Week 5: Turning Back the Hands on our Biological Clocks

A simple way to consider the costs/ and benefits of death is in the study of the Brook trout.

Over time, the lifespan of the trout was quadrupled from 6 years to 24 years after the stressful ‘cost’ of sexual maturation was delayed. In class we discussed these cost/ benefit trade-offs and we learned that in many cases, longevity and number of offspring are inverses of one another. Death or senescence, in many ways, is as a by-product selection for alleles that enhance growth and reproduction early in life. There is an inherent trade-off between investing in reproduction and investing in body maintenance. Old age, (as stated by Medawar in Life Ascending) is the decline of genes that go on operating well after they should be. For humans, the elimination of infectious diseases as well as the removal of predation risks allowed us to double our lifespan. Modern-day approaches to death correspond closely to Medawar’s concept of late-acting genes.

Have we done this without any obvious penalties?

Longer lifespans are known to be associated with accumulation of free radicals and decreased telomere length. Are free radicals and shortened telomeres symptoms of old age or the causes of old age?

In Life Ascending, Nick Lane argues that “death is not only inevitable: it is controlled by the fates programmed into the very fabric of life” (261).

So, is there no way we can avoid aging?

I would argue there are ways in which we can change the route of our programmed paths. One example of this is one we have touched on in class which is caloric restriction. By reducing the amount of food consumed, the body undergoes less stress (as well as produces less free radicals) to convert food to energy. In some ways, caloric restriction allows us to trick the body back into youth. There are also genes that cause predispositions to certain diseases depending on how risky we are (i.e lifestyle, eating habits ect.). However,  the genomic level blind to certain diseases. For example, selection cannot purge harmful mutations that have deleterious effects later in life such as Alzheimer’s disease and Hamilton’s disease. Also, if it takes two copies of the gene to cause deleterious effects to the individual, the gene will not be purged. Current findings suggest that genetically-caused diseases are linked to biological old age rather than chronological time, meaning our biological age is not time-dependent, but rather damage-dependent. Therefore, there is some hope for us to alter the effects of some but not all disease-related genes.

More to Consider:

1. Is aging inherently untreatable? Are we only able to enact change on the symptoms of aging?

2. What unit(s) of selection caused the invention of “death”? On the level of the individual? On the level of the gene?

3. Also, for those of you who are reading Life Ascending, did you feel like he was purposefully leaving things out of the discussion on death? I noticed this chapter was lacking information on diminishing telomere length in cell replication, which is a key component of cell deterioration and ageing. I am not sure if this was implicit or not?