Why do we age?

What is aging?

We all know what aging looks like in humans. Grey hair and wrinkles are the charming sides of getting old, but the fairy tale ends with that. In reality, with time, people deteriorate into frail beings, suffering from a series of diseases. Alzheimer’s, atherosclerosis, arthritis is just the beginning of the letter A. The full list is probably the size of a dictionary. The few “lucky” ones, who can claim they are healthy, still suffer from accelerated physical and cognitive decline, disability, and eventually death.

The book Evolutionary Biology of Aging from 1991 offered the following definition of aging: “A persistent reduction in the age-specific fitness components of an organism due to internal physiological deterioration.” We are born, we grow into developed adults, and then we take the steep slope to frailty and deterioration until we finally die. 

What most people think is the reason for aging?

The symptoms of aging are known to humanity for quite some time, but why is all of this happening? For millennia, humankind believed that this is just the way it is. “It’s in our nature,” “God made us this way,” “it’s just the way of life,” and so on. In fact, despite everything happening in the medical field, a lot of people for many generations to come will still believe those stories. Partly because of tradition, partly because of moral or religious beliefs, but not because of proved science. The research behind why we age started to unravel many secrets in the last decades, and this is only the beginning. We are yet to find our true genetic potential.

So, why are we aging?

Currently, David Sinclair’s Information Theory of Aging, inspired by the actual Information Theory initially proposed by Claude Shannon, is the best scientific explanation that we have. We will dive into the Information Theory and its biological offspring in a different article. For now, let’s keep it simple and focus on the big picture.

Let’s start with some definitions from biology. Our DNA is our genome. Every single one of our cells has the same DNA. The thing that differentiates a skin cell from a muscle cell, a nerve cell from a liver cell, and so on is the epigenome. The epigenome is the collective term for the control systems and cellular structures that operate the genome. Think of the epigenome as mechanics who use our DNA as a practical manual. With the progression of age, our epigenome starts making “mistakes.” Initially, they are small and unnoticeable. With time, our DNA is not that tightly packaged. The incorrect movement of the proteins disables or enables the wrong genes. The cell slowly deteriorates and loses its identity. After enough epigenetic “mistakes,” what is supposed to be a skin cell, transforms into a confused hybrid with an unclear purpose. “Mistakes” occur in all of our cells while we age. As a result, those groups of cells, which form tissues and organs, start losing their ability to perform the tasks that they were supposed to in the first place. With time your heart won’t be as efficient as it is now. Your liver won’t be processing as good as before. Your neurons won’t fire up as intensely as you were young. We slowly lose pieces of information, which makes the “mistakes” more and more apparent. The whole system frails until everything is so dysfunctional that your organs start to fail, and you die. 

Our DNA, operated by our epigenome, determines a significant part of what we are. If we translate this to computer science terms, the DNA will be the digital data, the source code, the instructions for the hardware, which enables it to do everything it does. The epigenome on the other side is the hardware, composed of resistors, capacitors, semiconductors, etc. Small problems with the physical components can be unnoticeable. In contrast, big ones can prevent it from even starting. But as long as the digital information stays intact, you can fix the problem, and you can have the same experience as before.

Another metaphor for aging from the book Lifespan, which we loved, is the comparison with digital compact disk (CD). The digital information (representing the DNA) is encoded on a layer of aluminum, placed on a transparent plastic disc (representing the epigenome). If you scratch the surface of the CD, you can have trouble reading it later on your device. The information on the CD, however, stays the same if the aluminum layer is intact. If you manage to polish the surface of the plastic disc and remove the scratches, you will be able to reread your disk as if nothing happened. However, if the damage also impacted the aluminum, parts of the data will be lost.

Why do we lose data?

David Sinclair explains this with DNA damage. Our cells have incredible survival circuits, which are triggered whenever DNA damage occurs. In normal conditions, our DNA has a gene that is silenced by a protein. Whenever DNA breaks, this protein moves from that gene and starts repairing the DNA. When the protein moves from the gene, the gene becomes active and prevents the cell from dividing. After all, if the cell divides while the DNA has damage, it will result in dysfunctional cells. After the protein has repaired the DNA damage, it returns to the same gene to silence it back again, so the cellular reproduction can continue. The above explanation is hugely simplified. In reality, we have several circuits like this one, some of them possibly correlated, but this is not important for this example. Now imagine that there is continuously some damage going on. The survival circuits are always active, and there is never-ending struggle to fix all of the harm that is happening. 

Excessive stress, in the genome and epigenome, is causing information loss in our cells. This loss of information is the reason behind cellular aging. Initially, those losses are insignificant, and they barely impact the function of the cell. Given enough time for the “mistakes” to accumulate, cells slowly lose their identity until they can no longer perform their tasks.

What causes DNA damage?

The list here is long and still incomplete. Radiation, toxins, and viruses are at the top, and they are capable of causing severe DNA damage, which can be irreparable. But what does that mean as a lifestyle? The sun is an obvious source of radiation, and human progress further added the x-ray, airport scanners, commercial flights, and a few more. You can find toxins in almost everything around you. A deadly concoction of toxins is present in tobacco, in the air of highly polluted cities and plastic. Every contact with those can and will give you irreparable DNA damage. Viruses are present everywhere around us, too, and despite that most of them are harmless to us, many of them can give you permanent DNA damage.

How can you protect yourself against DNA damage?

Unfortunately, it’s nearly impossible to avoid those threats. When your doctor says you need an x-ray, you most probably do, and not taking it may have an even worse impact on you, but you can do it only when necessary. You can skip a flight once in a while if it’s not essential. You can stop smoking and avoid places where people smoke. You can move to a less polluted city. You can (and you should) vaccinate. Minimizing the irreparable DNA damage can give you a few good years on top.

What more can you do?

With the metaphors, mentioned earlier we gave you a hint of what scientists are working on as we speak. Laboratories are researching ways to minimize loss of information and even restore the proper function of the epigenome (polishing the disk, repairing the hardware). Remember the survival circuits we discussed? Now that scientists identified some of those genes, we can think of ways to stimulate them. Giving our survival circuits an extra boost will enable them to perform better cellular repairs. This whole new area of biology is yet to give its best, but we already have a few discoveries that you can start using now. Continue reading our next article to understand how you can enable your body to tolerate more DNA damage and reduce the loss of information, which leads to aging.


To produce our articles, we use scientific documents and materials from acknowledged sources. By no means we want or can cover their entire content. We support the scientists who did the heavy lifting by buying their articles and books, as this is one of their few income sources. Scientific research is hard, and it barely has the support it deserves. If you want to help, read their books and publications.

  1. Aging, frailty and age-related diseases by T. Fulop, A. Larbi, J. M. Witkowski, J. McElhaney, M. Loeb, A. Mitnitski and G. Pawelec;
  2. What is Aging? by Michael R. Rose, Thomas Flatt, Joseph L. Graves, Lee F. Greer, Daniel E. Martinez, Margarida Matos, Laurence D. Mueller, Robert J. Shmookler Reis, and Parvin Shahrestani;
  3. Lifespan – Why We Age – And Why We Don’t Have To by David Sinclair and Matthew LaPlante;
  4. Telomeric DNA damage is irreparable and causes persistent DNA-damage-response activation by Marzia Fumagalli, Francesca Rossiello, Michela Clerici, Sara Barozzi, Davide Cittaro, Jessica M. Kaplunov, Gabriele Bucci, Miryana Dobreva, Valentina Matti, Christian M. Beausejour, Utz Herbig, Maria Pia Longhese and Fabrizio d’Adda di Fagagna;