## 3 Perspectives and Outcomes of the Presented RHMS with a Focus on Diet-Related Approaches
### Optimising Nutrition Interventions in Liver Cirrhosis  
#### 3.1.1 Aspects of Nutrition in Liver Cirrhosis--Pathophysiology and Recent Insights  
Malnutrition is present in 20% of patients with compensated LC and more than 50% of patients with decompensated liver disease at diagnosis and acts as an independent predictor of low survival [115]. The classical phenotype of malnutrition in LC is muscle wasting and loss of muscle mass (i.e., sarcopenia), but adipose tissue depletion may also occur, especially in patients with alcohol abuse and in women. Frailty, defined as loss of functional and cognitive capacity leading to a vulnerable state, is also considered a nutrition-related disorder, while deconditioning, a deterioration of muscle functional capacity secondary to sarcopenia and immobility is a hallmark of any chronic debilitating disease, including LC. There is a bidirectional relationship between nutritional status and decompensating events in LC--poor dietary management and malnutrition, especially sarcopenia, increase the risk of decompensation [116]--while each decompensating event is associated with a hypercatabolic state and altered nutritional intake (infections, gastrointestinal bleeding, altered mental status, dietary restrictions due to medical interventions, etc. ), contributing to significant denitrification, which further leads to increased morbidity and mortality. Although malnutrition predominantly refers to undernutrition, obesity is increasingly observed in newly diagnosed LC as a result of the growing incidence of LC cases related to MASLD and may mask the underlying muscle mass depletion, further contributing to higher morbidity and mortality [117]. Encouraging weight loss without a prior nutritional evaluation and overlooking the need for a personalized nutritional intervention in these patients may have a rather negative impact on their prognosis. As an emerging entity, novel nutrition evaluation methods and nutrition intervention strategies need to be implemented, as further research should focus on managing sarcopenia obesity and its associated metabolic comorbidities. Whether malnutrition can be reversed in LC patients is controversial, but there is certainly a need to improve the dietary intake of these patients, avoiding restrictions that are not evidence-based and encouraging health-promoting practices, including personalized diet optimisation and increased physical activity. The pathophysiology of malnutrition in LC is complex, and some aspects regarding nutritional intervention are still debatable. The liver plays a central role in the metabolism of carbohydrates, proteins, fat, vitamins, and minerals. Alterations in substrate utilisation for energy production are a main feature of LC and consist of depleted hepatic glycogen storage and impaired hepatic glycogenolysis, increased fat oxidation, and increased protein catabolism, resulting in protein-energy malnutrition even from the early stages of the disease. In addition, portal hypertension leads to malabsorption through impaired gut motility, intestinal dysbiosis, intestinal oedema, and mucosal changes. Evidence suggests recommending a high-energy and protein-rich diet (>1.2 g/kg/day) divided into three main meals and three snacks, the late-evening snack consisting of slow-release carbohydrates and proteins being the most important and most effective in improving nutritional status, risk of complications and mortality rates [118]. The use of branched-chain amino acid (BCAA) supplementation shows promise in reducing the risk and severity of hepatic encephalopathy but is limited by poor palatability and the need for further exploration of dietary manipulation for optimal BCAA disponibility [119]. Evidence is also accumulating that high-quality protein intake should not be restricted in patients with hepatic encephalopathy due to the subsequent risk of protein-energy malnutrition.