What comes to mind when you think of "a 100-year-old human"? Someone bent over a cane,
knees clicking against each other, complaining of chronic back pain with their sagging, freckled
skin and a face adorned with glasses and dentures? Well, that may not be the case in the future.
You see, while we are more prone to disease and ill health the older we get, there are
ways we may be able to proactively prevent this. Scientists the world over are trying
to understand whether we can slow down ageing or even "reverse" it to live healthier and longer.
So, what’s the inside scoop on this ageing research? And more importantly,
will it be possible to celebrate your 180th birthday with a skip in your step?
To start with, we need to understand why we age in the first place.
Aside from the existential dread it may cause, ageing is a complex process
whereby there is a progressive loss of the body’s ability to maintain itself.
Your body runs on finely tuned chemical machinery, proteins, and the cell's instruction
manual— DNA. Like all machinery, proteins break, malfunction and accumulate errors
over time. Highly reactive chemicals called free radicals are produced by metabolism,
and through exposure to the environment, such as UV rays, they can damage proteins and DNA.
To prevent this, cells constantly maintain order and cleanliness. The cell’s maintenance mechanisms
repair damaged DNA, discard old proteins, and signal the cell to make new proteins.
Eventually, the cell becomes too damaged and cannot work anymore. The body makes
more cells to replace these old ones. However, cells have an internal limit—defined
by their DNA—on how many times they can divide, meaning that we can't keep creating new cells
forever. Over time, with fewer new cells to replace old ones and with the damage piling up,
it becomes difficult to maintain our youth. This is part of what leads to the physical
manifestations of old age, as well as some common diseases, such as cancer and diabetes.
So, logically, if we could have more young cells and maintain our existing cells better,
we wouldn't get as sick and broken down when we're older.
Stem cells, with the potential for nearly unlimited divisions, are only present in some
areas of the body, like the liver or the skin of a grown adult. If we had a never-ending supply of
stem cells, we'd ideally be able to keep making new cells, but implementing this has proven quite
a challenge. It’s difficult to genetically engineer cells into the stem cells we need,
and stem cells require a very specific environment inside the body, without which they die.
Another strategy that has improved longevity in mice consists of killing
off old cells that accumulate as we age. These old cells, called senescent cells,
release toxins into their surrounding environment that harm neighbouring cells.
But what some scientists think might be more promising than stem cells or
getting rid of our senescent cells is activating our maintenance task force.
How do we do that? By playing with the cell’s metabolism.
A cell is constantly balancing building ( anabolism), and breaking down ( catabolism).
This balance is maintained by signals the cell gets from its environment. These signals consist
of the presence and amount of hormones and other molecules, such as proteins,
ATP—the energy currency of the cell— and oxygen. Molecular antennae, which are mostly made of
proteins, constantly sense the levels of these molecules both in and out of the cell.
When the receptor senses a change in the nutrition and energy level of the cell, for example, it
tells the cell to change its metabolic strategy. This communication is done by a protein version of
the telephone game called a signalling pathway. Ageing research is finding that pathways that
promote glucose and fat break down, prevent the cell from growing more, and stimulate repair,
such as getting rid of all those free radicals, will help increase longevity.
Research is also revealing various drugs that can affect these pathways. A very common drug
used to treat diabetes, called metformin, was also found to increase longevity in mice. Another drug,
rapamycin, has been shown to increase lifespan in mice, and might even help treat cancer.
However, these drugs are still in an experimental stage. Metformin has been
found to alter about 745 proteins in the human body, so scientists still don’t know
the extent of the changes it causes in humans. It might be easier to follow age-old wisdom
for delaying the onset of age. Calorie restriction—a strategy where you limit
the amount of calories you take in and when—has shown longevity-boosting effects
in mice. Exercising regularly was also found to activate repair and anti-ageing processes.
Another important factor is limiting stress, especially when it is sustained for long periods,
as this can have very negative effects that can damage your cells.
Now, if you do all this, how long should you really expect to live? Well,
we don't actually know yet. Much of this research has been conducted on mice, and human trials are
still too small to give us any real indication. Scientists are also studying centenarians—people
who have lived for over a century— to see what habits and genes they might have in common.
According to all this, reaching the unbelievable age of 180 might not be possible… yet. A healthy
100 is far from uncommon, and perhaps we will push that to 130 years of healthy living,
but we'll only find out when we, and our research, ages a bit further.