It is somewhat paradoxical that we cannot perform experiments on the animal we are most interested in studing, ourselves. It is difficult enough to deal with the moral implications of experimenting on non-humans. I frequently remind myself that the study of other creatures mitigates the suffering of my own species and this sometimes seems a paltry justification. Humans are investiaged non-invasively, or further when such intrusion is neccessary for medical purposes, but we are still limited in our understanding by such restrictions, the following science included.
It will come as no suprise that there is quite a bit of research into the possibility of extending the length of time that a living thing spends alive. To date, the only effective means of doing so have been based in some way on the concept of Calorie Restriction(CR), see ref. 1 for a review. This simply means that an animal takes in fewer calories than normal while maintaining adequate levels of nutrients. The results are reasonably unequivocal, from nematoads to mammals, lifespan is increased by this method. As one can see from the graph above, increased caloric restriction is effective up to around 65% fewer calories being taken in, at which point it plateaus.
Some recent research, however, (ref. 2) has found a seemingly non-CR-intertwined mechanism that also has an effect on mammalian lifespan. The authors of this study bred mice which lack the gene which codes for adenylyl cyclase 5 (AC5). ACs in general play a key role in beta-adrenergic receptor (β-AR) signaling. In the interest of brevity, I will not delve into the molecular biology of cell-to-cell communications, howiver it is important to know that the blockade of this particular signalling pathway has recently been demonstrated to sucessfully treat mild-to-moderate chronic heart failure (ref. 3). The research into mice which lack the AC5 gene shows that their lifespan is ~30% longer, “are protected from reduced bone density and susceptibility to fractures of aging. Old AC5 KO mice are also protected from aging-induced cardiomyopathy, e.g., hypertrophy, apoptosis, fibrosis, and reduced cardiac function.” (ref. 1)
With both of these examples of extended lifespan, however, a question arises. What quality of life do these animals have? This is perhaps more relevant for the research on calorie restriction, but the animals studied can never report to us how they are feeling though the scientist involved always take pains to minimize any outward signs of discomfort. Until such techniques have been tried in human beings the complete effects of these therapies remains a bit of a quesion mark in my mind. That is not to say that I’m not amazed and optimistic about this direction of progress, I simply find it incredible that such simple things as eating less or disrupting a single gene could have universally positive effects.
- D.A. Sinclair (2005) Toward a unified theory of caloric restriction and longevity regulation, Mech. Ageing Dev. 126, 987–1002.
- Lin Yan, Dorothy E. Vatner, J. Patrick O’Connor, Andreas Ivessa, Hui Ge, Wei Chen, Shinichi Hirotani, Yoshihiro Ishikawa, Junichi Sadoshima, and Stephen F. Vatner (2007) Type 5 Adenylyl Cyclase Disruption Increases Longevity and Protects Against Stress, Cell 130, 247-258
- M.R. Bristow (2000) beta-adrenergic receptor blockade in chronic heart failure, Circulation 101, 558–569.