changing stress from foe to friend (part 1)
the difference between acute and chronic stress and how to stop it from ruling your life
We generally refer to “stress” as any experience that challenges our ability to successfully cope with a situation. For the most part, we associate stress with strong feelings of anxiety, frustration, or burn-out - and there are an endless number of things that have the potential to act as a trigger for the onset of stress.
From day-to-day tasks of our personal lives like cooking, cleaning, looking after children, and going to work, to general lifestyle stressors such as financial worry, family issues, health concerns (lack of sleep), and the events happening in the world at any given time, there can be plenty of reasons to feel perpetually “stressed out.”
Many of us already know this well.
And while, individually, each one of the factors listed above might seem like no big deal, when the body becomes faced with many smaller, “acute” stressors over time, we can begin to develop chronic stress, and a slew of harmful health effects that go with it, as a result (1).
But to this we ask the question: what if there was another way to view stress? What if it was possible to change stress from foe to friend?
For years it has been the general understanding of both medical and psychological science that stress is harmful for our overall well-being and health. However, recent research suggests that there may be more to the idea of “helpful stress” than previously thought - and that sometimes all it takes is a simple switch in the way we manage it (2).
This article is part 1 in a series of 2 where we’ll be exploring just that. First, let’s talk about how we define stress.
understanding acute versus chronic stress
Acute stress is defined as having two main features:
- lasting only for a short duration of time
- a quick return to homeostasis (or calm), following the event.
Think of acute stress as something like being late for work; it can be extremely stressful in the moment, but as soon as you’ve arrived (and after finding out your boss isn’t mad), your reason for being stressed goes away and your body quickly reverts back to normal again. One way to imagine acute stress is to think of it as a bell curve.
Chronic stress, on the other hand, is characterised by the long-term, constant feeling of being stressed. This type of stress looks more like an elevated straight line and can last for months to years on end.
While occasionally chronic stress is the result of a single traumatic event, research suggests that it’s most common to develop chronic stress as a consequence of too many acute stressors building up over time (3).
This is thought to occur via three key conduits, conditions where acute stressors either:
- occur repeatedly
- are too slowly adapted to, or never overcome
- where a return to homeostasis following the event never occurs.
By considering acute and chronic stress as two different sides of the same coin, it becomes much easier to understand how they affect a variety of variables such as our emotional well-being, inflammatory response, and likelihood of developing disease, as well as how our bodies respond and react to them (4).
In this process, we can better uncover what shifts can be made in order to help change stress from a foe to a friend.
what happens to the body during stress
If there’s any one thing to remember about this section, it’s that our bodies have not changed much at all since the time our ancestors lived in caves.
What first emerged as a way for our ancient predecessors to assess risks to their survival such as coming face-to-face with a tiger or waging war with a neighboring tribe, still continues to control our physiological reaction to stress - just in a slightly different way.
Controlled by the sympathetic nervous system, we possess an evolutionary mechanism referred to as the “flight, fight, or freeze” response, that’s designed to perceive and put down on-coming threats.
But despite our social environment having changed so dramatically since the time we lived in caves, our flight, fight, or freeze response has not.
As a result, it’s not uncommon for us to experience the exact same physiological response as we would get when fighting a tiger, for much smaller, less threatening things like giving a presentation, going on a first date, or watching your work inbox pile up throughout the day.
Although these actions aren't typically real threats to our survival, our brain doesn’t quite know the difference and we can still experience them just as though they are.
This is what is looks like in the body:
First we experience a “threat” that triggers our stress response (and remember this can be something as minor as being stuck in traffic or receiving an angry text). Next a cascade of chemicals floods our system, increasing hormones such as cortisol and adrenaline within the bloodstream, and causing our blood pressure and heart rate to rise.
Our body redirects oxygen to our muscles, our breathing begins to speed up and we might even begin to break a sweat. Importantly, our parasympathetic nervous system switches off, we stop digesting our food, feeling sleepy, or thinking about things like romance or finding a mate.
In this sense, stress is not an experience “just in your head,” but a whole-body one where the sole focus is on fight, flight, or freeze, an evolutionary mechanism that’s designed to help us survive.
You can imagine that a person who chronically experiences high (or even low) levels of stress, would face consequences that manifest in a variety of ways.
Their blood pressure would stay high, their blood sugars would spike, their metabolisation would significantly change (it’s not uncommon for individuals with chronic stress to suffer from digestive issues and/or gain weight). They might develop anxiety or depression, would likely reduce the protection of their immune system against illness and disease, and would certainly miss out on a good night’s sleep - a lot.
Sleeping pills, anxiolytics, β-blockers, and antidepressants are all drugs that are used to counteract some of the problems associated with being stressed out - but they target only the symptoms of stress and not the source itself.
In this way, pharmaceuticals may be useful to some degree, but they have their own set of side effects and limitations because they work by taking over the natural function of the body, not necessarily the ability to help regulate and repair it (5).
Overall, it doesn’t seem like the body paints a very good picture of stress. Everything you read above largely screams, “avoid me” and “very bad!”
…but what about the times when stress can be used for good?
why stress doesn’t always have to be bad
Only very recently — within the last 10 years or so — did scientists realise that the experience of stress within the body doesn’t have to be bad. It’s a medical fact that there’s nothing inherently harmful about the physiological experience of acute stress, so long as it’s managed effectively, that is.
Click on to read part 2 of this article, and learn about one particularly ground-breaking study (and one body hack) that might change the way you view stress altogether.
Text References:
- (Smyth, J., Zawadzki, M., & Gerin, W. (2013). Stress and disease: A structural and functional analysis. Social and Personality Psychology Compass, 7(4), 217-227)
- McEwen B. S. (2006). Protective and damaging effects of stress mediators: central role of the brain. Dialogues in clinical neuroscience, 8(4), 367–381.
- Keller, A., Litzelman, K., Wisk, L. E., Maddox, T., Cheng, E. R., Creswell, P. D., & Witt, W. P. (2012). Does the perception that stress affects health matter? The association with health and mortality. Health psychology : official journal of the Division of Health Psychology, American Psychological Association, 31(5), 677–684)
- (Smyth, J., Zawadzki, M., & Gerin, W. (2013). Stress and disease: A structural and functional analysis. Social and Personality Psychology Compass, 7(4), 217-227)
- McEwen B. S. (2006). Protective and damaging effects of stress mediators: central role of the brain. Dialogues in clinical neuroscience, 8(4), 367–381.
