Results: Twenty-three studies were included in the final review. Thirty potentially modifiable determinants across seven domains (oral, psychosocial, medication and care, health, physical function, lifestyle, eating) were included. The majority of studies had a high risk of bias and were of a low quality. There is moderate evidence that hospitalisation, eating dependency, poor self-perceived health, poor physical function and poor appetite are determinants of malnutrition. Moderate evidence suggests that chewing difficulties, mouth pain, gum issues co-morbidity, visual and hearing impairments, smoking status, alcohol consumption and physical activity levels, complaints about taste of food and specific nutrient intake are not determinants of malnutrition. There is low evidence that loss of interest in life, access to meals and wheels, and modified texture diets are determinants of malnutrition. Furthermore, there is low evidence that psychological distress, anxiety, loneliness, access to transport and wellbeing, hunger and thirst are not determinants of malnutrition. There appears to be conflicting evidence that dental status, swallowing, cognitive function, depression, residential status, medication intake and/or polypharmacy, constipation, periodontal disease are determinants of malnutrition. Conclusion: There are multiple potentially modifiable determinants of malnutrition however strong robust evidence is lacking for the majority of determinants. Better prospective cohort studies are required. With an increasingly ageing population, targeting modifiable factors will be crucial to the effective treatment and prevention of malnutrition.

Acute leucine supplementation of the diet has been shown to blunt defects in postprandial muscle protein metabolism in old rats. This study was undertaken to determine whether the effect of leucine persists in a 10-d experiment. For this purpose, adult (9 mo) and old (21 mo) rats were fed a semiliquid 18.2 g/100 g protein standard diet during the 8-h dark period for 1 mo. Then, each group was given either a leucine-supplemented meal or an alanine-supplemented meal (as the control meal) for 1 h and the standard diet the rest of the feeding period. On d 10, rats were fed either no food (postabsorptive group) or the supplemented meal for 1 h. Muscle protein synthesis was assessed in vivo 90-120 min after meal distribution using the flooding dose method (1-(13)C phenylalanine). Leucinemia was similar in rats of both ages in the postabsorptive state. Postprandial plasma leucine concentrations were one- to twofold greater after the leucine meal than after the control meal. In the postabsorptive state, leucine supplementation did not modify the muscle protein synthesis rate in old rats but enhanced it to the postprandial rate in adult rats. As expected, muscle protein synthesis was stimulated by the control meal in adult rats but not in old rats. The leucine meal restored this stimulation in old rats but did not further stimulate muscle protein synthesis in adult rats. In conclusion, the beneficial effect of leucine supplementation on postprandial muscle protein anabolism persists for at least 10 d. The long-term utilization of leucine-rich diets may therefore limit muscle protein wasting during aging.

Skeletal muscle loss is observed in several physiopathological situations. Strategies to prevent, slow down, or increase recovery of muscle have already been tested. Besides exercise, nutrition, and more particularly protein nutrition based on increased amino acid, leucine or the quality of protein intake has generated positive acute postprandial effect on muscle protein anabolism. However, on the long term, these nutritional strategies have often failed in improving muscle mass even if given for long periods of time in both humans and rodent models. Muscle mass loss situations have been often correlated to a resistance of muscle protein anabolism to food intake which may be explained by an increase of the anabolic threshold toward the stimulatory effect of amino acids. In this paper, we will emphasize how this anabolic resistance may affect the intensity and the duration of the muscle anabolic response at the postprandial state and how it may explain the negative results obtained on the long term in the prevention of muscle mass. Sarcopenia, the muscle mass loss observed during aging, has been chosen to illustrate this concept but it may be kept in mind that it could be extended to any other catabolic states or recovery situations.