Starting off the year back at the beginning.
Resharing one of the first pieces – A Quick(ish) Lesson About Stress – since a whole bunch of you are new here (and because I took the holiday weeks off and am still working on fresh things to share.)
When this piece first went up, the goal was to set the groundwork for everything to come — introduce “stress” as a word and a biological response to the outside world while having a landing spot for the “how I view stress” reference that I knew might come up quite a bit. A year of applying the stress lens to the topics examined and explored here has confirmed that prediction. I reference back to A Quick(ish) Lesson About Stress A LOT.
Two companion pieces that pair nicely with this one:
And a good example of how my definitions of “stress” trap me in the “why is this a stressor?” conundrum when tackling the stressor map:
If this topic is of interest and/or if you have questions, I am doing a free1 Zoom webinar on all of this plus how it plays into women’s health and the ongoing work on the Maternal Stress Project. Plenty of time for Q&A too.
Join me on January 29th 9:30amPT/12:30pmET/5:30pmGMT. I will also record it if you want to catch up later.
Ok, moving on… below is the reshare of A quick(ish) lesson on stress (with light editing from the original version) and if you prefer ‘reading’ through your earholes, find the audio here:
A quick(ish) lesson about stress
Let’s reset the way we use the word stress.
First, I need to acknowledge that the term has always been problematic. I’ll save a deep dive into the history of the term for a later post (with a dash of it below) but here’s a spoiler: the word stress was never a great choice.
When one of the fathers of the field, Hans Selye, first used the term ‘stress’ in the context of health, he came under fire for attempting to define a field of study that captured everything and nothing. One of Selye’s contemporaries snarkily remarked:
“Therefore, stress, in addition to being itself and the result of itself, is also the cause of itself.” — Dr. Ffrangcon Roberts
I mean…. He wasn’t wrong.
In an attempt to avoid the ambiguity of the word stress, stress researchers, myself included, tend to lean more on the terms ‘stressors’, ‘stress response’, ‘acute stress’ and ‘chronic stress’.
But these terms can also fall victim to ambiguity and circular logic:
Stressor = any internal and external stimuli that trigger a stress response
Stress response = the physiological and behavioral response to a stressor
Acute stress = when the response to a stressor is isolated or brief such that the physiological/behavioral changes associated with the response are considered beneficial for health and survival (also, what I refer to as the adaptive stress response)
Chronic stress = when the response to stressors is elevated, prolonged, or consistent in a way that the physiological/behavioral changes become detrimental for health and survival (I might refer to this as a maladaptive response)
Some of you may have heard (or personally use) the terms eustress and distress or even allostasis and allostatic load with the Allostatic Model as an alternative to redefine stress in an identifiable, quantifiable, actionable way. All have their own use cases and benefits and limitations. But, in the interest of avoiding that rabbit hole, I’ll bounce back to defining stress, starting with the stress response…
What is the stress response?
While I’m tempted to get deep into the weeds of the physiological cascades that stressors tip off and how all the systems in the body respond accordingly… in the interest of brevity (ha!), I’ll attempt to keep it simple.
Let’s start by considering the adaptive stress response. Put aside modern human stressors for a second and look at why the stress system exists in our brains and bodies to begin with: survival.
Say you magically transplant into the body of an ancient human relative cruising the savannah. You spot a lion in the bush ready to pounce.
Your brain interprets the situation – predator equals stressor – and cues an acute stress response.
At that moment, your brain triggers two key arms of the acute stress response. On a blink-and-you’ll-miss-it timescale, the fight-or-flight2 response activates the sympathetic nervous system to release catecholamines (adrenaline + noraderenaline). In the context of the lion, this response has everything you need to get up and go or stay and fight – increased blood flow to shuttle oxygen across your body, energy mobilization to feed your muscles. We all know the physical sensations that accompany that fast reaction – heart racing, palms sweating, mind focused. You have probably experienced the feeling when getting up to talk in front of a crowd, or when a car plows through a crosswalk you are about to walk into, or when jumping out of an airplane while skydiving (we, modern-day humans, relate to adrenaline in funny ways.)
The slower arm of the acute stress response3 operates via hormones called glucocorticoids. In humans, the main glucocorticoid is cortisol (so I may reference this as the cortisol response, which, I know, will annoy some stress folks who prefer more precise terms).
Cortisol might ring familiar given that this hormone often gets the credit and blame as THE stress hormone. Since cortisol release does not get directly triggered by the nervous system but needs a whole signal cascade – a hormone to trigger a hormone to trigger a hormone – it takes a lot longer for this arm of the stress response to have an effect. Stress-induced cortisol does not become measurable in the bloodstream until three minutes after encountering a stressor and concentrations in the blood will not peak until 15-30 minutes after that.
Cortisol release requires a game of biological telephone with a lot of stopover points4. When compared to the nearly instantaneous sympathetic nervous system response, the cortisol response is a slowpoke.
In the time it takes for cortisol to rise in your bloodstream, you have either successfully escaped the lion, fought off the lion, or been completely devoured. Which makes cortisol seem useless in this classic stressor context. However, it is not cortisol’s job to help you fight or flight.
Cortisol mops up the mess after the catecholamines wreak havoc on your system in the interest of immediate survival. Cortisol prepares the body for the next stressor. Cortisol gets you through your slow limp to safety and prepares you for when the lion decides to continue stalking. Cortisol acts in the interest of the body’s return to healthy balance and long-term survival and this is where cortisol connects with immune function, metabolism, the reproductive system, etc. Cortisol pauses unnecessary processes and behaviors, diverts resources, changes functional priorities in the interest of long-term survival.
Cortisol is an incredible hormone. And yet it is the favorite punching bag when it comes to general discussions of stress (and the target of far too many ‘wellness’ products), but, it’s important to remember that cortisol’s role in the stress response adapted to help us survive stressors5. It’s us, modern humans, that push the stress response system too far, and then push those widespread connections between cortisol and nearly every system in the body in ways that gets us into health-related trouble.
Did I lose you? I’ll break down all of this in the webinar!
When does acute stress become chronic stress?
Clearly, the person who jumps out of airplanes for fun is not putting their life at risk because of the resulting acute stress response. As Dr. Bruce McEwen, a preeminent stress researcher once pointed out: it might be better to think about the difference between being ‘stressed’ and ‘being stressed out’. While acute stress is beneficial and healthy, chronic stress (being ‘stressed out’ or in allostatic overload for you allostasis folks) “serves no useful purpose and predisposes the individual to disease”.
Meaning: chronic stress = when you start seeing the health impacts of stressors… Or when you could see health impacts of stressors.
The body naturally seeks balance6. In the context of a stressor, the systems that are activated and elevated have counterbalancing mechanisms that also help return everything to pre-stress baseline once exposure to the stressor has ended. When these systems are activated in a way that does not allow full recovery or when they are maintained at a stress level for an extended period of time, counterbalancing mechanisms shift in an attempt to get the body back to some form of balance.
Picture the body operating as a seesaw — predictable weights balancing and counterbalancing. When the body responds to an acute stressor, an few extra pebbles may drop along with a counterbalance, but that weight is temporary. The stressor ends and the body recovers.
What happens when the pebbles and rocks start piling up without end or without time to recover? Individually, the pebbles (and even the rocks) may not weigh a whole lot and the seesaw may appear balanced. But, now there is quite a bit more weight on the board and the fulcrum. The balance is more precarious. The integrity of the board is weakened.
That pile up represents chronic stress. It’s added weight for an extended time. It’s increased instability. It’s wear-and-tear and slow degradation of the plank and fulcrum — a weakening of the balancing mechanisms. The health consequences from chronic stress related to tipping or breaking the seesaw with potential health implications related to the increased likelihood of tipping or breaking.
If it seems like I’m dancing around something here, I am.
Stress gets tricky in a clinical context because “stress” isn’t really a clinical term. Stress is not an illness3. Stress does not even directly cause illness. No medical professional will diagnose you with stress, chronic stress, or even allostatic overload. Stress exists in the subclinical space.
“It is never really the case that stress makes you sick, or even increases your risk of being sick. Stress increases your risk of getting diseases that make you sick, or if you have such a disease, stress increases the risk of your defenses being overwhelmed by the disease.” – Dr. Robert Sapolsky
This distinction all too often makes the potential health effects of stress invisible – a body operating just below the surface of illness until one more pebble or rock tips or breaks the seesaw… or doesn’t. However, even without visibility, we cannot ignore a body at risk for negative health outcomes or that real opportunities exist to prevent that body from tipping over the edge into an unhealthy state.
Even the smallest stressors can add up and impact health.
Decreasing the maternal stress load
First, I must point out and emphasize that, in the context of the Maternal Stress Project, ALL the stressors considered here — along with the triggers, the layers, the connections —represent potential psychological stressors. Even when a stressor node appears to have a physical component as well, for the purposes of this project, we are only exploring the psychological component – how the brain perceives, processes, and signals the existence of an external stressor rather than any associated internal stressors.
A psychological stressor is the lion in the bush as a potential threat, not the actual, physical threat when the lion catches you and leaves a gaping wound in your leg. It is the stress response related to the external anticipation of the event, not the internal response related to the actuality of the event. For example, in the stressor map, food insecurity is a source of stress that can be considered both a physical stressor (hunger, malnutrition) and a psychological stressor (the concept of missed meals+hunger+malnutrition). In the context of this project, we are focusing on the psychological stressor, narrowing in on how the brain interprets food insecurity and the related health consequences of that stress.
There is incredible variability in how individual humans respond to and are affected by stress, a result of the “psychological milieu” that external stressors filter through before the brain responds.
And this is where the opportunity for change comes in. I believe that classifying what makes a stressor a stressor while connecting as many dots as possible will open opportunities for new stress-related solutions at small and large scales.
But first, we have to define what makes a stressor a stressor…
What makes a stressor a stressor?
How we see and interpret ‘lions’ in our environment determines how our bodies physically respond.
When is a lion a lion? More complicatedly phrased as: What are the characteristics of an external stimuli that stimulate a stress response? Especially when that stressor does not directly affect survival.
Decades of research have categorized a few key psychological factors that trigger an acute stress response. These include: lack of control, unpredictability, novelty.
In the convoluted mess that is the human brain — the “psychological milieu” that is filtering and comparing and remembering and projecting — these simple key factors go right back to that adaptive system and the primitive context that differentiates stressor vs not stressor.
What makes a stressor not a stressor (or less of a stressor)?
As you can probably imagine, the flip side of those key psychological factors – control, predictability, familiarity – have the opposite effect on how stressors are interpreted by the brain.
Sense of control – Give animals a sense of control over whatever stressor they are exposed to (e.g. turning off a foot shock) and they will respond less and exhibit few to no ill effects compared to animals that experience the same exact stressor but lack control.
Predictability – When an animal knows precisely when a stressor will come around in their day, that same stressor stops initiating a physiological stress response.
Familiarity – If novelty = misaligned expectations, the opposite — familiarity — plays into both the sense of control and predictability.
In addition, certain behaviors and outside tools can modulate the interpretation of a threat and reduce how the brain and body responds in that moment. For example (from animal studies), having an outlet for frustration – a rat running on an exercise wheel, a baboon pounding on a lower-ranking member of the troop – decreases the magnitude of a stress response. A more human-centric stress response modulation tool is social affiliation. Strong bonds, friend and community support, reliable partnership all have some of the strongest effects on reducing a stress response7.
Other things to consider about how we internalize external stress
We perceive our outside world. We modulate the “appropriate” response. We can accumulate a stress load. All of these additional aspects of how we evaluate and respond to challenges are key to understanding our stress and key to understanding the opportunities to address this stress. Let’s look closer…
Perception matters
Humans are complicated animals. We feed external signals through more processing centers in our brain than nearly every other species. Our human brain interprets running late to school pickup as a ‘lion’ while also having the capacity to ignore the threat of an actual lion within a zoo enclosure.
In addition to sense of control and predictability, another way that context can change perception of a stressor is the brain’s consideration of: are things getting better or worse?
The school pick-up ‘lion’ might become less of a stressor (have a reduced stress response) if you receive a call from a friend who offers to pick up your kid for you. That same school pick-up ‘lion’ might become more of a stressor (with a greater stress response) if the school calls and your sad, forgotten kid screams for you in the background.
“The subtle and complex human correlates of the physiological stress response can be extraordinarily plastic. Stated more plainly, we have a heartening capacity to change.” – Robert Sapolsky
Tying back into the Maternal Stress Project – this is where connections between stressor nodes come in. The more connections or the stronger the connections or the more uncontrolled or unpredictable the stressor or connected stressors, the greater the health risk from the overall stress impact. BUT, when the load is lifted on connected stressors, when connections between stressors are weakened, when stressors occur with a perception of control or predictability, when stress buffers alleviate the gravity of the moment, the stress responses and the related health risk of the overall stress, can be reduced.
An example of the interconnected nature of stressors to better identify solutions, found here:
The stress response is not all or nothing.
If you feel your heart racing as you step up to a podium for a speech in front of a crowd, that feeling does not necessarily indicate that your body will also tee up cortisol release. In fact, different types of stressors result in different patterns of responses that operate separately via the nervous system versus the cortisol axis. A stress response is not all or nothing. And it’s not always a bad thing. It varies depending on the intensity of psychological factors.
The intensity of the psychological factors depends on how that external, potential stressor feeds through your complex brain, starting with perception. The brain considers contextual information, gauging if and how to respond, and then regulates cortisol release and recovery.
If your body does release cortisol, that hormone response comes in a variety of flavors: large spike or small spike, long spike or short spike, quick recovery or slow recovery, and everything in between.
As you might imagine, the body recovers with less of a lasting impact when the stress response is smaller and/or shuts off relatively quickly and all the affected systems return back to a pre-stress baseline.
I am not an expert in meditation and mindfulness as a stress management tool but I am fascinated by it and how it works on the level of perception, response modulation, and recovery. With that said, meditation and mindfulness is an individual solution and the focus on stress reduction for this project relate to solutions that go beyond the individual, especially given the gender time gap:
Not all baselines are the same
Elevated stress load across a lifetime = long-term wear-and-tear. The concept of ‘weathering’ posited by Dr. Arline Geronimus is a valuable way to understand health disparities as they relate to the stress of discrimination and racism and the psychological effects of other social determinants of health.
Individuals exposed to these stressors for their entire lives operate at a daily baseline that is closer to a chronic stress state, and, as a result, experience health complications at a higher rate. Discussed here in the context of the Black maternal health crisis with Dr.
:In the seesaw metaphor, those who experience lifelong stress and weathering have baseline load represented by a seesaw that always carries weight and has a higher likelihood of compromised board integrity from those years of being weighed down. These bodies operate closer to tipping or breaking than those who do not experience the same stress across their lives.
Solutions to improve women’s health exist in the grey space of stress
Reevaluating and centering stress in a different way allows a more impactful view for risk analysis and preventive care. New opportunities for health solutions exist in the space separating external stressors and internal illness. Space between all the pieces: potential threats in the external world → the perception of those threats as stressors → the physiological stress response to the perceived stimuli → downstream targets that break when the system is overwhelmed by the frequency, magnitude, timing of the stress responses → pathologies resulting from those systems breaking. Preventive care must start upstream — addressing potential threats, perception, and opportunities to modulate the stress response.
See this broken down in the context of resilience here:
For the Maternal Stress Project, revisiting the terminology and concept of ‘stress’ serves to acknowledge that we are all flirting with the line between healthy and unhealthy with regard to the stressors of modern American motherhood while recognizing that some of us have more weight on our seesaw than others.
In addition, evaluating and aligning the basic science of stress physiology aims to give weight to solutions that ameliorate, diminish, buffer, and/or eliminate exposure to stress in our personal journey, our community, our medical system, our society, and everything in between. This is a call for a universal shift of focus to extend ‘stress management’ in the context of health beyond personal responsibility and towards the structural, cultural, and systemic changes necessary to impact all birthing parents, all women, all mothers, all caregivers.
Quick summary of the key elements that I keep coming back to:
It’s not all in your head – psychological stressors have real physical effects
The human brain is a complex beast – what is ‘stress’ to one person may not be ‘stress’ to the next
Perception is your filter
Context matters – the stress signal can be modulated up or down based on negative associations or positive ones
For modern-day humans with modern-day lions, the line between beneficial stress responses and harmful chronic stress is a fine one.
Ok, now your turn — are you all getting this? how can I explain this better? Is this actually interesting and applicable for you?
Or, even better, join me on January 29th!
Note and a plea: The webinar is open to all but since I needed to update my Zoom account to a paid version, please consider bumping to a paid subscription to help me justify the expense!
I’d be remiss not to point out that the terminology and concept of ‘fight-or-flight’ came out of male-dominated research, which had a tendency to bias science in the masculine direction. The counter to fight-or-flight, argued that female animals respond with ‘tend-and-befriend’ behaviors when faced with a perceived threat. While I fully acknowledge that there are sex differences when it comes to stress physiology and behavioral responses, I don’t love the masculine/feminine gendering of the response imagery, especially when it comes to humans. Females have full capacity for ‘flight’ if faced with a predator and I know (from my own impulses) that a mother could put up a good fight if she or her children/offspring are threatened. On the flip side, males have the capacity to ‘tend’ (an area of neuroscience that has barely had its surface scratched… because of bias) and, similarly, ‘befriend’. It is critical to examine sex differences while also acknowledging the spectrum and considering the bias through which research findings are produced.
In lay descriptions of acute stress, I have seen the glucocorticoid response lumped in to reference a general the ‘fight-or-flight’ response. If it is helpful for your brain to categorize acute stress response = fight-or-flight response, go with it. Just remember, the glucocorticoid/cortisol response is not helping with the rapid response needed to fight or flight, it is helping with everything after the fighting and flighting.
and lots of ways to muck it up and muddy the water — not important to this explanation but a reason why I really do not love cortisol used as a key metric for quantifying “stress”.
Cortisol does other non-stress stuff too. Cortisol appreciation post coming soon!
ok, “balance” is a loaded word. Here, “balance” refers to how our bodies maintain homeostasis. NOT how we can externally manipulate, control, or regulate our own “balance” e.g. through whatever mumbo jumbo is sold as a way to “balance your hormones!” That is not a thing.
When I discuss solutions for reducing stress or stress buffering social affiliation and community start to come up a bunch. This is especially important when considering why stress may be gendered as it relates to access to stress buffering tools, like social time with friends and family:
You noted:
"Individuals who experience low levels of stress for their entire lives operate at a daily baseline that is closer to a chronic stress state, and, as a result, experience health complications at a higher rate."
Confused. Should it be "Individuals who experience *high* levels of stress?"