Irina Conboy's pithy description of what aging does to the operation of metabolism runs much as follows: "stem cells are sleeping, so damage is not regenerated. Instead you now make fibrous tissue, and deposit fat tissue to replace the damage. Then gradually over time, you just turn into this big scar and big fat blob." It is certainly the case that the older body seems to tend to hold on to lipids, create fat tissue, and put fats and other lipids into cells where they are usually not found in large amounts in youth. We might well ask why this happens. Is it the result of damage, some form of dysregulation of normal metabolism that is entirely harmful, or is it at least in part an evolved compensation that helps to attenuate some of the consequences of the underlying molecular damage that causes aging?

The authors of today's open access paper argue that both adaptive and maladaptive processes are in play. Nothing in biology is simple, and the observed redistribution of fat and changes in metabolism may be both harmful and protective when considered in various contexts, or when pieces of the whole are examined in isolation. That in later years it becomes challenging to maintain a good body weight, as the amount of work required to attain that goal ever increases, is no excuse for letting things slide, of course. While it may well be the case that some aspects of excess fat tissue are protective, the epidemiological evidence overwhelmingly demonstrates that, when taken as a whole, being even modestly overweight raises the risk of age-related disease, increases lifetime medical cost, increases mortality, and reduces life expectancy. Those negative effects scale up as the weight and excess fat tissue increase.

The Dual Role of the Pervasive "Fattish" Tissue Remodeling With Age