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As such, if you have this condition, what you eat and drink each day is especially important, particularly as components like protein, sodium, and sugar require your liver to work harder—a demand it may no longer be able to meet. A cirrhosis diet plan should be crafted with the help of your doctor and other members of your healthcare team, such as a registered dietitian, to ensure that you're adequately nourished and avoiding choices that can worsen your condition and otherwise impact your health. The liver has more than functions , making it one of the most vital organs. A cirrhosis diet can help provide adequate nutrition, reduce the amount of work your liver needs to do, thwart related complications, and prevent further liver damage.
Malnutrition encompassing both macro- and micro-nutrient deficiency, remains one of the most frequent complications of alcohol-related liver disease ArLD. Protein-energy malnutrition can cause significant complications including sarcopenia, frailty and immunodepression in cirrhotic patients.
Moreover, nutritional deficit increases the likelihood of hepatic decompensation in cirrhosis. Prompt recognition of at-risk individuals, early diagnosis and treatment of malnutrition remains a key component of ArLD management. In this review, we describe the pathophysiology of malnutrition in ArLD, review the screening tools available for nutritional assessment and discuss nutritional management strategies relevant to the different stages of ArLD, ranging from acute alcoholic hepatitis through to decompensated end stage liver disease.
Core tip: Malnutrition is a common complication of alcohol-related liver disease ArLD , which, if untreated, can adversely affect patient outcome and recovery.
Prompt recognition of nutritional depletion may identify those patients who are at higher risk of clinical decompensation, but there are few guidelines to inform the clinical management of these complex patients. In this article, we discuss the pathophysiology and treatment of micro- and macro-nutrient deficiency in ArLD, and provide recommendations for the management of patients at different stages of their illness.
The World Health Organization estimates that alcohol abuse accounts for approximately 3. Forty-one percent of liver deaths in Europe are related to harmful alcohol consumption [ 3 ]. Alcohol-related liver disease ArLD refers to a wide spectrum of liver pathologies, including steatosis fatty liver , steatohepatitis characterized by a combination of hepatic fat accumulation and inflammation , acute alcoholic hepatitis AAH and liver cirrhosis [ 4 ].
It is important to understand that whilst alcohol is the principle mediator of liver injury in many individuals with cirrhosis, it can play a significant contributory role in the progression of other liver diseases such as hereditary haemochromatosis and non-alcoholic steatohepatitis. The component of alcohol relating to conditions developing in such a setting are commonly described as alcohol-contributory liver disease AcLD.
Alcohol use disorders should be sought in all individuals presenting with chronic liver disease due to the prevalence of alcohol abuse across the diagnostic spectrum with both ArLD and AcLD requiring a common final pathway of management.
Whilst targeted pharmaceutical interventions are lacking in patients with alcohol-related cirrhosis [ 5 ] , sustained alcohol avoidance remains the cornerstone of ArLD and AcLD management and recovery [ 6 ]. Several studies have identified a strong relationship between poor nutrition and adverse outcomes in survival, quality of life and complications of alcohol-related cirrhosis, such as variceal bleeding, ascites, hepatic encephalopathy HE , infection and hepato-renal syndrome [ 7 - 9 ].
Protein-energy malnutrition PEM: Altered body composition due to an imbalance of energy, protein and micronutrients [ 10 , 11 ] is one of the most frequent complications of harmful alcohol use and can occur at all stages of ArLD [ 12 , 13 ]. Studies have shown that up to half of outpatients with alcohol-related cirrhosis, and almost all hospitalized patients with AAH exhibit evidence of clinically significant nutritional depletion [ 13 - 15 ].
In contrast, nutritional supplementation has been shown to be an effective means of improving liver function and patient survival in AAH [ 18 , 19 ]. There can be little doubt that the lack of clinical practice guidelines aimed at assessing and grading ArLD-related malnutrition accounts for the poor recognition, diagnosis and treatment of this condition in clinical practice. The aim of this article is to define the relevant pathophysiology, summarise modes of assessment and discuss optimal nutritional management in different forms of ArLD.
Malnutrition in ArLD and AcLD is multifarious and comprised of many interdependent elements, but simply increasing the availability of energy supplements is not enough to counteract the powerful forces that drive the catabolic state. Here we explore some of the elements that contribute to the condition Figure 1.
Loss of appetite and reduced food desire is related to the upregulation of inflammatory cytokines and appetite regulators in both acute and chronic liver disease. Whilst cytokines may act as a regulatory component of appetite in health, in disease states their dysregulation is a major contributor to the cachexia seen in all forms of acute and chronic disease [ 26 ].
Anorexia is worsened by physical symptoms of discomfort nausea, bloating and fatigue , dysgeusia and the mechanical effects of large ascites [ 28 ]. These factors may impact upon the food choices of patients and affect both the quality and quantity of nutrition as a result. Alcohol is absorbed by diffusion in the stomach and, to a lesser degree the duodenum and jejunum. Whilst acute and excessive alcohol consumption can cause gastric and duodenal erosions and villous-predominant epithelial loss in the upper jejunum [ 29 ] , the effects of chronic alcohol consumption on the intestinal mucosa are poorly understood.
They may include intestinal fibrosis and overgrowth of aerobic and anaerobic microorganisms which contribute to functional and morphological abnormalities of the small bowel [ 30 ]. Gerova et al [ 31 ] reported a higher frequency of small intestinal bacterial colonisation in patients with ArLD, with the changes occurring independently of the stage of liver dysfunction suggesting that the direct effect of alcohol on gut motility and immunity creates a permissive microenvironment for small bowel overgrowth at these sites.
In addition to changes in the gut microbiome, chronic alcohol ingestion can lead to a reduction in the adhesion of epithelial cell tight junctions [ 32 ] resulting in increased intestinal permeability, bacterial translocation and consequential increases in pro-inflammatory cytokines and lipopolysaccharides [ 33 ].
Chronic alcohol consumption impairs gut motility and alcohol-induced chemical gastritis delays gastric emptying, both of which significantly increase the oro-caecal transit time [ 34 ] leading to impaired absorption of nutrients. Furthermore, alcohol is an important risk factor for chronic pancreatitis and pancreatic exocrine insufficiency PEI which can exacerbate malabsorption [ 35 ]. Resting energy expenditure REE is the amount of energy an individual uses to perform vital organ functions free of activity and digestion.
REE can be calculated using the predictive formula of Harris-Benedict [ 36 ] however its calculation can be unreliable in patients with altered body composition by misconstruing the weight of extracellular fluid as dry body mass and overestimating the caloric requirements in cirrhotic patients with ascites.
Indirect calorimetry is not subject to this limitation as it measures REE without reference to body composition by basing its calculation on oxygen consumption and carbon dioxide production [ 37 ]. The ensuing increase in acetaldehyde production a toxic metabolite of alcohol puts stress on microsomal re-oxidation pathways which utilise more oxygen and ATP [ 40 ] to recover nicotinamide adenine dinucleotide, thereby perpetuating the hyperdynamic metabolism by increasing energy utilisation. AAH is a classical example of the alcohol-induced hypermetabolic state [ 41 , 42 ].
The accelerated catabolism typically seen in these patients is a composite of reduced oral energy intake with food as the individual becomes dependent on the calorific value of alcohol to provide their basal metabolic expenditure and subsequently becomes more protein-calorie deplete. Many patients reduce their alcohol intake before presenting with clinical manifestations of AAH [ 43 ] thus compounding the calorie debt and catalysing a chain of events leading to the establishment of a chemical and metabolic liver injury characterised by hepatitis and the sudden onset of jaundice and synthetic failure.
It is pertinent that the proven treatments for AAH include alcohol cessation and nutritional therapy with high protein and calorie supplementation. Another driver of hyper-metabolism is systemic low grade endotoxaemia [ 44 ] , driven by bacterial translocation, which can lead to upregulation of the sympathetic nervous outflow and worsening of the hypermetabolic state.
This results in clinical features such as fever, tachycardia, hyperglycaemia and muscle wasting [ 45 , 46 ]. In such patients, the accumulation of ascites further increases REE under indirect colorimetry testing due to the energy expense required to maintain the large fluid volumes at body temperature.
Improvements in energy expenditure are seen in patients after large volume paracentesis [ 47 ]. Excessive alcohol intake over a prolonged period results in impaired insulin resistance and increased cardiovascular morbidity and mortality [ 48 , 49 ].
In chronic alcohol consumption glycogen stores of the liver are depleted, whilst in acute episodes of heavy alcohol consumption binge drinking gluconeogenesis is inhibited and hepatic glycogenolysis stimulated to prevent hypoglycaemia. Therefore, whilst in a healthy individual acute alcohol consumption is unlikely to cause changes in the euglycemic state, in patients with chronic liver disease acute alcohol ingestion may precipitate hypoglycaemia [ 50 , 51 ].
Low to moderate doses of alcohol have little to no effect on muscle protein balance but acute ingestion of large doses of alcohol and chronic alcohol abuse causes changes to both whole-body and tissue-specific protein metabolism by increasing nitrogen excretion [ 52 ]. Myopathy is a common complication of chronic alcoholism and is the result of a prolonged imbalance between muscle protein growth and breakdown [ 53 , 54 ].
The liver plays a central role in lipid metabolism which follows a complex network of reactions and interplay of hormones, nuclear receptors, intracellular signalling pathways and transcription factors. Free fatty acids FAs are synthesised by the liver from glycolytic pathways and are directly mobilised from the gut and adipose tissue.
Alcohol also affects FA export from the liver by suppressing microsomal triglyceride transfer protein, as seen in livers of ethanol fed animals, which is required for the assembly of very low density lipoprotein prior to export [ 57 ].
The result is intrahepatic fat accumulation, which ultimately progresses to cirrhosis as a result of iterative cycles of injury and cell-death associated with sustained alcohol excess.
Thiamine vitamin B1 serves as a cofactor for the enzymes involved in glucose metabolism. Thiamine deficiency results in decreased activities of these pathways which can result in reduced ATP synthesis leading to cell damage and cell death. Chronic alcoholism leads to thiamine deficiency as a result of inadequate nutritional intake and decreased absorption of thiamine from the gastrointestinal tract [ 58 ].
Careful reintroduction of diet may need to be considered if refeeding syndrome is a concern, as the sudden increase in carbohydrate consumption causes a shift from fats to carbohydrate for energy production, increasing the demand for thiamine and compounding any deficiency by further depleting stores [ 59 ].
Wernicke encephalopathy is an acute neurological crisis which results from exhausted thiamine stores and is characterised by the clinical triad of encephalopathy, oculomotor dysfunction, and gait ataxia. Folate deficiency is also seen in these patients due to reduced dietary intake, intestinal malabsorption, reduced liver uptake, storage and increased urinary excretion [ 60 ].
Deficiencies in folate can cause defective DNA synthesis and repair which may manifest as macrocytic anaemia and muscle dysfunction. Chronic alcohol consumption and jaundice cause vitamin A levels to fall [ 61 ]. The metabolism of vitamin A is similar to alcohol metabolism in the human body as they both involve oxidative pathways and are therefore vulnerable to alterations in the basal redox-state of the liver [ 62 ]. Alcohol dehydrogenase activity and cytochrome 2E1 negatively affect retinoid homeostasis [ 63 ] and chronic alcohol consumption leads to depletion of hepatic and plasma retinoid levels and retinoid binding proteins [ 64 , 65 ].
Vitamin A deficiency can lead to the clinical presentation of night blindness. Various mechanisms, in addition to dietary insufficiency, have been postulated to account for vitamin C deficiency in the context of chronic alcohol consumption [ 67 ]. Alcohol-induced enterocyte toxicity leads to intestinal malabsorption and hepatotoxicity which inhibit hepatic transformation of various vitamins including vitamin C to their active metabolites [ 68 ].
The imbalance in vitamin C is exacerbated by increased urinary ascorbic acid excretion following episodes of alcohol excess [ 69 ]. Some studies suggest that pre-treatment with vitamin C significantly enhances blood ethanol clearance, possibly as a result of its ability to supply peroxide and thus allowing catalase to contribute to ethanol oxidation [ 70 ].
Clinical manifestation of vitamin C deficiency is namely scurvy and can present as poor wound healing, gingival swelling, gum bleeding, loss of teeth and mucocutaneous petechiae; late disease may be life-threatening with anasarca, haemolysis and jaundice [ 71 , 72 ]. Zinc is absorbed via metal binding transcription factors and plays a key role in the regulation of gene expression. In alcohol-fed mice, alcohol disrupts gut permeability and increases oxidative stress, predominantly at the level of distal small bowel which interferes with zinc homeostasis and leads to reduced ileal zinc concentrations [ 73 ].
In addition to reduced enteric absorption and increased urinary excretion of zinc, patients with alcohol-related cirrhosis often have diets lacking in protein and zinc, with zinc deficiency a common and easily rectified cause of dysgeusia. Zinc deficiency may manifest as acrodermatitis, anorexia, hypogonadism, altered immune function, poor wound healing, impaired night vision, diarrhoea, impaired mental function and portal systemic encephalopathy [ 75 , 76 ].
It is a critical determinant of metabolism, acting as a co-factor in more than enzymatic reactions involved in protein and nucleic acid synthesis and energy metabolism. Alcohol increases the urinary excretion of magnesium and total body stores of magnesium are depleted in nearly all patients with alcohol-related cirrhosis [ 77 ]. Further insensible losses occur as a result of alcohol-related diarrhoea, vomiting and concurrent use of drugs such as diuretics and aminoglycosides.
Hypomagnesemia predisposes to metabolic bone disease, cardiovascular co-morbidities and is associated with seizure, depression and neuromuscular abnormalities [ 78 , 79 ] Table 1. The interactions of divalent cation deficiencies such as selenium and magnesium are poorly understood but seem to play a key role in the immune-paresis seen in alcohol-related cirrhosis.
Selenium deficiency is common in alcohol-dependency [ 80 , 81 ] and proportionate to disease stage and increased levels of pro-inflammatory cytokines which play a role in liver injury and fibrosis. Current evidence suggests that micronutrient metabolism is impaired in decompensated liver disease and that by replacing these elemental deficiencies, clinicians may be able to counteract some of the immune-paresis and mood disorders commonly seen in these malnourished states [ 82 , 83 ].
Malnutrition and sarcopenia are important determinants of prognosis and survival in cirrhotic patients [ 84 , 85 ]. Poor nutrition increases the risk of complications and decompensation in liver disease patients [ 87 ]. Moreover, because muscle acts as an alternative site of ammonia detoxification [ 88 ] prospective studies in cirrhotic patients have shown that both overt and minimal HE are increased in patients with muscle depletion [ 89 ]. Nutrition has also been shown to have significant impact on ascites.
Cirrhosis and malnutrition produce an acquired state of immune paresis which negatively impacts upon patient recovery and survival [ 91 , 92 ]. In patients with ArLD, the presence of sarcopenia as recorded by the skeletal muscle index [ 94 ] is independently associated with an increased likelihood of an individual being removed from the transplant waiting list due to clinical deterioration HR 1.
The diagnosis and management of sarcopenia is therefore of paramount importance in the initial and subsequent assessment of liver-disease patients receiving clinical care.
There is no gold standard for assessment of malnutrition in liver disease and none specifically designed for patients with ArLD, but there are a number of screening tools [ 97 ] that have been developed to assess malnutrition risk, although most lack external validation. Given the high prevalence of malnutrition and sarcopenia in alcohol-related cirrhosis, all patients should undergo nutritional screening at the point of presentation, ideally using a standardised screening tool such as the RFH-NPT [ ].
Body mass index BMI is often distorted in patients with chronic liver disease by fluid retention states like anasarca or ascites. Moreover, sarcopenic-obesity is another entity characterised by excessive fat and poor muscle mass and function [ ]. In these settings, BMI proves to be an inadequate metric by which to predict complications and should be used in combination with objective measures of muscle mass and strength.
Muscle function tests are an important component of assessing nutrition risk. Hand-grip strength HGS has been well validated and is commonly used in clinical practice to record strength and muscle capacity [ ].
It is an inexpensive, easily replicated test and can be completed at the bedside or clinic. Observational studies have shown that HGS is strongly correlated with Child-Pugh score and can predict the risk of short-term morbidity in patients with alcohol-related cirrhosis [ ]. Moreover, HGS operates as a predictive tool for complications of cirrhosis and muscle function testing can be used as a predictive determinant of HE [ 97 ].
Malnutrition is a common finding in patients with chronic liver diseases. Recommended diets may be unpalatable because of required sodium restriction when treating ascites; moreover, dysgeusia associated with zinc or magnesium deficiency in cirrhotic patients has been reported. Fat malabsorption from reduced bile acid synthesis, increased intestinal protein losses, and relevant metabolic disturbances such as insulin resistance, increased fat turnover, and protein catabolism are also relevant factors contributing to the alteration of nutritional status in chronic liver disease. Malnutrition, particularly when the protein compartment is involved, has been shown to increase the risk of complications and to adversely affect the outcome in cirrhotic patients. A complete nutritional status assessment is always required at the time of diagnosis in cirrhotic patients. Although accurate quantitative measurements may be hindered by fluid overload and impaired hepatic protein synthesis, simple bedside methods such as anthropometry and subjective global assessment are deemed adequate to identify patients at risk and have been demonstrated to correlate with clinical outcomes. Energy expenditure can be estimated by standard formulas and dietary intake should be carefully evaluated through a detailed interview.
So, what should you eat to ensure that your liver can function normally? Still, here are some general food tips for a healthy or healthier liver:. Bile is a liquid made in the liver that helps break down fats in the small intestine. Bile duct disease keeps bile from flowing to the small intestine. Hepatitis C is a disease of the liver caused by the hepatitis C virus. You get the message because your liver is able to function properly and, provided your overall health is good, you feel in great physical shape. When you consume fatty or fried foods, and pile on the salt, your liver literally is under attack.
ISBN (PDF). Articles in this volume Bratova and Petr Wohl. Parenteral Nutrition-Associated Liver Disease: The Role of the Gut Microbiota.
Malnutrition encompassing both macro- and micro-nutrient deficiency, remains one of the most frequent complications of alcohol-related liver disease ArLD. Protein-energy malnutrition can cause significant complications including sarcopenia, frailty and immunodepression in cirrhotic patients. Moreover, nutritional deficit increases the likelihood of hepatic decompensation in cirrhosis.
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