Decades ago it was suggested that nutritional factors are important in
the development of alcoholic liver disease (ALD). However, several mo
dels of experimental alcoholism considered that the diets fed to anima
ls were nutritionally adequate, complete and balanced. Therefore, a co
ncept prevailed that the effects observed were due to alcohol per se a
nd that they occurred despite a nutritionally adequate status in the a
nimal. Examination of various models revealed that animals were malnou
rished because they ingested reduced levels of macro- and micronutrien
ts. Furthermore, they consumed only small amounts of carbohydrate and
a high level of unsaturated fat for long periods during the developmen
t of ALD. Alcoholic rats show many effects of inadequate nutritional s
tatus, such as a slow growth, depressed levels of liver glycogen and p
ancreatic amylase, enhanced protein degradation and circulating levels
of branched-chain amino acids, and increased levels of enzymes involv
ed in gluconeogenesis and alterations in the activities of enzymes rel
ated to the metabolism of carbohydrate as compared with controls. Chro
nic consumption of alcohol did not result in fatty liver, high blood a
lcohol concentration (BAG) or other observed effects when intake of en
ergy, carbohydrate and other nutrients was increased. Furthermore, pre
-existing effects of alcohol consumption, such as fatty liver, BAC and
delayed gastric emptying, were reversed in rats receiving increased e
nergy and carbohydrate intakes while continuing alcohol ingestion. Thu
s, nutritional status of the animal determines the production or preve
ntion of ALD or other effects that were considered to be due to alcoho
l alone.