The amount of ethanol consumed by the rats was staggering in this experiment, beginning at 10g/kg and moving to 16g/kg as the rats developed a tolerance. Their blood alcohol levels were kept between BAC 0.15 and 0.35 for six weeks, 24 hours per day, via a tube implanted in their stomachs. The legal driving limit in the United States is BAC 0.08, so the rats were always between double the legal driven limit and death, which occurs around 0.40 in most humans.
Researchers found that rats that were fed ethanol for six weeks developed fatty liver, necrosis, and inflammation. They found that within two weeks of adding L-Arginine to the diet of fish oil ethanol (in continued massive amounts), liver function began to reverse itself--"Collagen deposition and pericellular fibrosis are markedly decreased."
If these findings were to translate reasonably to human beings, it would indicate that liver disease is not a function of alcohol consumption, per se, but is instead mediated by a failure to ingest adequate amounts of protein (L-Arginine is the most common protein in the American diet). We already suspect that the malnourishment and disease found in chronic alcoholics is in part caused by their tendency to replace nutritious foods with calories from alcohol, and this study leads us one step closer to that conclusion.
CLIFF NOTES: Eating a lot of protein, or supplementing with L-Arginine, will probably prevent or reverse alcohol-induced liver damage.
