Jim Baen's Universe 1 Vol 1 Num 1: June 2006

COLUMNS Publisher's Podium

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Publisher's Podium

Written by Jim Baen



By Jim Baen

Note: The author would like to acknowledge the inestimable help received from conversations with Dr. John Lambshead, and for the enthusiastic support of Professor Eglund, whose analysis follows the article. There are probably several persons on the planet who will understand the analysis.

Many people have suggested that aging is a pre-programmed, genetically controlled function in higher animals. This appears to be confirmed by the research findings of Cynthia Kenyon, an eminently respectable scientist who publishes in peer-reviewed journals, on aging in nematodes. She reported extensions of nematode lifespan of five times normal, i.e. from around two weeks to ten, with their apparent vigour undiminished until shortly before death. In other words, they don’t just drag out old age but function properly for an extended period.

She accomplishes this by selectively blocking the expression of various “DAF” genes, including DAF-2 and DAF-16. DAF-2 suppresses the action of DAF-16, the latter triggers or suppresses at least six other genes the end result of which is to promote longevity. DAF-16 seems to influence the production of proteins that protect against free radical damage. So it could be said that DAF-2 has the function of deliberately limiting a nematode’s life span.

Of course, one has to be careful extrapolating from a nematode worm with a lifespan measured in weeks to something long lived like a human being. In nematodes, DAF-2 and DAF-16 are associated with moulting. Nematodes are Ecdysozoans (moulting animals) and these have the ability to go into a special ‘shut down’ state, known as ‘dauer larvae’ in the case of the Kenyon’s test animal, the nematode Caenorhabditis elegans.

Human beings neither moult nor go into a shut down mode (not even teenagers). However, the DAF-2 gene is similar to a gene in mammals called IGF-1 that is connected with insulin function. Martin Holzenberger created strains of mice in which one or both copies of the rodent gene for the IGF-1 receptor had mutations. Mice lacking any normal copies died as embryos. However, mice with one working copy developed normally and lived, on average, 26 percent longer than did animals with two normal copies of the IGF-1 receptor gene.

For the purposes of this article, let us assume that getting old and dying is a defined process, a process that is controlled by our genes; that our life span is deliberately limited. Why? This seems astonishingly counter-evolutionary. The two basic driving forces in evolution are (i) survival and (ii) success in mating (for sexual organisms). Surviving by definition implies extension of life span. However, it is also true that for many organisms that the longer an organism survives the more successful it will be at mating – even geeks will manage to reproduce if given enough chances.

So if our life span is deliberately limited by our genes then there must be some evolutionary advantage. The rest of this article will try and address this point.

One possibility is that we limit our lifespan by the need for optimal performance up to the time of successful reproduction. This is the racing car analogy. An engineer designing a Ford or a Peugeot tends to over-engineer to give reliability and a decent lifespan rather than optimise for performance. In contrast, the racing genius Colin Chapman used to examine his cars after a race and any component that was in too good a condition was promptly lightened. An ideal Chapman racing car would fall to pieces one inch after crossing the finish line – but in first place!

The racing car analogy does not really seem to explain Kenyon’s results because when DAF-2 is suppressed the worms stay younger longer; they do not stagger on in senility. It is almost as if the genes do not care how long a worm could live or what condition it might be in through most of that life but just decide it has lived long enough. What evolutionary mechanism could cause this?

In Utah, studies have been done that show that it is possible, in fact surprisingly easy, to track the presence of polygamous marriages by the occurrence of babies with birth defects. It turns out that having a few highly prolific males makes a surprisingly large impact on the occurrence of double recessives in the general population, and that this in turn leads to a surprisingly large number of birth-defects; children with Down’s Syndrome, cleft palate, club feet, various leukodystrophies and the like occur much more commonly than they would without the prior presence of these males. This observation is anecdotally common human experience. Inbreeding causes an increase in nasty recessive genes in the population and polygamy inevitably will increase inbreeding.

This is a common problem in conservation. Once a population of an organism drops below a certain level then the species is in terrible trouble. In theory, one could recreate a species from a single male and female. In practice, there are likely to be enormous genetic issues.

For human populations, inbreeding is likely to be especially dangerous for two reasons. The first is that the human genome is particularly messy compared to other mammals such as dogs or rats. The second reason is that reproductive success of males in human beings (who are highly social animals) tends to be correlated with status and status tends to increase with age. As the hypothetical TV interviewer put to the young blonde, ‘What first attracted you to this elderly, balding, multimillionaire, Miss Smith?’ The wealthy middle-aged man with a younger trophy wife is a phenomenon observed in all human society. A long life span in men is more of an issue because one high status man can impregnate many women. Reason one will tend to accentuate the impact of reason two.

So if a meta-population (a subgroup) of a species that has mutations that shorten its lifespan has offspring that are more successful than the offspring of a longer-lived meta-population then the former population will replace the latter. An evolutionary mechanism, therefore, exists that could promote death genes.

Just because this is logical and reasonable does not make it true, but I leave you with one final thought. Women commonly live longer than men and, in my model, it is long lived men that should be more dangerous to the species. If you are male, then nature could have it in for you.

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