NUTRITION AND LIVER DISEASE
NUTRITION AND LIVER DISEASE
Many chronic liver diseases are associated with malnutrition. Patients with advanced cirrhosis are often malnourished, with wasting of the muscle mass and an emaciated appearance. People who are well nourished, but drink alcohol, are also susceptible to alcoholic liver disease. It is known that a dramatic loss of weight (35-40%) can be associated with liver disease of any type.
It is vitally important that patients with liver disease maintain a balanced diet, one which ensures adequate intake of carbohydrates, fats and proteins. Such a diet will reduce the risks associated with malnutrition and help prevent muscle loss.
Protein restrictions are rarely indicated since there are no major benefits of limiting protein intake and a low-protein diet has not been shown to improve liver function or reduce ammonia levels. In fact, a low-protein diet hastens muscle breakdown. Protein requirements should be assessed on an individual basis and adjusted according to tolerance and illness severity.
Patients with the end-stage liver disease should be referred to a nutritionist or dietitian for counseling.
When are specific diet restrictions required?
Beyond the maintenance of a good, well-balanced diet, several conditions that develop in the later stages of cirrhosis require specific dietary management.
Hepatic encephalopathy is a condition of impaired mental function due to altered liver function. It is often seen when severe scar tissue formation (cirrhosis) in the liver prevents the normal flow of blood through the liver. The blood which contains toxins is “shunted” or redirected, back to the central circulation and into the brain without first going through the liver for detoxification. Cirrhosis with portal hypertension (an elevation of the portal pressure due to the obstruction of blood flow through the liver) may be treated surgically by shunting some of the blood around the liver, connecting the portal system with the systematic circulation. This “shunted” blood contains high concentrations of amino acids and ammonia and probably other, as yet unidentified, toxic substances that may cause altered mental function in some patients.
The treatment for hepatic encephalopathy is aimed at reducing toxins like ammonia, which is a by-product of protein digestion. Only a very few patients with disabling encephalopathy who have not responded to lactulose or nemycin therapy, which helps rid the body of ammonia, may require a lower protein dose. Severe protein restriction (20 grams a day or less) is impractical for long term therapy and is not recommended.
ascites and edema
Ascites is the accumulation of fluid in the abdominal cavity. Edema is fluid built up in the tissues, usually the feet, legs or back. Both conditions result from abnormal accumulation of sodium associated with portal hypertension and liver disease. Usually only “no added salt” is recommended for patients with cirrhosis. However, sodium intake is often restricted for patients who develop decompensated cirrhosis with ascites. Such a diet would allow only 2-3 grams of sodium and would exclude canned meats, soups and vegetables, cold cut meats, condiments such as mayonnaise and ketchup, and some cheeses. Most fresh foods are low in sodium. The best salt substitute is lemon juice (which is salt free).
Cholestasis is an inability of the liver to excrete bile. This may result in steatorrhea (fat malabsorption due to inadequate amounts of bile). Steatorrhea may go unnoticed by the patient or can be associated with weight loss due to lost fat calories. Stools may be oily in appearance and foul smelling. Fat supplements are available; the most commonly used being medium-chain triglycerides (MCT oil). Safflower oil can also be used. These oils are more readily absorbed since they are not as dependent upon bile for their digestion. They are often used as a caloric supplement. MCT oil is used like any other cooking oil, in salad dressings or in cooking. Patients with steatorrhea may also have difficulty absorbing fat-soluble vitamins (A, D, E, and K). However, water-soluble vitamins are absorbed normally. Supplementing the diet with fat-soluble vitamins is possible, though it should only be carried out under the guidance of a physician.
In Wilson disease there is a defect in copper metabolism. Patients affected by this disorder have an abnormal build-up of copper in the body due to the inability of the liver to excrete it. This inability allows the copper to accumulate in several organs: first the liver and then, usually the brain and the cornea of the eye. Treatment involves the use of a de-coppering agent, penicillamine, which removes the excess copper from the body. Dietary therapy for this disease includes the avoidance of copper-containing foods like chocolate, nuts, shellfish and mushrooms.
Hemochromatosis is a disease in which there is an inappropriate absorption of iron from the intestine. The excessive iron then accumulates in the liver, pancreas and other organs in the body. Patients with this disease should not be given iron supplements. Aside from this precaution, those with hemochromatosis may follow a normal diet. Treatment is achieved by frequent removal of blood from a large vein.
Fatty liver is related to alcohol, obesity, starvation, some drugs and other factors. It is not caused by eating fat and it should be treated with a well-balanced diet or the removal of the responsible chemical substance or drug.
Finally, patients with liver disease should be wary of supplements to the diet, particularly fad foods or packaged “nutritional” aids. Such foods can contain a lot of salt, potassium or inappropriate protein mixtures. Those that are safe should be taken only under a physician’s guidance
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