients receiving tube feeding.

Atherosclerotic cardiovascular disease (ASCVD) is the most common cause of death in most Western countries. Nutrition factors contribute importantly to this high risk for ASCVD. Favourable alterations in diet can reduce six of the nine major risk factors for ASCVD, i.e. high serum LDL-cholesterol levels, high fasting serum triacylglycerol levels, low HDL-cholesterol levels, hypertension, diabetes and obesity. Wholegrain foods may be one the healthiest choices individuals can make to lower the risk for ASCVD. Epidemiological studies indicate that individuals with higher levels (in the highest quintile) of whole-grain intake have a 29% lower risk for ASCVD than individuals with lower levels (lowest quintile) of whole-grain intake. It is of interest that neither the highest levels of cereal fibre nor the highest levels of refined cereals provide appreciable protection against ASCVD. Generous intake of whole grains also provides protection from development of diabetes and obesity. Diets rich in whole-grain foods tend to decrease serum LDL-cholesterol and triacylglycerol levels as well as blood pressure while increasing serum HDL-cholesterol levels. Whole-grain intake may also favourably alter antioxidant status, serum homocysteine levels, vascular reactivity and the inflammatory state. Whole-grain components that appear to make major contributions to these protective effects are: dietary fibre; vitamins; minerals; antioxidants; phytosterols; other phytochemicals. Three servings of whole grains daily are recommended to provide these health benefits.

Obese individuals are at increased risk from a range of metabolic diseases, including insulin resistance, dyslipidaemia and hypertension. Adipose tissue is an important endocrine organ, secreting a range of inflammatory mediators, including tumour necrosis factor a and interleukin 6. Circulating concentrations of these cytokines are increased in obesity and may contribute to the pathogenesis of metabolic diseases. The present review considers the evidence linking inflammation and obesity-related disease. The data show that an inflammatory phenotype, measured by serum sialic acid concentration, identifies individuals with insulin resistance, dyslipidaemia and hypertension. Serum sialic acid concentration increases progressively in obese individuals with none, one or multiple features of the metabolic syndrome, independent of BMI. Supplementation with long-chain n-3 polyunsaturated fatty acids has shown anti-inflammatory effects in studies of both healthy populations and in models of chronic inflammatory conditions. The effect on insulin sensitivity has been varied, with both positive and negative effects. This variability may relate to the metabolic characteristics of the study population; individuals with high background inflammation may derive greater benefits from n-3 polyunsaturated fatty acid supplements, suggesting a possible interaction between diet and phenotype. Future research is needed to fully evaluate the role of anti-inflammatory strategies in the dietary management of obesity.

Whole grains are important dietary constituents as they provide a plethora of nutrients and protective chemicals that may have synergistic actions in promoting health. Regular consumption of wholegrain foods has been associated with a reduced risk of several chronic diseases such as CHD and certain cancers, although their exact role in disease prevention is not yet fully elucidated. Studies reporting levels of whole grain consumption reveal that those subjects who include higher levels of whole grain foods in their diets also have many other favourable dietary and lifestyle practices. While the actions of these practices and whole grains may not be mutually exclusive, these variables do not appear to explain the reduction in risk of disease observed for high-whole grain consumers. Actual whole grain consumption levels are extremely low and many practical barriers exist to consumer uptake of these foods. Effective communication of the whole grain health message is an important strategy to increase awareness of the importance of whole grains in the diet. Increasing the variety and availability of acceptable wholegrain foods is also important. Whole grain consumption at breakfast can have an important impact on total daily nutrient intakes. This simple dietary modification is potentially relatively easy to achieve and could greatly contribute to increased whole grain intake for many individuals.

The epidemic of type 2 diabetes among children, adolescents and adults is increasing along with the increasing prevalence of overweight and obesity. Overweight is the most powerful modifiable risk factor for type 2 diabetes. Intake of whole-grain foods may reduce diabetes risk. Three prospective studies in 160 000 men and women examined the relationship of whole-grain or cereal-fibre intake with the risk of type 2 diabetes. Each study used a mailed Willett food-frequency questionnaire and similar methods of quantifying whole-grain foods and cereal fibre. The self-reported incident diabetes outcome was more reliably determined in the two studies of health-care professionals than in the study of Iowa women. Risk for incident type 2 diabetes was 21–27% lower for those in the highest quintile of whole-grain intake, and 30–36% lower in the highest quintile of cereal-fibre intake, each compared with the lowest quintile. Risk reduction persisted after adjustment for the healthier lifestyle found among habitual whole-grain consumers. Observations in non-diabetic individuals support an inverse relationship between whole-grain consumption and fasting insulin levels. In feeding studies in non-diabetic individuals insulin resistance was reduced using whole grains or diets rich in whole grains. Glucose control improved with diets rich in whole grains in feeding studies of subjects with type 2 diabetes. There is accumulating evidence to support the hypothesis that whole-grain consumption is associated with a reduced risk of incident type 2 diabetes; it may also improve glucose control in diabetic individuals.

Platelets play a substantial role in cardiovascular disease, and for many years there has been a search for dietary components that are able to inhibit platelet function and therefore decrease the risk of cardiovascular disease. Platelets can be inhibited by alcohol, dietary fats and some antioxidants, including a group of compounds, the polyphenols, found in fruits and vegetables. A number of these compounds have been shown to inhibit platelet function both in vitro and in vivo. In the present study the effects of the hydroxycinnamates and the flavonoid quercetin on platelet activation and cell signalling in vitro were investigated. The hydroxycinnamates inhibited platelet function, although not at levels that can be achieved in human plasma by dietary intervention. However, quercetin inhibited platelet aggregation at levels lower than those previously reported. Quercetin was also found to inhibit intracellular Ca mobilisation and whole-cell tyrosine protein phosphorylation in platelets, which are both processes essential for platelet activation. The effect of polyphenols on platelet aggregation in vivo was also investigated. Twenty subjects followed a low-polyphenol diet for 3 d before and also during supplementation. All subjects were supplemented with a polyphenol-rich meal every lunchtime for 5 d. Platelet aggregation and plasma flavonols were measured at baseline and after 5 d of dietary supplementation. Total plasma flavonoids increased significantly after the dietary intervention period (P=0·001). However, no significant changes in ex vivo platelet aggregation were observed. Further investigation of the effects of individual polyphenolic compounds on platelet function, both in vitro and in vivo, is required in order to elucidate their role in the relationship between diet and the risk of cardiovascular disease.

In response to the 1990 Nutrition Labeling and Education Act, the Food and Drug Administration approved seven health claims that addressed the relationship between broad food categories and risk of certain chronic diseases. These claims are based on scientific consensus that includes epidemiological, animal and clinical research. The Food and Drug Administration also established a process to petition for new health claims that address substance-disease relationships supported by adequate scientific and specific regulatory requirements. The whole grain-cancer and heart disease authoritative statement health claim approved in July 1999 followed a completely different process mandated by the Food and Drug Administration Modernization Act of 1997. It is based on an authoritative statement made by a government body that represents scientific consensus and is supported by other scientific agencies and organizations. The scientific basis for the claim published in Diet and Health reflects a comprehensive and deliberative review of epidemiological, animal and human studies by the National Academy of Sciences Committee on Diet and Health. Health claims used on whole-grain products can attract the attention of health-conscious consumers and are important tools in communicating health messages. However, the US public consumes substantially fewer whole-grain servings than recommended by US dietary guidance. Reasons given by consumers for not purchasing whole-grain foods include colour, price, softness, texture, moisture content and taste. Developing tastier value-added whole-grain foods along with simple coordinated messages from industry, the scientific community, public health experts and government will help consumers identify, purchase and consume more whole-grain products.

Wholegrain foods are important sources of nutrients and phyto-protective components, which are in short supply in many member states of the EU, including the UK. Encouraging the public to increase consumption of whole-grain foods is a positive health message that has critical public health implications. In February 2002 the UK Joint Health Claims Initiative (JHCI) published its authoritative endorsement that whole-grain foods are associated with a healthy heart (Joint Health Claims Initiative, 2002). This new health claim reflects a similar one in the USA based on the accumulation of epidemiological evidence between 1996 and 2001 from several very large cohort studies in the USA, Finland and Norway, which show a consistent protective effect of whole grain and reduced risk of CHD. The JHCI code of practice on health claims requires that the claimed benefit must be scientifically valid, with evidence supporting efficacy of the food in human consumers, under typical conditions of use. The evidence-based approach consists of the identification of studies, an evaluation of individual references, a critical evaluation of the totality of the evidence and a statement that there is significant scientific agreement to establish the validity of the claim. The studies suggest that an intake of three servings per d may have an important cardio-protective effect. The development of a process for the substantiation of health claims in the UK and in the EU is important to underpin regulatory developments, which should protect the consumer, promote fair trade and encourage innovation in the food industry. The present paper sets out the format of the scientific dossier that was presented to the JHCI and includes a call to promote further research to identify the important protective components in the whole grain ‘package’ and the biological mechanisms behind the observed beneficial effects on health. The major sources of whole grain in the UK are bread and breakfast cereals, and >90% of adults in the UK consume less than three servings per d. Increasing the variety and availability of acceptable whole-grain foods could lead to greater consumption levels, which has important public health implications and offers an attractive and food-based dietary strategy for targeting the whole population.

Homocysteine, derived from the demethylation of the ammo acid methionine, is either further catabolised by trans-sulfuration to cysteine or remethylated to methionine. Remethylation to methionine requires the cofactors, folate and vitamin B12. Folate is an effective homocysteine-lowering agent and, thus, homocysteine and folate status are inversely related. Hyperhomocysteinaemia is a strong independent risk factor for venous thromboembolism (VTE) and is associated with adverse pregnancy outcomes such as pre-eclampsia, placental abruption, early pregnancy loss and neural-tube defects. Pregnancy is a risk factor for VTE as a result of prothrombotic changes in levels of haemostatic factors. However, despite this hypercoagulable state, the incidence of pregnancy-associated VTE is relatively low. Hyperhomocysteinaemia is associated with abnormalities in markers of coagulation activation, and recent research suggests that folic acid supplementation, as well as lowering homocysteine, lowers markers of coagulation activation and increases levels of coagulation inhibitors. Tissue factor (TF) is the initiator of blood coagulation in vivo, and homocysteine induces TF expression in vitro. During pregnancy, monocyte TF expression is lower than that in the non-pregnant state, and this lowering of TF may act to counterbalance increases in coagulation activation. Furthermore, despite a high folate requirement, several studies have reported that homocysteine is lower in normal pregnancy than in the non-pregnant state. Although the exact mechanism of homocysteine lowering during pregnancy is unclear, one possible outcome of lower homocysteine may be the protection of women from pregnancy complications and VTE, and thus lower homocysteine may contribute to maintaining homeostasis in haemostasis.

Non-infectious diseases such as CHD and certain cancers have become major causes of death and disability in affluent countries. Probiotics (principally lactic acid bacteria; LAB) may assist in lowering the risk of these diseases. Experimental studies with probiotics have given generally inconclusive outcomes for infectious disease and for biomarkers for non-infectious disease. In part this situation may reflect their inability to colonise the adult human gut effectively. Prebiotics can assist in promoting colonisation, and resistant starch (RS), as a high-amylose starch, is a prebiotic and synbiotic. This starch exerts its synbiotic action through adhesion of the bacteria to the granule surface. Consumption of RS assists in recovery from infectious diarrhoea in man and animals. A rice porridge, high in RS, appears to modify the autochthonous porcine large-bowel microflora favourably through lowering Escherichia coli and coliform numbers. Many of the beneficial effects of RS on large-bowel function appear to beexerted through short-chain fatty acids (SCFA) formed by bacterial fermentation. In man LAB are found in relatively highest numbers in milk-fed infants where theprofile of fermentation products differs quite markedly from that in adults. It appearsunlikely that ingestion of current probiotics will alter either total SCFA or the proportions of the major acids. More emphasis needs to be given to the investigation of the effects of complex carbohydrates, including RS, on the autochthonous microflora of the human large bowel.

Raised blood pressure (BP) is a major cause of CHD and the leading cause of stroke. Although BP rises with age in most populations, there are remote populations around the world where BP does not rise with age and where the high prevalence of high BP and frank hypertension seen in the UK and other Western countries in the older age-groups is not found. However, when such populations migrate to urban settings, their BPs rise, indicating that the population-wide BP problem is largely environmental in origin. Thus, a substantial body of evidence has accumulated on the importance of dietary factors in BP (Na and alcohol intakes (direct relationship) and K intake (inverse relationship)) as well as body weight (direct relationship). More recently, attention has shifted to other dietary factors that might affect BP. Data from studies of vegetarians (who tend to have lower BP than meat-eating populations) as well as clinical data on the adverse effects of protein intake in patients with renal insufficiency led to the view in Western countries that dietary (animal or total) protein had an adverse effect on BP. By contrast, studies in Japan and China suggested that dietary protein might be protective of high BP and stroke. Recent epidemiological studies have found inverse associations between dietary protein intake and BP, consistent with this view, and supported by some evidence from animal studies. Recent controlled clinical trials of soyabean supplementation have also suggested a BP-lowering effect of protein intake. Results of further large-scale epidemiological studies of protein and BP are awaited.

Oligosaccharides, consisting of a mixture of hexose oligomers with a variable extent of polymerisation, are food products with interesting nutritional properties. They may be naturally present in food, mostly in fruits, vegetables or grains, or produced by biosynthesis from natural sugars or polysaccharides and added to food products because of their nutritional properties or organoleptic characteristics. The dietary intake of oligosaccharides is difficult to estimate, but it may reach 3–13 g/d per person (for fructo-oligosaccharides), depending on the population. The extent of resistance to enzymic reactions occurring in the upper part of the gastrointestinal tract allows oligosaccharides to become ‘colonic nutrients’, as some intestinal bacterial species express specific hydrolases and are able to convert oligosaccharides into short-chain fatty acids (acetate, lactate, propionate, butyrate) and/or gases by fermentation. Oligosaccharides that selectively promote some interesting bacterial species (e.g. lactobacilli, bifidobacteria), and thus equilibrate intestinal microflora, are now termed prebiotics. The pattern of short-chain fatty acid production in the caeco-colon, as well as the prebiotic effect, if demonstrated, are dynamic processes that vary with the type of oligosaccharide (e.g. extent of polymerisation, nature of hexose moieties), the duration of the treatment, the initial composition of flora or the diet in which they are incorporated. Experimental data obtained in vitro and in vivo in animals, and also recent data obtained in human subjects, support the involvement of dietary oligosaccharides in physiological processes in the different intestinal cell types (e.g. mucins production, cell division, immune cells function, ionic transport) and also outside the gastrointestinal tract (e.g. hormone production, lipid and carbohydrates metabolism). The present paper gives an overview of the future development of oligosaccharides, newly recognised as dietary fibre.

Dietary protein has several opposing effects on Ca balance and its net effect on bone is not well established. It has long been recognized that increasing protein intake increases urinary Ca excretion. More recently, it has been observed that increasing dietary protein raises the circulating level of insulin-like growth factor-1, a growth factor that promotes osteoblast formation and bone growth. Other effects of protein on the Ca economy have been suggested in some studies, but they are less well established. Several studies have examined associations between protein intake and bone loss and fracture rates. In the original Framingham cohort subjects with lower total and animal protein intakes had greater rates of bone loss from the femoral neck and spine than subjects consuming more protein. In another study higher total (and animal) protein intakes were associated with a reduced incidence of hip fractures in post-menopausal women. In contrast, a high animahplant protein intake has been associated with greater bone loss from the femoral neck and a greater risk of hip fracture in older women. Higher total and higher animal protein intakes have also been associated with increased risk of forearm fracture in younger post-menopausal women. In a recent study it was found that increasing dietary protein was associated with a favourable (positive) change in bone mineral density of the femoral neck and total body in subjects taking supplemental calcium citrate malate with vitamin D, but not in those taking placebo. The possibility that Ca intake may influence the impact of dietary protein on the skeleton warrants further investigation.

Bone growth and turnover results from the coordinated activities of two key cell types. Bone matrix is deposited and mineralised by osteoblasts and it is resorbed by osteoclasts, multinucleate cells that excavate pits on bone surfaces. It has been known since the early 20th century that systemic acidosis causes depletion of the skeleton, an effect assumed to result from physico-chemical dissolution of bone mineral. However, our own work has shown that resorption pit formation by cultured osteoclasts was absolutely dependent on extracellular acidification; these cells are inactive at pH levels above about 7·3 and show maximum stimulation at a pH of about 6·9. Bone resorption is most sensitive to changes in H+ concentration at a pH of about 7·1 (which may be close to the interstitial pH in bone). In this region pH shifts of <0·05 units can cause a doubling or halving of pit formation. In whole-bone cultures, chronic HCO3- acidosis results in similar stimulations of osteoclast-mediated Ca2+ release, with a negligible physico-chemical component. In vivo, severe systemic acidosis (pH change of about –0·05 to –0·20) often results from renal disease; milder chronic acidosis (pH change of about –0·02 to –0·05) can be caused by excessive protein intake, acid feeding, prolonged exercise, ageing, airway diseases or the menopause. Acidosis can also occur locally as a result of inflammation, infection, wounds, tumours or diabetic ischaemia. Cell function, including that of osteoblasts, is normally impaired by acid; the unusual stimulatory effect of acid on osteoclasts may represent a primitive ‘fail-safe’ that evolved with terrestrial vertebrates to correct systemic acidosis by ensuring release of alkaline bone mineral when the lungs and kidneys are unable to remove sufficient H+ equivalent. The present results suggest that even subtle chronic acidosis could be sufficient to cause appreciable bone loss over time.

Prebiotics have the potential to promote immediate and long-term effects on the health and well-being of infants. They have been added to infant formulas in Japan for 20 years and have only recently been used in Europe. The objective is to change the intestinal microflora in order to mimic the bacteriological effect and, thus, the functional effects of human milk. There is, however, a potential risk of long-term effects of the use of these infant formulas. The consequences of using prebiotics in infants, during the first months of life, on the composition and development of the intestinal microflora, and on the resulting bacterial–bacterial and bacterial–host interactions are not known. Attempts have been made to improve infant and follow-on formulas by prebiotic supplementation, but intervention studies are needed to evaluate their immediate and long-term beneficial effects and demonstrate the absence of harmful consequences from their use.

Body composition in children is of increasing interest within the contexts of childhood obesity, clinical management of patients and nutritional programming as a pathway to adult disease. Energy imbalance appears to be common in many disease states; however, body composition is not routinely measured in patients. Traditionally, clinical interest has focused on growth or nutritional status, whereas more recent studies have quantified fat mass and lean mass. The human body changes in proportions and chemical composition during childhood and adolescence. Most of the weight gain comprises lean mass rather than fat. In general, interest has focused on percentage fat, and less attention has been paid to the way in which lean mass varies within and between individuals. In the general population secular trends in BMI have been widely reported, indicating increasing levels of childhood obesity, which have been linked to reduced physical activity. However, lower activity levels may potentially lead not only to increased fatness, but also to reduced lean mass. This issue merits further investigation. Diseases have multiple effects on body composition and may influence fat-free mass and/or fat mass. In some diseases both components change in the same direction, whereas in other diseases, the changes are contradictory and may be concealed by relatively normal weight. Improved techniques are required for clinical evaluations. Both higher fatness and reduced lean mass may represent pathways to an increased risk of adult disease.

There is considerable loss of DM during wet heat treatment of vegetables, leading to an increase in dietary fibre. Correction for the loss of DM indicates that the effects on total dietary fibre are minor. There is, however, depolymerization of the dietary fibre polysaccharides. The degradation is related to the severity of the heat treatment. Souring, freezing and mild microwave treatment have no effects. The viscosity is in general related to the extent of polymerisation. Microwave treatment has different effects on various cultivars of green beans, and the addition of salt (NaCl and CaCl2) to the boiling water changes the physico-chemical properties of soluble fibre in carrots, depending on the cation. The higher viscosity of the soluble fibre in raw carrots may partly explain the lower glucose and hormonal responses observed in healthy subjects when compared with blanched and microwave-cooked carrots. In studies on rats the amount of butyric acid in the distal colon has been shown to be higher with dietary components containing high amounts of resistant starch. Further, the fermentability is lower and the butyric acid concentration higher with composite foods than with the corresponding purified fibre fractions. In human studies the faecal concentration of butyric acid has been shown to increase in patients with ulcerative colitis when β-glucan-enriched oat bran (20 g fibre) is added to the diet for 12 weeks. Also, an improvement of symptoms was reported.

Rye bran contains a high content not only of dietary fibre, but also of plant lignans and other bioactive compounds in the so-called dietary fibre complex. Blood concentrations of lignans such as enterolactone have been used as biomarkers of intake of lignan-rich plant food. At present, evidence from studies in human subjects does not warrant the conclusion that rye, whole grains or phyto-oestrogens protect against cancer. Some studies, however, have pointed in that direction, especially in relation to cancers of the upper digestive tract. A number of prospective epidemiological studies have clearly shown a protective effect of whole-grain cereals against myocardial infarctions. A corresponding protective effect against diabetes and ischaemic stroke (brain infarct) has also been demonstrated. It seems reasonable to assume that these protective effects are associated with one or more factors in the dietary fibre complex.

Energy balance can be estimated in tissues, body segments, individual subjects (the focus of the present article), groups of subjects and even societies. Changes in body composition in individual subjects can be translated into changes in the energy content of the body, but this method is limited by the precision of the techniques. The precision for measuring fat and fat-free mass can be as low as 0.5 kg when certain reference techniques are used (hydrodensitometry, air-displacement plethysmography, dual-energy X-ray absorptiometry), and approximately 0.7 kg for changes between two time points. Techniques associated with a measurement error of 0.7 kg for changes in fat and fat-free mass (approximately 18MJ) are of little or no value for calculating energy balance over short periods of time, but they may be of some value over long periods of time (18 MJ over 1 year corresponds to an average daily energy balance of 70 kJ, which is <1% of the normal dietary energy intake). Body composition measurements can also be useful in calculating changes in energy balance when the changes in body weight and composition are large, e.g. >5–10 kg. The same principles can be applied to the assessment of energy balance in body segments using dual-energy X-ray absorptiometry. Energy balance can be obtained over periods as short as a few minutes, e.g. during measurements of BMR. The variability in BMR between individuals of similar age, weight and height and gender is about 7–9%, most of which is of biological origin rather than measurement error, which is about 2%. Measurement of total energy expenditure during starvation (no energy intake) can also be used to estimate energy balance in a whole-body calorimeter, in patients in intensive care units being artificially ventilated and by tracer techniques. The precision of these techniques varies from 1 to 10%. Establishing energy balance by measuring the discrepancy between energy intake and expenditure has to take into consideration the combined validity and reliability of both components. The measurement error for dietary intake may be as low as 2–3% in carefully controlled environments, in which subjects are provided only with certain food items and bomb calorimetry can be undertaken on duplicate samples of the diet. Reliable results can also be obtained in hospitalised patients receiving enteral tube feeding or parenteral nutrition as the only source of nutrition. Unreliability increases to an unknown extent in free-living subjects eating a mixed and varied diet; thus, improved methodology is needed for the study of energy balance.