The actinic hypothesis generates more heat than lightIn a recent Current Comment published in Arthritis and Rheumatism (l), O'Brien and Regan review their concept of the pathogenesis of giant cell arteritis (GCA) and emphasize their commitment to the ''actinic hypothesis." This hypothesis proposes that the primary causative lesion in GCA is an alteration or degeneration of the elastic lamina of the temporal artery caused by solar radiation. O'Brien and Regan believe the degenerated elastin then triggers the development of the arteritis, and cannot understand why others do not share their enthusiasm for this idea.For many years elastic tissues of the aorta and its proximal branches have been thought to be somehow involved in the development of GCA (2). Various investigators have noted that the inflammatory reactions in positive biopsy specimens often appear more intense around the internal elastic lamina of the temporal artery (2-4). Multinucleated giant cells, which are characteristic of the disease, are often in direct