Recently Mundy et al1 have indicated that some statins, 3-hydroxy-3-methylglutaryl coenzyme A (HMG Co-A) reductase inhibitors in particular, have a potent stimulatory effect on bone formation in vitro and in experimental animals, possibly through increased expression of the bone morphogenetic protein 2 (BMP2) gene. Since the dosages of the statins in the study were much larger than would be used clinically, the significance of their stimulatory action in bone formation remains to be elucidated in humans. We investigated the relationship between statin use and lumbar bone mineral density (BMD) in a total of 440 Japanese subjects with type 2 diabetes (214 men and 226 women; mean [SE] age, 61.7 [0.9] years). Lumbar BMD was measured with dual-energy x-ray absorptiometry (QDR-4500; Hologic Co, Waltham, Mass), as previously described.2,3 Statins were used in 131 subjects: pravastatin in 88.5%, simvastatin in 9.2%, and fluvastatin in 2.3%. Surprisingly, the mean (SE) BMD was significantly lower in subjects receiving statins than in those not receiving statins (0.884 [0.15] vs 0.965 [0.11] g/cm2, P<.001). Furthermore, there was a negative correlation between BMD and the total serum cholesterol level in type 2 diabetes (r = 0.254, P<.001).