How nature, nurture & chance shape how we age

Published on May 31, 2016   49 min

Other Talks in the Series: Aging

0:00
Welcome to our lecture on How Nature, Nurture and Chance Shape How We Age. My name is George Martin. I am a Professor Emeritus at the University of Washington in Seattle, Washington, USA.
0:16
This slide provides a brief outline of the lecture. We will be dealing with three fundamental questions, why organisms age? Why various species age so differently? And, of special interest to our own species, why one observes such remarkable differences in patterns of aging among different members of the same species? As a pathologist, I have done many autopsies on geriatric subjects. I have never seen two individuals who have aged in exactly the same way, either qualitatively or quantitatively. All biology students fully appreciate that phenotypes result from both genes and environment, as well as their various interactions. But there is usually less interest in the issue of chance events, one reason why I will give that component a good deal of attention in this lecture.
1:15
Let's start with the question of why organisms age.
1:21
I shall be presenting what is often referred to as the classical evolutionary biological theory of why we age. It is important to first understand, however, that that theory is based upon what could be called age structured population of iteroparous organisms. By age structured, I mean that we are dealing with populations that consist of individuals of a wide range of ages. By iteroparous, I mean that these are populations that have multiple routes of reproduction during their adult lives. That scenario contrasts with groups of organisms that undergo what might be called semelparous, or big bang reproduction, namely single terminal episodes of reproduction, followed by death. This slide gives two such examples. On the left is a dying Spawning Salmon and on the right an Australian Marsupial Mouse. These mice only manage to reproduce in connection within a very short period of rainfall, an event that is essential for the growth of plants and thus sufficient food for progeny. When the season is right, males undergo a massive release of stress hormones while they fight for females, copulate and then die. One could use the term programmed aging for these two species and also for many flowering plants. Many of my colleagues, however, will argue that even iteroparous species like us undergo programmed aging. Many of them believe that aging is simply an extension of development. We should, of course, always welcome such alternative views, but one can make strong arguments against that proposition, which essentially states that aging is adaptive. That it is good for the species to have organisms die, as it preserves precious resources for the younger population. A famous late 19th century biologist, August Weismann published such views early in his career, but later changed his mind. Suffice it to say that the majority of geroscientists believed that aging is non-adaptive and that it cannot be explained by the type of determinative sequential adaptive alterations in gene expression that characterize development. This is not to say, however, that development is not an important determinant of health span and lifespan. I like to think of us as protein synthesizing factories. How well you build those factories and how well you design the quality controls will obviously make a big difference in how well these factories function, and how long they last.
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How nature, nurture & chance shape how we age

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