There are many health and nutrition implications of suffering from multimorbidity, which is a huge challenge facing health and social services. This review focuses on malnutrition, one of the nutritional consequences of multimorbidity. Malnutrition can result from the impact of chronic conditions and their management (polypharmacy) on appetite and nutritional intake, leading to an inability to meet nutritional requirements from food. Malnutrition (undernutrition) is prevalent in primary care and costly, the main cause being disease, accentuated by multiple morbidities. Most of the costs arise from the deleterious effects of malnutrition on individual’s function, clinical outcome and recovery leading to a substantially greater burden on treatment and health care resources, costing at least £19·6 billion in England. Routine identification of malnutrition with screening should be part of the management of multimorbidity together with practical, effective ways of treating malnutrition that overcome anorexia where relevant. Nutritional interventions that improve nutritional intake have been shown to significantly reduce mortality in individuals with multimorbidities. In addition to food-based interventions, a more ‘medicalised’ dietary approach using liquid oral nutritional supplements (ONS) can be effective. ONS typically have little impact on appetite, effectively improve energy, protein and micronutrient intakes and may significantly improve functional measures. Reduced treatment burden can result from effective nutritional intervention with improved clinical outcomes (fewer infections, wounds), reducing health care use and costs. With the right investment in nutrition and dietetic resources, appropriate nutritional management plans can be put in place to optimally support the multimorbid patient benefitting the individual and the wider society.

Infants born with low birth weights (<2500 g, LBW), accounting for about 15 % of newborns, have a high risk for postnatal growth failure and developing the metabolic syndromes such as type 2 diabetes, CVD and obesity later in life. Improper nutrition provision during critical stages, such as undernutrition during the fetal period or overnutrition during the neonatal period, has been an important mediator of these metabolic diseases. Considering the specific physiological status of LBW infants, nutritional intervention and optimisation during early life merit further attention. In this review, the physiological and metabolic defects of LBW infants were summarised from a nutritional perspective. Available strategies for nutritional interventions and optimisation of LBW infants, including patterns of nutrition supply, macronutrient proportion, supplementation of amino acids and their derivatives, fatty acids, nucleotides, vitamins, minerals as well as hormone and microbiota manipulators, were reviewed with an aim to provide new insights into the advancements of formulas and human-milk fortifiers.

Loss of body protein and hyperglycaemia represent typical features of the stress response to surgery and anaesthesia. This appears to be particularly pronounced in patients with diabetes mellitus type 2. The aim of the present study was to highlight the greater benefit of amino acids (AA) as represented by positive protein balance and maintenance of blood glucose homoeostasis compared with dextrose (DEX) in diabetic patients after colorectal surgery. A total of thirteen patients underwent a 5 h stable isotope infusion study (2 h fasted, 3 h fed with an infusion of AA (n 6) or DEX (n 7)) on the second post-operative day. Glucose and protein kinetics were assessed by using the stable isotopes l-[1-13C]leucine and [6,6-2H2]glucose. The transition from fasted to fed state decreased endogenous glucose production (P < 0·001) in both groups, with a more profound effect in the DEX group (P = 0·031). In contrast, total glucose production was increased by the provision of DEX while being lowered by AA (P = 0·021). Feeding decreased protein oxidation (P = 0·009) and protein synthesis in the AA group, whereas DEX infusion did not affect oxidation and even decreased protein synthesis. Therefore, only AA shifted protein balance to a positive value, while patients in the DEX group remained in a catabolic state (P < 0·001). Parenteral nutritional support with AA rather than with DEX is an effective strategy to achieve a positive protein balance while maintaining normoglycaemia in diabetic patients after colorectal surgery.

Cystic fibrosis (CF) is a complex multisystem disorder affecting mainly the gastrointestinal tract and respiratory system. Intestinal malabsorption occurs in approximately 90% of patients. In the past, malnutrition was an inevitable consequence of disease progression, leading to poor growth, impaired respiratory muscle function, decreased exercise tolerance and immunological impairment. A positive association between body weight and height and survival has been widely reported. The energy requirements of patients with CF vary widely and generally increase with age and disease severity. For many young adults requirements will be 120–150% of the age-related estimated average requirement. To meet these energy needs patients are encouraged to eat a high-fat high-energy diet with appropriate pancreatic enzyme supplements. Many patients are unable to achieve an adequate intake as a result of a variety of factors including chronic poor appetite, infection-related anorexia, gastro-oesophageal reflux and abdominal pain. Oral energy supplements and enteral tube feeding are widely used. Nutritional support has been shown to improve nutritional status and stabilise or slow the rate of decline in lung function. With such emphasis on nutritional intake and nutritional status throughout life, poor adherence to therapies and issues relating to body image are emerging. The median survival of patients with CF is increasing. CF is now considered a life-limiting disease of adulthood rather than a terminal childhood illness. With increased longevity new challenges are emerging that include the transition of young adults with CF to adult services, CF-related diabetes, disordered eating, osteoporosis, liver disease and transplantation.

Energy balance is the difference between energy consumed and total energy expended. Over a given period of time it expresses how much the body stores of fat, carbohydrate and protein will change. For the critically-ill patient, who characteristically exhibits raised energy expenditure and proteolysis of skeletal muscle, energy balance information is valuable because underfeeding or overfeeding may compromise recovery. However, there are formidable difficulties in measuring energy balance in these patients. While energy intake can be accurately recorded in the intensive care setting, the measurement of total energy expenditure is problematic. Widely used approaches, such as direct calorimetry or doubly-labelled water, are not applicable to the critically ill patient. Energy balance was determined over periods of 5–10 d in patients in intensive care by measuring changes in the fat, protein and carbohydrate stores of the body. Changes in total body fat were positively correlated with energy balance over the 5 d study periods in patients with severe sepsis (n24, r 0.56, P=0.004) or major trauma (n 24, r 0.70, P<.0001). Fat oxidation occurred in patients whose energy intake was insufficient to achieve energy balance. Changes in body protein were independent of energy balance. These results are consistent with those of other researchers who have estimated total energy requirements from measurements of O2 consumption and CO2 production. In critically-ill patients achievement of positive non-protein energy balance or total energy balance does not prevent negative N balance. Nutritional therapy for these patients may in the future focus on glycaemic control with insulin and specialised supplements rather than on energy balance per se.

Enteral tube feeding remains an indispensible strategy to treat disease-related malnutrition. In the present study we evaluated in clinical practice whether prescribed feeding volumes correspond with administered quantities and we highlight possible causes for discrepancies. During a 4-month observation period data from all patients fully depending on tube feeding (1·5–2·5 litres/d) were collected in a Dutch 900-bed academic hospital. The range for administered feeds to be adequate was set at 100 ± 10 % of the prescribed dose. Fifty-five patients (mean age 57 (sd 30) years) were included. Tube feeding was given continuously via pump (n 37) or drip (n 3), in portions (n 14) or by combined modes (n 1). Administered tube feeding amounts were significantly lower than prescribed in 40 % of all patients (P ≤ 0·001). The mean ratio of administered v. prescribed energy was 87 (sd 21) % (all modes), 85 (sd 24) % (pump), 94 (sd 12) % (portions) and 88·3 (sd 18·1) % (drip), respectively. The mean energy deficit amounted to 1089 kJ/d (range − 7955 to +795). Only on intensive care unit wards did feeding administration meet the set goal. Feeding interruptions because of diagnostic or therapeutic procedures were the main reason for decreased intakes. Our findings show that many patients relying on tube feeding do not meet their nutritional goals during hospital stay. This problem can be addressed by adapting feeding schedules and the use of formulations with a higher energy density.

Common to both acute and chronic disease are disturbances in energy homeostasis, which are evidenced by quantitative and qualitative changes in dietary intake and increased energy expenditure. Negative energy balance results in loss of fat and lean tissue. The management of patients with metabolically-active disease appears to be simple; it would involve the provision of sufficient energy to promote tissue accretion. However, two fundamental issues serve to prevent nutritional demands in disease being met. The determination of appropriate energy requirements relies on predictive formulae. While equations have been developed for critically-ill populations, accurate energy prescribing in the acute setting is uncommon. Only 25–32% of the patients have energy intakes within 10% of their requirements. Clearly, the variation in energy expenditure has led to difficulties in accurately defining the energy needs of the individual. Second, the acute inflammatory response initiated by the host can have profound effects on ingestive behaviour, but this area is poorly understood by practising clinicians. For example, nutritional targets have been set for specific disease states, i.e. pancreatitis 105–147 KJ (25–35 kcal)/kg; chronic liver disease 147–168 kj (35–40 kcl)/kg, but given the alterations in gut physiology that accompany the acute-phase response, targets are unlikely to be met. In cancer cachexia attenuation of the inflammatory response using eicosapentaenoic acid results in improved nutritional intake and status. This strategy poses an attractive proposition in the quest to define nutritional support as a clinically-effective treatment modality in other disorders.

There is ongoing debate about the respective roles of enteral and parenteral nutrition. The present short review suggests that these two feeding modalities are not mutually exclusive and that optimal nutritional support may necessitate the concomitant administration of enteral together with parenteral nutrition.

The prevalence of obesity in the general population is high and it is inevitable that artificial feeding will be needed from time to time in the obese patient, particularly in the critical care setting. Against a background of generous endogenous stores of energy as adipose tissue and the ability of obese individuals to survive starvation longer than non-obese individuals, emphasis is placed on preserving lean body mass and optimizing physiological function. Insulin resistance is typical of the obese individual and is exacerbated by stress; overfeeding is dangerous, particularly if it results in hyperglycaemia. Refeeding syndrome also has to be avoided. Weight may be difficult to measure and lean body mass difficult to assess. Calculation of energy requirements is therefore problematic in practice in the obese individual and there is substantial evidence from controlled clinical trials of the safety of feeding at or below resting energy expenditure. If this approach is taken it is wise to provide a more generous than normal protein intake and to beware of patients with a very high baseline urinary N excretion.

There is a clear rationale for elucidating effective ways of identifying and treating disease-related malnutrition (DRM), given the physiological and financial consequences of this common condition and its treatability. Evidence indicates the efficacy of nutritional support methods (oral, tube and intravenous) in increasing total nutritional intake while having little effect on appetite, satiety, appetite mediators (e.g. leptin) and voluntary food intake. When used as the only source of nutrition, artificial nutrition can effectively maintain nutritional intake, and yet many patients find enteral or parenteral feeding alone is unable to relieve distressing appetite sensations, and unusual temporal patterns (including dissociation between hunger and desire to eat) occur. Despite the positive impact of these feeding methods on intake, controversy about whether nutritional support can affect patient outcome has remained. Systematic reviews and meta-analyses indicate that improvements in function and clinical (mortality, complication rates) outcome can occur in a number of patient groups (including hospitalised patients, the elderly, patients who have had gastrointestinal surgery, patients at risk of pressure ulcers). In order to target those patients who will benefit from nutritional support, and overcome the ongoing problem of poor detection and recognition of DRM, simple routine screening to identify risk followed by practical evidence-based treatment is recommended.

The World Health Organization's (1990) definition of palliative care describes an holistic approach to care for patients with advanced progressive illness. Issues relating to nutrition, lack of appetite and the subsequent weight loss the individuals may experience present a challenge to all concerned with providing both formal and informal care to this patient group. The philosophy of palliative care requires a multidisciplinary approach to the constellation of issues and problems related to food that are faced by both patients and carers in receipt of palliative care. The literature in this area is mainly related to those patients with a cancer diagnosis. The developing role of palliative care in patients with non-malignant disease provides further challenges for health care professionals. The present paper aims to reflect an entire philosophical approach to care through an examination of one area of practice.

Undernutrition is commonly associated with chronic disease in children and the elderly. Overnutrition is also, but less commonly, associated with chronic illness. In most diseases malnutrition arises because energy intake does not match energy output. Traditionally, the focus of research has been on abnormalities in energy expenditure, in the belief that these factors were the main determinants of energy imbalance. Recent studies using the doubly-labelled-water method to measure total energy expenditure, combined with more complex study design, have suggested an alternative conclusion. In many chronic diseases patient behaviour, and particularly energy intake, is responsible for energy imbalance and malnutrition. Energy balance studies have therefore provided a useful foundation for the design of strategies aimed at preventing or managing chronic malnutrition. However, modifying patient behaviour is an ambitious undertaking which may not be within the scope of existing clinical nutrition services. A number of non-traditional models of managing chronic malnutrition in children and the elderly are promising. Increasing recognition of the value of systematic review will also provide improved strategies for prevention and management of chronic malnutrition.

Surgery plays a key role in the management of both acute and, less frequently, chronic intestinal failure. Acute intestinal failure frequently requires surgical treatment when it arises as a consequence of intestinal fistulation or obstruction. In specialised clinical practice approximately 50% of acute intestinal failure is associated with intestinal fistulas and in approximately 50% of patients, this condition arises as part of the natural history or complicating treatment for Crohn's disease. A considerable proportion of such patients have abdominal infection and present complex nutritional and metabolic problems. The most important aspect of the surgical management of patients with acute intestinal failure associated with intra-abdominal infection is management of sepsis, since recovery is unlikely in the presence of active infection. Moreover, effective nutritional support and restoration of body composition is not possible if sepsis remains unresolved. Surgical strategies to deal with intra-abdominal infection may involve percutaneous drainage, laparotomy and resection of fistulating segments of intestine and, when infection is persistent and contamination extensive, laparostomy (a technique in which the abdomen is left open and allowed to heal by secondary intention). Surgical treatment should not only be timely and effective, but also aimed at preventing secondary damage to the small intestine, in order to minimise the risk of short bowel syndrome. In some cases a proximal defunctioning stoma may be required, with prolonged nutritional support, using either home total parenteral nutrition or feeding via the defunctioned distal gut (fistuloclysis), pending restoration of intestinal continuity. The role of surgical treatment for patients with short bowel syndrome is less clear. While surgery is frequently required for the management of complications of short bowel syndrome (including gallstones and possibly peptic ulcer disease), the role of intestinal lengthening and tapering procedures (to increase functional intestinal length), and artificial valves, reversed segments and colonic interposition (to reduce intestinal transit) remains controversial. For some patients with short bowel syndrome and, in particular, those with combined intestinal and hepatic failure, intestinal transplantation may become the treatment of choice as long-term results continue to improve.

A new definition of intestinal failure is of reduced intestinal absorption so that macronutrient and/or water and electrolyte supplements are needed to maintain health or growth. Severe intestinal failure is when parenteral nutrition and/or fluid are needed and mild intestinal failure is when oral supplements or dietary modification suffice. Treatment aims to reduce the severity of intestinal failure. In the peri-operative period avoiding the administration of excessive amounts of intravenous saline (9 g NaCl/l) may prevent a prolonged ileus. Patients with intermittent bowel obstruction may be managed with a liquid or low-residue diet. Patients with a distal bowel entero-cutaneous fistula may be managed with an enteral feed absorbed by the proximal small bowel while no oral intake may be needed for a proximal bowel enterocutaneous fistula. Patients undergoing high-dose chemotherapy can usually tolerate jejunal feeding. Rotating antibiotic courses may reduce small bowel bacterial overgrowth in patients with chronic intestinal pseudo-obstruction. Restricting oral hypotonic fluids, sipping a glucose-saline solution (Na concentration of 90–120 mmol/l) and taking anti-diarrhoeal or anti-secretory drugs, reduces the high output from a jejunostomy. This treatment allows most patients with a jejunostomy and >1 m functioning jejunum remaining to manage without parenteral support. Patients with a short bowel and a colon should consume a diet high in polysaccharides, as these compounds are fermented in the colon, and low in oxalate, as 25% of the oxalate will develop as calcium oxalate renal stones. Growth factors normally produced by the colon (e.g. glucagon-like peptide-2) to induce structural jejunal adaptation have been given in high doses to patients with a jejunostomy and do marginally increase the daily energy absorption.

Critical illness is associated with a marked increase in metabolic rate and progressive wasting, despite aggressive nutritional support. The metabolic events which are responsible for these phenomena are unclear, but are characterised by marked impairment of the anabolic effects of insulin on glucose metabolism and excessive activation of the sympathetic nervous system. It has been suggested that critical illness may be associated with impaired carbohydrate oxidation and a marked increase in the loss of heat energy associated with glucose administration (glucose-induced thermogenesis). This situation may result in impaired efficiency of nutrient assimilation. Studies employing combinations of nutrient infusions both at clinically-relevant rates and in association with euglycaemic hyperinsulinaemia have, however, demonstrated that nutrient-induced thermogenesis is unaffected in critical illness in human subjects, and that defective glucose utilization occurs as a consequence of impaired insulin-mediated glucose storage rather than oxidation. Although the cellular and molecular mechanisms underlying these changes are controversial, the recent validation of a human model of insulin resistance in critical illness should provide a means of studying this response in future, and allow the identification of therapeutic targets. This information should increase the efficacy of nutritional support in some of our most seriously-ill patients.

The metabolism of critical illness is characterised by a combination of starvation and stress. There is increased production of cortisol, catecholamines, glucagon and growth hormone and increased insulin-like growth factor-binding protein-1. Phagocytic, epithelial and endothelial cells elaborate reactive oxygen and nitrogen species, chemokines, pro-inflammatory cytokines and lipid mediators, and antioxidant depletion ensues. There is hyperglycaemia, hyperinsulinaemia, hyperlactataemia, increased gluconeogenesis and decreased glycogen production. Insulin resistance, particularly in relation to the liver, is marked. The purpose of nutritional support is primarily to save life and secondarily to speed recovery by reducing neuropathy and maintaining muscle mass and function. There is debate about the optimal timing of nutritional support for the patient in the intensive care unit. It is generally agreed that the enteral route is preferable if possible, but the dangers of the parenteral route, a route of feeding that remains important in the context of critical illness, may have been over-emphasised. Control of hyperglycaemia is beneficial, and avoidance of overfeeding is emphasised. Growth hormone is harmful. The refeeding syndrome needs to be considered, although it has been little studied in the context of critical illness. Achieving energy balance may not be necessary in the early stages of critical illness, particularly in patients who are overweight or obese. Protein turnover is increased and N balance is often negative in the face of normal nutrient intake; optimal N intakes are the subject of some debate. Supplementation of particular amino acids able to support or regulate the immune response, such as glutamine, may have a role not only for their potential metabolic effect but also for their potential antioxidant role. Doubt remains in relation to arginine supplementation. High-dose mineral and vitamin antioxidant therapy may have a place.