I was just seeing a patient in liver transplant clinic today with end stage liver disease secondary to fatty liver disease leading to Non Alcoholic Steatohepatitis (NASH) and cirrhosis. She was miffed with her primary care physician because he had told her to limit her dietary protein intake because of her cirrhosis and our Transplant Nutritionist just finished telling her that dietary protein is okay. All those missed opportunities for hamburgers and steak! I am sympathetic to both this patient and her physician.
Most medical students since the 1940s have been taught that hepatic encephalopathy (a state ranging from confusion to full on coma) can be exacerbated by eating protein rich foods. The theory is that the amino acids in protein contain nitrogenous compounds that can be converted into ammonia, which goes to the brain and causes encephalopathy. Normally, ammonia and other neurotoxins are filtered out by the liver. But when the liver is scarred down (cirrhotic) and otherwise not functioning well, the toxin containing blood from the intestines bypasses the liver via collateral circulation and directly enters the systemic vascular system. The brain does not like ammonia and other junk from the intestinal circulation and encephalopathy ensues. So no meat for the cirrhotic patient the dogma goes.
A study published by Cordoba, et al., in the July 2004 issue of Journal of Hepatology randomized 30 cirrhotics hospitalized because of encephalopathy and fed half of them a low protein diet and the other half a normal protein diet. Both groups had similar outcomes despite the different diets. Although both groups were found to have the same rate of protein synthesis in their bodies, those fed the low protein diet had a higher rate of protein breakdown. The implication being that low protein diets make the already malnourished states of the cirrhotic patients worse.
What made this paradigm shift possible is that these days we are very good at managing hepatic encephalopathy with two medicines: lactulose and rifaxamin. Lactulose is a liquid that causes one to have frequent bowel movements and thereby decreases that amount of bacteria in the colon that convert protein (or other nitrogen containing foods) to ammonia and other toxins. It also changes the pH in the intestines so that toxin formation is less efficient. There are probably other mechanisms afoot, but this is what we teach our medical students today. Rifaxamin is an oral antibiotic that is not absorbed into the circulation, so it stays in the intestines and kills toxin producing bacteria. Both medicines are reasonably well tolerated (well, lactulose makes you poop a lot, so too much can make you dehydrated, and rifaxamin is expensive) and they are very good at controlling encephalopathy.
So the current clinical thinking is to have cirrhotics eat well (including normal protein intake) to combat the muscle wasting and generalized malnutrition associated with end stage liver disease and manage the encephalopathy with effective medications. Tell your doctor, but be gentle: we know what we are taught and knowledge is always changing all around us!