Of the total body reserve of vitamin A, the liver is the major repository (greater than or equal to 90%); plasma contains only 1% of the total amount. Although the median liver concentration in well-nourished American adults is approximately 100 micrograms/g, a minimally adequate concentration is suggested to be 20 micrograms/g. Physiologic, nutritional, clinical, and genetic factors affect plasma retinol levels by a variety of mechanisms. Of total body carotenoids, most are associated with adipose tissue (greater than 80%), and a lesser amount is associated with liver (10%). Vitamin A concentrations in the liver are low at birth but then rise to adult levels at 1-4 years of age. Liver carotenoid concentrations are not proportional to liver vitamin A reserves. Total liver retinol is proportional to dietary retinol but not in a purely linear fashion. When liver reserves exceed 30 micrograms/g, the excretion of vitamin A metabolites in bile is much increased. Plasma vitamin A is homeostatically controlled over the physiologic range of liver vitamin A concentrations, e.g., 20-300 micrograms/g. Below 20 micrograms/g liver, plasma vitamin A values tend to fall; above 300 micrograms/g liver, plasma values tend to increase. At very high intakes, plasma vitamin A values can be greater than or equal to 300 micrograms/dl. In such cases most of the plasma vitamin A is in the form of retinyl ester. Thus, except in cases of deficiency or excess, vitamin A levels in the plasma are not good indicators of vitamin A status. Other methods of evaluating vitamin A status include relative dose response, analysis of liver autopsy or biopsy samples, isotope-dilution approach, and pseudoequilibrium approach. The first two of these methods have proven to be very useful in specific circumstances, whereas the others are under development.