Rosacea is a chronic inflammatory condition of unknown etiology. Although individuals of all ethnic backgrounds can develop rosacea, it primarily affects patients of Irish, Scottish, Scandinavian, and English descent. The earliest pathophysiologic change is vascular instability, with flushing attributable to a heat-regulating reflex involving the countercurrent thermal exchange between the common carotid artery and the internal jugular vein; substance P and vasoactive peptides may also play a role. Recent linkages to increased amount and activity of cathelicidin and kallikrein 5 have also been suggested. Ultraviolet damage with microscopic evidence of dermal elastotic degeneration is noted in most patients. Demodex folliculorum and Demodex brevis mites have been found at higher concentrations in patients with rosacea, especially those with topical steroid-induced rosacea. Helicobacter pylori infection may contribute to rosacea, possibly through the release of vasoactive substances such as gastrin. Studies on H. pylori have prompted consideration of an association between rosacea and gastritis. A statistically significant incidence of migraine headaches accompanying rosacea has been reported, perhaps indicating a background of vascular reactivity.