Abdominal aortic aneurysms (AAAs) have traditionally been attributed t
o atherosclerosis, although there is increasing epidemiological, bioch
emical and genetic evidence that aneurysmal arterial disease is differ
ent from occlusive atherosclerosis. One of the most consistent biochem
ical findings in the aneurysmal aorta is a significant reduction in el
astin protein; the cause, for this remains unclear. There is in vitro
evidence that vitamin D-3 (1,25 dihydrocholecalciferol) inhibits the p
roduction of elastin by smooth muscle cells. On the basis of this obse
rvation and the possibility that some subjects may be exposed to exces
s vitamin D-3, the hypothesis that vitamin D-3 may be a previously un
recognized aetiological factor in the pathogenesis of AAA is developed
.