Unlock the Truth: High Protein Diet’s Impact on Ascites in Liver Cirrhosis Revealed!

Cirrhosis, a condition characterized by the replacement of normal liver architecture with nodules and diffuse hepatic fibrosis, represents the final pathway for various chronic liver diseases. Protein-calorie malnutrition (PCM) is a common and serious complication in patients with cirrhosis, occurring in 50%-90% of cases and is associated with increased morbidity and mortality. While the pathogenesis of PCM is multifactorial, alterations in protein metabolism play a significant role. This article aims to provide a comprehensive overview of the relationship between a high-protein diet and ascites in the context of liver cirrhosis, considering nutritional recommendations, assessment methods, and potential interventions.

Understanding Liver Cirrhosis

Progression of chronic liver disease to cirrhosis can vary from weeks to years, depending on the etiology. Cirrhosis is classified as either compensated or decompensated. Compensated cirrhosis is often asymptomatic, while decompensated cirrhosis is characterized by complications such as hepatic encephalopathy, variceal bleeding, ascites, or jaundice.

A wide variety of chronic liver diseases lead to cirrhosis, the most common are toxic/metabolic (alcohol, MASLD, hemochromatosis), viral (hepatitis B and C), and autoimmune (autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis). Less common etiologies include biliary (atresia, cholangiopathies), vascular (Budd-Chiari, cardiac), genetic (cystic fibrosis, lysosomal acid lipase deficiency, alpha-1-antitrypsin deficiency, galactosemia, Wilson’s disease), and iatrogenic (medications, supplements) conditions.

The Role of Protein in Liver Health

The liver plays a crucial role in the metabolism of proteins, carbohydrates, and fats. Its main functions include amino acid interconversion, deamination (breakdown), and urea synthesis. Amino acids are categorized as essential (obtained from the diet) and non-essential (synthesized by the body). In liver disease, these metabolic processes are disrupted, contributing to PCM.

Protein-Calorie Malnutrition (PCM) in Cirrhosis

PCM is a common complication of cirrhosis, often undiagnosed due to the presence of edema and ascites, which complicate weight change detection. The pathogenesis of PCM is multifactorial, involving changes in protein metabolism and function.

Read also: High-Fiber Diet for Better Health

Factors Contributing to PCM

Several factors contribute to PCM in liver disease:

Decreased Oral Intake: Anorexia, common in patients with liver disease, can be secondary to changes in the liver's control of appetite. Gastrointestinal symptoms like early satiety, nausea, vomiting, diarrhea, constipation, indigestion, abdominal pain/distension, ascites, and reflux further decrease oral intake.
Fatty Acid Malabsorption: The liver's inability to produce adequate bile and decreased micelle formation lead to fatty acid malabsorption, reducing the calories available for the body's use.
Hypozincemia: Zinc deficiency, caused by decreased intake of zinc-rich foods and increased GI and urinary losses, is associated with liver disease. Low albumin levels, common in liver disease, further impair zinc transport to body tissues.
Metabolic Alterations: Impaired glycogen synthesis and storage lead to an early "fasting state," utilizing glycerol and amino acids for gluconeogenesis, resulting in continuous fat and muscle breakdown.
Hypermetabolism: Increased β-adrenergic activity and activation of the sympathetic nervous system (SNS) contribute to hypermetabolism, leading to increased muscle breakdown.

Consequences of PCM

PCM in cirrhosis leads to a poor prognosis and various complications such as:

Tissue Wasting: Constant breakdown of fat and muscle leads to tissue depletion and muscle wasting.
Visceral Protein Depletion: Malnourished cirrhotic patients experience depletion of visceral protein sources.
Muscle Depletion: Body composition studies show significant fat breakdown early in liver disease, progressing to significant muscle depletion with severe liver dysfunction, especially in decompensated cirrhosis.

Nutritional Assessment in Cirrhosis

Accurate assessment of nutritional status is crucial for managing PCM in cirrhotic patients. Various methods are employed, each with its limitations:

Dietary Intake Evaluation: Methods like 24-hour food recalls, food frequency questionnaires, calorie counts, and food diaries are used to evaluate food intake.
Serum Protein Levels: Albumin and prealbumin levels, though commonly used, are affected by factors other than nutrition status, such as inflammation and infection.
Anthropometric Measurements: Height, weight, and BMI are quick methods, but unreliable in patients with edema and ascites. Corrective measures have been developed to subtract 5%, 10%, or 15% of the measured weight for mild, moderate, or severe ascites, respectively, with an additional 5% subtracted for pedal edema.
Bioelectrical Impedance Analysis (BIA): BIA is considered an accurate tool in cirrhosis patients without ascites, calculating body composition based on the water content of different tissues.
Subjective Global Assessment (SGA): SGA considers changes in weight and dietary intake, GI symptoms, functional capacity, and physical assessment of subcutaneous fat, muscle wasting, edema, and ascites.

High Protein Diet: Considerations and Recommendations

Earlier dietary recommendations for cirrhotic patients suggested a restricted protein diet, primarily due to concerns about hepatic encephalopathy (HE). However, current evidence suggests that protein restriction is not beneficial and may even be detrimental.

Protein Intake and Hepatic Encephalopathy

Studies have shown that restricting protein intake does not significantly reduce serum ammonia levels and can lead to increased muscle breakdown. A normal to high protein diet (1.2-1.5 g/kg/day) is now recommended to avoid PCM and tissue wasting.

Cordoba et al. divided patients with HE into two groups: one receiving a normal protein diet (1.2 g/kg/day) and the other a low-protein diet. No significant difference was found in serum ammonia levels between the groups.
Gheorghe et al. demonstrated that protein restriction was not required for the improvement of HE, with 80% of participants showing significant improvements on a high-protein, high-calorie diet (1.2 g protein/kg/day and 30 kcal/kg/day).
Swart et al. determined that the minimum protein requirement for patients with cirrhosis to be in positive nitrogen balance was 1.2 g/kg/day.

Current Protein Recommendations

Patients with cirrhosis should consume 25-40 kcal/kg/day based on their dry body weight and 1.0-1.5 g/kg protein per day to prevent muscle catabolism. It is advised to consume six small, frequent meals throughout the day to meet their higher needs.

Branched-Chain Amino Acids (BCAA)

The ratio of branched-chain amino acids (BCAA) to aromatic amino acids (AAA) is often altered in cirrhosis, potentially contributing to complications like HE. Supplementation with BCAA has been used to normalize this ratio.

Vegetable vs. Animal Protein

Some studies suggest that vegetable proteins may be beneficial for patients with cirrhosis, possibly due to their amino acid composition and fiber content.

Ascites Management and Dietary Considerations

Ascites, the accumulation of fluid in the abdominal cavity, is a common complication of cirrhosis. Management typically involves sodium restriction and diuretics.

Sodium Restriction

Limiting sodium intake is a cornerstone of ascites management. A conventional target of 2,000 mg/day is often recommended.

Diuretics

Diuretics help to reduce fluid retention and ascites. However, their use requires careful monitoring to avoid complications like electrolyte imbalances and renal impairment.

Nutritional Interventions for Ascites

Several studies have investigated the role of nutritional interventions in the management of ascites:

Bunout et al. found no significant difference in ascites resolution with a high-carbohydrate, normal-protein diet compared to a normal diet.
Bernardi et al. reported that moderate sodium restriction (40-60 mEq/day) combined with diuretics was more effective than strict sodium restriction (20 mEq/day) alone.
Gauthier et al. showed that a sodium-free diet combined with diuretics led to greater weight loss and decreased girth compared to a normal diet with sodium restriction.
Nasrallah et al. found that keto acid therapy led to greater complete resolution of ascites and greater improvement in patients with moderate to severe alcoholic hepatitis.
Simon et al. observed that a BCAA evening snack had lower mortality and fewer paracentesis procedures in patients with cirrhosis and ascites.

Unconventional Nutritional Interventions

Some trials have explored unconventional nutritional interventions:

Descos et al. used ultrafiltration combined with reinfusion of concentrated ascitic fluid to remove excess water and electrolytes.
Calvey et al. evaluated the effect of an amino acid infusion on nitrogen balance in patients with alcoholic hepatitis.
Sorrentino et al. assessed the impact of glutamine supplementation on outcomes after paracentesis.

General Dietary Recommendations for Liver Cirrhosis

If you’re living with liver cirrhosis, prioritize high protein foods and incorporate both plant- and animal-based protein sources into your diet. Limit or avoid alcohol and foods high in unhealthy fats or sodium.

While specific recommendations should be tailored to individual needs, some general guidelines include:

Prioritize Nutrient-Dense Foods: Fruits, vegetables, nuts, seeds, and legumes should form the basis of the diet.
Include High-Quality Protein: Eggs, dairy products, seafood, lean meats, poultry, beans, lentils, and chickpeas are excellent sources.
Limit Unhealthy Fats: Avoid trans fats found in fried foods and processed snacks.
Avoid Alcohol: Alcohol can worsen liver damage and scarring.
Moderate Sodium Intake: Limiting salty foods can prevent fluid retention and ascites.
Eat Small, Frequent Meals: This can help prevent malnutrition and maintain energy levels.
Consider Supplementation: Vitamin and mineral deficiencies are common in cirrhosis, so supplementation may be necessary.

Foods to Eat

Fruits: apples, oranges, berries, pears, peaches, plums
Vegetables: broccoli, cauliflower, asparagus, tomatoes, peas, potatoes
Protein foods: eggs, dairy products, seafood, lean cuts of meat and poultry
Legumes: beans, lentils, chickpeas
Nuts: walnuts, almonds, cashews, pistachios, macadamias
Seeds: pumpkin seeds, flaxseed, chia seeds, hemp seeds
Whole grains: quinoa, oats, brown rice, buckwheat
Heart-healthy fats: olive oil, avocados, avocado oil, salmon, nuts, seeds
Beverages: water, coffee, tea
Herbs and spices: black pepper, cumin, dill, parsley, thyme

Foods to Avoid

Highly processed foods: fast food, convenience meals, canned soups, packaged snacks
Unhealthy fats: margarine, vegetable shortening, fried foods
Salty snacks: chips, crackers, pretzels, microwave popcorn
Processed meats: hot dogs, sausage, deli meats, bacon, beef jerky
High sodium condiments: soy sauce, teriyaki sauce, steak sauce, spaghetti sauce
Undercooked foods: raw or undercooked meat, poultry, eggs, fish, oysters, or mussels
Alcohol: wine, beer, spirits, cocktails

Additional Nutritional Considerations

Malnutrition can be present in up to 20% of patients with compensated cirrhosis and 50% of patients with decompensated cirrhosis and is associated with increased morbidity and mortality. There is no universally accepted definition of malnutrition, but it is often defined as loss of skeletal muscle mass and strength, in addition to diminished subcutaneous and visceral fat mass (adipopenia), due to reduced protein and energy consumption.

Patients with cirrhosis also have decreased hepatocyte mass and thereby decreased glycogen stores, which promotes gluconeogenesis. Aromatic amino acids and branched-chain amino acids are released from skeletal muscle via proteolysis for gluconeogenesis. A decrease in circulating branched-chain amino acids, as well as increased skeletal muscle ammonia production, endotoxemia, and low testosterone levels, all promote increased protein catabolism and decreased protein synthesis.

A comprehensive nutritional assessment in cirrhosis includes subjective global assessment (SGA), in addition to anthropometric and biochemical measurements. Given that edema and ascites can falsely elevate the BMI, corrective measures have been developed to subtract 5%, 10%, or 15% of the measured weight for mild, moderate, or severe ascites, respectively, with an additional 5% subtracted for pedal edema. Functional testing using hand-grip strength as a tool to assess muscle strength has been shown to have the highest accuracy for detecting nutritional compromise in chronic liver disease.

In addition to overall malnutrition, patients with cirrhosis often have micronutrient deficiencies. Fat-soluble vitamin deficiencies (vitamins A, D, E, and K) are common, especially in patients with cholestatic liver disease, due to malabsorption, decreased intake, and reduced production of carrier proteins. Patients may also be deficient in water-soluble vitamins, including thiamine (B1), and, less commonly, pyridoxine (B6), folate (B9), and cobalamin (B12) due to reduced hepatic storage. Zinc and magnesium deficiencies are also common. Supplementation with 150-175 mg/day of zinc can lower ammonia levels when used as monotherapy or when combined with vitamin A, C, and E supplementation. A daily multivitamin with minerals can address most of these deficiencies.

Malnourished cirrhosis patients should consume 35-40 kcal/kg/day (using body weight corrected for ascites) to promote anabolism. Macronutrient recommendations are for 1.2-1.5 g/kg/day of protein, 50-70% of calories from carbohydrates, and 10-20% of calories from fat. Supplementation with 4 g of oral branched-chain amino acids daily can increase albumin and protein synthesis and decrease risk for major adverse liver events.

The Royal Free Hospital Nutrition Prioritizing Tool (RFH-NPT)

The Royal Free Hospital Nutrition Prioritizing Tool (RFH-NPT) can be used to screen for malnutrition among patients with cirrhosis, classifying patients into low, moderate, and high nutritional risk. It should be assumed that any patient with a BMI under 18.5 and those with advanced decompensated cirrhosis (Child-Pugh C) have high risk of malnutrition.

Recommendations

Patients who have screened positive for frailty or sarcopenia and those at risk for malnutrition should receive a personalized “prescription” for intake that is tailored to their individual needs. This prescription should involve management of their underlying medical conditions, boosting macronutrient intake, consideration of micronutrient intake and treatment of other systems to maximize nutrition and improve muscle mass.

According to AASLD guidelines, patients should undergo multidisciplinary team management, ideally including the patient’s primary care provider, gastroenterologist/hepatologist, registered dietician, certified exercise physiologist/physical therapist, and health behavior specialist especially if they have progressive frailty or sarcopenia.

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