Malnutrition and chronic heart failure

Abstract

Malnutrition in patients with chronic heart failure (CHF) is not always as severe as muscle wasting in the same patients. Our data showed that 24% of patients with CHF had malnutrition (serum albumin < 3.5 g/dl) while 68% had muscle atrophy. This apparent discrepancy can be explained by considering the metabolic role of the striate muscle. The striate muscle maintains body metabolic performance by continuous exchange of fuel (amino acids) with other organs such as the liver. This happens when the subject is suffering from malnutrition or is starving, and it is regulated by the ratio of catabolic to anabolic molecules such as hormones or cytokines. Glucose is produced when amino acids are metabolized in the liver by gluconeogenesis. Malnutrition, muscle wasting and the frequent progression to cachexia can be reduced by the use of specific therapeutic agents such as cytokines and/or catabolic hormone antagonists. This is because cytokines and catabolic hormones, with consequent insulin resistance (IR), can cause muscle wasting. An alternative and/or complementary therapy may be exogenous supplementation with amino acids. Amino acids: are rapidly absorbed independent of pancreatic activity, reduce IR, induce production in the liver of anabolic molecules such as growth hormone and insulin-like growth factor, and modulate catabolic hormone-mediated effects on adipocytes. Research on the most suitable qualitative and quantitative amino acid composition for an alternative and/or complementary therapy is being undertaken in different research centres.