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The (Scientific) Origins of Stress

    Stress. Even the work itself evokes feelings, perhaps even emotion. Thoughts, mostly negative, enter our minds about how stress impacts our daily life; the bills we have to pay, the appointments we need to keep, the work we have to do. This is the layman’s view of stress. It’s a negative reaction that leaves us feeling anxious, sad, or overwhelmed. We believe it leads to sickness, depression, or any number of health issues, and often have ready-made phrases like “relax, don’t stress it, find stress relief” ready and at our fingertips to utilize.

    If you have a scientific background, your view of the word may be slightly different. Instead of the negative view, the idea of the stress response takes center stage. Fight or flight, homeostasis, stimulus and response, cortisol and adrenaline; all phrases which describe our general understanding of the scientific concept of stress. We’re familiar with the idea that if we encounter a stressor, be it a lion or a robber or even a scary movie, a cascade of events take place in our body that prepare us for the impending danger. In this context, stress is not a danger but can save our lives. If you are familiar with athletic development, you might see stress as a way towards adaptation. Apply a stress, through a hard workout, and then recover and wait to see your muscles grow, your heart pumps more blood, and your performance improves.

With all these concepts, what does stress mean? The reality is it can be all of these concepts and it can be none. It’s a complicated word that keeps collecting a variety of meanings as we grow to understand the concept. The problem is these meanings get lodged in our minds as truths, regardless of whether they have validity or not. We carry around these concepts, likely because of their popularity, and we have a hard time dispensing of them.  If they are overturned or changed, the original popularized concept sticks in our mind.

    The concept of stress, through its meandering journey towards understanding, is one ripe with misunderstanding. The impact is we have been left with a word, that carries an abundance of context on it’s back, which has shackled us from utilizing the concept of stress as the body and mind intended. To elucidate where we went wrong, we need to go back to the start.

Fight or Flight: The Origins of Stress

In 1915, a young Harvard Physiologist named Walter Cannon described “the necessities of fighting or flight” in his now classic book, Bodily Changes in Pain, Hunger, Fear and Rage. With the turn of a phrase, Cannon began the process of ingraining the now famous “fight or flight” instinct into our consciousness. As often occurs with scientific breakthroughs, the now common concept was a result not of deliberate examination but one of serendipity.

As a young medical student, Cannon used the newly discovered X-ray to investigate the mechanism of swallowing; did food reach the stomach because of muscles in the mouth or esophagus? Starting with geese and then moving to cats, Cannon X-rayed animals as they swallowed a variety of liquids and foods. The results were a success, as Cannon discovered how peristalsis helped move food through digestion. While putting the cats through his experiment, Cannon noticed a peculiarity. When the cats got scared or alarmed, the movement of the food through the gastrointestinal tract came to a halt. Even stranger, if the cats were consoled and comforted, GI tract movement resumed. 

From this simple observation of digestion, Cannon and his colleagues at the Harvard lab researched the wider impact of what occurred when animals were alarmed. After a series of wide-ranging experiments focusing on what happens to different organs when animals experienced alarm, Cannon centered on the sympathetic nervous system, and the hormone that it triggered, adrenaline. With the administration or uptick of adrenaline through emotional disturbance, the animal’s body transformed, as if preparing for battle. He saw all of the now-classic signs; increases in heart rate, breathing rate, and glucose mobilization, as well as the redistribution of blood flow. With these observations, Cannon was convinced that in response to any acute emergency, the body had a singular response, and it was all because of adrenaline; Prepare to fight or flight.

Cannon wasn’t finished with stress. In 1932 in his book The Wisdom of the Body, he outlined the other side of the stress coin, how one returns to normal. Influenced by the ideas of Claude Bernard decades earlier, Cannon sought to discover how stability in the body was maintained. How did breathing rates, heart rate, and blood pressure return to normal after a stress-inducing disturbance in these systems? He believed that the body had a natural control system, that was based on the stability of the internal environment. Through innovative animals experiments looking at hunger, thirst, Cannon outlined the concept of homeostasis or the maintenance of a relatively stable environment. 

Cannon had his grand theories. In response to emergencies, adrenaline was the key. When faced with a disturbance, the body sought to prepare and then return itself to balance, regardless of what type of stressor it was. In other words, the system was reactive, the emotional or physical trigger caused a downstream reaction. With the two major concepts of stress, fight or flight and homeostasis, in place, Cannon changed our understanding of emergencies and emotional disturbance forever. But it took another scientist to bring the ideas to the mainstream.

Stress Enters the Mainstream

Like his predecessor, Hans Selye didn’t set out to understand stress, he was after something far different–a new sex hormone. He began his experimentation by injecting ovarian extract into rats, hoping to discover the new hormone being released as a reaction to the extract. With each reaction, he saw a distinct response, but it wasn’t his sought after hormone. Instead, there was a signature response, the adrenal cortexes enlarged and the immune system reacted. Frustrated and downtrodden by his lack of hormone discovery, Selye began to think about this standard response in a different way.

He tried injecting different substances, shocking the rats, and a whole slew of other activities, and each time, the same signature response occurred.  Selye believed that in response to any noxious stimulus, the body had a generalized response. Selye termed the stimulus a stress.

In his work, Selye built upon Cannon’s research and found that it wasn’t only adrenaline that caused the body to be ready for battle. The Hypothalamic-Pituitary Axis (HPA) played a large role. The HPA axis results in the release of Cortisol and other hormones that we now commonly refer to as ‘stress hormones.’ Selye believed the body went through an alarm stage (similar to Cannon’s fight or flight stage) in which it marshaled a reaction to a stimulus. Cortisol acted as the main trigger, which resulted in the signature response that Selye kept observing. Crucially, Selye believed that this was a nonspecific reaction. No matter what the stressor–be it burns, cold, infection or trauma– the body responded in the same way. And if it occurred too frequently, the body would eventually become ‘exhausted.’

With the believed universality of Selye’s concept, he called the General Adaptation Syndrome, Selye began applying it to everything. Any environmental stressor had to cause the same reaction. He took to popular writing to explain his concept and the harm that could potentially occur. Too much stress and your organs could be damaged or even fail. Despite calls for Selye to term this negative reaction as something other than “stress” by the journal Nature, Selye’s choice phrase grew into an empire. Stress was negative, and it was a singular reaction.

The evolution of the concept of stress didn’t occur in a physiologist vacuum. Ideas grow from the context of their times. And in many ways, the evolution of the concept of stress is the result of the simultaneous growth and battle of physiology versus psychology. In the start of Bodily Changes in Pain, Hunger, Fear, and Rage, Cannon’s Darwinian influence can be seen: 

“the doctrine of human development from sub-human antecedents has done much to unravel the complex nature of man. As a means of interpretation, this doctrine has been directed chiefly towards the solving of puzzles in the peculiarities of anatomical structure…expressive actions and gestures– the facial appearance in anger, for example–observed in children and in widely distinct races, are found to be innate, and are best explained as the retention in human beings of responses which are similar in character in lower animals.”

    Cannon saw himself as extending the explosion of Darwinian explanation in the physical sciences to the world of emotions and what we now call stress. He believed that we could best understand these reactions as a simple response coming from our ancient ancestry.

During the middle of the 20th century, with Ivan Pavlov and B.F. Skinner’s influence, the concept of Behaviorism took root in the understanding of psychology. The theory posited that behaviors could best be understood as a reflex or a reaction to our environment. Whenever a stimulus was presented, we had a response that was either ingrained or conditioned.  It shouldn’t come as a surprise that Cannon was a friend of Pavlov, the man who popularized the notion of conditioning, which relied on ingraining a response to a stimulus. Cannon and Pavlov exchanged correspondence over Pavlov’s ideas of a conditioned reflex. As Cannon outlined his theories and Selye then built upon them, it’s little doubt that the ideas that held a prominent place in the conceptual framework of psychology at the time, influenced these thinkers. Whether it was Darwin or the Behaviorist, the framework at the time provides a glimpse of the lens that most scientists saw during their time. During this unique time, the physiology and the psychology were on the same page, reactive response driven systems dominated.

A Simplistic View

Scientific rigor or acceptance doesn’t guarantee translation to the lay public. To make that jump requires something else, a capturing of the public imagination. The concept needs to invade our mental space, capturing part of our collective consciousness just as any viral meme would today. And that’s what separates the work of Selye and Cannon apart. Their legacy in popular culture can be seen in the words and phrases we still use today. Anytime we invoke the powers of adrenaline, be it in pushing a football player to extraordinary performance in the final moments of a game, or an adventurer saving himself in a life or death situation, we have Cannon to thank. Similarly, when we blame stress for our recent trip to the doctors or even our greying hair, it’s a clear reflection of the lasting impact of Hans Selye.

    Their joint ideas of a non-specific response became a fixture of both scientific and popular understanding of stress. Whenever we were faced with a stressful event or alarming situation, our bodies initiated a cascade of events to prepare us. Whether it was through the GPA axis and cortisol or the Sympathetic Nervous System and adrenaline, both Cannon and Selye believed the response was the same. We had a general stress response, with both Cannon and Selye leaving only a little room for minor adjustments based on the specific stressor we encountered.

Furthermore, our one general response system was reactive. We needed the stressor or stimulus to trigger this cascade. The ideas were so fervently implanted in our minds that it wasn’t until fifty years after Selye introduced his concept of a General Adaptation Syndrome, that his idea of non-specificity was scrutinized with experimental testing (Pacak et al. 1998). By this time, it was too late, the concept of stress, as Selye envisioned it, was firmly planted in our conscious minds. Like a catchy theme song that wormed its way into our minds, once ideas have taken hold, it’s difficult to let them go, even if their flaws later become clear.

    Let’s go back to the scenes described at the beginning of the chapter; the encounter with the bear in Tennessee and the surprise run that went through a potential meth camp. If Selye and Cannon’s general reactive response is correct, then we all would experience the same adrenaline or cortisol driven response. Yet, individuals facing similar circumstances, experience different reactions and display different behaviors. When the group of six of us came upon the meth camp, we all didn’t sprint away. Some froze, others ran, a few searched for more information. But, the behaviors weren’t the only things that differed. If you asked each individual, his or her internal experiences were just as varied. Some were scared and frightened, others filled with excitement, and a few were calm, cool and collected.  Did the same general response cause all of these varied feelings and behaviors? Or did each individual experience their own distinct stress response, guided by a unique combination of nervous system activation and hormonal output?

    As is often the case, our body is smarter than we like to give it credit for.

The Fast or Slow Road to Responding to Danger

    Glass, fine china, porcelain; all substances that we’d agree are fragile. Drop them from almost any height, or maybe even nudge them so that they barely tip over on a shelf, and they all will potentially shatter. Fragile items have little flexibility. The concept of fragility extends beyond physical items but to systems of the body as well. A fragile system is akin to the fine china dish that sat in your grandmother’s kitchen drawers, it has little flexibility and a high risk of failing. Fragile systems are rigid, in that they have one route towards success, and if deviated off this route, no matter what direction, failure is imminent. Opposite of a fragile system is what author Nassim Taleb calls an antifragile one. To be antifragile is to not only be flexible and resilient but to be able to adapt and grow under times of stress. When it comes to the human body, the simple stress response is a fragile system. It contains an inflexible generic response to a stressor. If that pathway doesn’t work, if our one squirt of cortisol or adrenaline doesn’t do the job, well, best of luck.

    But human beings wouldn’t have survived millions of years, escaping stressors along the way, with such a fragile system. While people tend to imagine the fragile, thankfully for us, the fine tuning of natural selection over millions of years results in a system that can adapt and withstand change. The stress response didn’t pop into existent as we reached modern human form, it’s a system that has been forged and developed through our animal ancestors. To be able to serve a diverse range of functions–preparing us to face a fearsome lion, as well as a first date– our bodies response to stress had to be adaptable.

    Just as we have different energy systems to provide fuel to our working muscles during a race, so that we aren’t reliant on slow to burn fat or our limited carbohydrate stores, our body has multiple different ways to get it prepared to handle whatever we encounter.

The Autonomic Nervous system guides our immediate reaction. It’s two divisions, the Sympathetic Nervous System (SNS) and Parasympathetic Nervous System (PNS) act in accord, starting the cascade of neural and then hormonal responses to stress. It’s best to think of the SNS as the accelerant and the PNS as the counterbalancing brake. SNS activation will result in an increase in heart rate, dilation of both pupils and your lungs, reducing blood flow to non-essential organs and a whole host of other reactions preparing your body for battle. The PNS has the opposite effect, lowering heart rate, causing constriction and relaxation. These two counterbalancing nervous system reactions push and pull, activate and withdraw, to provide the desired result. The nervous system is the first line of defense, and direct innervation of the nervous system to organs causes a fast, almost immediate response. This is thanks in large part to the fact that the signal from the brain to the target organ is entirely neural. There’s no need for a hormone to carry the message further, and slow the process down. As a result, direct activation by the SNS and PNS are the superhighways of our body. As we move away from the highways to major thoroughfares to small country roads, the resulting flow of hormones carry out the desired downstream actions. At each step along the way we lose speed, but we gain something else.

Walter Cannon’s original work focused on the SNS and its stimulation of the adrenal glands to release the aptly named hormone adrenaline, or as it is known in the scientific community, epinephrine. Cannon ascribed epinephrine as the key ingredient to the entire fight or flight system, but its counterpart norepinephrine was discovered soon after. These two hormones combine to make up what we call the catecholamines. The catecholamines have many of the same effects of direct SNS activation–arousal, increases in blood flow, vasodilation in the muscles– but it takes an extra 20-30 seconds from stimulus to response for these hormones to take action. They are the slightly slower versions of direct nervous system stimulation. Yet, the effects tend to last ten times as long.  As a result, we get to keep the much-needed excitatory response for longer. We’re beginning to see the flexibility within the body.

    While often lumped together, Epinephrine and Norepinephrine have contrasting effects. Just like the PNS and SNS counterbalance each other, these two catecholamines can function in much the same way. Norepinephrine can act to cause a decrease in heart rate or vasoconstriction of the blood vessels, while epinephrine can have the opposite results. Additionally, their paths to appearance in our body differ. Norepinephrine can be released from both the SN¬S–acting as a neurotransmitter– and the adrenal glands. This combined release means that Norepinephrine circulates even at rest, thanks to a continuous low-level activation of the SNS, but also can increase during times of stress. On the other hand, epinephrine, which is primarily released from the adrenal glands, shows a rapid and dramatic response to stressors. Even more so than its close cousin, norepinephrine. This ever-changing mixture of epinephrine to norepinephrine in the body allows the body to balance its response to anything we encounter. This becomes apparent when we face a challenge or a threat.

Whenever we face a stressor, we made a quick appraisal; is this something that could endanger us or should we be excited about facing it? Regardless of what the actual stressor is– be it a physical attack, a speech we have to give, or a game we are about t play– whether we view it is a threat or challenge shifts our bodies reaction. When we feel threatened,  more norepinephrine is released.   On the other hand, if we experience a stressor as a challenge, the ratio tips in favor of epinephrine, resulting in increased vasodilation, among other changes intended to protect us from the impending battle. The ratio doesn’t just change our internal biological reaction, but also how we handle feelings and behavior. In one study, researchers found that a high N/E ratio is related to people expressing the anger externally, while a lot ratio leads to an inward direction of anger. Some research has even suggested that this ratio is related to suicides and assault behavior.

The Slow Road to Stress

    Since Selye’s discoveries, cortisol and stress have been tied at the hip. Even those of us with a patchy understanding of hormones, know that cortisol is the stress hormone, and that, by and large, it’s one that we don’t want a lot of. If Cortisol has a reputation, it’s as an evil cause of a myriad of diseases and maladies. Cortisol is the source of our anxiety and the cause of our stress-induced health maladies. If our cortisol goes too high, adrenal fatigue, weight gain, hair loss, and mood swings are just around the corner. An entire industry of stress relieving, cortisol dropping supplements, books, exercises, and fad-diets has risen out of this story. It might surprise you then, that cortisol is not a stress-causing hormone, but a remedy to stress.

Complementing catecholamines and the SNS, cortisol, and the HPA axis that delivers it, represent the “slow response.” Cortisol’s effects aren’t felt until 20-30min after the onset of a stressor. In other words, if we were relying on cortisol to prime us to run away from the lion we just encountered, we might be left waiting. Instead, it’s best to think of cortisol as our bodies remedy, readying us for recovery. It’s preparing us to deal with the aftermaths of whatever it is we encounter. Cortisol liberates energy and shuts down non-essential functions like the reproductive system so that the body can throw all its resources into recovering. The effect can even be seen in our behavior, as high cortisol levels post –game results in a gradual quieting of our competitive instinct. Cortisol is designed to bring us back down to baseline.

Cortisol’s bad rap is due to what occurs when cortisol remains elevated, failing to return to their baseline, even after the stress is gone. With prolonged exposure, we see a link to the health issues that we all are accustomed to hearing that stress causes. Our body mistakenly thinks that we still need to recover from a stressor, so it keeps pumping cortisol into the bloodstream to try to fix the problem. After a while, our body seems to adapt, making the always stressed state that we reside our new normal. The cortisol related maladies are therefore a problem with coming down off the stressor, not necessarily the stress itself. It’s a problem of shutting it off and recovering.

These three systems, the Hypothalamic-pituitary axis (HPA), the Adrenomedullary hormonal system (AHS), and the Sympathetic Nervous System (SNS), represent the traditional stress response. They have their own unique characteristics and roles. Whether we need an instant reaction or a delayed and potentially nuanced one, our body has multiple routes to get there. 

The Tools of a Flexible System

While these three systems represent the traditional “stress” hormones, the reality is more complex. A whole host of hormones and neurotransmitters can be released depending on the situation. It’s best to see these chemical messengers as the tools the body has available to accomplish its goal of protecting itself. Instead of falling pretty to the old adage of if all you have is a hammer, everything looks like a nail, the body comes packed with a full set of tools which it can utilize to make sure we create or fix whatever it is that comes our way. While understanding the exact mechanisms of each of these neurotransmitters or hormones is beyond the scope of this post, the key is understanding the diverse reactions the body can have, and the complexity of their interactions.

Testosterone is commonly thought of as the hormone tied to muscle growth, roid rage, and teenage boys hard to understand minds. Due to these associations, it’s often considered an “anger” hormone. But, as pointed out in their book Top Dog, Po Bronson and Ashley Merryman classify it as a hormone of intensity, not anger. As Testosterone floods our body pre-game, our fear subsides and our competitiveness takes over. That doesn’t mean rage, it means doing what we need to make sure we win the game. This distinction explains why contrary to our intuitive sense, an increase in testosterone actually increases the amount of teamwork and cooperation players display on the field. Testosterone amplifies, not necessarily angers.

It should come as no surprise then that pre-game levels of naturally occurring levels are tied to player performance. That’s lead players in a variety of sports attempting to manipulate their athlete’s pre-game levels. No, not by drugs, but by natural means. Interventions such as making sure to see the game as a challenge, performing a warm-up that they like, or even spending quality time with teammates, all lead to momentary bumps in testosterone levels. And this small bump is often enough to make a difference in a players performance.

In other words, if we can convince our body to release testosterone during a stressful time, it can help ensure success. The opposite effect can also occur, with prolonged stress, we often see a decrease in testosterone levels, as your body tries to divert resources elsewhere. Testosterone responds to stress in much the same way as any other hormone if it is needed to protect us, it might get released. It’s not just out on the field or track that we see this testosterone shift with stress, doctors performing demanding surgeries can see an almost 500% increase before surgery.

On the opposite end of the hormone spectrum is oxytocin, a molecule commonly linked to bonding with our close friends and family. For decades, oxytocin’s function remained related to breastfeeding and pregnancy. As our understanding grew, scientists discovered that oxytocin wasn’t just a hormone that arose in pregnant women, but instead played a large role in social bonding, the formation of trust, and, if animal studies are correct, even cementing the connection felt between lovers.

Oxytocin’s reputation began to shift thanks to a small grayish-brown mammal; the prairie vole. In the early 1990’s neuroscientist, Tom Insel began using two types of voles to understand pair bonding. In the wild, the montane vole is best described as a loner, preferentially nesting and living by itself. In contrast, the closely related prairie vole would be described as a model of family values. After mating, they form a close pair bond, spending time with their mate and getting defensive to anyone who intrudes on their special relationship. Insel wondered why was their such a contrast in the behavior from these two genetically similar voles. His answer lied in two hormones, oxytocin, and its close cousin vasopressin.

In a series of experiments, Insel and his colleagues began collecting measures of both hormones and their behavior in the lab. What they quickly noticed was that these two hormones, vasopressin more so in males, and oxytocin more so in females, largely determined whether the voles displayed behavior of affiliation or aggression. Taking their experiments a step further, the research team implanted a mini-pump in the prairie vole that would flood the rat’s body with oxytocin whenever the researchers wanted. When the female vole received the hormone in the presence of a male, they selected this male over and over when given a choice to spend time with a number of other voles. When the female vole spent time with a male without oxytocin being released, the female didn’t preferentially pick the male afterward.  In other words, the hormone was necessary to create a lasting bond with the opposite sex. With these innovative experiments concluded, oxytocin rapidly became the answer to all of our bonding related questions, and perhaps even the secret to monogamy.

Thanks to the vole, research in humans accelerated, and, perhaps too ambitiously, began tying it to an expansive array of pro-bonding ideals in humans, including empathy, love, and even monogamy. The fever over oxytocin grew so quickly, that it even earned the nickname the “love hormone” and was the feature of viral Ted Talks encouraging everyone to hug their neighbors to receive a hit of this lovely hormone.  Like most new discoveries that reach viral status, the early enthusiasm for this all-positive, wonder hormone, was a bit too much. Oxytocin no doubt plays a large role in bonding, and even concepts like empathy, but the functions of this hormone are much more nuanced and complex. In particular, it functions in times of stress paint a contrasting picture to the “love hormone.”

While the mysteries of oxytocin are still being unraveled, it appears to play a role in identifying and responding to various types of stress. In particular, social stress seems appears to be a major trigger for the hormone. Like the other hormones disgusted, its effects are not singular in nature but instead, vary based on the situation. Periods of social contact or isolation both can deliver a burst of the hormone. Researchers speculate that when pro-social behavior occurs, oxytocin acts to reinforce the positive experience, helping to create a sense of well-being. On the other side, during isolation or loneliness, oxytocin is released to push people towards filling their social needs. 

This dual action of oxytocin acting in both pro and anti-social environments might be surprising. How does a hormone originally tied to monogamy also help to induce anger? But it’s a demonstration of the body utilizing hormones in a context-dependent way. In one such example, oxytocin has been shown to both enhance and reduce the feeling of fear.   In attempting to further elucidate the mechanisms of oxytocin’s effects during stress, researchers give participants a hit of the hormone via a nasal spray and then track their behavior. In one such study, scientists found that oxytocin increased the subjects ability to recognize facial cues. Subjects were able to quickly identify fear, but not other emotions.  In a similar study, oxytocin administration increased the salience of social stimuli.  Oxytocin seems to not only help push us towards social behavior but also in boosting our ability to attend to and identify social cues.

When we look at stress, not as a negative but simply a stimulus that disturbs our body, the picture gets a bit clearer. Whether it’s a novel social environment, the sensation that accompanies isolation, or even the effects of sex, they all induce a type of stress response. Oxytocin seemingly plays a role in helping prepare the body and mind to be prepared and adapt. Whether that is in creating a social bond, or in helping to identify and facilitate a sense of anger, so that we may perhaps protect our children or mate. The wide-ranging effects of oxytocin demonstrate a common theme of the hormones released during times of stress. They are context dependent, and not only can bias us towards particular behaviors, but also bias our sensory abilities towards attending to certain internal or external feedback.

    The bodies stress tool kit isn’t limited to adrenaline, testosterone, oxytocin, and cortisol, there is a myriad of other hormones and neurotransmitters that get released when we encounter something that takes outside of our norm. The chemical responses vary greatly when they are released, their actions, and in the length of their effects. Growth Hormone, for instance, can see an almost 10x increased when we are under physical duress while having little to no response under psychological stress (Ranabir and Reetu, 2011). Thyroid hormones, on the other hand, can increase during psychosocial encounters, while actually decreasing during other types of stress.

    Another trendy hormone called dopamine, which plays a role in desire and motivation, can have a varying response depending on the magnitude of the stress. During moderate levels, it can increase, while during extreme stress the body can experience dopamine depletion, leading to feelings of apathy.  Similarly, the hormone prolactin can have a varying response, either increasing or decreasing.

    With each mixture of hormones, neurotransmitters, and nervous system activity, we have a varying response that is reflected in the bodily organs. The immune system can activate and put on high alert for impending damage, or it can be almost completely shut down, diverting resources elsewhere. Blood flow to various organs can be accelerated or diverted elsewhere. The muscular system can be primed for action, increasing tension in the glutes or hamstrings to run away. And our attention and senses can be tuned towards specific kinds of information. Our brain up or down-regulates what cues reach awareness, such as a specific color, smell, or feeling, and which ones our brain filters out; such as ignoring the sensations of pain when we’ve been hurt and are in a life or death situation. In other words, our body can shift its response at almost every level depending on what gives us the best chance of survival or success.

The key isn’t in having an intricate understanding in every chemical that can be released and utilized during stress but to understand the tools we have in our possession to craft the appropriate response. The variation exists for a simple reason. Our bodies have a flexible system to respond to the demands that we encounter. The context of the situation shapes the response we have, and the hormonal shifts both reflect and carry it out.

The flexibility the body displays is not unique to the stress response, it’s present in other systems of the body. One instance is in how we provide energy to our working muscles. If we break out in a fast run over a mile, our immediate energy needs are met by the phosphocreatine system. A quick reacting system that provides energy for a few seconds at best. To fill in the gap in energy demands once the PCR system is exhausted, anaerobic glycolysis will kick in. The anaerobic system revs up pretty quickly and has the capacity to last minutes instead of seconds. All the while, our aerobic system has been attempting to rev up from our first step, but won’t be fully activated until almost two minutes has passed. If we extend our run out from one mile to one that takes hours, we’ll gradually switch to processing more fat instead of sugar. In other words, our body is prepared for whatever the exercise demands are. It has a quick solution and a long term one. There’s overlap between all systems, to make sure that gaps are closed and we are rarely in a situation where we have no way to supply energy to our working muscles. The stress response system works in much the same way. We have flexibility and options, a fast and a slow route, signals that affect us immediately and others that kick in after minutes or hours have passed.

If we need a boost in excitation or heart rate, we can have direct SNS stimulation, or on the other, we can dampen down the PNS stimulation. If the PNS response is dampened, then it’s like taking our foot off the brake in an idling car, the car will start to move forward without us having to apply any pressure to the gas, or in this example the SNS. If these responses aren’t enough, we can stimulate the adrenals and get epinephrine or norepinephrine released. Depending on the ratio of these two hormones, we either have an excitatory state, with an increase in heart rate, or a quieting down, with a decrease in heart rate. On we could go in the myriad of ways the body can impact something as simple as physiological arousal. Flexibility, not rigidity, is the philosophy our body lives by.

Flight, Fight, or Tend and Befriend?

    In a 2007 review on the subject, researchers David Goldstein and Irwin Kopin completed the challenging task of summarizing how people’s bodies responded to over a dozen different stressful situations. In response to a myriad of stressors, the researchers evaluated the reactions of the three main stress response systems of the body we just covered: the HPA, AHS, and SNS. These three different systems each resulted in the secretion of a different “stress” hormone, ranging from cortisol to epinephrine to norepinephrine. Each hormone can result in a different body response, from increasing or decreasing blood flow to altering glucose or fluid balance. If Selye and Cannon’s theory held true, then the researchers should have seen the same general hormonal response, regardless of the stressor encountered.

    Goldstein and Kopin left no stone unturned, they looked at stress in humans and animals, ranging from daunting physical stressors like electroconvulsive shock, cold exposure or surgery, to mental ones, including social stress, inducing of fear, and active escape situations. In short, they evaluated 15 different stressors and the hormonal reactions to each. Contrary to what Selye and Cannon hypothesized, the response of the three stress systems was wide and varied. To cold exposure, the SNS was active, while the HPA and AHS were almost non-existent.  On the other hand, fainting had a non-existent SNS, while the AHS and to a lesser extent the HPA system was activated. In the case of Immobilization of rats, all three systems seemed to be revved up to the max. Each individual stressor resulted in a varied hormonal response.

To make sense of these various reactions, researchers have attempted to categorize the variety of stress responses based on both hormones and behavior. What combination of HPA, AHS, and SNS activation occurs and then whether our response is to approach, avoid, or flee whatever stressful situation we encounter. Building upon Cannon’s original flight or fight response, we now have responses described as fight, flight, freeze, threat or challenge, and tend and befriend. Each response represents a different combination of hormones and subsequent behavioral response.

For example, the popularized tend-and-befriend response relies mainly on oxytocin. With oxytocin flowing, heart rate and cortisol actually decreasing and in turn, individuals seek social contact and to protect loved ones.   Under times of stress, this response helps to push us to care about our social group, often times putting others before ourselves. It might be the response that pushes us to protect our children, to search for others during the house fire, or for the army medic to ensure his or her patients are taken care of, instead of selfishly abandoning them during a crisis. It’s easy to see why protecting the group as a whole, and in particular, our offspring would be an evolutionary advantage.

    Similarly, how we perceive a stressor alters our response. Whether we see it as a threat or challenge, shifts our behavioral and hormonal response. For instance, if you see your next race as a challenge, an opportunity to see how good we have a challenge response: our cardiac output increases, while our peripheral resistance decreases. If we view that same race as a threat (i.e. if we have a fear of failure), our body has a completely different reaction, our peripheral resistance, and blood pressure increases.

In comparing the HPA and the Adrenomedullary hormonal system (AHS), they found that activation of the AHS occurred when the situation involved effort without distress, while HPA predominated when distress without effort was involved. Both systems were activated when effort with distress was the situation. A different stress response, all based on how we view the stressor.

We’re left with a classification system. We take the behavior and the hormones and try to fit each into a catchy title, fight or flight, tend and befriend. The reality though is a much more nuanced system. While, the details are difficult to unravel, based on Goldstein’s different responses to fifteen stressors, we seem to be able to fine tune our reactions to anything we encounter. Our body is not limited to a generalized reactive system like Selye envisioned, or even a few stress response categories to fit a few situations. Instead, we have a flexible system. One that can encounter a myriad of situations, and make sure we have an appropriate response. It’s a system that has the flexibility to mix ingredients to reach the desired outcome.

The stress response turns out to be not only our way of ensuring survival but to make sure that we take appropriate reactions to anything we encounter. Not just crisis, like the originators of the concept envisioned, but even small encounters. Our body has a slight sympathetic nervous system response to eating a big meal, or a small change in temperature, or even simply standing up after lying down. In fact, we have a small SNS activation even while at rest, as if our body keeps the car on idle, ready to press on the gas if it needs to.

In a way, our stress response system can be seen as baking cookies. Depending on the ingredients we mix, the temperature we bake them at, and how long we leave them in the oven, and a slew of other factors, we may be left with gooey or crisp ones, chocolate chip or peanut butter, or any number of other cookies we all love. They may all be categorized as cookies, but they are vastly different.

Up until now, we’ve worked on the assumption that our body responds to whatever stress we encounter with a response to it. See a snake on the ground, a certain combination of hormones is released, step onto the stage for a speech, another mix of hormones flows through your body.  Is that truly the case?

I have a confession to make; I’ve been leading you slightly in the wrong direction. The mental framework we’ve been working under is that the stimulus causes the hormonal response. But, what happens, if instead of the response is a reaction, it’s the result of a prediction. The brain doesn’t simply react, instead it uses context–the environment, feelings, past experience, and bodily state– to decide what the best response is. Using our cookie example, our individual preferences–whether we like chocolate or peanut butter, crunchy or soft textures– our past experiences that caused us to hone what we liked, and our current hunger pangs and cravings, all guide what ingredients we’ll use and cookie we will try to create. We don’t mix together all of the ingredients in hope that we’ll end up with our gooey chocolate chip favorites. We predict the exact ingredients and baking time that will give us that result.

And that’s the concept of Allostasis. A predictive model, instead of a reactive one. While Cannon and Selye focused on a simplistic reaction. The reality is it’s much more complex. Our modern understanding of stress is far more complex. Yes, the same hormones and neural responses hold true, but we don’t just respond to the environment. We utilize the environment, past experience, and the sensory information coming in to PREDICT our response. Our brain is a simulating machine.

It’s why walking a street at 2pm elicits a completely different reaction than walking the same street at 2am. In the latter example, the context of the environment heightens our awareness, causing us to be a little on edge.

The same idea can be applied to athletic contexts. Our stress response is dependent on not only the stress of the workout, but the context surrounding it. A low key practice will elicit a different response than one in which pressure is increased and we are challenge. A coach who utilizes fear and punishment based workouts will elicit a different response than one who relies on positive reinforcement. Even for the same workout.

In our understanding of stress, we can now see our journey across a number of models. We started with Cannon and a simple reactionary one, before branching out to a system that had a not only a general response, but also some sort of individual variation. From there, we’ve moved toward a predictive one, where we don’t wait for the stimulus, but instead guess what the best response is based on context. Finally, we’ve made it to the adaptive predictive model. Where meaning is layered on to context and experience, and our body attempts the best possible guess of how to handle what is coming. And when our experience is complete, we take the actual feedback, and have the ability to adapt and learn. Which is the final stage. A predictive mechanism, where our predictions are updated based on if they turned out to be correct or not.

  1. Reactive=   Stimulus –> General Response
  2. Varied Reactive=  Context –> Stimulus –> Varied Response
  3. Predictive=   Context–> Prediction–> Response (and Learning Response from predictive accuracy.)

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    1 Comment

    1. MW on March 30, 2019 at 4:16 pm

      This information is very enlightening and useful. We *have* been conditioned as a culture to fear stress, and I think part of it is because we believe that being stressed about giving a speech generates the same dire biochemical cascade as facing a lion, which in and of itself is rather a scary notion. To extrapolate on the cookie analogy, it is like thinking that if you have one cookie, it commits you to eating every cookie on the tray (biochemically), when in reality, stress comes in different amounts and types, depending on the stimulus, which means that you are not committed to eating every cookie when you give a speech or toe the line at a race–in fact, you need only take a bite if that’s all that is required. Thanks for the great post.

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