NUTRITION IN LIVER DISEASES

Liver is regarded as the chemical factory of the body based on its involvement in the body’s
chemical reaction. The liver constitutes about 3% of the body’s weight. 27% of the body’s total
blood flow takes place in the liver.
Liver is one of the most important organs of the body, it secretes bile and take part in metabolic
processes. It manufactures many important substances. Digested amino acids are received, new
proteins are synthesized in the liver. Many metabolic processes of protein take place in the liver.
It also plays an important role in carbohydrate metabolism. Liver is the chief storehouse of
carbohydrate and it regulates the blood glucose level by converting excess sugar into glycogen.
Triglycerides and phospholipids are synthesized in the liver. Liver incorporates them into
lipoproteins for transport.
Liver has a prominent role in lipid metabolism. It converts absorbed fatty acids into circulating
phospholipids. It also synthesizes cholesterol and converts it into bile salts. Fats in the liver are
oxidized into energy. Again, protein, carbohydrate and fats are interconverted. Bile salt are
essential for fat digestion and liver detoxicates poisonous substances from the body. Conversion
of beta carotene into vitamin A and storage of vitamin A and D are other functions. Plasma
proteins are also synthesized by the liver. Worn out red blood cells are broken down and the liver
extracts useful substances. It also stores iron and copper. The intrinsic factor or the anti-anaemic
factor is produced by the liver. There is no other organ in our organ in our body which takes part
in so many vital functions. Thus, a healthy liver is essential for healthy living.
Deamination, transamination and gluconeogenesis related to protein and carbohydrate
metabolism takes place in the liver.
Disorder of liver are jaundice or hepatitis, hepatic percoma and coma, hepatic cirrhosis and fatty
liver.
Dietary deficiencies produce liver disorders like fatty liver and cirrhosis of the liver. Protein
deficiency, choline deficiency, cystine deficiency, methionine deficiency and B vitamin
deficiencies produce either fatty liver or necrosis of liver. Liver injury occurs due to alcoholism.
Acute hepatic damage and jaundice occur in malnourished alcoholic patients. Lipid metabolism
changes in alcoholics by enhancing fatty acid synthesis and decreasing its oxidation. Triglyceride
formation is stimulated by alcohol. Cirrhosis of liver occurs among chronic alcoholics.
Iron and copper for hemoglobin synthesis is stored in the liver. Disintegrated red blood cells
leave their iron content in the liver for reuse. Intermediary metabolism, synthesis of many new
substances, excretion of many end products of metabolism, toxic substances and drugs,
immunological substances, formation and storage of many nutrients are done by the liver. Thus,
a healthy liver is essential for healthy living.
Virus causes infection and it slowly damages the liver. Alcohol consumption reduces food intake
and develops deficiency of proteins, vitamins and minerals. In an alcoholic person, vitamins like
thiamine, vitamin B12, folic acid and ascorbic acids are not absorbed properly.
JAUNDICE
Jaundice is a symptom which denotes abnormal liver function due to diseases. In jaundice, the
skin and mucous membranes show a yellow pigmentation due to rise in the serum bilirubin.
Jaundice occurs from haemolysis of red blood cells as in yellow fever and pernicious anemia.
Obstruction in bile flow either through intra or extra hepatic obstruction results in jaundice. A
malignant growth, stones or inflammation of the mucous ducts produce obstructive hepatitis.
Hepatocellular jaundice results from damage to the parenchymal cells due to viral infection or
due to toxic origins such as poison or drugs.
VIRAL HEPATITS
Viral hepatitis is otherwise known as infectious hepatitis. This is the common cause of jaundice.
Through food or water, the virus enters the body. Anorexia, fever, headache, rapid weight loss,
loss of muscle tone and abdominal discomforts are the earlier symptoms. These develop into
jaundice. The symptoms may continue for 4-8weeks. If proper treatment is not given it leads to
permanent liver damage. Living in crowded areas and living on inadequate diet especially on low
protein diet and consumption of alcohol while ill, produce complications. Recovery is possible
even with restricted diet, rest and supplementation of deficient nutrients especially vitamins.
Prolonged convalescence results in relapse or fatal conditions because of liver cellular collapse.
Mortality due to jaundice occurs mainly among malnourished people because an already
damaged liver due to malnourishment is further affected by infection. Neglected hepatitis leads
to cirrhosis of the liver.
Viral hepatitis is caused by hepatitis A (HAV) and hepatitis B (HBV). HAV is transmitted
through faecal or oral route and HBV is transmitted through blood transfusion.
Dietary Management
Modification in dietary treatment depend on the liver damage. Since anorexia is an important
symptom, normal feeding is difficult at the initial stage. In hospitalized cases, intravenous
feeding with 10% glucose solution is recommended. As soon as there is improvement in the
appetite, simple foods of high nutritional quality should be given.
The objective of the dietary treatment is to avoid further injury and strain to the liver and provide
nutrients for regeneration of liver tissues. A high protein, high carbohydrate, moderate fat diet is
recommended. Small feeds of attractive meals at regular intervals are suggested.
In nasogastric feeding stage, about 1,000kcals are supplied for a person weighing 60kg. In severe
cases, 1,600-2,000kcals are suggested. Once convalescence stage is reached 45kcals/kg body
weight helps to regain normalcy.
Protein requirement varies according to severity of the disease. With severe jaundice, an intake
of 40g protein and in mild jaundice 60-80g of protein is permitted. If hepatic coma or percoma
accompanies it, then protein -containing foods are not given as the liver metabolizes the end
products of intestinal protein. Cereal proteins ate better suggested during this condition.
An average consumption of fat along with normal protein intake is recommended. In hepatic
percoma and in coma, hepatic cellular failure takes place. Liver cells are not able to metabolize
fats, therefore fat is restricted in such cases. In severe jaundice, 30g of fat is permitted and 50-
60g of fat in moderate jaundice.
High carbohydrate content in the diet is essential to supply enough calories so that tissue proteins
are not broken down for energy purpose. For 1,600kcals, a diet of 300-340g carbohydrate is
recommended.
Vitamins are essential to regenerate liver cells, 500mg of vitamin C, 10mg of vitamin K and
supplements of B complex vitamins are essential to meet daily needs. However, if anorexia and
vomiting after consumption of these supplements are present, intravenous administration should
be adopted.
Mineral deficiency occurs if normal food consumption is not possible. Normal serum level of
sodium and potassium must be maintained through supplement use.
Foods allowed: Foods allowed in viral hepatitis are cereal porridges, bread, rice, millet
preparations, milk preferably skimmed milk, soups from tender vegetables, roots like tapioca,
potato, yam, fruits and fruit juices, biscuits, sugar, custard and light non-stimulating beverages
etc.
Foods avoided: Foods to be avoided in the diet of a hepatitis patient are pulses, beans, meat,
fish, chicken, eggs, baked products, dried fruits, nuts, spices, alcoholic beverages, fried foods,
cooking fats, whole milk, sardines, fried fish or fish rich in fat. Liberal intake of water is
allowed.
The patient needs bed rest but slightly movement in the room to improve the appetite. In
moderate jaundice, pulses or beans, meat, fish or chicken and eggs are allowed. Though fried
foods are restricted but cooking fat is permitted. Dried fruits, fruit juices, water or other
beverages except alcoholic beverages are allowed.
Hepatitis in infancy and childhood is not complicated if the therapeutic dietary pattern is strictly
observed. But hepatitis in pregnancy especially in the second and third trimester is harmful to
both the mother and the unborn child.
HEPATIC PERCOMA AND COMA
Complications of viral or acute alcoholic hepatitis, accidental damage to the hepatic artery,
anaesthetic agents and certain drugs, encephalopathy or surgery of the liver produce hepatic
coma or percoma.
Common symptoms of these disorders are confusion, disordered consciousness, tremor of the
outstretched hands, psychosis, apathy and personality changes. Gradually, these symptoms may
lead to death.
The exact cause is that the liver is incapable of detoxicating ammonia from bacterial
decomposition of protein foods. In a healthy person’s body, the liver converts ammonia into urea
and excretes it through kidneys. In liver disorders or in hepatic surgery, nitrogenous materials
especially ammonia get into systemic circulation and reach the central nervous system. The
blood ammonium ion level is increased in coma. Along with ammonia, indoles and phenols are
also not detoxicated from the body by the damaged liver. There are many toxic products of
metabolism in minute quantities which are detoxicated by a healthy liver. All these are
accumulated in the body in the coma stage. Again, urine is not eliminated properly which affects
the concentration of waste products in the urine and blood. Electrolyte balance is also upset.
Dietary Management
For a coma patient, 1,000kcal are recommended. A low protein diet is prescribed. The
endogenous breakdown of protein can be minimized by a carbohydrate diet. An improvement in
coma suggests 30-40g protein/day. In acute coma, protein in the diet is withheld. As fats are not
metabolized, they are not given for a coma patient. Carbohydrate rich foods are included
liberally to prevent endogenous breakdown of protein. Glucose is recommended as it is easy to
assimilate. Vitamin and mineral supplementation is essential. Fruit juices, vegetable soups
without seasoning may be fed to coma patient. In most cases, nasogastric feeding is carried out
which consist of 1000ml orange juice, 200g Glucose and 1000ml water.
Sample Menu for Hepatic Coma
Time Meal Menu
6:00am ----- Apple juice

8:00am Breakfast Oats porridge

10:00am Mid-time Lemon juice

12:00pm Lunch Cornflakes or rice gruel

2:00pm Mid-time Orange juice

4:00pm Tea Tomato juice

6:00pm Mid-time Coconut water

8:00pm Dinner Vegetable soup

9:00pm ------ Watermelon juice

10:00pm Bedtime Skimmed milk

CIRRHOSIS OF LIVER
Cirrhosis is a common disease of liver which usually affects alcoholics. Previous occurrence of
hepatitis also causes cirrhosis of liver. Undernutrition causes necrosis of liver cells and fatty
liver. Fatty liver produces cirrhosis of liver. Toxins of foods like aflatoxins also cause cirrhosis.
Injury and degeneration of liver reach its final stage as cirrhosis. Drug or chemical poisoning,
HBV, metabolic disorders and cystic fibrosis or biliary obstruction causes cirrhosis.
In cirrhosis, normal liver tissue is slowly destroyed and fibrous connective tissues develop
nodules which impair liver functions. In cirrhosis of liver, parenchyma is destroyed and it is
replaced by fibrous tissues. Gradually all active parenchymal tissues are destroyed and liver
function is seriously affected. Morphological changes occur and the liver is contracted and
irregularly distorted. In advanced cirrhosis, complications arise and one of the common
complications is retention of water in the tissues due to hypoalbuminemia. Synthesis of albumin
by liver is reduced in cirrhosis which leads to reduced osmotic pressure of the plasma. Due to
high portal pressure, fluid is accumulated in the abdominal cavity and ascites occur.
There are three (3) types of cirrhosis
1. Diffuse hepatic fibrosis which is also known as alcoholic cirrhosis or portal or Laennec’s
cirrhosis.
2. Post-necrotic scarring in liver
3. Biliary cirrhosis which occurs due to obstruction, infections or toxin.
Wasting of tissues, low serum albumin, oedema, ascites and retention of sodium are some of the
symptoms. Portal hypertension and lymphatic obstruction cause oedema. In infantile biliary
cirrhosis, diminished appetite, flatulence, liver enlargement and jaundice occur first. In later
stages, oedema and ascites occur.
Symptoms: Gastro-intestinal disturbances such as anorexia, nausea, vomiting, pain and
distension of abdomen.
Dietary Management
A high calorie, high protein, high carbohydrate, low fat diet with vitamins and mineral
supplementation is recommended for cirrhosis patients. Calorie content of the diet for a cirrhosis
patient is 2000-2500kcal. Consumption of food is difficult because of anorexia and ascites. But
the patient requires highly nutritious foods because of prolonged undernourishment.
A high protein diet helps regeneration of the liver cells. Depending on the symptoms of the
disease and malnourishment of the patient quality and quantity of protein is decided. Milk
protein concentration with low fat and vegetable protein sources are better. The protein content
of the diet varies according to the symptoms. If hepatic coma accompanies, protein is restricted.
Otherwise a high protein diet of about 2g of protein per kg of body weight is advisable.
Fat is restricted in cirrhosis of liver but 0.5g-1g per kg of the body weight is harmless if enough
protein is included in the diet.
Carbohydrate should provide more than 60% of the total calories so that liver damage is
minimized. Sodium is restricted in oedema and ascites. If there are no ascites very little salt is
permitted. Potassium salt is administered for ascites and oedema to prevent hypokalemia.
Anemia is common among cirrhosis patients. So, iron supplementation is essential. Vitamin
supplementation especially of B vitamins is required to prevent anemia. Choline and methionine
are useful if fatty infiltration is present.
Foods included in cirrhosis diet are cereals in any soft form, pulses, beans, meat, fish and
chicken, soft cooked eggs, vegetables, cooked or pureed fruits, fruit juices and light beverages.
Cooking salt is not added. A smooth or liquid diet is suggested if there is difficulty in swallowing
food. Fried items, rich desserts, strongly flavoured vegetables, nuts, milk, salad and seasoned
gravies should be avoided in a cirrhosis diet.

GALL BLADDER DISEASE

Gall bladder is situated in the middle of the liver to the right side. Bile ducts collect the bile and
store it in the gall bladder. In liver disorders, biliary ducts and gall bladder are also affected. Bile
helps the digestion and absorption of fats and fat-soluble vitamins and minerals, iron and
calcium. As and when bile is required the intestinal mucosa secretes a hormone -cholecystokinin.
Sphincter helps gall bladder to contract and release bile.
The formation of gall bladder stone or cholelithiasis is a common disease of the gall bladder.
Gallstones are mainly found in women. Obese women are more susceptible to this disease.
Gallstones slip into the common bile duct producing obstruction. Only then the patient feels the
pain and cramps.
Gall stones have to be treated as in the absence of bile, fat is not absorbed and is excreted in the
stools. It is white in colour. If the stone is big, surgery is the remedy. If small, then they can be
treated by using oral administration of bile acids.
Bile acid administration dissolves gall bladder stones. The gall bladder wall becomes red and
swollen and sometimes pus is formed. If the stone is untreated jaundice may occur.
A low-fat diet is prescribed for gall stones. Low-fat enteral formula diets are available.
Pasteurized egg white powders or egg white solids with sucrose or malt dextrin and sodium
caseinate and casein are used along with electrolytes.
Foods allowed are skimmed milk and products of skimmed milk, coffee, tea, fruit juices and
cocoa, cereals like rice, enriched bread, fried and sautéed vegetables.