Alcohol is one of the most common causes of all categories of liver disease – fatty infiltration, hepatitis, and cirrhosis. It is estimated that one of 12 chronic users of alcohol develops cirrhosis which, if the individual does not abstain from alcohol, can progress to end-stage hepatic failure. The development of alcoholic cirrhosis appears to be related to the duration of alcohol intake and the amount consumed daily. Research indicates that the mean duration of alcohol intake to produce cirrhosis is 10 years and the dose is estimated to be in excess of 160 g. of alcohol daily, e.g., 16 ounces of Scotch whiskey.
For many years it was thought that all forms of alcoholic liver disease were not caused by alcohol per se but by the inadequate diets consumed by many chronic alcoholics, and it has been common practice to advise individuals who drink appreciable amounts of alcohol daily to eat an adequate diet to avoid liver disease. However, recent research strongly suggests that alcohol is the causative agent. Through an experiment, scientists have concluded that adequate nutrient intake with the continued intake of excessive quantities of alcohol will not prevent the development of fatty livers, alcoholic hepatitis, or cirrhosis.
Alcohol And The Behavior
Concurrent with liver disease, the patient who is a chronic alcoholic is likely to exhibit severe malnutrition because he does not eat. Weight loss may not be marked because an individual can derive 1500 to 2500 calories a day from alcoholic beverages. With abstinence from alcohol, adequate energy and nutrient intake corrects the malnutrition of chronic alcoholism and, at the same time, supports the regenerative activity of the liver cells provided the disease process has not progressed to end-stage hepatic failure.
Diet Therapy For Liver Cirrhosis
ENERGY. All patients with liver disease require adequate energy intake. Without adequate energy supplied by carbohydrate and fat, amino acids from food and body cells will be daemonized in intermediary metabolism to contribute to energy needs through the gluconeogenic pathway. This will decrease the number of amino acids available for liver cell regeneration; and, in advanced cirrhosis, increase the amount of ammonia available for ureagenesis.
PROTEIN. Protein intolerance can develop acute hepatitis or advanced cirrhosis. The characteristic biochemical aberration is hyperammonemia caused by severe liver cell damage in acute hepatitis and by cell damage and portal blood shunting in advanced cirrhosis.
VITAMINS AND MINERALS. With the restriction of protein, and, if low protein wheat starch products are used as a major source of calories, it is strongly recommended that nutrient intake from food be supplemented with vitamin and mineral preparations including all the B vitamins, iron, and trace minerals.
ELECTROLYTES AND FLUIDS. Id ascites is present, sodium intake is restricted to 200 to 500 mg per day and fluid is restricted to the amount lost each day. The limited sodium and fluid intake may also be combined with some level of protein restriction.
FREQUENCY OF MEALS. The patient with advanced cirrhosis sold consumes frequent feedings. Also, the patient with severe ascites will need frequent small feedings because the fluid collection in his abdomen makes it impossible for him to eat large quantities of food at a meal.
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