Last week we talked about a wrong turn taken by 20th Century evolutionary theory. \u00a0Foundation for the theory was laid in the 1930s in a model put forward by a towering figure of statistical science, R. A. Fisher. \u00a0Fisher\u2019s model was based upon competition among individual genes distributed through members of a breeding population. \u00a0He 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.<\/p>\n
This is a narrow and one-sided interpretation of Darwin\u2019s original theory, but it is regarded by most researchers in the field today as axiomatic. \u00a0Though the \u201cselfish gene\u201d was introduced only thirty years later (by Richard Dawkins<\/a>), this term perfectly describes Fisher\u2019s model.<\/p>\n There is no provision for cooperation in this model. \u00a0In fact, the ubiquitous webs of cooperation that we find in nature are paradoxical and mysterious for 20th-century evolutionary theory.<\/p>\n Fisher was influenced by two things that we might now regard as peripheral distractions, or worse. \u00a0First, there were no computers in his day, and he was looking for equations that were simple enough to be solved by hand. \u00a0Second, Fisher was a Social Darwinist and a eugenicist, and (perhaps subconsciously) he was creating a scientific system that would support his social beliefs.<\/p>\n 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. \u00a0In 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. \u00a0As the etymology implies, it is about a \u201cfit\u201d between an individual\u2019s traits and the ecological niche in which it lives. \u00a0Fitness is relative, and evolutionary processes can only be properly understood in terms of a system of changing individual genes and changing ecosystems.<\/p>\n 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. \u00a0This was a vindication of Fisher\u2019s model.<\/p>\n Much more recently, ecosystems have been observed changing<\/a> just as fast or faster than the organisms within them. \u00a0But 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 \u201cselfish gene\u201d is a narrow, incomplete way of looking at evolution, and describes only one piece of the story.<\/p>\n What has this to do with aging?<\/strong><\/p>\n Within the \u201cselfish gene\u201d paradigm, aging is worse than useless to an individual. \u00a0Aging always decreases fitness. \u00a0It is inconceivable that there could be \u201caging genes\u201d, evolved mechanisms of self-destruction on a fixed timetable.<\/p>\n \u201cThe 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.\u201d<\/p>\n<\/blockquote>\n stated thus in a 2004 Scientific American article<\/a> by Leonard Hayflick and Jay Olshansky.<\/p>\n 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. \u00a0Indeed, such genes have been around since the Cambrian Explosion, and have been preserved by natural selection over a vast stretch of evolutionary history. \u00a0Modern 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. \u00a0Usually, 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. \u00a0But when these stories are collected and considered together, a pattern emerges: there is broad, overwhelming evidence for programmed aging in the biosphere. \u00a0I have collected and described some of this evidence in a recent book chapter<\/a>\u00a0 For example:<\/p>\n The range of life spans in nature spans a factor of a million. \u00a0Some of the same mechanisms of aging are involved on vastly different time scales. \u00a0Bats live ten times longer than mice, while burning up a lot more energy and generating more free radicals. \u00a0This 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.<\/p>\n<\/li>\n Genes that regulate aging have been conserved for a billion years, since the dawn of eukaryotic life. \u00a0All other known genes that have conserved on such a scale relate to core metabolic processes that are absolutely essential to life. \u00a0It seems that natural selection has treated aging as a process absolutely essential to life.<\/p>\n<\/li>\n Life span is extended not by helping the body along or shielding it from damage but by challenging the body. \u00a0For example (to describe a familiar process in a provocative way), life span is shortened by having enough to eat. \u00a0What 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?<\/p>\n<\/li>\n There are two ancient modes of programmed death at the cellular level, namely apoptosis and telomere shortening. \u00a0These 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.<\/p>\n<\/li>\n<\/ul>\n Why does it matter whether aging is programmed?<\/strong><\/p>\n 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\u2019s as well.<\/p>\n If you believe that aging is a process of accumulated damage, then you want to help<\/span> the body\u2019s natural defenses. \u00a0But if you believe in programmed aging, then you want to thwart<\/span> the body\u2019s natural self-destruction – \u00a0jam the signaling that controls self-destruction, or trick the body into a younger gene expression profile.<\/p>\n 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. \u00a0Things 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.<\/p>\n 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\u2019s signaling language to learn how the assault is triggered.<\/p>\n Here are some of the ways in which the body actively self-destructs. \u00a0These 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.<\/p>\n Inflammation turns against healthy cells, destroying joints and arteries and brain cells, as well as increasing cancer risk.<\/p>\n<\/li>\n The immune system shuts down over time, making us more vulnerable to infections and cancer.<\/p>\n<\/li>\n Telomeres shorten with age, and the stem cells we need for healing and regrowth are fewer in number and less active.<\/p>\n<\/li>\n Apoptosis – programmed cell death – destroys healthy tissue, especially muscles and neurons.<\/p>\n<\/li>\n<\/ul>\n 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.<\/p>\n \u00a0For basic information about healthy living for a long life,\n
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\nsee the author\u2019s permanent page at\u00a0AgingAdvice.org<\/a>.<\/strong><\/p>\n","protected":false},"excerpt":{"rendered":"