Systematic review: the effect of prunes on gastrointestinal function.

BACKGROUND: Prunes (dried plums) are high in fibre and are perceived to promote healthy gastrointestinal (GI) function. AIM: To assess the effect of prunes on GI function through a systematic review of randomised controlled trials (RCTs). METHODS: Sixteen electronic databases were searched, a hand search was performed and key opinion leaders were contacted. RCTs investigating the effect of prunes on GI function were included. Two reviewers independently screened relevant articles, extracted data and assessed risk of bias. RESULTS: Four trials met the inclusion criteria, one in constipation and three in non-constipated subjects. In constipation, 3 weeks of prune consumption (100 g/day) improved stool frequency (3.5 vs. 2.8 CSBM per week, P = 0.006) and stool consistency (3.2 vs. 2.8 on Bristol stool form scale, P = 0.02) compared with psyllium (22 g/day). In non-constipated subjects, prunes softened stool consistency in one trial and increased stool weight (628 g vs. 514 g/72 h wet weight, P = 0.001) in another trial, compared with control. No trials found differences in GI symptoms between prunes and comparator. Meta-analysis was not appropriate due to heterogeneity in populations and methods. Two of the trials were limited by unclear risk of bias. CONCLUSIONS: In constipation, prunes appear superior to psyllium for improving stool frequency and consistency, however, the evidence for other outcomes and the effects in non-constipated subjects is weak. Although prunes may be a promising intervention for the management of constipation and increasing stool weight, this needs to be confirmed by further rigorous research.

The prevalence of PFS and prevalence and characteristics of reported food allergy; a survey of UK adults aged 18-75 incorporating a validated PFS diagnostic questionnaire.

BACKGROUND: Pollen-food syndrome (PFS), a food allergy affecting pollen-sensitized individuals, is likely to be the most prevalent food allergy in adults, estimated to affect 50-90% of people allergic to birch tree pollen. OBJECTIVE: A validated PFS diagnostic questionnaire (PFSDQ2) was used to determine the prevalence of PFS and also to characterize those who report reactions to foods. METHODS: Five UK General practices each sent the PFSDQ2 by post to 2000 patients aged 18-75 years randomly selected from their practice database. The validated questionnaire was accompanied by an additional set of questions to ascertain the demographic of the population, the foods involved and the age of onset. RESULTS: There were 3590 subjects who returned completed questionnaires, with an average return rate from each practice of 36% (range 22-47%). Of these, 73 were diagnosed with PFS according to the questionnaire (PFS+ve) giving a population prevalence of 2%. A further 482 subjects reported reactions to foods but did not fulfil the diagnostic criteria for PFS. The greatest prevalence of PFS was in the Croydon (SE England) urban practice (4.1%) and the lowest in the Aberdeen (Scotland) urban practice (0.8%) (P < 0.001).The most frequently reported trigger foods were apples, hazelnuts and kiwifruit and the majority of those with PFS first experienced symptoms below the age of 20 years. PFS+ve subjects were also more likely to be female and have a higher socio-economic status than those who did not report reactions to foods. CONCLUSIONS: The UK prevalence of PFS was 2%, although this varied according to the location of the practice population. The majority of PFS+ve subjects first reported symptoms in their teens. The reported age of onset has important implications for the diagnosis of primary and cross-reactive peanut and tree nut allergies in teenagers and young adults. The continuing rise in aeroallergen sensitization is likely to result in an increased frequency of PFS presenting in both primary and secondary care.

Faecal microbiota and short-chain fatty acids in patients receiving enteral nutrition with standard or fructo-oligosaccharides and fibre-enriched formulas.

BACKGROUND: Prebiotics potentially increase the growth of bifidobacteria, which may minimise the risk of diarrhoea in patients receiving enteral nutrition (EN). The present study aimed to compare the concentrations of faecal microbiota and short-chain fatty acids (SCFA) in patients receiving EN with either a standard formula or one enriched with fructo-oligosaccharides (FOS) and fibre. METHODS: Forty-one hospitalised adult patients (25 males, 16 females) who were on exclusive EN for at least 12 days were recruited to a cross-sectional study. Faecal samples were collected and analysed for major groups of microbiota using fluorescent in situ hybridisation and SCFA concentrations were analysed using gas liquid chromatography. RESULTS: There were generally low concentrations of the major bacterial groups, including bifidobacteria, in all patients receiving either standard or FOS/fibre-enriched formula [bifidobacteria: 6.6 (1.3) versus 7.0 (2.0) log(10) cells g(-1) dry faecal, P=0.199]. However, faecal butyrate concentrations were higher in patients receiving the FOS/fibre-enriched formula compared to standard formula [20.5 (21.6) versus 4.6 (6.7) µmol g(-1) dry faecal, P=0.006]. CONCLUSIONS: Low concentrations of faecal bifidobacteria were identified in these patients, which potentially increases their risk of diarrhoea. Other microbiota groups may utilise FOS/fibre, leading to different butyrate concentrations between the two cohorts.

A review of the evidence for the impact of improving nutritional care on nutritional and clinical outcomes and cost.

BACKGROUND: The association between malnutrition and poor clinical outcome is well-established, yet most research has focussed on the role of artificial nutritional support in its management. More recently, emphasis has been placed on the provision of adequate nutritional care, including nutritional screening and the routine provision of food and drink. The aim of this literature review is to establish the evidence for the efficacy of interventions that might result in improvements in nutritional and clinical outcomes and costs. METHODS: A structured literature review was conducted investigating the role of nutritional care interventions in adults, and their effects on nutritional and clinical outcomes and costs, in all healthcare settings. Ten databases were searched electronically using keywords relating to nutritional care, patient outcomes and healthcare costs. High quality trials were included where available. RESULTS: Two hundred and ninety-seven papers were identified and reviewed. Of these, only two randomised, controlled trials and six other trials were identified that addressed the major issues. A further 99 addressed some aspects of the provision of nutritional care, although very few formally evaluated nutritional or clinical outcomes and costs. CONCLUSIONS: This review reveals a serious lack of evidence to support interventions designed to improve nutritional care, in particular with reference to their effects on nutritional and clinical outcomes and costs. The review suggests that screening alone may be insufficient to achieve beneficial effects and thus more research is required to determine the most cost-effective interventions in each part of the nutritional care pathway, in a variety of healthcare settings and across all age ranges, to impact upon nutritional and clinical outcomes.

The effect of protein malnutrition on the capacity for protein synthesis during wound healing.

OBJECTIVES: It has been shown that wound healing in the rat is associated with increased protein synthesis at the site of the wound 48 hours after surgical trauma. The aim of the current study was to examine the effect of protein malnutrition prior to abdominal surgery on the capacity for muscle protein synthesis both at the site of the wound and in undamaged abdominal muscle. DESIGN AND MEASUREMENTS: Thirty-two rats were randomly assigned to a low or high protein diet (3% and 20% casein respectively). After two weeks, half the rats in each group underwent abdominal surgery. Forty-eight hours after the operation all the animals were killed and tissues were analysed for RNA and protein contents. RESULTS: The capacity for protein synthesis, as indicated by the RNA:protein ratio, was increased at the site of the healing wound. The low protein diet caused a decrease in the capacity for protein synthesis in unoperated animals but did not prevent the increase associated with wound healing. CONCLUSION: The capacity to increase protein synthesis during wound healing is protected against the effects of malnutrition, indicating that it has a high biological priority.

Dietary counselling and food fortification in stable COPD: a randomised trial.

BACKGROUND: Malnutrition in chronic obstructive pulmonary disease (COPD) is associated with a poor prognosis, yet evidence to support the role of dietary counselling and food fortification is lacking. A study was undertaken to assess the impact of dietary counselling and food fortification on outcome in outpatients with COPD who are at risk of malnutrition. METHODS: A randomised controlled unblinded trial was performed in 59 outpatients with COPD (6 months intervention and 6 months follow-up). The intervention group received dietary counselling and advice on food fortification and the controls received a dietary advice leaflet. Outcome measures were nutritional status, respiratory and skeletal muscle strength, respiratory function, perceived dyspnoea, activities of daily living (ADL) and quality of life. RESULTS: The intervention group consumed more energy (difference 194 kcal/day; p = 0.02) and protein (difference 11.8 g/day; p<0.001) than controls. The intervention group gained weight during the intervention period and maintained weight during follow-up; the controls lost weight throughout the study. Significant differences were observed between the groups in St George's Respiratory Questionnaire total score (difference 10.1; p = 0.02), Short Form-36 health change score (difference 19.2; p = 0.029) and Medical Research Council dyspnoea score (difference 1.0; p = 0.03); the difference in ADL score approached statistical significance (difference 1.5; p = 0.06). No differences were observed between groups in respiratory function or skeletal and respiratory muscle strength. Improvements in some variables persisted for 6 months beyond the intervention period. CONCLUSION: Dietary counselling and food fortification resulted in weight gain and improvements in outcome in nutritionally at-risk outpatients with COPD, both during and beyond the intervention period.

Health benefits of isoflavones in functional foods? Proteomic and metabonomic advances.

There is currently considerable interest in the potential health benefits of isoflavones in functional foods and in the future prospects for the development of new products of benefit to the consumer. The potential health benefits of isoflavones may include protection against age-related diseases including cardiovascular disease, osteoporosis, hormone-dependent cancer and loss of cognitive function. The mechanisms involved may include weak oestrogenic action and antioxidant activity. Our proteomic investigations of changes in the human serum profile in response to the consumption of isoflavones in soya functional foods suggest potentially beneficial modulation of the levels of a number of serum proteins, including increased apolipoprotein E (involved in lipid metabolism) and caeruloplasmin (antioxidant and copper regulatory properties) levels and decreased alpha-1-acid glycoprotein (involved in immunomodulation) levels that may contribute to vascular protection. Furthermore, preliminary metabonomic data indicates an alteration in the urinary metabolite profile after isoflavone consumption, which may be of significance.

Molecular and cellular events in alcohol-induced muscle disease.

Alcohol consumption induces a dose-dependent noxious effect on skeletal muscle, leading to progressive functional and structural damage of myocytes, with concomitant reductions in lean body mass. Nearly half of high-dose chronic alcohol consumers develop alcoholic skeletal myopathy. The pathogenic mechanisms that lie between alcohol intake and loss of muscle tissue involve multiple pathways, making the elucidation of the disease somewhat difficult. This review discusses the recent advances in basic and clinical research on the molecular and cellular events involved in the development of alcohol-induced muscle disease. The main areas of recent research interest on this field are as follows: (i) molecular mechanisms in alcohol exposed muscle in the rat model; (ii) gene expression changes in alcohol exposed muscle; (iii) the role of trace elements and oxidative stress in alcoholic myopathy; and (iv) the role of apoptosis and preapoptotic pathways in alcoholic myopathy. These aforementioned areas are crucial in understanding the pathogenesis of this disease. For example, there is overwhelming evidence that both chronic alcohol ingestion and acute alcohol intoxication impair the rate of protein synthesis of myofibrillar proteins, in particular, under both postabsorptive and postprandial conditions. Perturbations in gene expression are contributory factors to the development of alcoholic myopathy, as ethanol-induced alterations are detected in over 400 genes and the protein profile (i.e., the proteome) of muscle is also affected. There is supportive evidence that oxidative damage is involved in the pathogenesis of alcoholic myopathy. Increased lipid peroxidation is related to muscle fibre atrophy, and reduced serum levels of some antioxidants may be related to loss of muscle mass and muscle strength. Finally, ethanol induces skeletal muscle apoptosis and increases both pro- and antiapoptotic regulatory mechanisms.

Metabolic changes in malnutrition.

This paper is concerned with malnutrition caused by inadequate intake of all the major nutrients rather than deficiency diseases relating to a single micronutrient. Three common situations are recognised: young children in third world countries with protein-energy malnutrition; adults in the same countries who are chronically adapted to subsisting on marginally inadequate diets; and patients who become malnourished as a result of chronic diseases. In all these situations infectious diseases are often also present, and this complicates the interpretation of biochemical and physiological observations. The metabolic response to starvation is primarily concerned with maintaining a supply of water-soluble substrates to supply energy to the brain. Thus there is an initial rise in metabolic rate, reflecting gluconeogenic activity. As fasting progresses, gluconeogenesis is suppressed to minimise muscle protein breakdown and ketones become the main fuel for the brain. With chronic underfeeding the basal metabolic rate per cell appears to fall, but the mechanistic basis for this is not clear. The main adaptation to chronic energy deficiency is slow growth and low adult body size, although the reduction in energy requirement achieved by this is partially offset by the preservation of the more metabolically active organs at the expense of muscle, which has a lower metabolic rate. The interaction between malnutrition and the metabolic response to trauma has been studied using an animal model. The rise in energy expenditure and urinary nitrogen excretion following surgery were significantly attenuated in malnourished rats, suggesting that malnutrition impairs the ability of the body to mobilise substrates to support inflammatory and reparative processes. However, the healing process in wounded muscle remained unimpaired in malnutrition, suggesting that this process has a high biological priority.

Effect of folic acid supplementation on genomic DNA methylation in patients with colorectal adenoma.

BACKGROUND AND AIMS: A low dietary folate intake can cause genomic DNA hypomethylation and may increase the risk of colorectal neoplasia. The hypothesis that folic acid supplementation increases DNA methylation in leucocytes and colorectal mucosa was tested in 31 patients with histologically confirmed colorectal adenoma using a randomised, double blind, placebo controlled, parallel design. METHODS: Subjects were randomised to receive either 400 microg/day folic acid supplement (n = 15) or placebo (n = 16) for 10 weeks. Genomic DNA methylation, serum and erythrocyte folate, and plasma homocysteine concentrations were measured at baseline and post intervention. RESULTS: Folic acid supplementation increased serum and erythrocyte folate concentrations by 81% (95% confidence interval (CI) 57-104%; p<0.001 v placebo) and 57% (95% CI 40-74%; p<0.001 v placebo), respectively, and decreased plasma homocysteine concentration by 12% (95% CI 4-20%; p = 0.01 v placebo). Folic acid supplementation resulted in increases in DNA methylation of 31% (95% CI 16-47%; p = 0.05 v placebo) in leucocytes and 25% (95% CI 11-39%; p = 0.09 v placebo) in colonic mucosa. CONCLUSIONS: These results suggest that DNA hypomethylation can be reversed by physiological intakes of folic acid.

Influence of folate status on genomic DNA methylation in colonic mucosa of subjects without colorectal adenoma or cancer.

DNA hypomethylation may increase the risk of colorectal cancer. The main aim of this study was to assess the influence of folate status (serum and erythrocyte folate and plasma homocysteine concentrations) on DNA methylation. Methylenetetrahydrofolate reductase (MTHFR 677C --> T and 1298A --> C), methionine synthase (MS 2756A --> G) and cystathionine synthase (CBS 844ins68) polymorphisms were measured to account for potential confounding effects on folate status and DNA methylation. A total of 68 subjects (33 men and 35 women, 36-78 years) free from colorectal polyps or cancer were recruited in a cross-sectional study. Tissue biopsies were obtained at colonoscopy for the determination of DNA methylation in colonic mucosa using an in vitro radiolabelled methyl acceptance assay. Serum and erythrocyte folate were inversely correlated with plasma homocysteine (r=-0.573, P<0.001 and r=-0.307, P=0.01 respectively) and DNA hypomethylation in colonic mucosa (r=-0.311, P=0.01 and r=-0.356, P=0.03). After adjusting for gender, age, body mass index, smoking and genotype, there were weak negative associations between serum and erythrocyte folate and colonic DNA hypomethylation (P=0.07 and P=0.08, respectively).

Plasma taurine and cysteine levels following an oral methionine load: relationship with coronary heart disease.

OBJECTIVE: To test the hypothesis that endogenous synthesis of taurine from methionine is impaired in people with coronary heart disease (CHD). DESIGN: Nested case-control. SUBJECTS: Indian Asian and white European males aged 35-60 y. Both racial group included patients with CHD and healthy controls. Samples from 20 subjects in each of the four groups were selected at random. INTERVENTION: Fasting blood samples were taken before and 6 h after consumption of methionine (100 mg/kg body weight) MEASUREMENTS: Plasma concentrations of taurine, cysteine, pyridoxal-5-phosphate and 4-pyridoxic acid. RESULTS: Fasting plasma taurine values were higher in Indian Asian cases than controls, but not significantly different between European cases and controls. Postload taurine values were higher in cases than controls in both racial groups (P=0.002). Fasting plasma cysteine was higher in cases than controls (P=0.002) and higher in Indian Asians than Europeans (0.007), but there were no significant differences between any of the groups in postload cysteine values, nor in plasma pyridoxal-5-phosphate or 4-pyridoxic acid. CONCLUSIONS: Taurine production from methionine was not impaired in patients with CHD, but fasting plasma cysteine was higher in CHD cases than controls.

Separation and identification of rat skeletal muscle proteins using two-dimensional gel electrophoresis and mass spectrometry.

Skeletal muscle plays a major role in whole body protein metabolism, and changes in the rates of synthesis and degradation of proteins are likely to lead to characteristic changes in the amounts of different proteins in muscle under various physiological and pathological conditions. This paper demonstrates the feasibility of a proteomic approach to analyzing the protein composition of skeletal muscle. We report here the initial establishment of two-dimensional gel electrophoresis (2-D PAGE) reference maps for mixed skeletal muscle taken from the abdominal wall of a normal adult rat. We used immobilized pH gradients of 3-10 (non-linear) and 4-7 (linear), and matrix assisted laser desorption/ionization--time of flight mass spectrometry for protein identification by peptide mass fingerprinting. More than 600 protein spots were detected on each gel, of which 100 were excised and characterized. In-gel digestion followed by peptide mass fingerprinting enabled tentative identification of 74 of these, which included a wide range of myofibrillary and sarcoplasmic proteins. This database should provide the nucleus of a valuable resource for investigation of the biochemical basis of skeletal muscle pathologies in general and such specific disorders as alcoholic myopathy and injury.

The postprandial rates of glycogen and lipid synthesis of lean and obese female Zucker rats.

OBJECTIVE: To determine the relative rates of glycogenesis and lipogenesis following administration of a test meal in lean and obese Zucker rats. PROTOCOL: Nine-week-old lean and obese Zucker rats were fasted overnight, then tube-fed a test meal of balanced composition amounting to 16kJ (lean rats and one group of obese rats) or 24kJ (one group of obese rats) and containing 200 mg 1-(13)C glucose. Immediately after the meal the rats were injected intraperitoneally with 5 mCi of 3H2O and killed 1 h later. METHODS: Glycogenesis was calculated from the incorporation of 3H into liver glycogen divided by the specific activity of plasma water. Lipogenesis was calculated similarly from the incorporation of 3H into saponifiable lipids in liver and perirenal adipose tissue. The proportion of glycogen synthesized by the indirect pathway via pyruvate was determined from the ratio of 3H labelling at positions C6 and C2 in the glycogen glucose residues. Glycogen synthesis from glucose was determined from the ratio of 13C enrichment in liver glycogen to that in plasma glucose. RESULTS: The rate of synthesis of glycogen was considerably lower in the livers of obese rats than those of lean controls, with the larger meal causing a small but significant increase in glycogenesis. The proportion of glycogen synthesized via pyruvate showed a non-significant increase in the obese rats, while the amount of glycogen synthesized from glucose was significantly decreased. Hepatic lipogenic rates were about five times higher in both groups of obese rats than the lean controls. In adipose tissue, lipogenesis per g tissue was slightly reduced in the obese rats, although there was clearly an increase in adipose tissue lipogenic activity per whole animal. The larger meal caused a greater rise in plasma glucose and insulin concentrations but did not affect lipogenic rates, although it did cause a greater suppression of lipolysis, as indicated by a lower plasma glycerol concentration. CONCLUSION: Ingested carbohydrate is partitioned predominantly into hepatic fatty acid synthesis in obese Zucker rats. Hepatic glycogen synthesis is suppressed and comes mainly from precursors other than glucose. The suppression of hepatic glycogen synthesis may contribute to the increased energetic efficiency of obese Zucker rats.

The effect of malnutrition on the metabolic response to surgery.

The effect of previous malnutrition on the metabolic response to surgical hysterectomy was investigated in adult female rats. Malnutrition was achieved by feeding a 20 g protein/kg diet and restricting food intake to 50% of normal. This dietary regimen was maintained for 3 weeks before surgery and for 4 d after surgery. Unoperated control rats were pair-fed with the hysterectomized rats after surgery. Energy balance was measured by the comparative carcass technique and, in a second experiment, urinary N excretion was measured. Surgery caused energy expenditure to increase by 37% in ad libitum-fed rats but in malnourished rats it increased by only 22%. Urinary N excretion rose immediately after surgery. In the ad libitum-fed rats it was on average 85% greater in hysterectomized rats than controls for the first 3 d after surgery, whereas in the restricted rats it was 74% greater on the first day and not significantly elevated thereafter. Thus, malnutrition attenuated the metabolic response to surgery but did not abolish it completely.

Cachexia in experimental models.

Cachexia refers to a state of severe malnutrition characterized by anorexia, weight loss, and muscle wasting. Although it is most commonly considered in the context of cancer, it may occur as a consequence of a variety of chronic diseases. Cachexia appears to differ from "semistarvation" in that there is evidence of metabolic changes that are different from the normal response to reduce food intake. Animal models are useful in the study of cachexia because they allow homogeneous groups of subjects, free from confounding influences, to be studied. Accurate control of diet is possible, and pair-fed controls can be used to allow specific investigation of the metabolic component. However, the model must show features that are appropriate for the disease being studied. In the case of cancer this means using a model in which cachexia occurs without too high a tumor burden or growth rate or too severe a reduction in food intake. Studies in the author's laboratory have used a transplantable Leydig cell tumor in Fischer rats. Food intake decreases by 20-40% and energy expenditure is greater than that of pair-fed controls. One mechanism that may be responsible for this relates to the postprandial metabolism of carbohydrate, since after a test meal there appears to be a greater rate of hepatic glycogen synthesis via the indirect pathway in tumor-bearing rats than in controls. The indirect pathway involves gluconeogenic enzymes, and studies using a variety of different tracers and enzyme inhibitors suggest that amino acids are important precursors. An increased rate of hepatic glycogen synthesis also appears to be maintained for a longer time after the meal in tumor-bearing rats, and this may act to delay the onset of the next meal, thereby explaining the decreased meal frequency that has been observed.

The effect of meal size on postprandial carbohydrate metabolism in normal and tumor-bearing rats.

Doubling the size of a meal causes less than a two-fold increase in the thermic effect of feeding. One possible reason for this is that larger meals may be associated with a change in the pathway of postprandial hepatic glycogen synthesis from the indirect pathway, involving gluconeogenesis, to the more energetically efficient direct pathway. We have therefore investigated the effect of meal size on the relative contributions of those two pathways both in normal rats and in tumor-bearing rats, which have previously been shown to utilize the indirect pathway to a greater extent. Rats bearing a transplantable Leydig cell tumor and freely fed controls were fasted overnight and given a test meal amounting to 12 or 24 kJ of their normal diet. They were then injected with 3H2O and 14C-glycerol and killed one hour later. The total amount of 3H incorporated into liver glycogen was not affected by meal size, although it was greater in tumor-bearing rats than controls. Analysis of the 3H labelling at different positions in the glycogen glucose residues showed that the proportion of glycogen synthesized via pyruvate, which tended to be greater in tumor-bearing rats, was significantly reduced by increasing the size of the meal. Glycogen synthesis from glycerol was not affected by either meal size or tumor growth. Increasing the size of the meal increased the rate of fatty acid synthesis in both the liver and the epididymal fat pad, but not the tumor. Thus increasing the size of the meal appeared to increase the proportion of glycogen synthesized by the direct pathway from glucose in both tumor-bearing and control animals.

Glycogen synthesis in tumor-bearing rats after ingestion of a high-glycerol meal.

Tumor-bearing rats have a high rate of postprandial hepatic glycogen synthesis by the indirect pathway that involves gluconeogenesis. This study was designed to investigate the role of glycerol as a precursor for postprandial glycogen synthesis in tumor-bearing rats. Rats bearing a Leydig cell tumor and freely fed controls were fasted overnight, then fed a 16-kJ meal with or without 50 mg of glycerol by gavage. [U-14C]glycerol (1 microCi) was also administered intragastrically, and 7 mCi of 3H2O were injected intraperitoneally. The rats were killed one hour later, and the specific activities at different positions within the glycogen glucose residues in the liver were measured. Increasing the glycerol content of the meal had no significant effect on the overall incorporation of 3H into liver glycogen or on the proportion of glycogen synthesized via pyruvate in tumor-bearing or control rats. There was no difference between tumor-bearing and control rats in the amount of glycerol incorporated into glycogen, although this was increased by the high-glycerol meal. Thus glycerol appeared to make a small contribution to postprandial glycogen synthesis in tumor-bearing and control rats.

Two phase randomised controlled clinical trial of postoperative oral dietary supplements in surgical patients.

BACKGROUND: Previous work has shown that the administration of oral dietary supplements to patients who have undergone gastrointestinal surgery results in clinically significant short term benefits. AIMS: This study aimed firstly to re-evaluate these short term effects, and secondly to establish whether there are any long term benefits. SUBJECTS: One hundred patients admitted for elective moderate or major gastrointestinal surgery. METHODS: In the inpatient phase, patients were randomised to receive a normal ward diet postoperatively, or the same diet supplemented with an oral dietary supplement. In the outpatient phase, patients were further randomised to receive their home diet, or their home diet supplemented with the oral dietary supplement for four months. RESULTS: During the inpatient phase, patients treated with oral supplements had a significantly improved nutritional intake and lost less weight (2.2, 95% confidence interval (95% CI) 0.9 kg) compared with control patients (4.2 (0.78) kg, p < 0.001). Supplemented patients maintained their hand grip strength whereas control patients showed a significant reduction in grip strength (p < 0.01). Subjective levels of fatigue increased significantly above preoperative levels in control patients (p < 0.01) but not in the supplemented group. Twelve patients in the control group developed complications compared with four in the supplemented group (p < 0.05). In the outpatient phase, supplemented patients had improved nutrient intakes but there were no significant differences in indices of nutritional status or wellbeing between the groups. CONCLUSIONS: The prescription of oral dietary supplements to patients who have undergone gastrointestinal surgery results in clinically significant benefits. These benefits, however, are restricted to the inpatient phase.