Chronic alcohol consumption has a biphasic effect on hepatic retinoid homeostasis, as is shown in this summary of our biphasic model describing alcohol’s effect on hepatic and extrahepatic retinoid homeostasis. The first phase is characterized by a relatively small but significant decline in hepatic retinoid stores, a relatively large increase in extrahepatic retinoid levels, and a transient increase in serum retinol, reflecting the mobilization of hepatic retinoid stores. The second phase, which commences with continued alcohol consumption, is characterized by a quantitatively large decline in hepatic retinoid stores reflecting CYP-mediated catabolism of retinoid within the liver, with no further mobilization to the extrahepatic tissues.