Why do we age?
There have been many theories of aging over the centuries.
The ancient Greek, Galen of Pergamum, who served as official court physician to Roman Emperor Marcus Aurelius, believed aging was a loss of two of the four bodily “humors,” heat and moisture, over time.
More recently, Erasmus Darwin (grandfather of Charles) suggested a theory that aging was a loss of “irritability” and response to sensation in the tissues.
Since then all manner of different theories on why we age have been proposed and, spoiler alert, there is no agreement in the scientific community on which (if any) of these is true.
In fact, some scientists even question if such a thing as “aging” actually exists, or if it’s just a term we use to try and lump together several wildly different processes into a single, artificial category.
We briefly discussed the nine different hallmarks of aging in our very first article about the possibility of human life extension, and while there is pretty broad agreement in the scientific community that these are indicators of aging, there’s still no consensus on if they are the cause(s) of aging itself, or simply the visible result of the aging process.
Since we’ve just finished up our section of articles on how to measure and track your own body and are about to dive into the first section on actual longevity interventions next month (on diet—stay tuned!), we figured this was the perfect time to step back and examine the main theories of what aging is, because this can help us contextualize why certain longevity interventions may have the effects they do.
For instance, might rejuvenation from young blood infusions work by disrupting the programmed, pro-aging signals in the blood?
Or could caloric restriction extend life by slowing down the rate of oxidative damage caused by free radicals?
These are still open questions, but by thinking about them you can hopefully make better decisions about what, if any, longevity interventions to try, and you may be better able to understand your results as well.
Table of Contents
Why do we age?
As I mentioned there are as many theories of aging as there are scientists working on the problem, but most of them can be grouped into two broad categories:
- Damage accumulation theories
- Programmed aging theories
I used some basic criteria to select representative sample theories from each category to discuss below. These were:
- The theory still has current (within the last five years) peer-reviewed research in support of it (e.g. Galen of Pergamum’s humors theory is not included).
- The theory is actively being tested by current longevity research.
Theories of aging
The aging theories below are organized by category (damage accumulation vs. programmed), and then ordered by age of theory (older first).
Damage accumulation theories of aging
At their most basic level, damage accumulation theories of aging—sometimes also referred to as error theories of aging or “wear and tear” theories of aging—postulate that aging is the result of a slow build-up of damage in the body over time.
As we age, external and internal factors like cosmic radiation, infections by harmful bacteria and viruses, and even toxins like air pollution cause lots of little breaks and errors in the complex cellular machinery that keeps us alive and repairs our body. As these errors build up, they compound and cause more errors and damage, resulting in a cascading effect that leaves us weaker and more susceptible to diseases like cancer, Alzheimer’s, and infections.
1. The free radical theory of aging
Remember when antioxidants were all the rage and everyone was telling you to take antioxidant supplements to live longer?
That was all because of this theory.
Also referred to as the oxidative damage theory of aging (and occasionally the in the 1950s). While it was very popular 10-15 years ago, it has recently fallen out of favor with many scientists for a number of reasons.theory of aging), this theory is one of the older ones on this list (originally proposed
Free radicals (also referred to in this situation as “reactive oxygen species” (ROS)) are molecules with an unpaired electron that causes them to “steal” electrons from neighboring molecules. The free radical theory of aging proposes free radicals cause aging by damaging the function of the molecules they steal electrons from. This can cause a chain reaction as the molecules that had their electron stolen must now steal an electron from another nearby molecule.
Since many biological molecules are very specifically built, stealing an electron from them can cause them to not be able to function correctly. Eventually (goes the theory), this damage builds up over time and more and more parts of a cell become non-functioning, leading to eventual cell death or.
While initial experiments of this theory in mice models and fruit flies were promising, showing mice with lower levels of free radicals lived longer, and fruit flies exposed to more oxidative damage lived less long, recent research results have been more mixed.
For instance, in humans, several antioxidants like beta carotene, vitamin A, and vitamin E—far from preventing the damage caused by free radicals—may actually increase mortality, and lots of large studies have shown that antioxidants do not reduce age-related diseases like cancer or heart disease. More studies have shown that in some cases, increasing the numbers of free radicals in test animals actually increases longevity. Additionally, it’s now postulated that reactive oxygen species are important signaling molecules in the body.
So while the free radical theory of aging still has its adherents, it seems far from the dominant aging theory it was in the early 2000s.
2. The DNA damage theory of aging
Our DNA and genetics determine a whole heck of a lot about our health and longevity so it shouldn’t be surprising that they may also be responsible for how and why we age.
The DNA damage theory of aging, originally proposed in the 1960s, hypothesizes that as we age, the cellular repair machinery that usually fixes DNA strand breaks, cross-linkages, and transcription errors stops working as well as it used to. This means all these little bits of DNA damage—which are caused by everything from accidental copying errors, to radiation, to those free radicals we discussed above—slowly start to build up in your cells.
As this DNA damage gets worse in millions and billions of different cells in your body, many of them either die, stop functioning correctly, or turn into zombie senescent cells that send out harmful signals to their nearby healthy neighbors. The combined effect of all this is that as you age your body becomes less functional, weaker, and more susceptible to disease.
A well-known proponent of this theory is longevity expert Dr. Aubrey de Grey, who discusses a detailed version of the damage accumulation theory of aging in his longevity book from 2007, Ending Aging.
In the book, de Grey discusses what he sees as the seven crucial types of damage that cause aging:
- Extracellular aggregates (like the plaques that cause Alzheimer’s)
- Accumulation of senescent cells
- Extracellular matrix stiffening (crosslinks from sugar molecules that can lead to cardiovascular disease)
- Intracellular aggregates
- Mitochondrial DNA mutations
- DNA mutations that lead to cancerous cells
- Cell loss, tissue atrophy
Not all of these are directly caused by DNA damage, but it forms a large part of the reason behind some of the most destructive results of aging.
The DNA damage theory of aging also has quite a bit of research backing it up, including studies showing that centenarians have higher levels of DNA repair enzymes in their bodies and that mice with mutations that don’t allow them to repair DNA damage very well tend to age faster. Additionally, certain premature aging diseases in humans, called progeria, are caused by DNA defects and result in people who are chronologically young suffering from many of the symptoms of old age, including wrinkles, cardiovascular disease, and bone strength issues.
That said, some conflicting evidence in mice, namely that mutated mice without certain DNA repair genes didn’t age any faster than controls, suggests that maybe it’s only specific types of DNA damage that matter for aging.
3. The information theory of aging
Also known as the epigenetic theory of aging, this is a fairly new theory, proposed by prominent life-extension researchers like Harvard’s Dr. David Sinclair and Dr. Steve Horvath, the creator of the epigenetic clock for measuring biological age. You can think of it in some respects as a subset of the DNA damage theory of aging, but it’s distinct enough that I think it’s worth considering separately.
As I’m sure you’ll recall from our discussion of DNA and genetics previously, epigenetics refers to how DNA and genes are packaged around proteins called histones; wrapped around them like a garden hose on a reel. When DNA is wrapped up tight around a histone, that section doesn’t express its genes. It’s only when DNA is unwound that its genes are accessible and active. All this, plus some factors like molecules called methyl groups that attach to histones, is called your epigenome.
According to the information or epigenetic theory of aging, damage to your epigenome—how your DNA is packaged and expressed—causes aging. The epigenome determines what type of cell a cell is by expressing and suppressing specific genes. A skin cell will express certain genes but not others, while a heart cell will express and suppress entirely different genes.
However, as damage like toxins, radiation, and free radicals upsets the epigenome, cells start to “forget” what kind of cell they are. If this damage is not repaired, skin cells may start to act like heart cells and vice versa, leading to all sorts of problems and eventually to cell death or senescence.
What’s promising about this theory is that, unlike your DNA, which doesn’t really change throughout your life, your epigenome is constantly changing and is actually (relatively) easy to modify. All sorts of lifestyle habits, from smoking, to drinking, to exercise, to diet have been shown to influence and alter your epigenetics.
Dr. Sinclair likens DNA information to the data encoded on a DVD, whereas the epigenome is the clear plastic cover on top of that DVD. If the plastic cover gets scratched, the DVD will skip or become unreadable, but if you polish away the scratches on the cover you can watch the DVD again because all the encoded information is still there.
It’s a good metaphor, though I think I prefer my colleague Rachel’s:
“Your DNA can’t change—think of it like the script of King Lear. No matter which playhouse you might watch the drama, the lines all remain uniform. However, the director, the actors, the stagehands—your epigenetics, to continue the metaphor—might change. If you eat poorly and exercise irregularly, your DNA’s performance might seem more akin to a high school production than a masterpiece produced by London’s Royal Shakespeare Company.”
There’s some recent research (especially using Horvath’s epigenetic clocks) correlating epigenetic damage and changes with susceptibility to age-related diseases as well as just increased mortality risk, and cellular senescence, but with as new as this theory is there’s still a lot of research and work to be done.
Programmed theories of aging
As opposed to damage accumulation theories of aging, programmed theories of aging hold that aging is a process that is programmed by the body, or by evolution, to purposefully shut down repair mechanisms and allow the body to age and decay and eventually die.
While there are several different programmed theories of aging, they differ mainly in the mechanisms of how the “program” is “run” in the body, e.g. gene expression vs. hormone signals etc., not in the reasoning for why the program exists in the first place, so I’ve only included one programmed theory below that I think is representative of the other theories as a whole.
4. The group selection theory of aging
If aging is a central program that the body runs on purpose, the biggest question we need to answer is: why?
According to Darwinian theory, evolution should select for traits that allow an individual to survive long enough to reproduce and pass on their genes. So why would it instead select for a biological program that makes the individual weaker and more susceptible to disease and death over time?
The group selection theory of aging answers that question by removing the evolutionary focus from the individual, to the group.
Essentially this theory (sometimes also called the kin selection theory of aging) argues that group survival is more important for passing on genetics over time, and so one of the reasons aging may have evolved is that it is beneficial for the group even if it is harmful to the individual.
Longevity influencer Josh Mitteldorf holds this view, and it is the subject of his 2016 book, Cracking the Aging Code.
“[T]hough aging is bad for the individual, it is important for the community. Aging creates opportunities for the young and thus it promotes population turnover for adaptive change. Another communal benefit of aging is the stabilization of populations. Aging levels the death rate so individuals don’t all die at once, as in famines and epidemics.”
Though it should be noted that belief in any programmed aging theory is still a minority view, there is some experimental evidence to back up this evolutionary aging theory.
For instance, the discovery of “longevity genes” in organisms like yeast as well as in humans that, when turned on, can slow down the aging process and even in some cases rejuvenate the aged organism, suggests there may be an evolutionary reason these genes get switched off as we age. The existence of what looks like a universal, evolutionarily conserved “biological clock” across multiple species, using a variation of Steve Horvath’s epigenetic, methylation-based clock, might also suggest there’s a central program that regulates aging at the organism level. And the finding that diluting blood in old mice with, essentially, a saline solution caused aging reversal and tissue rejuvenation suggests there may be pro-aging signaling molecules in the blood that “tell” all the other parts of the body to get old.
Additionally, both yeast and roundworms display biological processes which actively cause senescence and death, and recent computer modeling studies have suggested such processes could increase worm colony fitness as a whole. Some older research on bird and mammal death rates also provides support for the idea that aging may be an evolutionary tool to keep population death rates constant to prevent overpopulation that could lead to mass group die-off.
Critiques of the group selection theory of aging focus on the relative strengths of individual vs. group selection in evolution, arguing group selection is normally a much weaker force than individual selection.
Additionally, critics suggest there are alternative reasons that longevity genes might be “switched off” as we age, such as “antagonistic pleiotropy.” Pleiotropy is ancient Greek meaning “more ways” and here refers to the phenomenon of one gene influencing multiple, seemingly unrelated traits. The antagonistic pleiotropy theory of aging says that there’s a tradeoff to be made with some longevity genes that, while they may help us stay healthy when we’re young, actually have harmful effects over a long enough time frame, but that those harmful effects only happen after we’ve reproduced so evolution doesn’t select for mitigating them.
Other theories of aging?
I know I only covered a representative subset of theories on why we age here. There are several I didn’t include including the disposable soma theory, and the Hayflick limit and telomere shortening theories.
Are there others you think are worth covering or that have solid recent scientific evidence? Add them in the comments!
I’m the co-founder of Longevity Advice and have been passionate about radical life extension ever since I was a teenager. Formerly I was a content marketing director in the B2B software space. I’m also a sci-fi novelist, wargame rules writer, and enthusiast for cooking things in bacon fat. My sister once called me “King of the Nerds” and it’s a title I’ve been trying to live up to ever since.
Your question is wrong. You are asking a metaphysical question of “WHY” we age. That implies a purpose, which is a teleological issue. What this article describes are theories of mechanisms by which we age, or “HOW” we age. That’s a totally different issue. We will never know why we age. You would have to ask the “creator” why aging and death are planned for humans and other animals. We can study mechanisms, but why these mechanisms exist we will never know. And since there may be a purpose for aging, which is the why of aging, then we may not be able to circumvent that purpose. Perhaps there are many aging mechanisms, all working to achieve the purpose of individual death. If death is “meant” to happen, then perhaps there is nothing we can do about it. Stopping one mechanism of dying might just lead to other ways to die. If we are supposed to die, we may not be able to do anything about it. That’s the difference between “why” and “how”.
Hey Sydney, it may be a semantic issue. Often we use “why” to ask about the root or proximate cause of something. I.e. “Why did I get lung cancer? Because cigarettes cause harmful effects to my lungs” etc. A why in this case doesn’t require a purpose, just a mechanistic explanation.
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