Aging may be unavoidable, but the science behind it is something which is not yet fully understood, writes James Kelly
Ageing as a concept is so familiar to us that we hardly question it at all. Assuming life-long health and a little luck, we’re born, we grow and develop, we decline, and then we die. As it’s extremely impractical (read impossible) to be born fully-grown and ready for the world, a stage of growth and development is obviously necessary. Decline with age, senescence, is where it all gets confusing. The grand architect of life, evolution, saw fit that we should eventually perish. My question is: why?
Putting the idea of God’s will aside, historically, ageing was thought to be analogous to wear and tear. We were just worn down eventually, like a dull knife or a rusted gate. However, with greater scientific understanding this idea was eventually disregarded. Unlike the knife and the gate, we are not closed systems subjected to increasing entropy (disorder) by the laws of thermodynamics. We could develop, maintain and repair ourselves. Following even more scientific endeavour, evolution was discovered and formalized. Could knowledge of our origins elucidate the murky waters of ending? Possibly.
Before going any further, an understanding of evolution is necessary. Evolution is the process by which different kinds of living organisms have developed and diversified from earlier forms throughout the history of the Earth. It is important to remember that evolution is not a goal-driven process, but rather the result of the accumulation of random advantageous changes over generations. I only mention advantageous changes, as those that inferred no advantage or disadvantage usually resulted in the death of the organism, through being out-competed for resources. The development of organisms then, is the result of the acquisition of useful genes; genes being the replicable and transmittable units that give rise to physical traits.
The first to attempt to explain senescence, with reference to evolution, was August Weismann. The German evolutionary biologist, who was practically a contemporary of Darwin (being only twenty-five years his junior), theorised that decline and death were necessary in order to support the population, i.e. the old decline and die to make room for the young. While this theory has much appeal, offering a reason for senescence, it fails to explain how senescence as a trait could be required; how it would infer an advantage on the organisms containing ageing genes, allowing them to out-compete individuals lacking the ageing genes, and as such propagate. Weismann abandoned this theory before his death.
In the 1950’s, the next major theory of ageing was proposed by Peter Medawar. Known as ‘mutation accumulations’, the theory posited the idea that as nature is a highly competitive place and as almost all animals die before they attain old age, there would be no selective pressure for acquiring traits that combated senescence. Following from this, it was theorised that a number of semi-lethal and lethal genes may be responsible for senescence and the resulting death. As these genes only cause an adverse effect later in life, the organism would be able to reproduce and pass the genes on before they died from the effect. As such, these genes would not have been removed by natural selection. While this would remain an important concept in all subsequent theories of aging, Medawar’s theory overall is discredited (mostly due to its inability to explain the need for certain genes only in later life).
A few years after Medawar, George C. Williams proposed his theory of ageing, ‘Antagonistic Pleiotropy’. The main tenet of Williams’ theory was that genes with an advantageous function in early life later had a detrimental function, making their exploitation a trade-off. An example would be a gene that enhanced fertility in early life but may result in decline later on. This theory fits in with modern genetics in that there are genes that have different effects, even at different stages in life. However, when breeding experiments were carried out using fruit flies selected for long-life, it was observed that the flies produced not only lived longer, but were more fertile. The theory also falls down when we consider that there are certain genes whose only apparent effect is to cause senescence.
The final major theory posed was the Disposable Soma Theory, in which Thomas Kirkwood argued that ageing was the result of economising resources. He suggested that metabolism, reproduction and repair and maintenance competed with minimal resources, and that repair and maintenance lost. While this theory seems plausible, it’s contradicted by research carried out since the thirties. The well-established principal of caloric restriction states that organisms subject to reduced food intake (though not malnourishment) show slower ageing.
While each of the major theories offered were subsequently shown to be fundamentally flawed, they gave us greater insight into the ageing process and allowed scientists room to expand based on convergent research in the related field. No proper theory has been posited since Kirkwood’s, but the topic still gets eluded to often, resulting in a mesh of ideas presently afloat in the scientific sea. The prevailing opinion today is that some mechanism of non-programmed ageing is responsible for senescence, meaning that each individual’s ability to maintain and repair itself is what dictates the degree to which senescence affects it. Hopefully greater understanding in the areas of group selection and genomics will result in a complete theory of ageing.