“Stressed out” has only been pressure-tested as a concept for less than 100 years.
That sounds crazy, considering that all human advancements were designed to improve life.
Why would we have finally borrowed “stress” from the realm of physics to apply to human life in the 20th century? Why not in the 18th century? The 15th?
There are theories about that… But the consensus is that those who worked in the field of psychology in 1936 were at their wit’s end trying to describe what was happening to people all over.
The industrialization of life hadn’t freed us from labor. In fact, it had just created space for more labor — and different kinds than most people were used to. Urbanization, depression recovery, the rise of chronic illness…
Pick your favorite set of modern conditions and they probably culminated in the cultural revolution of stress referring to people — not bridges and other infrastructure.
Simply naming what was happening to people led to the rise of personal psychology, accessible therapy, and popularized professional introspection.
It also allowed us to study the effects that overwhelming stress has on us biologically. It’s how we were eventually able to learn about adrenal fatigue and overrun nervous systems.
And it’s how we figured out that it was aging us, via protective caps at the end of our chromosomal DNA called telomeres.
When those caps become damaged and shortened, we feel and look less youthful.
Let’s get into the weeds.
Telomeres from the Micro to the Macro
The concept of telomeres has been around since the 1930s…
But one woman — who has been studying them since the ’70s — shared a Nobel Prize for her discoveries in 2009. Elizabeth Blackburn, a molecular biologist, far advanced our understanding of cellular aging with her research.
And like much in the world of academia, that’s where her breakthroughs stayed… struggling to reach the masses.
What she found was that we actually have a fair bit of control over the way we age.
The key to managing our aging is not just protecting our telomeres from damage, but lengthening them as well.
Think about the aglets at the ends of your shoelaces that keep the string from fraying.
That’s what your telomeres do, effectively. They cap the end of DNA strands. Telomeres get shorter and more frayed when we live unhealthy lives with overwhelming stress.
The shorter those telomeres are, the less likely it is that DNA cells will divide and multiply.
If they cannot divide and multiply, they simply die. The presence of too many senescent cells — cells that cannot divide and instead grow old and expire — shortens the expanse between where you are now and where you’ll eventually end up.
If your genes carry encoding for heart disease, and there are too many senescent cells, you’ll experience heart disease sooner than you otherwise have to.
Essentially, it accelerates your descent into aging. It removes the barrier between where you are and where you will likely end up. It propels you into your aged future before you’re ready for it.
So the trick becomes focusing on lengthening telomeres…
But it’s not as simple as it sounds.
Proving Cause and Effect
The science of telomeres and aging is deeply complicated. While the burgeoning research presented by Blackburn and her co-author Elissa Epel is compelling and solid, many conclusions are still at the “presumptive association” stage rather than mainstream best practices.
Many of the risk factors that shorten telomeres are existing risk factors for other degenerative diseases, like smoking and eating empty calories for years.
There are a few salient points to keep in mind…
- Lifestyle changes are far more influential in protecting and lengthening telomeres than medicinal intervention.
- You’re not the same age throughout your body — lengthening your telomeres won’t change that.
- Aging is more than just telomeres. As cellular expert Judith Campisi says, “If all aging was due to telomeres, we would have solved the aging problem a long time ago.”
Scientists estimate that cells can replicate around 50 times before the telomeres become too short to do it anymore. (Important note: not everyone experiences telomere shortening — some people simply don’t. Additionally, stem cells, sperm cells, and white blood cells produce an enzyme called telomerase that automatically adds to telomere length after each replication.)
So what causes telomere shortening?
It’s the stuff we already know to avoid. We just have an even better reason now.
Smoking, drinking alcohol, leading a sedentary lifestyle void of movement, oxidative damage, a diet of processed and nutritionally empty foods, and stress are the biggest factors associated with shortening your telomeres.
We know that’s a paradox — in order to not stress about aging, you must first try not to be stressed — but at least we can quantify why excessive cortisol production contributes to the rapid acceleration of the aging process now!
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