Both gene array and protein expression studies found vitamin A metabolism altered in models of alopecia areata (AA). To test if dietary vitamin A alters the progression of AA we fed C3H/HeJ graft recipient mice purified AIN93M diets containing 0, 4, 12, or 28 IU vitamin A/g diet or chow starting two weeks before receiving a full thickness skin graft. Body weight, food intake and hair loss were measured weekly. Samples were collected 5, 10, 15, and 20 weeks post grafting. H&E slides were graded blinded (by JPS) for hair cycle stage, AA lesions, and severity (epidermal hyperplasia, granulocytes, lymphocytes, outer root sheath hyperplasia, and follicular dystrophy) on a four-point scale. AA lesions and infiltrating immune cells appeared 5 weeks after grafting in mice fed the recommended level of vitamin A (4IU/g), significantly sooner than mice fed either 0IU/g or chow. Mice fed 12IU/g had significantly more gross ventral hair loss than chow fed mice 12-15 and 18 weeks post graft and more than mice fed 0IU/g diet at 14 weeks post graft and significantly more epidermal hyperplasia than mice fed 0IU/g diet at 15 weeks. By 20 weeks after grafting AA was less severe in mice fed 12IU/g diet than those fed 0IU/g diet. This suggests that feeding no vitamin A in the diet, and relying only on liver stores, delays the onset of AA, but once it appears it is more severe. Feeding the recommended level of dietary vitamin A (4IU/g) resulted in AA sooner and the disease remained severe throughout the time course. AA progressed slowly in mice fed 3 times the recommended level (12IU/g), peaked at 15 weeks, then resulted in less severe disease by 20 weeks. Mice fed 7 times the recommended level (28IU/g) had moderate progression of disease and severity.