Previous studies have shown that plasma concentrations of HDL cholesterol decline with age, most likely as a result of hormone changes, inflammation, and metabolic dysfunction.  M. Walter, from Charite-Universitatsmedizin (Berlin, Germany), and colleagues suggest, however, that “beyond these effects specific aging processes may be involved.” Namely, the team posits that replicative aging, in which a cell’s capacity to divide is limited by its telomere length, may serve as a specific aging mechanism that may decrease HDL concentration and function.  Additionally, in acknowledging the age-related HDL decline, the team suggests that a HDL-lowering genetic variation may exist.   Applying these arguments, the researchers propose that  “HDL may modulate the aging process, not only by its well-known antiatherogenic effects, eg, its ability to remove cellular lipids and by antiatherogenic pleiotropic effects on cell survival, but possibly also by direct interfering with aging signaling or survival factor KLOTHO.”