Multi-level Selection and the Evolution of Aging, II
Last week we talked about a wrong turn taken by 20th Century evolutionary theory. Foundation for the theory was laid in the 1930s in a model put forward by a towering figure of statistical science, R. A. Fisher. Fisher’s model was based upon competition among individual genes distributed through members of a breeding population. He measured success of a gene by the number of copies of that gene in the population, and he equated Darwinian fitness with the rate at which that number would increase from generation to generation.
This is a narrow and one-sided interpretation of Darwin’s original theory, but it is regarded by most researchers in the field today as axiomatic. Though the “selfish gene” was introduced only thirty years later (by Richard Dawkins), this term perfectly describes Fisher’s model.
There is no provision for cooperation in this model. In fact, the ubiquitous webs of cooperation that we find in nature are paradoxical and mysterious for 20th-century evolutionary theory.
Fisher was influenced by two things that we might now regard as peripheral distractions, or worse. First, there were no computers in his day, and he was looking for equations that were simple enough to be solved by hand. Second, Fisher was a Social Darwinist and a eugenicist, and (perhaps subconsciously) he was creating a scientific system that would support his social beliefs.
Decades after Fisher, there was a worldwide community of evolutionary scientists who were trained and experienced in thinking within his framework, and skilled in solving equations involving the variable (gene frequency) that Fisher had deemed important. In the 1970s and 80s, the field of Evolutionary Ecology was established, mathematically acknowledging what Darwin had told us all along, that fitness is not an objective characteristic of an individual gene, but a function of the interaction between an organism and its ecosystem. As the etymology implies, it is about a “fit” between an individual’s traits and the ecological niche in which it lives. Fitness is relative, and evolutionary processes can only be properly understood in terms of a system of changing individual genes and changing ecosystems.
In the 1970s, the belief became established that ecological change was generally much slower than the change in gene frequency, so that the ecology might usefully be regarded as a fixed background in which gene frequency of a (constant) population could be followed and analyzed. This was a vindication of Fisher’s model.
Much more recently, ecosystems have been observed changing just as fast or faster than the organisms within them. But today it is still a minority of evolutionary theorists who believe that ecological change is not generally slower than genetic change, so that the two must properly be regarded as a system more complex and intractable than the one Fisher described. To them, the “selfish gene” is a narrow, incomplete way of looking at evolution, and describes only one piece of the story.
What has this to do with aging?
Within the “selfish gene” paradigm, aging is worse than useless to an individual. Aging always decreases fitness. It is inconceivable that there could be “aging genes”, evolved mechanisms of self-destruction on a fixed timetable.
“The way evolution works makes it impossible for us to possess genes that are specifically designed to cause physiological decline with age or to control how long we live.”
stated thus in a 2004 Scientific American article by Leonard Hayflick and Jay Olshansky.
But since 1990, many such genes have been discovered: genes that cause self-destruction, and genes that regulate the timetable of aging based on environmental cues. Indeed, such genes have been around since the Cambrian Explosion, and have been preserved by natural selection over a vast stretch of evolutionary history. Modern evolutionary science is in denial about the existence of such families of genes, and evidence for programmed aging has been dismissed piecemeal every time it pops up. Usually, some loophole is identified through which the phenomenon in question might have been evolved via a process of individual selection, consistent with the standard model. But when these stories are collected and considered together, a pattern emerges: there is broad, overwhelming evidence for programmed aging in the biosphere. I have collected and described some of this evidence in a recent book chapter For example:
The range of life spans in nature spans a factor of a million. Some of the same mechanisms of aging are involved on vastly different time scales. Bats live ten times longer than mice, while burning up a lot more energy and generating more free radicals. This says that the rate of aging is not controlled by (for example) the natural rate at which proteins become oxidized or sugars cross-linked, but rather that the repair mechanisms for these processes are shut down on a schedule that the body chooses.
Genes that regulate aging have been conserved for a billion years, since the dawn of eukaryotic life. All other known genes that have conserved on such a scale relate to core metabolic processes that are absolutely essential to life. It seems that natural selection has treated aging as a process absolutely essential to life.
Life span is extended not by helping the body along or shielding it from damage but by challenging the body. For example (to describe a familiar process in a provocative way), life span is shortened by having enough to eat. What could it be that the body is capable of doing to protect itself when it is half-starved, but not capable of doing when food energy is plentiful?
There are two ancient modes of programmed death at the cellular level, namely apoptosis and telomere shortening. These are the primary modes of aging in protozoans, and both these mechanisms seem to have been preserved and modified over time, so that they are both implicated in human aging today.
Why does it matter whether aging is programmed?
Our concept of what aging is and where it comes from has a profound effect on our approach to anti-aging medicine, and has influenced the course of research on diseases of old age such as cancer, atherosclerosis and Alzheimer’s as well.
If you believe that aging is a process of accumulated damage, then you want to help the body’s natural defenses. But if you believe in programmed aging, then you want to thwartthe body’s natural self-destruction – jam the signaling that controls self-destruction, or trick the body into a younger gene expression profile.
If you believe that evolution has already optimized the body for the longest possible life span, then improving on Mother Nature is going to be difficult indeed. Things that go wrong with age must be because evolution has tried and failed to find a solution, and it is up to us to engineer something that is cleverer and more effective than nature was able to find.
But if you believe that evolution has programmed the body to self-destruct on a time schedule, then you look for the clock that sets off the time bomb, you study the body’s signaling language to learn how the assault is triggered.
Here are some of the ways in which the body actively self-destructs. These are ripe targets for research that will not only lengthen life spans, but also lighten the burden of diseases of old age, lessen suffering, and relieve an overtaxed system of medical care.
Inflammation turns against healthy cells, destroying joints and arteries and brain cells, as well as increasing cancer risk.
The immune system shuts down over time, making us more vulnerable to infections and cancer.
Telomeres shorten with age, and the stem cells we need for healing and regrowth are fewer in number and less active.
Apoptosis – programmed cell death – destroys healthy tissue, especially muscles and neurons.
Re-channeling just a small portion of medical research funding into these areas holds the possibility for simultaneous and enormous benefits in many aspects of our health.
For basic information about healthy living for a long life,
see the author’s permanent page at AgingAdvice.org.
Aging is neither a process of accumulated damage, nor programmed. It is both. As natural evolution tends towards optimising survival (through increased fitness within a specific environmental niche) it becomes more economical to allocate resources to the survival of the germ line at the expense of somatic cells. Therefore, somatic cells accumulate damage which is not being repaired properly. This damage affects genetic function, apoptotic cascades, as well as down-regulates telomere function. It is futile to try and influence any of these processes, as the root of the problem is an imbalance in resource allocation, and not excessive damage or genes that cause the body to ‘self-destruct’ . The only solution is to reverse the rate of energy allocation (from germ-line back to somatic cells), through modulation of the rate of entropy loss. The processes are much more complex and sophisticated than generally believed.
“There is no provision for cooperation in this model.”
That’s completely wrong! The Selfish Gene (the book) talks extensively about how and why cooperation happens. Learn the basics of what you’re criticizing before you criticize it.