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What is longevity?

The study of longevity is the study of the aging process. Aging can be studied in many different ways. Currently many scientists are interested in what happens at a cellular level to cause living things to age. You may have heard that antioxidants are good for you. These compounds repair oxygen damage that would otherwise cause more accelerated cellular aging. This is just one of the exciting pieces of the aging puzzle.  Another way to study aging is to look at it from an evolutionary point of view.

We are interested the maintenance of genetic variation for traits that should be under strong natural selection. Evolutionary theory predicts that the individuals that can live and reproduce the longest will out-compete others. It will be their offspring that make up the bulk of the next generation. Eventually, all individuals should evolved to be long-lived and reproductively successful to late age, but this is not seen in nature. Why not?

Does this mean evolutionary theory is wrong? 

No. Evolutionary theory says that aging is expected in organisms with separate soma and germ lines. Two different genetic models that predict aging are the Mutation Accumulation and Antagonistic Pleiotropy theories. Both theories are based in Neodarwinian evolution, and both are based on the fact that the strength of natural selection will decrease with age (reviewed by Charlesworth, 1994). 

The basis of the Mutation Accumulation (MA) theory is that since the strength of natural selection declines with age, a population can accumulate harmful genetic mutations that only have late-life effects. Once an individual has had the opportunity to reproduce, genetic ‘defects’ (mutations) that have harmful effects late in life will not affect that individual’s fitness. The net result is that there is little natural selection on those types of mutations, and they are successfully passed on to subsequent generations.

The Antagonistic Pleiotropy (AP) theory is similar in concept.  It also relies on the idea that the strength of natural selection decreases with age. Pleiotropy is a term that refers to one gene having more than one phenotypic effect.  In the case of antagonistic pleiotropy, the idea is that genes than have beneficial effects early in life may have some sort of deleterious late life effects. For example, a hormone expressed in large amounts during development might yield a larger, more fit individual, but might also cause disease at late ages. There is a lot of experimental evidence for both of these theories (for examples, see Hughes and Charlesworth 1994; or Chippendale et al. 1994). 

What is left to discover?

Recently, despite the evidence for them, both theories have been called into question. Common experience and data on humans and other organisms suggest than in a group of adult organisms of the same age, the mortality rate will increase over time. In fact, this decrease in survival (or other traits) is what we mean by aging.

Both the MA and AP theories are consistent with mortality rate increases early in adulthood, and this is indeed what is seen. However, data taken on C. elegans, D. melanogaster, H. sapiens, C. capitata and other organisms suggest that mortality rates plateau or even decline at late ages (Carey 1994, Curtsinger 1994, Brooks et al. 1994).  These findings caused some to suggest that perhaps organisms do not have finite life spans, or that perhaps existing evolutionary theories of aging are incorrect. If the mortality rates actually do decline at late ages, current evolutionary theory must be adjusted, refined, or replaced.

Goals

• Determine if mortality rates do indeed decline at late ages, and why.  Examine the roles that (1) behavior, (2) environment, (3) reproduction, and (4) genetics play in determining aging patterns.

• Find evidence for or against MA theory by looking for the existence of age-specific mutations.

Interested in Causes of Aging?

Neither the Hughes Laboratory nor the University of Illinois is responsible for the content on the web pages listed below. Here are some other aging-related web sites you might enjoy:

Literature Cited:

Brooks, A.; G.J. Lithgow; T.E. Johnson. 1994. Mortality rates in a genetically heterogeneous population of Caenorhabditis elegans. Science 263: 668-671.

Carey, J.; P. Liedo; D. Orozco; J. Vaupel. 1994. Slowing of mortality rates at older ages in large medfly cohorts. Science 258: 457-461.

Charlesworth, B. 1994. Evolution in age-structured populations, 2^nd ed. Cambridge University Press, New York.

Chippendale, A.K.; D.T. Hoang; P.M. Service; M.R. Rose. 1994. The evolution of development in Drosophila melanogaster selected for postponed senescence. Evolution 48: 1880-1889.

Curtsinger, J.W.; H.H. Fukui; D.R. Townsend; J.W. Vaupel. 1994. Demography of genotypes: failure of the limited life-span paradigm in Drosophila melanogaster.  Science 258: 461-463.

Hughes, K.A.; B. Charlesworth. 1994. A genetic analysis of senescence in Drosophila. Nature 367: 64-66.