How genomic instability affects aging and what we can do to combat it
Our bodies are amazingly complex. At a cellular level, they complete billions of processes every second, mostly without us even noticing. However sometimes those processes go wrong, leading to diseases, degeneration, and signs of premature aging. One factor that plays an important role in how we age is genomic instability. But what is it, and how can it be prevented? Find out now.
What are genomes?
Our bodies are made up of trillions of cells — about 30 trillion according to scientists’ best estimates. That’s a number so big it’s almost beyond imagining. If we unraveled our bodies and stretched out each part, we’d have 25 feet of intestines, 100,000 miles of blood vessels, and 10 billion miles of DNA. That’s enough to travel to the edge of the solar system and back. And most amazingly of all, the DNA in each cell fits into just 6 microns of space.
Put simply, our bodies are more complicated than we can imagine, and DNA is about the most complicated part of all. DNA is the instruction manual for making our bodies. It contains all the code we’ll ever need to build the proteins, molecules, and acids that form each part of us. In humans, DNA is coiled into 23 structures called chromosomes. These are like filing systems that keep all the relevant parts of DNA together in small groups called genes. We have a gene for our hair color, another for our eye color, a third for our height, and so on. Our genes determine almost everything about how our bodies are made.
A genome is a complete set of genetic instructions, the sum total of all those genes and chromosomes and miles of DNA. The human genome contains 3.2 billion base pairs of DNA.
How genomes become unstable
Each genome contains an extraordinary amount of information. What’s most amazing, however, is that most of it isn’t used. “Junk” DNA, properly known as noncoding DNA, is all the information we’ve collected over our evolutionary history that we don’t really use. That actually forms the vast majority of our DNA — up to 98% of all the genetic information we carry.
Although noncoding DNA isn't directly useful to us, a lot of it is still “read” (“transcribed”) by our bodies. Some estimates, such as that conducted by ENCODE, the Encyclopedia of DNA Elements, suggests that as much as 80% of noncoding DNA gets transcribed. Sometimes this DNA is used to make components of the molecules our bodies need, such as transfer RNA, regulatory RNA, and ribosomal RNA.
Whether we use it or not, all our DNA is at risk of damage. Mistakes made during cell replication, mutations caused by oxidative stress, and age and environment-related stressors can all be harmful to DNA.
Think of DNA like an instruction manual for a very complicated computer (our bodies). However this manual contains instructions for all the things that came before that computer it’s written for — everything from the abacus to the microchip is written into this manual. Each part of the manual is split into its own sections (genes) so it’s easy to tell what instructions are relevant to working the computer.
When the DNA is damaged, it’s like taking that manual and mixing up all the pages. Trying to build a new computer from all the jumbled instructions is almost impossible, and mistakes are going to be made. That’s what happens to our bodies when our DNA gets damaged. The useful DNA and the noncoding DNA get mixed up, and our bodies start to produce dysfunctional cells.
What happens when we make dysfunctional cells?
Cell dysfunctions are super common in our bodies. We make about 10 million new cells every second, so even with a 99.999999999% success rate, there are going to be occasional mistakes. Our bodies have a system for dealing with these cells. This is called apoptosis, and it’s a form of controlled cell death that keeps us healthy by removing and replacing old or damaged cells.
Unfortunately, this failsafe isn’t perfect. Again, we’re dealing with numbers so big we can’t really comprehend them, so some mistakes are unavoidable. Most of the dysfunctional cells that escape apoptosis are senescent. That means they don’t replicate. Senescent cells can cause signs of premature aging by sending out signals to surrounding cells that make them enter senescence too. Once cells stop replicating in significant numbers, structures begin to break down and tissues stop being repaired. This causes visible signs of aging such as wrinkles, and is also associated with age-related degenerative diseases like Parkinson’s.
A very small number of dysfunctional cells don’t enter senescence but continue to replicate. Because they’re damaged to begin with, each replication can become more mutated than the last. Some mutations lead to the destruction of the cells, while others lead to unchecked growth — cancer. In fact, cancer is the best-known result of genomic instability, although it causes all kinds of other degenerative diseases.
What can we do to repair genomic damage?
Unfortunately, there is no medicine that can fix damaged DNA. The good news is, our bodies do a lot of repair work for us. Our immune systems are constantly taking out damaged cells and patching up DNA in others. However these natural repair mechanisms slow over time, and the damage to our DNA accumulates with age. That means that DNA mutations are ultimately unavoidable. Aging is a natural, inevitable process that we all have to go through — however much we wish that wasn’t true!
That doesn’t mean there’s nothing we can do about genomic instability. The best option available to us is to prevent the accumulation of damage that leads to unstable DNA. Some of this damage is unavoidable because it’s the result of bodily processes we can’t control, but a lot of it comes from our lifestyles and environment. Eating a healthy, balanced diet, and getting regular exercise is important to maintaining a healthy body.
DNA is particularly susceptible to damage from oxidative stress. This is a result of free radicals from pollution and tobacco smoke, and from reactive oxygen species (ROS). Our bodies create ROS when we metabolize greasy, fried foods, so avoiding these foods reduces oxidative damage. To combat other causes of oxidative stress, get lots of antioxidants in your diet. These are molecules that neutralize free radicals and prevent them from causing damage. You can find antioxidants in fruit, vegetables, nuts, black tea, and dark chocolate.
The final step you can take to support your DNA is to wear sunscreen and avoid harmful UV rays. UV light causes direct DNA damage by mutating thymine, one of the base substances of DNA. Even on cloudy days you should wear sunscreen in order to reduce your UV light exposure from sunlight.
Looking after our DNA is about taking care of our overall health. When we nourish our bodies, we improve cellular function and reduce the risk of genomic instability.