Conjugated linoleic acid (CLA) is a collective term for positional and geometric isomers of octadecadienoic acid in which the double bonds are conjugated, i.e. contiguous. CLA was identified as a component of milk and dairy products over 20 years ago. It is formed as an intermediate in the course of the conversion of linoleic acid to oleic acid in the rumen. The predominant naturally occurring isomer is the cis-9, trans-11 modification. Treatment of linoleic acid-rich oils such as safflower oil, soyabean oil, or maize oil with base and heat will result in the formation of CLA. Two isomers predominate in the synthetic preparation, c9,t11 and t10,c12. CLA has been shown to inhibit chemically-induced skin, stomach, mammary or colon tumours in mice and rats. The inhibition of mammary tumours in rats is effective regardless of type of carcinogen or type or amount of dietary fat. CLA has also been shown to inhibit cholesterol-induced atherosclerosis in rabbits. When young animals (mice, pigs) are placed on CLA-containing diets after weaning they accumulate more body protein and less fat. Since CLA is derived from the milk of ruminant animals and is found primarily in their meat and in products derived from their milk there is a concerted world-wide effort to increase CLA content of milk by dietary means. Its effect on growth (less fat, more protein) is also a subject of active research. The mechanisms underlying the effects of CLA are still moot.

A 2-month follow-up of nutritional status was performed in forty elderly patients with recent hip fracture. Patients were nutritionally assessed on admission to our rehabilitation unit (day 0), then monthly (day 30, day 60) by measurement of resting energy expenditure (REE), anthropometric, impedance and biological variables. Patients were defined as undernourished (n 13) or normally nourished (n 27) on the basis of mid-arm circumference (MAC) and triceps skinfold thickness (TST) measurements. Seven patients recovered a walking autonomy and were discharged from the hospital before day 30 (group I) whereas thirteen patients were discharged after day 30 (group II); twenty patients remained in the study at day 60 (group III). MAC and TST decreased in normally nourished patients from group III throughout the study whereas they did not change in group II or in undernourished patients from group III. REE values in relation to fat-free mass were increased compared with normal values and were similar in the three groups on day 0; they did not change during the study. Daily energy intake in relation to body weight was higher in group I and increased in group II and in undernourished patients from group III throughout the study. In contrast, it was below the recommended value at day 0 and it did not significantly improve in normally nourished patients from group III. Serum albumin, transthyretin and transferrin levels on day 0 were below reference intervals in the three groups. Albumin levels increased in group III throughout the study. Inflammatory proteins decreased in groups II and III, with C-reactive protein levels returning to normal values in group II by day 30 and in group III at day 60, while orosomucoid levels did not become completely normal over this period. Our findings indicate no improvement in nutritional status in undernourished patients after surgery for recent hip fracture, despite an adequate energy intake. An insufficient spontaneous energy intake for normally nourished patients was associated with a delayed favourable outcome resulting in a prolonged duration of hospitalization. A hypermetabolic state persisted during the 3 months after surgery.

Despite the almost universal clinical observation that inflammation of the gut is frequently associated with inflammation of the joints and vice versa, the nature of this relationship remains elusive. In the present review, we provide evidence for how the interaction of dietary lectins with enterocytes and lymphocytes may facilitate the translocation of both dietary and gut-derived pathogenic antigens to peripheral tissues, which in turn causes persistent peripheral antigenic stimulation. In genetically susceptible individuals, this antigenic stimulation may ultimately result in the expression of overt rheumatoid arthritis (RA) via molecular mimicry, a process whereby foreign peptides, similar in structure to endogenous peptides, may cause antibodies or T-lymphocytes to cross-react with both foreign and endogenous peptides and thereby break immunological tolerance. By eliminating dietary elements, particularly lectins, which adversely influence both enterocyte and lymphocyte structure and function, it is proposed that the peripheral antigenic stimulus (both pathogenic and dietary) will be reduced and thereby result in a diminution of disease symptoms in certain patients with RA.

In ruminants, Co is required for the synthesis of vitamin B12, which in turn is needed for the resynthesis of methionine by methylation of homocysteine and thus, cobalamin deficiency may induce hyperhomocysteinaemia which is brought into context with perturbations of the antioxidative–prooxidative balance. The present study was conducted to explore whether Co deficiency in cattle is also associated with homocysteine-induced disturbances of oxidative status. Co deficiency was induced in cattle by feeding two groups of animals on either a basal maize-silage-based diet that was moderately low in Co (83 μg Co/kg DM), or the same diet supplemented with Co to a total of 200 μg Co/kg DM, for 43 weeks. Co deficiency was apparent from a reduced vitamin B12 status in serum and liver and an accumulation of homocysteine in plasma which was in excess of 4·8 times higher in Co-deprived cattle than in controls. The much increased level of circulating homocysteine did not indicate severe disturbances in antioxidant–prooxidant balance as measured by individual markers of lipid peroxidation, protein oxidation, and the antioxidative defence system. There were no quantitative difference in plasma thiol groups, nor were there significant changes in concentrations of α-tocopherol, microsomal thiobarbituric acid-reactive substances and carbonyl groups in liver. However, there was a trend toward increased plasma carbonyl levels indicating a slight degradation of plasma proteins in the hyperhomocysteinaemic cattle. Analysis of the hepatic catalase (EC 1.11.1.6) activity revealed an 11 % reduction in Co-deficient cattle relative to the controls. These results indicate that long-term moderate Co deficiency may induce a severe accumulation of plasma homocysteine in cattle, but considerable abnormalities in oxidative status failed to appear.

Elevated levels of coagulation factor VII activity (FVIIc) are associated with increased risk of CHD. FVIIc is strongly determined by two polymorphisms (R353Q and 0/10 base pairs (bp)) and plasma triacylglycerol (TAG) concentrations. The Q and 10 bp polymorphisms show strong linkage disequilibrium and have been associated with lower levels of fasting FVII, but there has been little investigation of the effect of these genotypes on the postprandial FVII metabolism. The present study demonstrated that fasting activated factor VII (FVIIa) and factor VII antigen (FVIIag) levels were significantly lower in the heterozygotes carrying the Q and 10 bp alleles (n 12), than in the R/0 bp homozygotes (n 12) (43·0 (SE 4·8) v. 23·9 (SE 6·5) mU/ml and 85·7 (SE 5·4) v. 71·6 (SE 7·5) % respectively). During postprandial lipaemia there was a significant increase in FVIIa in R/0 bp homozygotes but not in the heterozygotes carrying the Q and 10 bp alleles. The proportion of FVIIa (FVIIa : FVIIag) increased in the homozygotes but not in the heterozygotes (2·04 (SE 0·35) v. 1·20 (SE 0·26) respectively). Therefore possession of the relatively common Q and 10 bp alleles is not associated with postprandial activation of FVII, which may in turn have a protective effect against CHD.

A diet history method for estimating energy and N intakes was validated against 24 h urinary N excretion and energy expenditure measured by the doubly-labelled water (DLW) method. Forty-eight women aged 50–65 years were studied over 1 year. Weighed diet records from 4 d and two 24 h urine collections, for measurement of urinary N excretion, were obtained in each of four seasons. At the end of the year, a diet history was obtained, BMR was measured by whole-body calorimetry, and, in sixteen women, total energy expenditure (EE) was measured by DLW. Energy intake (EI) and N intake (NI) were calculated using food tables. Using weighed records and diet history respectively mean NI were 11·21 (SD 2·09) G AND 11·47 (sd 2·40) g (NS) and EI were 8·08 (sd 1·54) MJ and 8·20 (sd 1·86) MJ (NS). Mean urine N : NI and EI : BMR values indicated bias to under-reporting by weighed record and diet history techniques in some individuals, but there was no significant difference between these measures at the group level. The Pearson correlation coefficient (r) for urine N v. NI was 0·81 for the weighed record and 0·38 for the diet history. The correlation of EE v. EI was r 0·48 for weighed record and r 0·11 for diet history. In this study the diet history gave the same estimate of mean intake, but the weighed record appeared to perform better in ranking individuals.

Since the food habits of many elderly people are inadequate, the first experiment of the present study tested whether flavour amplification induces changes in preferences for and consumption of food and thus might result in a nutritional benefit. Two panels, one of 260 and one of 120 subjects, aged 19–98 years, took part in the study in which preferences for flavour-amplified yoghurt and Quorn® were measured. For both products, only a few of the young subjects (20 %) preferred the high flavour level; the percentage of subjects preferring the high flavour levels increased with age. These changes were highly significant. In a second experiment, participants received, under ad libitum conditions over 2 d in random order, a dish of yoghurt with either a high or a low flavour level. When adjusted for total consumption quantity, consumption of the highly flavoured yoghurt was not significantly correlated with age (r -0·03, P = 0·35). In a third experiment, odour perception was measured by determining the detection threshold for isoamylacetate. BMI values were obtained and the relationships between BMI and odour perception, age, preference and consumption were assessed in the age group 40–65 years. A significant correlation was observed between age and BMI (r 0·51, P < 0·0005). No significant correlation was observed between BMI and relative consumption of highly flavoured yoghurt (r -0·14, P = 0·14). A significant correlation was observed between BMI and preference for flavour-amplified yoghurt (r 0·35, P < 0·001). However, no significant correlation was observed between BMI and odour perception (r 0·07, P = 0·32). With increasing age, a combined influence of age, sex, BMI and odour perception on food preference is to be expected. According to our multiple regression analysis, BMI showed a significant partial regression coefficient (standardized β 0·36, P = 0·03). In conclusion, flavour amplification of food for older adults deserves attention, but specific approaches, which are tailored to the candidate food systems and older adult target groups, are needed.

Impaired nutritional status has been frequently reported in surveys estimating its prevalence amongst patients in hospital. While there is no doubt that protein–energy undernutrition has serious implications for health, recovery from illness or surgery and hospital costs, lack of nationally or internationally accepted cut-off points and guidelines for most nutrition-related variables make nutritional assessment difficult and proper comparisons between studies impossible. In reviewing published work in which the prevalence of undernutrition has been assessed, it can be seen that each study defined undernutrition, or nutritional risk, using different methodology. This present review aims to highlight the problems which arise when deciphering these studies, and the resulting difficulty in determining the true prevalence of undernutrition and nutritional risk, amongst both general and specific groups of hospital in-patients. It is widely agreed that routine hospital practices can further adversely affect the nutritional status of sick patients in hospital. How this occurs, and the potential effects of impaired nutritional status on clinical outcome are examined. The methods currently available to assess nutritional status are evaluated in the knowledge that such assessments are difficult in clinical practice. The review concludes by proposing that if we want the medical and nursing professions to consider the nutritional status of hospital patients seriously, definitions of undernutrition and nutritional risk, and cut-off values for the nutritional variables measured must be agreed to allow evidence-based practice. Outcome measures which allow clear comparisons between groups and treatments must be used in studies assessing the effects of nutritional interventions.

Obesity is now commonly defined in adults as a BMI > 30 kg/m2. The prevalence of obesity in established market economies (Europe, USA, Canada, Australia, etc.) varies greatly, but a weighed estimate suggests an average prevalence in the order of 15–20 %. The prevalence in these countries generally shows increasing trends over time. Obesity is also relatively common in Latin America, but much less so in sub-Saharan Africa and Asia where the majority of the world population lives. Nevertheless obesity rates are increasing there as well and, more importantly, rates of diabetes are increasing even more quickly, particularly in Asian countries. The risks of type 2 diabetes mellitus in these countries tend to increase sharply at levels of BMI generally classified as acceptable in European and North American white people. There have been suggestions to adopt specific classifications of obesity in Asians (e.g. BMI 23 for overweight and 25 or 27 kg/m2 for obesity) and this will greatly affect the prevalence estimates of obesity worldwide (currently at about 250 million people). Particularly for health promotion purposes BMI may be replaced by a classification based on waist circumference, but also specific classifications for different ethnic groups may be necessary. The number of diabetics has been projected to increase from 135 million in 1995 to 300 million in 2025. Much of this increase will be seen in Asia. In summary, both obesity and type 2 diabetes are common consequences of changing lifestyles (increased sedentary lifestyles and increased energy density of diets). Both are potentially preventable through lifestyle modification on a population level, but this requires a coherent and multifaceted strategy. Such strategies are not developed or implemented. These developments point toward the great urgency to develop global and national plans for adequate prevention and management of obesity and type 2 diabetes mellitus.

Since the food habits of many elderly people are inadequate, the first experiment of the present study tested whether flavour amplification induces changes in preferences for and consumption of food and thus might result in a nutritional benefit. Two panels, one of 260 and one of 120 subjects, aged 19–98 years, took part in the study in which preferences for flavour-amplified yoghurt and Quorn® were measured. For both products, only a few of the young subjects (20 %) preferred the high flavour level; the percentage of subjects preferring the high flavour levels increased with age. These changes were highly significant. In a second experiment, participants received, under ad libitum conditions over 2 d in random order, a dish of yoghurt with either a high or a low flavour level. When adjusted for total consumption quantity, consumption of the highly flavoured yoghurt was not significantly correlated with age (r -0·03, P = 0·35). In a third experiment, odour perception was measured by determining the detection threshold for isoamylacetate. BMI values were obtained and the relationships between BMI and odour perception, age, preference and consumption were assessed in the age group 40–65 years. A significant correlation was observed between age and BMI (r 0·51, P < 0·0005). No significant correlation was observed between BMI and relative consumption of highly flavoured yoghurt (r -0·14, P = 0·14). A significant correlation was observed between BMI and preference for flavour-amplified yoghurt (r 0·35, P < 0·001). However, no significant correlation was observed between BMI and odour perception (r 0·07, P = 0·32). With increasing age, a combined influence of age, sex, BMI and odour perception on food preference is to be expected. According to our multiple regression analysis, BMI showed a significant partial regression coefficient (standardized β 0·36, P = 0·03). In conclusion, flavour amplification of food for older adults deserves attention, but specific approaches, which are tailored to the candidate food systems and older adult target groups, are needed.

The Tanita body-fat analyser is a novel device to estimate body fat, based on the principles of bioelectrical impedance. It differs from other impedance systems which use surface electrodes in that the subjects stand bare-footed on a metal sole-plate which incorporates the electrodes, hence impedance is measured through the legs and lower trunk. In 104 men and 101 women (16–78 years and BMI 16–41 kg/m2) the mean bias in body-fat mass measured using the Tanita body-fat analyser was 0·8 (2SD 7·9) KG RELATIVE TO A FOUR-COMPARTMENT MODEL. THIS IS COMPARABLE TO THE OTHER PREDICTION TECHNIQUES TESTED (CONVENTIONAL TETRAPOLAR IMPEDANCE -1·3 (2sd 6·9) kg, skinfold thicknesses 0·3 (2sd 7·4) kg, and BMI-based formulas -0·2 (2sd 9·0) kg and -0·6 (2sd 8·5) kg), but the agreement was poorer than for ‘reference’ methods to measure body fat (density 0·2 (2sd 3·7) kg, total body water -0·9 (2sd 3·4) kg and dual-energy X-ray absorptiometry 0·1 (2sd 5·0) kg). The present paper also describes the derivation of a new prediction equation for the calculation of body composition from the Tanita body-fat analyser. The equation incorporates sex, age, and a log-transformation of height, weight and the measured impedance to predict body fat measured by a four-compartment model. This approach is recommended in the derivation of other prediction equations in body composition analysis. Using this novel prediction equation the residual standard deviations were 4·8 % for men and 3·3 % for women. A similar analysis using data collected with a conventional tetrapolar system yielded residual standard deviations of 4·3 % for men and 3·1 % for women. This demonstrates that the practical simplicity of the novel Tanita method is not associated with a clinically significant decrement in performance relative to a traditional impedance device.

The purpose of the present study was to estimate whole-body fatty acid and cholesterol synthesis in weight-stable adults and to determine the likely effect on the doubly-labelled water (DLW) method for measuring energy expenditure. Synthesis was measured by 2H incorporation over 14 d in six adult males in approximate energy balance following noradrenaline infusion to maximize mobilization of free fatty acid from adipose tissue. The inter-individual variation in synthesis rates was large and in one subject the proportion of free fatty acid synthesized was ten times that of the mean of the rest of the group; the fasting concentration of esterified fatty acid in this subject was five times that of the rest of the group indicating likely violation of the assumptions underlying the calculation of whole-body synthesis. After 14 d of labelling in the other five subjects, 0·9 (SEM 0·3) % OF THE CIRCULATING FREE FATTY ACID, 9·3 (sem 3·0) % of the esterified fatty acid, 14·6 (sem 2·4) % of the free cholesterol and 28·3 (sem 3·7) % of esterified cholesterol had been synthesized de novo. A high rate of synthesis correlated with a low pre-dose 2H abundance both within and between lipid classes suggesting that natural 2H abundance variations in some lipid classes may be used to determine their metabolic origin. Whole-body synthetic rates were 8 g/d for fatty acid and 0·3–0·5 g/d for cholesterol. These values correspond to very small errors on DLW-derived estimates of CO2 production; -2·5 litres/d for fatty acid and -0·1 to -0·2 litres/d for cholesterol. These results, obtained in subjects typically consuming a diet with a lower fat and cholesterol content that the typical Western diet, suggest that the DLW method is unlikely to be affected by fatty acid and cholesterol synthesis in subjects in energy balance consuming a typical Western diet.

Two studies were designed to compare the effects on post-ingestive satiety of manipulating the degree of saturation of fatty acids, at a fixed chain length (18 C atoms), in a fixed energy (5·68 MJ for males; 3·97 MJ for females), high-fat (55 % energy) lunch meal. Two different groups of twenty subjects (ten males and ten females) took part in each study. All forty subjects were of normal weight and aged between 18 and 36 years. Study 1 compared the effects of fat A (oleic blend, high in monounsaturated fatty acids (MUFA)) with those of fat B (linoleic blend, high in polyunsaturated fatty acids (PUFA)) and fat C (stearic–oleic blend, high in saturated fatty acids (SFA)). Study 2, which was designed to confirm and extend the findings of Study 1, compared the effects of fats A, B and C with those of fat D (a linoleic–oleic blend). Energy and nutrient intakes were monitored for the rest of the day and for the following day. Profiles of hunger, fullness and other sensations were monitored by continuous tracking and end-of-day questionnaires. In each meal the fat content was exclusively composed of one particular type (A, B, C or D) and was divided equally between the main course and dessert. Study 1 revealed a significant effect of fat type (degree of saturation) on intake of nutrients at the following (dinner) meal (smallest F[2,36] 3·38, P < 0·05), on post-ingestive ratings of motivation to eat (smallest F[2,36] 4·18, P = 0·02) and on energy intake over the whole test day (F[2,36] 3·39, P < 0·01). Subjects consumed significantly more energy after consumption of the lunch containing fat A than after the lunches containing fats B or C and there was a trend for these effects to continue into the second day. In Study 2, fat C produced more similar effects on appetite to fat A and there was a tendency for subjects to consume more over the whole test day when they had consumed the lunch containing fat A than when they had consumed the lunch containing fat B. Furthermore, when the data from fat conditions A and B in both studies were combined (n 40) the results of Study 1 were confirmed. Overall, the results of these short-term studies indicate that PUFA may exert a relatively stronger control over appetite than MUFA and SFA.

The objectives of the present study were to examine the effects of (1) ingesting mandatory snacks v. no snacks and (2) the composition of isoenergetically-dense snacks high in protein, fat or carbohydrate, on food intake and energy intake (EI) in eight men with ad libitum access to a diet of fixed composition. Subjects were each studied four times in a 9 d protocol per treatment. On days 1–2, subjects were given a medium-fat maintenance diet estimated at 1·6 × resting metabolic rate (RMR). On days 3–9, subjects consumed three mandatory isoenergetic, isoenergetically dense (380 kJ/100 g) snacks at fixed time intervals (11.30, 15.30 and 19.30 hours). Total snack intake comprised 30 % of the subjects' estimated daily energy requirements. The treatments were high protein (HP), high carbohydrate (HC), high fat (HF) and no snack (NS). The order was randomized across subjects in a counterbalanced, Latin-square design. During the remainder of the day, subjects had ad libitum (meal size and frequency) access to a covertly manipulated medium-fat diet of fixed composition (fat: carbohydrate: protein, 40:47:13 by energy), energy density 550 kJ/100 g. All foods eaten were investigator-weighed before ingestion and left-overs were weighed after ingestion. Subjective hunger and satiety feelings were tracked hourly during waking hours using visual analogue scales. Ad libitum EI amounted to 13·9 MJ/d on the NS treatment compared with 11·7, 11·7 and 12·2 MJ/d on the HP, HC and HF diets respectively (F(3,21) 5·35; P = 0·007, sed 0·66). Total EI values were not significantly different at 14·6, 14·5, 15·0 and 14·2 MJ/d respectively. Snack composition did not differentially affect total daily food intake or EI. Average daily hunger was unaffected by the composition of the snacks. Only at 12.00 hours did subjects feel significantly more hungry during the NS condition, relative to the other dietary treatments (F(3,18) 4·42; P = 0·017). Body weight was unaffected by dietary treatment. In conclusion, snacking per se led to compensatory adjustments in feeding behaviour in lean men. Snack composition (with energy density controlled) did not affect the amount eaten of a diet of fixed composition. Results may differ in real life where subjects can alter both composition and amount of food they eat and energy density is not controlled.

The aim of the present study was to determine whether dietary peptide concentration had an effect on endogenous ileal amino acid flow in the growing pig. Eight 33 kg live weight entire male pigs had post-valve T-caecum (PVTC) cannulas surgically implanted for the collection of ileal digesta. The pigs were fed twice daily at 100 g/kg metabolic body weight per d and were given diets containing enzyme-hydrolysed casein (EHC) at 0, 50, 100 and 200 g/kg in a Latin-square design. A basal casein-based diet was fed to the pigs for 6 d periods between receiving the experimental diets. The pigs received the experimental diets for 8 d periods, with continuous collection of digesta for 24 h on each of the fifth and eighth days. The endogenous ileal amino acid flows were determined with reference to recovery of the marker, Cr, directly for pigs receiving the protein-free diet or after centrifugation and ultrafiltration (10 000 Da molecular mass cut-off) for pigs on the EHC-based diets. Mean endogenous ileal N flows were 1753, 1948, 2851 and 5743 μg/g DM intake when the pigs received diets containing 0, 50, 100 and 200 g EHC/kg respectively. There was a significant (P < 0·05) effect of dietary peptide concentration on the endogenous ileal flows of N and all of the amino acids, with an increase in endogenous ileal amino flow with increasing dietary EHC concentration.

Although the rapid increase in the prevalence of obesity in many countries suggests that environmental factors (mainly overeating and physical inactivity) play the most important role in the development of overweight, it is very likely that genetic factors also contribute. It appears that one major gene in combination with one or several minor genes constitute the genetic components behind excess accumulation of body fat in most obese individuals. However, monogenic obesity has been described in a few families due to changes in leptin, leptin receptor, prohormone convertase, pro-opiomelanocortin or melanocortin-4 receptor. None of the monogenic variants is of great importance for common human obesity; the latter genes are unknown so far. Results from genomic scans suggest that major obesity genes are located on chromosomes 2, 10, 11 and 20. Studies of candidate genes indicate that the minor obesity genes control important functions of adipose tissue, and that structural variance in these genes may alter adipose tissue function in a way that promotes obesity. Such genes are β2- and β3-adrenoceptors, hormone-sensitive lipase, tumour necrosis factor alpha, uncoupling protein-1, low-density lipoprotein receptor, and peroxisome proliferator activator receptor gamma-2. Some of these genes may promote obesity by gene–gene interactions (for example β3-adrenoceptors and uncoupling protein-1) or gene–environment interactions (for example β2-adrenoceptors and physical activity). Some are important for obesity only among women (for example β2- and β3-adrenoceptors, low-density lipoprotein receptor and tumour necrosis factor alpha). Few ‘non-adipose’ genes have so far shown a firm association to common human obesity, which could suggest that the important genes for the development of excess body fat also control adipose tissue function.