Why We Age – Part I: The Evolution of Aging

Welcome to Part I in a Series on Human Aging

If you had to guess how you were going to die, you could narrow it down pretty quickly. It takes only a handful of diseases to account for over half of the deaths of Americans each year. Only five in fact – heart disease, cancer, stroke, Alzheimer’s disease, and diabetes. Though these disparate diseases affect different organ systems and develop as a result of different mechanisms, they all share a common underlying cause – the aging of the human body. It is aging that is the real killer here – aging kills more people on Earth than anything else. Maybe that’s obvious, maybe it’s not.



For a condition that kills so many, most of us don’t have the slightest understanding of how aging works or why it happens. This series will ask the deceptively simple question, “Why do we age?” To tackle this, we will break this question into three distinct parts: “Why do we age?”, “How do we age?”, and “Is it possible to live longer?” The first will explore aging from the perspective of evolution, the second will delve into the actual mechanisms within our bodies that cause us to age, and the third will discuss scientific research into lifespan extension. Stay with me.

If you think about it, nearly all things age. Your car. Wine. Cheese. The electronic device you’re reading this on. Aging is more than a fact of life. It’s a core feature of almost every complex system on Earth. At its most basic level, aging is no more than the accumulation of changes over time. In many cases, these changes manifest as various forms of damage that slowly build up and eventually lead to the demise of the system in question. Your car breaks down; your laptop’s hard drive fails; your life ends.

But, this is unsatisfying. If aging is just the accumulation of damage, why do some animals live 100 years and others 100 minutes? There has got to be more to it.

To begin answering this question, its helpful to understand how it has been answered over the course of scientific history. The first modern theory of aging was formalized in the wake of the publication of Darwin’s On the Origin of SpeciesThis theory, posited by August Weismann, proposed that we age as a part of a genetic program that causes the old to die out in order to leave more resources for the young. Though Weismann presented a good idea with a lot of intuitive appeal, the problem is that evolution doesn’t really work this way. Life does not “decide” to do something – rather, certain genes, arising from innate genetic variation in a population, render greater fitness to an organism, leading to the propagation of the gene. Re-framing the aging debate in this context was necessary for a more complete, and accurate understanding.

It was not until 60 years later that a better theory was proposed. Peter Medawar, a British biologist, hypothesized that the pressure of natural selection fades rapidly after an organism reaches sexual maturity. Genes only get propagated through reproduction, so after an organism is expected to reproduce, there isn’t much benefit in keeping it alive any longer. Basically, in a simplified sense, after we reach our prime reproductive age, evolution essentially gives up on us. We live as long as we do because our genes promote our growth and health up until reproduction, but after that they abandon us to the ravages of time. (Pretty selfish huh?) 

Medawar’s theory was further developed five years later by George Williams. At this time, biologists started identifying genes that were tied to the aging process and were surprised to find that they were shared among nearly all organisms. This got Williams thinking. What if the genes that make us weak in old age are actually the same genes that make us fit and strong in our youth? This theory became known as the antagonistic pleiotropy theory of aging (a mouthful I know). A generally accepted theory today, antagonistic pleiotropy means that in the fight to reproduce, our genes sacrifice longevity for virility. The beautiful thing is, this theory not only accounts for why we age, but it also provides an explanation for how these aging genes could arise in the population to begin with – they bestow us with greater fitness.

Now that we understand some of the most important ideas within aging theory, we can think a little deeper about a fundamental debate underlying the aging process: does aging result from a pre-programmed process or simply from the accumulation of damage over time? If you think about it, it is both really, and is fairly analogous to the Nature vs. Nurture debate. Our genetic program dictates our general lifespan by allocating resources between growth, repair, and reproduction, but damage accumulation ultimately leads to our demise. We live within a relatively narrow lifespan, which is based on our genetic program, but each individual’s unique genetic code and pattern of damage accumulation dictates his/her specific lifespan. 

So why do some species live for 100 years and others only minutes? Different traits are required of different organisms of different niches. Flies need only live long enough to lay a bunch of eggs as quickly as possible, while humans must live long enough to grow significantly before sexual maturity and also care for young for a long time after birth (see K vs R strategists). As a result, longer-lived species must possess genetic mechanisms for offsetting damage and promoting growth and survival for much longer periods of time. In shorter lived organisms, this selective pressure is not exerted, and as a result, these organisms devote significantly fewer resources to growth, repair, and maintenance, leading to shorter lifespan. Some common factors that promote a longer lifespan across organisms include increased reproductive success, low adult mortality (permitting more reproductive events per lifetime), and high juvenile mortality (making it necessary for adults to live longer so they can  compensate for such loss). 

Going deeper into this topic, interesting trends and patterns have been observed with regards to how long different species live. For one, the larger the organism, the longer it tends to live. This makes sense intuitively, bigger animals take longer to grow and reach maturity and thus should have longer lifespans.  On the other hand, animals with faster heart beats tend to have shorter lives. The thought here is that the basal metabolic rate of organisms with faster heart beats is higher, which leads to faster damage accumulation, and ultimately aging and death.

But what about organisms that don’t seem to age at all? A few select organisms exhibit what has been termed “negligible senescence” – they don’t age. These animals can reproduce indefinitely and have an equal chance of dying at every point in their lives. Some examples include tortoises and the sturgeon fish. In fact, some creatures, like the “immortal jellyfish” can actually age in reverse! These jellies astonishingly regress to a larval state and regrow into adults multiple times.

So how do these strange organisms fight off aging? What are telomeres? Why do so many food companies market antioxidants? Do they work? Can I live forever? All this next week.

9 thoughts on “Why We Age – Part I: The Evolution of Aging

  1. Pingback: 1p – Why We Age | Exploding Ads

  2. I don’t think antioxidants that are marketed work. I mean, just because a product has antioxidants does not mean it is absorbed and used by the body. Like with many vitamin supplements…


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