The purpose of this study was to investigate the immediate and long-term effects of early feed restriction (ER) on morphology and gene expression of lateral gastrocnemius muscle. Newly hatched crossbred broiler chickens were allocated into control and ER groups, the latter being free-fed on alternate days from hatch to 14 days of age (14 d), followed by ad libitum feeding as the control group until 63 d. The lateral gastrocnemius muscle was taken at 14 and 63 d, respectively for myofibre typing by both myosin ATPase staining and relative quantification of myosin heavy chain (MyHC) mRNA for slow-twitch (SM), red fast-twitch (FRM) and white fast-twitch (FWM) myofibres. The body weight and lateral gastrocnemius weight were significantly lower in the ER group, accompanied by significantly reduced serum triiodothyronine. The ER group exhibited significantly higher SM and FRM MyHC expression at 14 d, but lower SM expression at 63 d. Myosin ATPase staining revealed a similar pattern. The percentage of SM was higher at 14 d while lower at 63 d in the ER group. These morphological changes were accompanied by changes of mRNA expression for growth-related genes. The ER group expressed lower insulin-like growth factoar I (IGF-I) and higher IGF-I receptor (IGF-IR) at 14 d, yet significantly increased growth hormone receptor and IGF-IR mRNA at 63 d. These results indicate that ER may delay the slow to fast myofibre conversion as an immediate effect, but would result in a lower percentage of slow fibres owing to compensatory growth in the long term, which involves changes of mRNA expression for the growth-related genes in the muscle.

Visceral adipose tissue and skeletal muscle have central roles in determining whole-body insulin sensitivity. The peroxisome proliferator-activated receptor-γ (PPARγ) is a potential mediator of insulin sensitivity. It can directly modulate the expression of genes that are involved in glucose and lipid metabolism, including GLUT4, lipoprotein lipase (LPL) and adipocytokines (leptin and adiponectin). In this study, we aimed to determine the effects of obesity-associated insulin resistance on mRNA expression of PPARγ and its target genes. Dogs were studied when they were lean and at the end of an overfeeding period when they had reached a steady obese state. The use of a sensitive, real-time PCR assay allowed a relative quantification of mRNA expression for PPARγ, LPL, GLUT4, leptin and adiponectin, in adipose tissue and skeletal muscle. In visceral adipose tissue and/or skeletal muscle, mRNA expression of PPARγ, LPL and GLUT4 were at least 2-fold less in obese and insulin-resistant dogs compared with the same animals when they were lean and insulin-sensitive. The mRNA expression and plasma concentration of leptin was increased, whereas the plasma level and mRNA expression of adiponectin was decreased, by obesity. In adipose tissue, PPARγ expression was correlated with leptin and adiponectin. These findings, in an original model of obesity induced by a prolonged period of overfeeding, showed that insulin resistance is associated with a decrease in PPARγ mRNA expression that could dysregulate expression of several genes involved in glucose and lipid metabolism.

Fatty acids are known to play diverse roles in immune cells. They are important as a source of energy, as structural components of cell membranes, as signaling molecules and as precursors for the synthesis of eicosanoids and similar mediators. Recent research has suggested that the localization and organisation of fatty acids into distinct cellular pools has a direct influence on the behaviour of a number of proteins involved in immune cell activation, including those associated with T cell responses, antigen presentation and fatty acid-derived inflammatory mediator production. This article reviews these studies and places them in the context of existing literature in the field. These studies indicate the existence of several novel mechanisms by which altered fatty acid availability can modulate immune responses and impact upon clinical outcomes.

Enterotoxigenic Escherichia coli (ETEC) is an important cause of diarrhoea in children and piglets. Infection of ETEC results in fluid secretion and electrolyte losses in the small intestine. In this study the effects of tempeh, a traditional fungal fermented soyabean product, on fluid losses induced by ETEC infection in piglets was investigated. Pairs of ETEC-infected and non-infected small intestinal segments of piglets were perfused simultaneously for 8 h with pre-digested tempeh, its supernatant and saline as an internal control. In saline perfused segments, ETEC infection reduced net fluid absorption by more than 500 μl/cm2, whereas this reduction was significantly less for pre-digested tempeh and its supernatant (75 and 282 μl/cm2, respectively). The supernatant of pre-digested tempeh was also compared with its permeate and retentate fractions. These fractions were created by ultra-filtration and contained respectively low and high molecular weight (>5 kDa) compounds. Again ETEC infection caused a significant reduction of net fluid absorption when perfused with saline (386 μl/cm2) and also with the permeate fraction (300 μl/cm2), but much less with the supernatant and the retentate fraction (125 and 140 μl/cm2, respectively). The reduction in net fluid absorption upon ETEC infection when perfused with supernatant of either undigested or pre-digested tempeh was not different. Therefore from this study it can be concluded that a high molecular weight soluble fraction of tempeh is able to protect against fluid losses induced by ETEC, suggesting that this could play a potential role in controlling ETEC-induced diarrhoea.

Potassium (K) organic anion salts, such as potassium citrate or potassium malate in plant foods, may counteract low-grade metabolic acidosis induced by western diets, but little is known about the effect of other minor plant anions. Effects of K salts (chloride, citrate, galacturonate or tartrate) were thus studied on the mineral balance and digestive fermentations in groups of 6-week-old rats adapted to an acidogenic/5 % inulin diet. In all diet groups, substantial amounts of lactate and succinate were present in the caecum, besides SCFA. SCFA were poorly affected by K salts conditions. The KCl-supplemented diet elicited an accumulation of lactate in the caecum; whereas the lactate caecal pool was low in rats fed the potassium tartrate-supplemented (K TAR) diet. A fraction of tartrate (around 50 %) was recovered in urine of rats fed the K TAR diet. Potassium citrate and potassium galacturonate diets exerted a marked alkalinizing effect on urine pH and promoted a notable citraturia (around 0·5 μmol/24 h). All the K organic anion salts counteracted Ca and Mg hyperexcretion in urine, especially potassium tartrate as to magnesuria. The present findings indicate that K salts of unabsorbed organic anions exert alkalinizing effects when metabolizable in the large intestine, even if K and finally available anions (likely SCFA) are not simultaneously bioavailable. Whether this observation is also relevant for a fraction of SCFA arising from dietary fibre breakdown (which represents the major organic anions absorbed in the digestive tract in man) deserves further investigation.

Gallic acid (GA) is a naturally abundant plant phenolic compound in the human diet and is known to reduce the risk of disease. In this study, the anti-obesity effect of GA in an animal model of diet-induced obesity was investigated. Obesity was induced in male Wistar rats by feeding them a high-fat diet (HFD). GA was given as a supplement at the levels of 50 and 100 mg/kg rat for a period of 10 weeks. The results showed that the body weight, organ weight of the liver and adipose tissue weights of peritoneal and epididymal tissues in the HFD+GA groups were significantly decreased as compared with the HFD group. Serum TAG, phospholipid, total cholesterol, LDL-cholesterol, insulin and leptin levels in the HFD+GA groups were significantly decreased as compared with the HFD group. Histological study showed that the lipid droplets of rats with HFD+GA diets were significantly smaller than those with HFD diets. Hepatic TAG and cholesterol levels in HFD+GA groups were significantly decreased as compared with the HFD group. Moreover, the consumption of GA reduced oxidative stress and GSSG content and enhanced the levels of glutathione, GSH peroxidase, GSH reductase and GSH S-transferase in the hepatic tissue of rats with HFD-induced obesity. These results demonstrate that intake of GA can be beneficial for the suppression of HFD-induced dyslipidaemia, hepatosteatosis and oxidative stress in rats.

The aim of the present study was to verify whether the oral administration of cyanidin 3-O-β-d-glucoside (C3G) might counteract damage induced by chronic exposure (28 d) to ochratoxin A (OTA) in rats and if its effect may be mediated by haeme oxygenase-1 (HO-1). Forty male Sprague–Dawley rats, individually caged, were divided into four groups of ten animals. A control group received a commercial diet, group C3G received the control diet supplemented with C3G (1 g/kg feed), group OTA received the control diet supplemented with 200 parts per billion of OTA, and group OTA+C3G received the OTA group diet supplemented with C3G (1 g/kg feed). After 4 weeks of treatment animals were killed and the liver, kidneys and brain of each rat were collected and homogenised to evaluate non-proteic thiol groups (RSH), lipid hydroperoxide (LOOH) levels, HO-1 expression and DNA fragmentation. Rats of the OTA group showed a significant (P < 0·001) decrease in RSH content of kidney and liver and a significant (P < 0·001) increase of LOOH in all the examined tissues compared with the control group. In the OTA+C3G group both RSH content and LOOH levels were similar to those observed in the control group, demonstrating that C3G was able to counteract the effects of OTA. A significant (P < 0·001) induction of HO-1 was evident in kidney and liver of both OTA and C3G groups. DNA damage occurred in all the examined tissues of the OTA group, whereas C3G was able to prevent it. The present study confirmed that the effects of OTA are mediated by oxidative stress and demonstrated that C3G efficiently counteracted deleterious effects of OTA because of its antioxidant and HO-1-inducing properties.

Three groups of five wethers with ruminal and duodenal cannulas and maintained as either fauna-free (FF) or inoculated with total mixed fauna (TF) or Entodinium caudatum as a single-species monofauna (EN) were used in an experiment with two 28 d periods. In the first period, the sheep were fed a control barley-based diet (40:60 concentrate to silage DM) and in the second period the diet was supplemented with 187 g DM of Enterolobium cyclocarpum for the last 12 d of the period. The diets of period 1 and 2 were isonitrogenous. There was no effect of fauna on apparent ruminal and total tract organic matter and fibre digestion, but bacterial and microbial N flow and efficiency were improved in FF sheep compared to TF sheep. In period 2, protozoal numbers were reduced between 31 and 88 % 2 h after feeding E. cyclocarpum for the third to twelfth day of supplementation and by an average of 25 % in samples collected over the 24 h feeding cycle. Supplementation of the diet with E. cyclocarpum and the consequent protozoal reduction in TF and EN sheep improved the flow of non-ammonia N and bacterial N to the small intestine and the efficiency of microbial synthesis. However, E. cyclocarpum reduced ruminal organic matter digestion, especially in faunated sheep, and total tract organic matter, N and fibre digestion. Thus, a reduction in the protozoal cell numbers of 25 % was sufficient to achieve the beneficial effects of reduced fauna on the bacterial protein supply, but diet digestibility was reduced.

Epidemiological, biochemical, animal model and clinical trial data described in this overview strongly suggest that polyunsaturated fatty acids, particularly n-6 fatty acids, have a role in the pathogenesis and treatment of multiple sclerosis (MS). Data presented provides further evidence for a disturbance in n-6 fatty acid metabolism in MS. Disturbance of n-6 fatty acid metabolism and dysregulation of cytokines are shown to be linked and a “proof of concept clinical trial” further supports such a hypothesis. In a randomised double-blind, placebo controlled trial of a high dose and low dose selected GLA (18 : 3n-6)-rich oil and placebo control, the high dose had a marked clinical effect in relapsing-remitting MS, significantly decreasing the relapse rate and the progression of disease. Laboratory findings paralleled clinical changes in the placebo group in that production of mononuclear cell pro-inflammatory cytokines (TNF-α, IL-1β) was increased and anti-inflammatory TGF-β markedly decreased with loss of membrane n-6 fatty acids linoleic (18 : 2n-6) and arachidonic acids (20 : 4n-6). In contrast there were no such changes in the high dose group. The improvement in disability (Expanded Disability Status Scale) in the high dose suggests there maybe a beneficial effect on neuronal lipids and neural function in MS. Thus disturbed n-6 fatty acid metabolism in MS gives rise to loss of membrane long chain n-6 fatty acids and loss of the anti-inflammatory regulatory cytokine TGF-β, particularly during the relapse phase, as well as loss of these important neural fatty acids for CNS structure and function and consequent long term neurological deficit in MS.

The effect of dietary conjugated linoleic acid (CLA) on body composition and energy metabolism was investigated in broiler chickens. Male broiler chicks were assigned to receive either a control diet (1 % sunflower oil) or a diet containing CLA (1 % of a 1:1 mixture of trans-10, cis-12 and cis-9, trans-11 isomers of octadecadienoic acid). The diets were fed ad libitum for 3 weeks and there were eight replicates per diet, each replicate including four chickens so that each treatment had thirty-two animals. The proportion of body fat was lower in the control group than in the CLA group. No significant differences as to the proportions of body water, ash and protein were observed. Feed and energy intake were significantly lower in CLA-fed birds. The percentage of ingested energy lost in excreta was higher after CLA feeding and heat expenditure as a percentage of ingested energy was lower in the CLA-fed group. The CLA-fed group showed a higher percentage of SFA and lower percentages of MUFA and PUFA in carcass fat. It is concluded that CLA stimulated de novo fatty acid synthesis and lowered desaturase activity.

The present study aimed to evaluate the effects of a post-weaning high-fat (HF) diet upon hepatic morphology in rats subjected to perinatal protein restriction. Pregnant Wistar rats were assigned to a normal-protein diet (NP; with 19 % of protein) or a low-protein (LP) diet (with 5 % of protein). At weaning, the following groups were formed: NP and NP-HF, males and females, which were fed standard chow and an HF diet, respectively. Likewise, LP rat dams originated LP and LP-HF offspring, both sexes. Euthanasia was performed at 6 months of age. Three-way ANOVA disclosed a three-factor interaction among sex, perinatal diet and HF diet in relation to body mass, retroperitoneal fat pad, liver mass:tibia length ratio, binucleation rate and hepatocyte area at 6 months old (P < 0·05). The high-fat diet intensified the effects of perinatal protein restriction concerning systolic blood pressure, genital fat pad and hepatocyte number (P < 0·05; two-way ANOVA). Furthermore, higher steatosis rates and insulin and leptin concentrations were found in males fed on the HF diet, indicating a sex–post-weaning diet interaction (P < 0·05; two-way ANOVA). Fetal programming and HF diet as a single stimulus caused mild hypertension at 3 months, an important reduction in hepatocyte number as well as stage 1 steatosis at 6 months. However, hypertension and hepatocyte number deficit were worsened and grade 2 steatosis occurred after exposure to the HF diet. All of these serve to highlight the paramount importance of intra-uterine conditions and postnatal diet quality when it comes to the pathogenesis of chronic diseases.

Undernutrition is common in surgical patients, is frequently unrecognised and is strongly associated with adverse outcomes such as high rates of complications and mortality, worsening functional status and prolonged hospitalisation. Owing to the associated infection and symptoms such as repeated vomiting, a high prevalence of undernutrition is expected in hydrocephalus patients, which may contribute to their poor surgical outcomes. The aim of this study was to evaluate the influence of preoperative nutritional status on the outcome of Indian patients with hydrocephalus undergoing neurosurgical shunt surgery. One hundred and twenty-four consecutive patients undergoing scheduled hydrocephalus shunt surgery were studied prospectively. All patients underwent nutritional screening according to different parameters prior to surgery. The patients were classified into normally nourished and undernourished groups. The undernourished group was further subdivided into moderately and severely undernourished. The surgical outcome was compared between these groups. A high prevalence (53 %) of undernutrition was observed in these patients. Postoperative complications such as shunt infection (P = 0·0023), shunt revision (P = 0·0074) and mortality (P = 0·0003) were significantly more common in undernourished patients compared with normally nourished patients. Serum albumin emerged as the most significant independent predictor of postoperative mortality. The present study demonstrated a high prevalence of undernutrition in hydrocephalus patients in India and its adverse influence on the outcome of shunt surgery. Early preoperative nutritional status screening and its optimisation may decrease the morbidity and mortality of shunt surgery for hydrocephalus.

Fetal undernutrition programmes risk of later metabolic disorders. Postnatal factors modify the programmed phenotype. This study aimed to assess the effects of a postnatal high-fat (HF) challenge on body weight gain, adiposity and gene expression following prenatal undernutrition. Pregnant rats were fed either a control diet or a low-protein (LP) diet, targeted at days 0–7 (LPE), days 8–14 (LPM), or days 15–22 (LPL) gestation. At 12 weeks of age offspring were either fed standard laboratory chow diet (4·13 % fat), or a 39·5 % fat diet, for 10 weeks. LP exposure had no effect on weight gain or abdominal fat in males. Females exposed to LP diet in utero exhibited a similar weight gain on HF diet as on the chow diet. Programming of fat deposition was noted in LPE females and males of the LPM and LPL groups (P = 0·019). Hypothalamic expression of galanin mRNA was similar in all groups, but expression of the galanin-2 receptor was modified by LP exposure in female offspring. Hepatic expression of sterol response element binding protein (SREBP-1c) was decreased by LP at both the mRNA (P = 0·008) and protein (P < 0·001) level. HF feeding increased expression of SREBP-1c mRNA three-fold in controls, with little response noted in the LP groups. Interactions of factors such as postnatal diet, age and sex act together with prenatal factors to determine metabolic function and responsiveness at any stage of postnatal life. This study further establishes a role for prenatal nutrition in programming the genes involved in lipid metabolism and appetite regulation.

The aim of this study was to evaluate the effect of a synbiotic containing Lactobacillus acidophilus ATCC 4962, fructooligosaccharide, inulin and mannitol on plasma lipid profiles and erythrocyte membrane properties in hypercholesterolaemic pigs on high- and low-fat diets. Twenty-four white male Landrace pigs were randomly allocated to four treatment groups for 8 weeks (n 6). Treatment factors were the supplementation of synbiotic (with and without) and dietary fat (5 and 15 %). The supplementation of synbiotic reduced plasma total cholesterol (P = 0·001), TAG (P = 0·002) and LDL-cholesterol (P = 0·045) for both dietary fats. A higher concentration of esterified-cholesterol in HDL of pigs supplemented with synbiotic than the control regardless of dietary fat (P = 0·036) indicated that cholesterol was reduced in the form of cholesteryl esters. Reduced concentration of cholesteryl esters (P < 0·001) and increased concentration of TAG (P = 0·042) in LDL of pigs on synbiotic suggested that LDL-cholesterol was reduced via the hydrolysis of smaller and denser LDL particles. The erythrocytes of pigs without any synbiotic showed more prevalence of spur cells than those given the synbiotic, as supported by the higher cholesterol: phospholipid ratio in erythrocytes (P = 0·001). Also, membrane fluidity and rigidity were improved as supported by the decreased fluorescence anisotropies in the Hb-free erythrocyte membrane of pigs given synbiotic (P < 0·001). The administration of the synbiotic reduced plasma TAG, total cholesterol and LDL-cholesterol in hypercholesterolaemic pigs, possibly in the form of cholesteryl esters, via the interrelated pathways of lipid transporters (VLDL, LDL and HDL). The synbiotic also reduced deformation of erythrocytes via improved membrane fluidity and permeability.

The guinea-pig was previously reported as being sensitive to a niacin-deficient (ND), high-protein diet, suggesting that it is a suitable model for the low tryptophan to NAD+ conversion observed in human subjects. However, these studies were based on growth rates and mortality. The objective of the present study was to determine whether guinea-pigs are suitable for ND studies based on measurements of blood and bone marrow NAD+. Using a 20 % casein diet, ND decreased blood NAD+ after 4 weeks, but this parameter returned to normal after 9 weeks of feeding, while bone marrow was decreased by 35 % at this time point. Using a 15 % casein diet, 7 weeks of ND caused 44 and 42 % decreases in blood and bone marrow NAD+. Using a 10 % casein diet, ND decreased NAD+ by 32 % in blood and 62 % in bone marrow at 7 weeks. Growth rates were directly related to the dietary tryptophan content, with the lowest growth rates seen with the 10 % casein diet. Changes in guinea-pig NAD+ are comparable with the rat model at similar levels of dietary tryptophan, while mortality rates were dramatically higher in the guinea-pig model. The present study concludes that mortality in ND guinea-pigs is not indicative of poor tryptophan conversion, but is due to environmental stresses in guinea-pigs that are not observed with rats. We conclude that guinea-pigs are not suitable for research on niacin deficiency and they present challenges for any study requiring purified diets and wire-bottomed cages.

The effects exerted by polyunsaturated fatty acids (PUFA) on immune system functions have been investigated in recent years. These studies have reported the important role that n-3 PUFA play in the diminution of incidence and severity of inflammatory disorders. Nevertheless, less attention has been paid to the action of monounsaturated fatty acids (MUFA) upon the immune system. The administration of a diet containing a high amount of olive oil in experimental animals produces a suppression of lymphocyte proliferation, an inhibition of cytokine production and a reduction in natural killer (NK) cell activity. Despite these alterations in immune functions, it has been reported that olive oil-rich diets are not as immunosuppressive as fish oil diets. An important aspect in immunonutrition is focused on the relationship between fats, the immune system and host resistance to infection, particularly when these nutrients are supplied to patients at risk of sepsis. Different studies have determined that olive oil-rich diets do not impair the host resistance to infection. Therefore, olive oil constitutes a suitable fat that may be applied in clinical nutrition and administered to critically ill patients. In the present review, we summarize the current knowledge on olive oil and immune system functions, the biological consequences derived from the administration of diets containing olive oil and the impact of olive oil on immune defence.

Trivalent chromium (Cr3+) is an essential trace element involved in insulin function. Cr deficiencies result in decreased insulin sensitivity, glucose intolerance and an increased risk of diabetes. Cr status decreases with age suggesting that the elderly may be at high risk of Cr deficiency. This study aimed to provide information about the Cr content of foods in France and the Cr intake in French free-living elderly. We measured the food Cr content and daily Cr intake of freely chosen diets for 3 d in twelve French free-living elderly people and their Cr excretion and plasma hormonal related variables, leptin, insulin and cortisol. Considering the relationship between insulin resistance and oxidative stress, we also determined plasma thiobarbituric acid reactive substance, thiol groups and total and reduced glutathione. Although these subjects had well-balanced diets, their daily Cr intakes did not reach the French recommendations. The low Cr intakes were due to the low Cr density of the foods. We found a negative correlation between Cr intakes and insulin, BMI and leptin.

The present study evaluated the pharmacokinetics of three different grapefruit flavanone forms in dog plasma and demonstrated their absorption after an oral intake of a grapefruit extract; pharmacokinetic parameters of these forms were also determined. Ten healthy beagles were administered 70 mg citrus flavonoids as a grapefruit extract contained in capsules, while two additional dogs were used as controls and given an excipient. The grapefruit flavanone naringin, along with its metabolites naringenin and naringenin glucuronide, was detected in dog plasma. Blood samples were collected between 0 and 24 h after administration of the extract. Naringin reached its maximun plasma concentration at around 80 min, whereas naringenin and naringenin glucuronide reached their maximun plasma concentrations at around 20 and 30 min, respectively. Maximum plasma concentrations of naringin, naringenin and naringenin glucuronide (medians and ranges) were 0·24 (0·05–2·08), 0·021 (0·001–0·3) and 0·09 (0·034–0·12) μmol/l, respectively. The areas under the curves were 23·16 l (14·04–70·62) min × μmol/for nariningin, 1·78 (0·09–4·95) min × μmol/l for naringenin and 22·5 (2·74–99·23) min × μmol/l for naringenin glucuronide. The median and range values for mean residence time were 3·3 (1·5–9·3), 2·8 (0·8–11·2) and 8·0 (2·3–13·1) h for naringin, naringenin and naringenin glucuronide, respectively. The results of the present study demonstrate the absorption of grapefruit flavanones via the presence of their metabolites in plasma, thus making an important contribution to the field since the biological activities ascribed to these compounds rely on their specific forms of absorption.

Dietary microparticles are non-biological bacterial-sized particles of the gastrointestinal lumen that occur due to endogenous formation (calcium phosphate) or following oral exposure (exogenous microparticle). In the UK, about 40 mg (1012) of exogenous microparticles are ingested per person per day, through exposure to food additives, pharmaceutical/supplement excipients or toothpaste constituents. Once ingested, exogenous microparticles are unlikely to pass through the gastrointestinal tract without adsorbing to their surfaces some ions and molecules of the intestinal lumen. Both entropy and ionic attraction drive such interactions. Calcium ions are especially well adsorbed by dietary microparticles which then provide a positively charged surface for the attraction (adsorption) of other organic molecules such as lipopolysaccharides, peptidoglycans or protein antigen from the diet or commensal flora. The major (but not only) sites of microparticle entry into intestinal tissue are the M-cell rich lymphoid aggregates (termed Peyer's patches in the small bowel). Indeed, it is well established that this is an efficient transport route for non-biological microparticles although it is unclear why. We hypothesise that this pathway exists for “endogenous microparticles” of calcium phosphate, with immunological and physiological benefit, and that “exogenous dietary microparticles”, such as titanium dioxide and the silicates, hijack this route. This overview focuses on what is known of these microparticles and outlines their potential role in immune tolerance of the gut (endogenous microparticles) or immune activation (exogenous microparticles) and inflammation of the gut.

Four hundred and forty-five randomly selected hospitalised patients had their nutritional status assessed from anthropometric, haematological and biochemical data. Nutritional status was compared between survivors and non-survivors at baseline, 6 weeks and 6 months. Using Cox's proportional hazard analysis, we measured the association between nutritional assessment variables and 1-year mortality after adjusting for disability, chronic illness, medications, smoking and tissue inflammation. Nutritional status was significantly worse amongst non-survivors compared with survivors, and non-survivors showed marked and significant deterioration in all measures of nutritional status compared with survivors. After adjusting for poor prognostic indicators the hazard ratios of death in the fourth, third and second quarters of both baseline serum albumin and mid-upper arm circumference distributions relative to the first were 0·68, 0·77 and 0·58 (trend P = 0·013) and 0·61, 1·0 and 0·87 (trend P = 0·005) respectively. Intervention studies are needed to determine whether the relationship between malnutrition and the poor outcome highlighted by the present study is causal or a mere association.