An association between processed and red meat consumption and total mortality has been reported by epidemiological studies; however, there are many controversial reports regarding the association between meat consumption and CVD and IHD mortality. The present meta-analysis was carried out to summarise the evidence from prospective cohort studies on the association between consumption of meat (total, red, white and processed) and all-cause, CVD and IHD mortality. Cohort studies were identified by searching the PubMed and ISI Web of Knowledge databases. Risk estimates for the highest v. the lowest consumption category and dose–response meta-analysis were calculated using a random-effects model. Heterogeneity among the studies was also evaluated. A total of thirteen cohort studies were identified (1 674 272 individuals). Subjects in the highest category of processed meat consumption had 22 and 18 % higher risk of mortality from any cause and CVD, respectively. Red meat consumption was found to be associated with a 16 % higher risk of CVD mortality, while no association was found for total and white meat consumption. In the dose–response meta-analysis, an increase of 50 g/d in processed meat intake was found to be positively associated with all-cause and CVD mortality, while an increase of 100 g/d in red meat intake was found to be positively associated with CVD mortality. No significant associations were observed between consumption of any type of meat and IHD mortality. The results of the present meta-analysis indicate that processed meat consumption could increase the risk of mortality from any cause and CVD, while red meat consumption is positively but weakly associated with CVD mortality. These results should be interpreted with caution due to the high heterogeneity observed in most of the analyses as well as the possibility of residual confounding.

Epidemiological studies have shown an inverse association between dietary intake of whole grains and the risk of chronic disease. This may be related to the ability to mediate a prebiotic modulation of gut microbiota. However, no studies have been conducted on the microbiota modulatory capability of whole-grain (WG) cereals. In the present study, the impact of WG wheat on the human intestinal microbiota compared to wheat bran (WB) was determined. A double-blind, randomised, crossover study was carried out in thirty-one volunteers who were randomised into two groups and consumed daily 48 g breakfast cereals, either WG or WB, in two 3-week study periods, separated by a 2-week washout period. Numbers of faecal bifidobacteria and lactobacilli (the target genera for prebiotic intake), were significantly higher upon WG ingestion compared with WB. Ingestion of both breakfast cereals resulted in a significant increase in ferulic acid concentrations in blood but no discernible difference in faeces or urine. No significant differences in faecal SCFA, fasting blood glucose, insulin, total cholesterol (TC), TAG or HDL-cholesterol were observed upon ingestion of WG compared with WB. However, a significant reduction in TC was observed in volunteers in the top quartile of TC concentrations upon ingestion of either cereal. No adverse intestinal symptoms were reported and WB ingestion increased stool frequency. Daily consumption of WG wheat exerted a pronounced prebiotic effect on the human gut microbiota composition. This prebiotic activity may contribute towards the beneficial physiological effects of WG wheat.

Curcumin is the active ingredient of turmeric. It is widely used as a kitchen spice and food colorant throughout India, Asia and the Western world. Curcumin is a major constituent of curry powder, to which it imparts its characteristic yellow colour. For over 4000 years, curcumin has been used in traditional Asian and African medicine to treat a wide variety of ailments. There is a strong current public interest in naturally occurring plant-based remedies and dietary factors related to health and disease. Curcumin is non-toxic to human subjects at high doses. It is a complex molecule with multiple biological targets and different cellular effects. Recently, its molecular mechanisms of action have been extensively investigated. It has anti-inflammatory, antioxidant and anti-cancer properties. Under some circumstances its effects can be contradictory, with uncertain implications for human treatment. While more studies are warranted to further understand these contradictions, curcumin holds promise as a disease-modifying and chemopreventive agent. We review the evidence for the therapeutic potential of curcumin from in vitro studies, animal models and human clinical trials.

This paper results from the final phase of the ENDO project (DGXII AIRII-CT94-1095), a European Commission-funded project on non-digestible oligosaccharides (NDO). All participants in the programme met to perform a consensus exercise on the possible functional food properties of NDO. Topics studied during the project (including a workshop on probiotics and prebiotics) and related aspects, for which considerable evidence has been generated recently, were evaluated on the basis of existing published scientific evidence. There was a general consensus that: (1) there is strong evidence for a prebiotic effect of NDO in human subjects. A prebiotic effect was defined as a food-induced increase in numbers and/or activity predominantly of bifidobacteria and lactic acid bacteria in the human large intestine; (2) there is strong evidence for the impact that NDO have on bowel habit; (3) there is promising evidence that consumption of inulin-type fructans may result in increased Ca absorption in man; (4) there are preliminary indications that inulin-type fructans interact with the functioning of lipid metabolism; (5) there is preliminary evidence in experimental animals of a preventive effect against colon cancer. Human nutrition studies are needed to substantiate these findings. It was concluded that the nutritional properties of NDO may prove to be a key issue in nutritional research in the future.

There is a growing appreciation that it is not just the total intake of dietary Se that is important to health but that the species of Se ingested may also be important. The present review attempts to catalogue what is known about Se species in foods and supplements and the health effects in which they are implicated. The biosynthetic pathways involved in Se assimilation by plants and the way in which Se species are metabolised in animals are presented in order to give an insight into the species likely to be present in plant and animal foods. Known data on the species of Se in the food chain and in food supplements are tabulated along with their concentrations and the analytical methodology used. The latter is important, since identification that is only based on retention-time matching with authentic standards must be considered as tentative: for evidence of structural confirmation, fragmentation of the molecular ion in addition to MS data is required. Bioavailability, as normally defined, is higher for organic Se species. Health effects, both beneficial and toxic, thought to be associated with specific Se species are described. Potent anti-tumour effects have been attributed to the low-molecular-weight species, Se-methyl-selenocysteine and its γ-glutamyl-derivative, found in a number of edible plants of the Allium and Brassica families. There remain considerable gaps in our knowledge of the forms of Se that naturally occur in foods. Without adequate knowledge of Se speciation, false conclusions may be drawn when assessing Se requirements for optimal health.

Nudging or ‘choice architecture’ refers to strategic changes in the environment that are anticipated to alter people’s behaviour in a predictable way, without forbidding any options or significantly changing their economic incentives. Nudging strategies may be used to promote healthy eating behaviour. However, to date, the scientific evidence has not been systematically reviewed to enable practitioners and policymakers to implement, or argue for the implementation of, specific measures to support nudging strategies. This systematic review investigated the effect of positional changes of food placement on food choice. In total, seven scientific databases were searched using relevant keywords to identify interventions that manipulated food position (proximity or order) to generate a change in food selection, sales or consumption, among normal-weight or overweight individuals across any age group. From 2576 identified articles, fifteen articles comprising eighteen studies met our inclusion criteria. This review has identified that manipulation of food product order or proximity can influence food choice. Such approaches offer promise in terms of impacting on consumer behaviour. However, there is a need for high-quality studies that quantify the magnitude of positional effects on food choice in conjunction with measuring the impact on food intake, particularly in the longer term. Future studies should use outcome measures such as change in grams of food consumed or energy intake to quantify the impact on dietary intake and potential impacts on nutrition-related health. Research is also needed to evaluate potential compensatory behaviours secondary to such interventions.

Previous research has shown that nutrients and certain food items influence inflammation. However, little is known about the associations between diet, as a whole, and inflammatory markers. In the present study, we examined the ability of a FFQ-derived dietary inflammatory index (DII) to predict inflammation. Data from a Belgian cross-sectional study of 2524 generally healthy subjects (age 35–55 years) were used. The DII is a population-based, literature-derived dietary index that was developed to predict inflammation and inflammation-related chronic diseases. The DII was calculated from FFQ-derived dietary information and tested against inflammatory markers, namely C-reactive protein (CRP), IL-6, homocysteine and fibrinogen. Analyses were performed using multivariable logistic regression, adjusting for energy, age, sex, BMI, smoking status, education level, use of non-steroidal anti-inflammatory drugs, blood pressure, use of oral contraceptives, anti-hypertensive therapy, lipid-lowering drugs and physical activity. Multivariable analyses showed significant positive associations between the DII and the inflammatory markers IL-6 (>1·6 pg/ml) (OR 1·19, 95 % CI 1·04, 1·36) and homocysteine (>15 μmol/l) (OR 1·56, 95 % CI 1·25, 1·94). No significant associations were observed between the DII and the inflammatory markers CRP and fibrinogen. These results reinforce the fact that diet, as a whole, plays an important role in modifying inflammation.

The hypothesis tested in the present study is that dietary fructans are able to modulate gastrointestinal peptides involved in the control of food intake, namely glucagon-like peptide (GLP)-1 (7-36) amide and ghrelin. After 3 weeks of treatment with a standard diet (control) or the same diet enriched with 100 g fructans varying in their degrees of polymerization (oligofructose (OFS), Synergy 1 (Syn) or long chain inulin)/kg, male Wistar rats were deprived of food for 8 h before sample collection. Dietary energy intake throughout the experiment was significantly lower (P>0·05) in fructans-fed rats than in control rats, leading to a significant decrease (P>0·01) in epidydimal fat mass at the end of the treatment in OFS- and Syn-treated rats. GLP-1 (7-36) amide concentration in portal vein serum was higher in OFS- and Syn-fed than in control rats. Both GLP-1 (7-36) amide concentration and proglucagon mRNA concentrations were significantly greater (P>0·05) in the proximal colonic mucosa of fructans-fed rats v. controls. Normally active ghrelin concentration in plasma increases during food deprivation and rapidly falls during a meal. In the present study, after 8 h of food deprivation, active ghrelin in the plasma remained significantly lower (P>0·05) in OFS and Syn-fed than in control rats. These results are in accordance with the modifications of dietary intake and fat-mass development in short-chain fructans-treated rats and demonstrate the potential modulation of GLP-1 (7-36) amide and ghrelin by fermentable fibres such as fructans, which are rapidly and extensively fermented in the proximal part of the colon.

Enhancing the n-3 polyunsaturated fatty acid (PUFA) content of beef is important in view of the generally saturated nature of fatty acids in ruminant meats and the negative effect this can have on human health. This study examined the effects of different sources of dietary n-3 PUFA on the performance of steers and the fatty acid composition of m. longissimus thoracis muscle and associated subcutaneous adipose tissue. Animals were fed ad libitum on grass silage plus one of four concentrates (60:40 forage:concentrate on a DM basis) containing differing sources of lipid: Megalac (16:0), lightly bruised whole linseed (18:3n-3), fish oil (20:5n-3 and 22:6n-3) and a mixture of linseed and fish oil (1:1, on an oil basis). Diets were formulated so that total dietary oil intake was 6 %, approximately half of which was from the experimental test oil. Linseed feeding not only increased the levels of 18:3n-3 in muscle phospholipid from 9·5 to 19 mg/100 g muscle but also enhanced the synthesis of 20:5n-3, the level of which increased from 10 to 15 mg/100 g muscle. Linseed also increased the proportion of 18:3n-3 in muscle neutral lipid and in adipose tissue lipids by a factor of 1·64 and 1·75 respectively. Fish oil feeding doubled the proportion of 20:5n-3 and 22:6n-3 in muscle phospholipids. The proportion of 18:1 trans in muscle neutral lipid was higher on the n-3 PUFA diets than the control diet, 0·04 and 0·02 respectively. Despite the implied modification to rumen metabolism, lipid source did not affect feed intake, growth rate, cold carcass weight or carcass fatness, but carcass conformation score was higher on fish oil treatments (P<0·05). However, total muscle fatty acid content was not different between treatments and ranged from 3·5–4·3 % of tissue weight. The increase in n-3 PUFA in the meat produced by feeding linseed or fish oil lowered the n-6:n-3 ratio but had little effect on the P:S ratio.

The gut microbiota has been implicated in host nutrient absorption and energy homeostasis. We studied the influence of different diets on body composition in germ-free (GF) and conventional (CV) mice. GF and CV male adult C3H mice were fed ad libitum a semi-synthetic low-fat diet (LFD; carbohydrate–protein–fat ratio: 41:42:17; 19·8 kJ/g), a high-fat diet (HFD; 41:16:43; 21·4 kJ/g) or a commercial Western diet (WD; 41:19:41; 21·5 kJ/g). There was no difference in body weight gain between GF and CV mice on the LFD. On the HFD, GF mice gained more body weight and body fat than CV mice, and had lower energy expenditure. GF mice on the WD gained significantly less body fat than GF mice on the HFD. GF mice on both HFD and WD showed increased intestinal mRNA expression of fasting-induced adipose factor/angiopoietin-like protein 4 (Fiaf/Angptl4), but they showed no major changes in circulating Fiaf/Angptl4 compared with CV mice. The faecal microbiota composition of the CV mice differed between diets: the proportion of Firmicutes increased on both HFD and WD at the expense of the Bacteroidetes. This increase in the Firmicutes was mainly due to the proliferation of one family within this phylum: the Erysipelotrichaceae. We conclude that the absence of gut microbiota does not provide a general protection from diet-induced obesity, that intestinal production of Fiaf/Angptl4 does not play a causal role in gut microbiota-mediated effects on fat storage and that diet composition affects gut microbial composition to larger extent than previously thought.

It is essential to have a thorough knowledge of the bioavailability and metabolism of dietary flavonols to understand their role in disease prevention. Lightly fried onions containing 275μmol flavonols, principally quercetin-4′-glucoside and quercetin-3,4′-diglucoside, were fed to healthy human volunteers and plasma and urine were collected over a 24h period. Samples were analysed by HPLC with diode array and tandem mass spectrometric detection. Five flavonol metabolites, quercetin-3′-sulphate, quercetin-3-glucuronide, isorhamnetin-3-glucuronide, a quercetin diglucuronide and a quercetin glucuronide sulphate, were detected in plasma in quantifiable amounts with trace quantities of six additional quercetin metabolites. Sub-micromolar peak plasma concentrations (cmax) of quercetin-3′-sulphate, quercetin-3-glucuronide, isorhamnetin-3-glucuronide and quercetin diglucuronide were observed 0.6–0.8h after ingestion. In contrast, the cmax of quercetin glucuronide sulphate was 2.5h. The elimination half-lives (t1/2) of quercetin-3′-sulphate, quercetin-3-glucuronide and quercetin diglucuronide were 1.71, 2.33 and 1.76h respectively, while the t1/2 of isorhamnetin-3-glucuronide was 5.34h and that of quercetin glucuronide sulphate was 4.54h. The profile of metabolites excreted in urine was markedly different to that of plasma with many of the major urinary components, including quercetin-3′-glucuronide, two quercetin glucoside sulphates and a methylquercetin diglucuronide, absent or present in only trace amounts in the bloodstream indicative of substantial phase II metabolism. Total urinary excretion of quercetin metabolites was 12·9μmol, corresponding to 4·7% of intake. If these samples had been subjected to hydrolysis, as in many previous studies, only quercetin and isorhamnetin would have been detected and quantified. The bioactivity of these metabolites should be considered.

Intestinal barrier integrity is a prerequisite for homeostasis of mucosal function, which is balanced to maximise absorptive capacity, while maintaining efficient defensive reactions against chemical and microbial challenges. Evidence is mounting that disruption of epithelial barrier integrity is one of the major aetiological factors associated with several gastrointestinal diseases, including infection by pathogens, obesity and diabetes, necrotising enterocolitis, irritable bowel syndrome and inflammatory bowel disease. The notion that specific probiotic bacterial strains can affect barrier integrity fuelled research in which in vitro cell lines, animal models and clinical trials are used to assess whether probiotics can revert the diseased state back to homeostasis and health. This review catalogues and categorises the lines of evidence available in literature for the role of probiotics in epithelial integrity and, consequently, their beneficial effect for the reduction of gastrointestinal disease symptoms.

We have recently developed a simple algorithm for the classification of household and locomotive activities using the ratio of unfiltered to filtered synthetic acceleration (gravity-removal physical activity classification algorithm, GRPACA) measured by a triaxial accelerometer. The purpose of the present study was to develop a new model for the immediate estimation of daily physical activity intensities using a triaxial accelerometer. A total of sixty-six subjects were randomly assigned into validation (n 44) and cross-validation (n 22) groups. All subjects performed fourteen activities while wearing a triaxial accelerometer in a controlled laboratory setting. During each activity, energy expenditure was measured by indirect calorimetry, and physical activity intensities were expressed as metabolic equivalents (MET). The validation group displayed strong relationships between measured MET and filtered synthetic accelerations for household (r 0·907, P < 0·001) and locomotive (r 0·961, P < 0·001) activities. In the cross-validation group, two GRPACA-based linear regression models provided highly accurate MET estimation for household and locomotive activities. Results were similar when equations were developed by non-linear regression or sex-specific linear or non-linear regressions. Sedentary activities were also accurately estimated by the specific linear regression classified from other activity counts. Therefore, the use of a triaxial accelerometer in combination with a GRPACA permits more accurate and immediate estimation of daily physical activity intensities, compared with previously reported cut-off classification models. This method may be useful for field investigations as well as for self-monitoring by general users.

The effects of different polyphenol-containing beverages on Fe absorption from a bread meal were estimated in adult human subjects from the erythrocyte incorporation of radio-Fe. The test beverages contained different polyphenol structures and were rich in either phenolic acids (chlorogenic acid in coffee), monomeric flavonoids (herb teas, camomile (Matricaria recutita L.)), vervain (Verbena officinalis L.), lime flower (Tilia cordata Mill.), pennyroyal (Mentha pulegium L.) and peppermint (Mentha piperita L.), or complex polyphenol polymerization products (black tea and cocoa). All beverages were potent inhibitors of Fe absorption and reduced absorption in a dose-dependent fashion depending on the content of total polyphenols. Compared with a water control meal, beverages containing 20–50 mg total polyphenols/serving reduced Fe absorption from the bread meal by 50–70 %, whereas beverages containing 100–400 mg total polyphenols/serving reduced Fe absorption by 60–90 %. Inhibition by black tea was 79–94 %, peppermint tea 84 %, pennyroyal 73 %, cocoa 71 %, vervain 59 %, lime flower 52 % and camomile 47 %. At an identical concentration of total polyphenols, black tea was more inhibitory than cocoa, and more inhibitory than herb teas camomile, vervain, lime flower and pennyroyal, but was of equal inhibition to peppermint tea. Adding milk to coffee and tea had little or no influence on their inhibitory nature. Our findings demonstrate that herb teas, as well as black tea, coffee and cocoa can be potent inhibitors of Fe absorption. This property should be considered when giving dietary advice in relation to Fe nutrition.

White adipose tissue is a key endocrine and secretory organ, releasing multiple adipokines, many of which are linked to inflammation and immunity. During the expansion of adipose tissue mass in obesity there is a major inflammatory response in the tissue with increased expression and release of inflammation-related adipokines, including IL-6, leptin, monocyte chemoattractant protein-1 and TNF-α, together with decreased adiponectin production. We proposed in 2004 (Trayhurn & Wood, Br J Nutr92, 347–355) that inflammation in adipose tissue in obesity is a response to hypoxia in enlarged adipocytes distant from the vasculature. Hypoxia has now been directly demonstrated in adipose tissue of several obese mouse models (ob/ob, KKAy, diet-induced) and molecular studies indicate that the level of the hypoxia-inducible transcription factor, hypoxia-inducible factor-1α, is increased, as is expression of the hypoxia-sensitive marker gene, GLUT1. Cell- culture studies on murine and human adipocytes show that hypoxia (induced by low O2 or chemically) leads to stimulation of the expression and secretion of a number of inflammation-related adipokines, including angiopoietin-like protein 4, IL-6, leptin, macrophage migration inhibitory factor and vascular endothelial growth factor. Hypoxia also stimulates the inflammatory response of macrophages and inhibits adipocyte differentiation from preadipocytes. GLUT1 gene expression, protein level and glucose transport by human adipocytes are markedly increased by hypoxia, indicating that low O2 tension stimulates glucose utilisation. It is suggested that hypoxia has a pervasive effect on adipocyte metabolism and on overall adipose tissue function, underpinning the inflammatory response in the tissue in obesity and the subsequent development of obesity-associated diseases, particularly type 2 diabetes and the metabolic syndrome.

Under commercial conditions, weaning of piglets is associated with social, environmental and dietary stress. Consequently, small-intestinal barrier and absorptive functions deteriorate within a short time after weaning. Most studies that have assessed small-intestinal permeability in pigs after weaning used either Ussing chambers or orally administered marker probes. Paracellular barrier function and active absorption decrease when pigs are weaned at 3 weeks of age or earlier. However, when weaned at 4 weeks of age or later, the barrier function is less affected, and active absorption is not affected or is increased. Weaning stress is a critical factor in relation to the compromised paracellular barrier function after weaning. Adequate feed intake levels after weaning prevent the loss of the intestinal barrier function. Transcellular transport of macromolecules and passive transcellular absorption decrease after weaning. This may reflect a natural intestinal maturation process that is enhanced by the weaning process and prevents the pig from an antigen overload. It seems that passive and active absorption after weaning adapt accurately to the new environment when pigs are weaned after 3 weeks of age. However, when weaned at 3 weeks of age or earlier, the decrease in active absorption indicates that pigs are unable to sufficiently adapt to the new environment. To improve weaning strategies, future studies should distinguish whether the effect of feed intake on barrier function can be directed to a lack of a specific nutrient, i.e. energy or protein.

Although high α-linolenic acid flaxseed (Linum usitatissitmum) is one of the richest dietary sources of α- linolenic acid and is also a good source of soluble fibre mucilage, it is relatively unstudied in human nutrition. Healthy female volunteers consumed 50 g ground, raw flaxseed/d for 4 weeks which provided 12–13% of energy intake (24–25 g/100 g total fat). Flaxseed raised α-linolenic acid and long-chain n-3 fatty acids in both plasma and erythrocyte lipids, as well as raising urinary thiocyanate excretion 2.2- fold. Flaxseed also lowered serum total cholesterol by 9 % and low-density-lipoprotein-cholesterol by 18%. Changes in plasma α-linolenic acid were equivalent when 12 g α-linolenic acid/d was provided as raw flaxseed flour (50 g/d) or flaxseed oil (20 g/d) suggesting high bioavailability of α-linolenic acid from ground flaxseed. Test meals containing 50 g carbohydrate from flaxseed or 25 g flaxseed mucilage each significantly decreased postprandial blood glucose responses by 27%. Malondialdehyde levels in muffins containing 15 g flaxseed oil or flour/kg were similar to those in wheat-flour muffins. Cyanogenic glycosides (linamarin, linustatin, neolinustatin) were highest in extracted flaxseed mucilage but were not detected in baked muffins containing 150 g flaxseed/kg. We conclude that up to 50 g high-α-linolenic acid flaxseed/d is palatable, safe and may be nutritionally beneficial in humans by raising n-3 fatty acids in plasma and erythrocytes and by decreasing postprandial glucose responses.

1. The rates of passage of markers of fluid and particulate digesta through the sheep alimentary tract have been described mathematically in single-injection experiments by analysing the concentration curves of marker excretion in faecal dry matter and then predicting these concentrations by means of an equation containing two exponential terms. Three components related to this equation are a transit time for digesta in the intestines, a half-time of marker in the reticulo-rumen and a half-time tentatively associated with the passage of marker through the caecum and proximal colon. With this approach no surgical interference with an animal is required to obtain meaningful information about gut function.

2. Abomasal cannulation did not affect the rate of passage of 51Cr EDTA through the gut.

3. The mean half-times (T1/2) for 51Cr EDTA in the reticulo-rumen and hind-gut, respectively, were 646 and 236 min for a roughage diet and 890 and 607 min for a diet consisting mainly of wheat grain, both diets providing approximately the same amounts of digestible dry matter. These results indicated that the changes in half-times were proportionately much greater in the caecum and proximal colon than in the reticulo-rumen. The mean transit time of marker through the digestive tract also increased from 721 to 1345 min when the concentrate diet was given.

4. The complex of chromium-51 with EDTA was excreted faster in faeces than cerium-144–praseodymium-144 when both were given together as a single injection into the reticulorumen. This was caused mainly by differential rates of elimination of water and particulate matter from the reticulo-rumen.

The association between abdominal fat accumulation and risk of chronic diseases, including type II diabetes and coronary heart disease, has long been recognized. Insulin resistance may be a key factor in this link. Many studies have pointed to an association between insulin resistance and intra-abdominal fat accumulation (visceral obesity). However there is no clear proof of a causal link between visceral fat accumulation and insulin resistance. In assessing the probability of a causal link, it is useful to consider potential mechanisms. One such potential causal link is the release of non-esterified fatty acids from visceral fat into the portal vein, so that they have direct effects on hepatic metabolism. Visceral fat has been shown in many studies to exhibit a high rate of lipolysis compared with subcutaneous fat depots. However, if the idea that visceral fat releases fatty acids into the portal vein at a high rate is examined critically, a number of difficulties appear. Not least of these is the fact that continued high rates of lipolysis should lead to the disappearance of the visceral fat depot, unless these high rates of fat mobilization are matched by high rates of fat deposition. There is far less evidence for high rates of fat deposition in visceral adipose tissue, and some contrary evidence. Evidence for high rates of visceral lipolysis in vivo from studies involving catheterization of the portal vein is not strong. If this potential link is discounted, then other reasons for the relationship between visceral fat and insulin resistance must be considered. One is that there is no direct causal link, but both co-correlate with some other variable. A possibility is that this other variable is subcutaneous abdominal fat, which usually outweighs intra-abdominal fat several-fold. Subcutaneous fat probably plays the major role in determining systemic plasma non-esterified fatty acid concentrations, which are relevant in determining insulin resistance. In conclusion, there is at present no proof of a causal link between visceral fat accumulation and insulin resistance, or the associated metabolic syndrome. The possibility of co-correlation with some other factor, such as subcutaneous abdominal fat accumulation, must not be forgotten.

Obesity is a serious health problem because of its co-morbidities. The solution, implying weight loss and long-term weight maintenance, is conditional on: (i) sustained satiety despite negative energy balance, (ii) sustained basal energy expenditure despite BW loss due to (iii) a sparing of fat-free mass (FFM), being the main determinant of basal energy expenditure. Dietary protein has been shown to assist with meeting these conditions, since amino acids act on the relevant metabolic targets. This review deals with the effects of different protein diets during BW loss and BW maintenance thereafter. Potential risks of a high protein diet are dealt with. The required daily intake is 0·8–1·2 g/kg BW, implying sustaining the original absolute protein intake and carbohydrate and fat restriction during an energy-restricted diet. The intake of 1·2 g/kg BW is beneficial to body composition and improves blood pressure. A too low absolute protein content of the diet contributes to the risk of BW regain. The success of the so-called ‘low carb’ diet that is usually high in protein can be attributed to the relatively high-protein content per se and not to the relatively lower carbohydrate content. Metabolic syndrome parameters restore, mainly due to BW loss. With the indicated dosage, no kidney problems have been shown in healthy individuals. In conclusion, dietary protein contributes to the treatment of obesity and the metabolic syndrome, by acting on the relevant metabolic targets of satiety and energy expenditure in negative energy balance, thereby preventing a weight cycling effect.