Recent studies have challenged core stress concepts taught in graduate classes. We cannot turn off our physiological reactions to stressors like a light switch. Furthermore, we shouldn't attempt to do so, as arousal can improve our performance.
Kelly McGonigal compellingly presents evidence that major life changes will not shorten life expectancy if we reinterpret our activation as bravely facing challenges. In addition, our prosocial actions can protect us from the harmful effects of major life changes. Dr. Inna Khazan persuasively argues that a mindfulness approach to stress can enhance our cardiovascular and neuroendocrine responses to stressors.
Challenges to Homeostasis
Claude Bernard, Walter Cannon, and Hans Selye were influential scientists who contributed significantly to the development and understanding of the concept of homeostasis, which refers to the ability of living organisms to maintain internal stability and balance in the face of changing external conditions.
Claude Bernard (1813-1878) was one of the first scientists to recognize the importance of maintaining a stable internal environment for the proper functioning of the body's cells and organs. He introduced the concept of the "milieu intérieur" (internal environment) and argued that the role of physiological processes is to maintain a constant internal environment, which is necessary for life. Bernard's work laid the foundation for the concept of homeostasis and emphasized the importance of the body's ability to regulate its internal conditions.
Walter Bradford Cannon (1871-1945) built upon Bernard's work and coined the term homeostasis to describe the dynamic equilibrium that living organisms maintain to ensure their survival. He identified several key physiological mechanisms responsible for maintaining homeostasis, such as the regulation of body temperature, blood sugar levels, and pH. Cannon also introduced the "fight or flight" response, which refers to the body's acute stress response and the physiological changes that occur to prepare an organism for action in the face of a threat.
János Hugo Bruno "Hans" Selye (1907-1982) is best known for his research on stress and its effects on the body. He developed the concept of the "general adaptation syndrome" (GAS), which describes the body's three-stage response to stress: alarm, resistance, and exhaustion. Selye's work contributed to our understanding of how the body strives to maintain homeostasis in the face of stressors and how chronic stress can lead to maladaptive responses, negatively affecting overall health.
Together, the work of Claude Bernard, Walter Cannon, and Hans Selye has helped shape our understanding of homeostasis as a fundamental principle governing the function of living organisms. Their research has provided valuable insights into the complex regulatory systems that enable organisms to adapt and respond to their environments, ensuring their survival and well-being.
We will discuss powerful challenges to homeostasis, including cataclysmic events, early life stress/adversity, and childhood trauma.
Cataclysmic Events
Lazarus and Cohen (1977) described cataclysmic events as "sudden, unique, and powerful single life-events requiring major adaptive responses from population groups sharing the experience” (p. 91).
Intentional and unintentional, these events can impact local communities (e.g., mass shootings), geographic regions (e.g., earthquakes, fires, hurricanes, and tsunamis), and the entire planet (e.g., the COVID-19 pandemic. These catastrophes can produce death, dislocation, fear, grief, trauma, and Post-Traumatic Stress Disorder. Graphic © Syda Productions/Shutterstock.com.
Many factors influence survivor response to these powerful stressful events, including perceived discrimination, resources, support, vulnerability to future harm, distance from the devastation, and media coverage. The stressfulness of an event is influenced by geographic proximity, its recency, and whether it was intended. Intentional events are more traumatic than natural disasters because the perpetrators targeted the victims and could do so again (Brannon et al., 2022).
Traumatic Stress and Post-Traumatic Stress Disorder (PTSD)
Traumatic stress is produced by a highly intense stressor that disrupts coping and endangers ourselves or others. Post-Traumatic Stress Disorder (PTSD) is a severe and long-lasting trauma and stressor-related disorder that often develops within three months of a traumatic event. DSM-5 (APA, 2013) divides its symptoms into four clusters: intrusion, avoidance, negative alterations in cognition and mood, and alterations in arousal and reactivity. Graphic © John Gomez/Shutterstock.com.
The exposure can also be second-hand, such as witnessing domestic violence or learning about a family tragedy (Crider, 2004; Lamprecht & Sack, 2002). The lifetime prevalence of adult PTSD in the United States is about 6.8% (Kessler et al., 2005).
While the earliest model of PTSD focused on trauma during combat, subsequent research has shown that crime, domestic violence, natural disasters, sexual assault, and terrorism can precipitate PTSD symptoms. Since women are more likely than men to experience these stressful events, it should not be surprising that they are more often diagnosed with this disorder (Stein et al., 2000). Children and adolescent victims and witnesses of violence also share an elevated risk of PTSD (Silva et al., 2000).
A single traumatic event can reshape synapses and increase electrical activity in the amygdala 10 days later. The N-methyl-D-aspartate receptor (NMDA-R) protein, which plays a central role in long-term memory, mediates these changes (Yasmin et al., 2016). Amygdala graphic © Kateryna Kon/ Shutterstock.com.
Early Life Stress/Adversity (ELA)
Birnie and colleagues (2023) reported that early-life stress could disrupt reward circuitry, resulting in anhedonia or loss of pleasure and motivation. They discovered a corticotropin-releasing hormone (CRH)/gamma-aminobutyric acid (GABA) pathway from the basolateral amygdala to the nucleus accumbens in mice. Adverse experiences overactivated this pathway, disrupting reward-seeking behaviors. Silencing this pathway restored reward behaviors.
In humans, the amygdala's central nucleus activates the hypothalamus' paraventricular nucleus (PVN), increasing CRH release to the pituitary gland in response to stressful stimuli.
Chronic, elevated CRH levels in the bloodstream may enhance learning classically conditioned fear responses, heighten arousal and attention to increase readiness to respond to a stressor, intensify the startle response, and reduce appetite and body weight, sexual behavior, and growth.
Childhood Trauma and PSTD
The overall one-year prevalence of childhood trauma is around 14% (SAMHSA, 2022). This number is likely an underestimation. Graphic © fasphotographic/Shutterstock.com.
Intentional acts may produce more widespread distress than natural disasters because they threaten future and more devastating attacks. The impact of a catastrophic event depends on your distance from the event, the time interval since the event, and the perpetrators' perceived intentions (Brannon et al., 2022).
PTSD can permanently damage the systems that regulate our stress response, particularly the amygdala and hypothalamic-pituitary-adrenal (HPA) axis. Patients experience increased cortisol level fluctuation and persistent epinephrine, norepinephrine, testosterone, and thyroxin elevation (Taylor, 2006).
PTSD may promote medical illness through persistent immunosuppression (Kawamura et al., 2001). Military veterans diagnosed with PTSD are more likely to develop severe diseases following discharge than veterans without PTSD (Deykin et al., 2001). PTSD may also exacerbate pre-existing health problems. PTSD resulting from the September 11, 2001, World Trade Center attacks may have helped worsen asthmatic symptoms in New York residents (Fagan et al., 2003).
Stress and Anxiety
Studies have shown that stress and anxiety share common neural circuits, particularly involving the basolateral amygdala (BLA) and the locus coeruleus (LC). Graphic © Vasilisa Tsoy/Shutterstock.
Acute stress can induce anxiety through norepinephrine inputs from the LC to the BLA. Additionally, mitochondrial function within the nucleus accumbens (NAc) has been implicated in individual trait anxiety and the stress-anxiety link (Daviu et al., 2019).
The Physiological Impact of Chronic Stress
Researchers have studied the deleterious effects of chronic stress on the microbiome and immune system. Consistent with Hans Selye's General Adaptation Syndrome, chronic stress can produce allostatic load, and exhaustion, resulting in depletion and death.
Allostasis is a concept that complements homeostasis, describing the adaptive processes the body uses to maintain stability or balance during times of stress or change. While homeostasis refers to maintaining relatively constant internal conditions, allostasis focuses on the body's ability to adapt and adjust to various stressors to maintain overall stability.
In the context of Hans Selye's General Adaptation Syndrome (GAS), allostasis plays a crucial role in the body's response to stress. GAS describes the body's three-stage response to stress: alarm, resistance, and exhaustion.
Alarm stage: This is the initial response to a stressor, where the body activates the "fight or flight" response, which Walter Cannon described. This involves the release of stress hormones such as adrenaline and cortisol, leading to increased heart rate, blood pressure, and other physiological changes that prepare the body to react to the threat. Allostasis is at work during this stage as the body adapts to the new stressor and deviates from its normal balance to deal with the immediate challenge.
Resistance stage: If the stressor persists, the body enters the resistance stage, attempting to adapt to the ongoing stress and maintain a new level of stability. Allostasis continues to play a role as the body adjusts its physiological processes to manage the stressor. This may include the continued release of stress hormones, adjustments in immune function, and alterations in metabolism.
Exhaustion stage: If the stressor continues for an extended period, the body's adaptive resources may become depleted, leading to the exhaustion stage. Allostasis may no longer be effective at this point, as the body's ability to adapt to the stressor is overwhelmed. This can result in a breakdown of physiological systems and an increased risk of illness and disease.
Allostasis highlights the dynamic nature of the body's response to stress and underscores the importance of adaptability in maintaining stability. However, prolonged or chronic stress can lead to allostatic load, which describes the cumulative wear and tear on the body due to repeated or excessive adaptation to stressors. This can negatively affect overall health, increasing the risk of various physical and mental health conditions. Graphic adapted from Biostrap.
Stress and the Microbiome
The human body primarily comprises single-celled organisms, which outnumber our human cells 1.3-to-1 (Sender et al., 2016). Viruses vastly outnumber bacteria and could sharply increase the microbe-to-human cell ratio (Saey, 2016). The microbiome is a collection of microorganisms (including bacteria, viruses, fungi, and other microscopic organisms) that live in and on our bodies. Most human bacteria are located in our gut. Graphic © Kateryna Kon/Shutterstock.com.
Research using rodents suggests that the 40 trillion bacteria in our microbiome may influence brain development, neurotransmitter synthesis, emotions, pain thresholds, and response to stressors. In rodents, shifts in the microbiome's ecology can produce more exploratory or cautious behavior. Illustration 168610495 © Burgstedt | Dreamstime.com
The relationship between the brain and gut biome appears to be bidirectional. While the brain and gut microbiome probably communicate using several pathways, the 100 million enteric system neurons that regulate the GI tract may be a crucial nexus. Mild stress can reduce the number of beneficial bacteria.
Chronic stress can significantly impact the human microbiome. The gut microbiome, in particular, plays a crucial role in many aspects of our health, including digestion, immune function, and even mental health.
Chronic stress can affect the human microbiome in several ways:
Altered composition: Chronic stress has been shown to cause alterations in the composition of the gut microbiota, leading to imbalances between beneficial and potentially harmful microorganisms. This dysbiosis can disrupt the normal functioning of the gut microbiome and contribute to various health issues, including inflammatory bowel diseases, obesity, and immune dysregulation.
Increased permeability: Chronic stress can lead to increased gut permeability, often called "leaky gut." This occurs when the tight junctions between the cells lining the gut weaken, allowing bacteria, toxins, and undigested food particles to pass into the bloodstream. This increased permeability can lead to inflammation and exacerbate immune-related conditions.
Weakened immune function: A significant proportion of the immune system is located in the gut, and the gut microbiome plays a vital role in modulating immune responses. Chronic stress can impair immune function, making it harder for the body to control potentially harmful microorganisms and increasing the risk of infection and inflammation.
Impact on mental health: The gut microbiome communicates with the brain through the gut-brain axis, a complex network involving the nervous system, hormones, and immune signaling. Chronic stress can disrupt this communication, contributing to anxiety, depression, and other mental health disorders. Conversely, alterations in the gut microbiome can also influence stress responses, creating a bidirectional relationship between stress and the gut microbiome. Disorders like anxiety and depression may be associated with abnormal microbiota (Carpenter, 2012).
Lifestyle factors: Chronic stress can lead to unhealthy lifestyle choices, such as poor diet, lack of exercise, and insufficient sleep, which can negatively impact the gut microbiome. For example, a diet high in processed foods and low in fiber can lead to a less diverse gut microbiota, which has been associated with various health problems.
In summary, chronic stress can significantly affect the human microbiome, particularly in the gut, leading to imbalances in microbial composition, increased gut permeability, weakened immune function, and impacts on mental health. Maintaining a healthy microbiome through a balanced diet, regular exercise, and stress management techniques can help promote overall health and well-being.
Stress and the Immune System
Although brief stress does not suppress immunity and may strengthen it (Dhabhar, 2018), chronic stress can reduce immunocompetence.
Klopack and colleagues (2022) reported an archival study involving responses from over 5,700 US adults 50 and older about stress from discrimination, their jobs, life events, and traumatic experiences. They cross-referenced responses with immune cell counts from their blood. Higher stress levels were associated with accelerated immune aging, as measured by CD4+ and CD8+ cells. T lymphocytes (T cells) are white blood cells and crucial components of the immune system. CD4+ and CD8+ T cells play essential roles in adaptive immunity, which is a highly specific and long-lasting defense against pathogens and foreign substances. Also known as helper T cells, CD4+ T cells primarily assist in the immune response by coordinating and regulating the activities of other immune cells. They are crucial for activating and directing B cells to produce antibodies, stimulating cytotoxic T cells to kill infected cells, and recruiting other immune cells, like macrophages and neutrophils, to the site of infection.
Also known as cytotoxic T cells or killer T cells, CD8+ T cells are responsible for directly killing infected or abnormal cells, such as virus-infected cells or cancer cells. Graphic © Juan Gaertner/Shutterstock.com.
The Brain Mediates Stressor Effects on Health
Neuroimaging studies have identified neural systems involved in threat processing, safety processing, and social cognition as key contributors to stress-related physiological changes (Muscatell & Einsenberger, 2012).
Threat Processing
The neural systems involved in threat processing include the amygdala, dorsal anterior cingulate cortex (dACC), and anterior insula (AI). These regions function as part of a "neural alarm system" that detects potential threats and coordinates responses. The amygdala responds to salient and relevant stimuli to the perceiver's goals and motivations, particularly those related to fear and threat. It is connected to the sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal (HPA) axis. The dACC is associated with distress and cognitive control during threat or pain, and the AI is linked to interoceptive awareness, reflecting the conscious representation of the body's physiological state.
Safety Processing
The neural systems involved in safety processing prominently feature the ventromedial prefrontal cortex (VMPFC). The VMPFC plays a critical role in signaling safety and inhibiting threat-related responses. It is active during situations like fear extinction when a previously feared stimulus is associated with safety. The VMPFC's inhibitory connections to the amygdala may decrease threat perception and reduce physiological stress responses. Additionally, studies indicate that individuals experiencing low stress or pain conditions show increased VMPFC activity, suggesting its involvement in reducing stress and enhancing perceptions of safety.
Social Cognition
Neural systems involved in social cognition include the medial prefrontal cortex (MPFC), perigenual anterior cingulate cortex (pACC), dorsomedial prefrontal cortex (DMPFC), and posterior cingulate cortex (PCC). These regions are associated with processing thoughts, feelings, and traits related to oneself and others. The MPFC, pACC, and PCC are activated when individuals reflect on their own traits or emotions, while the MPFC and DMPFC are particularly engaged in understanding others' mental states. These areas connect to regions like the amygdala and hypothalamus, which are important for generating sympathetic nervous system (SNS) and hypothalamic-pituitary-adrenal (HPA) axis responses.
Stress and Functional Connectivity
Mental stress significantly reduced functional connectivity within the prefrontal cortex (PFC), particularly in the dorsolateral PFC (DLPFC). This reduction is observed in both inter- and intra-hemispheric regions and involves synchronized electrical (EEG alpha rhythms) and hemodynamic (fNIRS oxygenated and deoxygenated hemoglobin) responses (Al-Shargie, 2021).
Dorsolateral prefrontal cortex graphic © Songkram Chotik-anuchit/Shutterstock.com.
The right DLPFC was identified as the most stress-sensitive region, showing significant connectivity disruptions under stress. The ventrolateral and frontopolar areas also exhibited reduced connectivity but to a lesser extent.
Physiological Versus Psychosocial Stress
Recent meta-analyses have highlighted the differential neural engagement during physiological and psychosocial stress. Both types of stress activate the inferior frontal gyrus (IFG) and the anterior insula (AI), indicating a global neural stress reaction (Kogler et al., 2015). Insular cortex graphic Ide JS and Li C-S R (2011) Creative Commons Attribution 3.0. Error-related functional connectivity of the habenula in humans. Front. Hum. Neurosci. http://journal.frontiersin.org/article/10.3389/fnhum.2011.00025/fu
However, physiological stress tends to activate regions associated with pain processing, such as the insula and striatum (e.g., caudate nucleus and putamen). In contrast, psychosocial stress activates the right superior temporal gyrus and deactivates the striatum, particularly the ventral striatum involved in reward processing.
This differentiation underscores the importance of considering the type of stressor when studying neural responses to stress.
Positive Perspectives on Stress
Although challenge is an inescapable and often energizing part of living, stress does not have to produce illness and premature death. In this section, we will discuss the effect of reframing the stress response as courage, the protective effects of prosocial behavior, hardiness, and the benefits of a mindfulness perspective.
Reframe the Stress Response
Cannon (1942) studied voodoo deaths in shamanistic cultures and published speculation about how beliefs can produce lethal cascades of system failure in the American Anthropologist. Graphic © Fer Gregory/Shutterstock.com.
The Belief That Stress Is Harmful
Keller et al. (2012) conducted a regression analysis of the 1998 National Health Interview Survey and prospective National Death Index data from 28,753 adults. Both elevated levels of reported stress and the perception that stress negatively impacted health independently and jointly predicted poor physical and psychological health outcomes. While neither variable independently predicted premature death, those who reported high levels of stress and the perception that stress impacts health experienced a 43% greater risk of early death.
Reframing Physiological Arousal
Jamieson and colleagues (2012) investigated whether reframing or "reappraising" physiological arousal during stressful events can improve cardiovascular responses and attentional focus. Previous theories and research suggest how individuals mentally frame their physical stress responses can significantly impact their well-being, but the mechanisms underlying these effects are unclear.
In this study, participants were assigned to one of three groups: (1) a reappraisal group, which was instructed to view stress-induced physiological arousal as beneficial, (2) an attention reorientation group, which was told to redirect their attention to external cues to reduce stress, or (3) a control group that received no specific instructions. All participants then engaged in a stressful task, the Trier Social Stress Test (TSST), involving public speaking and mental arithmetic under evaluative scrutiny, during which their cardiovascular responses were recorded. They also completed an emotional Stroop task afterward to measure attentional bias toward negative information.
The theoretical framework behind this study is the Biopsychosocial (BPS) Model of Challenge and Threat. According to this model, stress responses differ based on whether people perceive they have enough resources to handle a stressful situation ("challenge" state) or whether the demands of the situation exceed their resources ("threat" state).
Developed in part by researchers like Jim Blascovich and Wendy Mendes, the model posits that stress responses fall into one of two states: "challenge" or "threat," depending on whether people perceive their resources as sufficient to meet situational demands.
In the "challenge" state, individuals feel that they have the skills or resources to handle the stressor. Physiologically, this is characterized by activation of the sympathetic-adrenal-medullary (SAM) axis, leading to increased cardiac efficiency (measured as higher cardiac output) and vasodilation, which improves blood flow and supports an "approach" or engagement orientation. The challenge state is generally associated with adaptive outcomes, such as better performance and positive health effects.
In contrast, the "threat" state arises when people perceive that the demands of the situation exceed their resources. Although the SAM axis is still activated, the cardiovascular response differs: individuals show lower cardiac efficiency and increased vasoconstriction, which reduces blood flow to the periphery. This response signals an "avoidance" orientation, preparing the body for potential damage or defeat. Threat states are linked with poorer cognitive functioning in the short term and, over time, with negative health outcomes, such as cardiovascular disease and accelerated cognitive decline.
The BPS Model suggests that reappraising stressful situations to perceive them as more manageable (shifting from a threat to a challenge state) can lead to healthier physiological and psychological responses.
Physiologically, challenge states are linked with increased cardiac efficiency and vasodilation, which enhance blood flow and signal an approach-oriented response. In contrast, threat states are characterized by reduced cardiac efficiency and vasoconstriction, indicating an avoidance-oriented response, potentially predisposing individuals to negative health outcomes like cardiovascular disease.
The findings indicated that those in the reappraisal group showed more adaptive physiological responses: their bodies demonstrated increased cardiac efficiency (measured as cardiac output) and reduced vascular resistance (indicating lower total peripheral resistance). This suggests that viewing stress as beneficial may foster a challenge-oriented physiological profile, which has been associated with better health outcomes. Additionally, reappraisal participants displayed less attentional bias toward negative, threat-related stimuli compared to other groups. This bias, often marked by a heightened focus on negative information, is linked to anxiety and other stress-related disorders.
This study's implications are promising for clinical contexts, especially in fields like cognitive-behavioral therapy (CBT). Reappraisal techniques echo components of CBT, where patients are often trained to reinterpret stressful bodily signals more constructively. For example, anxiety therapies sometimes use reappraisal to reduce "fear of fear"—a self-amplifying response where individuals feel anxious about their anxiety symptoms. By modifying how patients interpret their physiological arousal, reappraisal could be used to help reduce anxiety, particularly in disorders associated with attentional biases toward threats, such as social anxiety or PTSD.
Check out Kelly McGonigal's TED Talk How to Make Stress Your Friend. McGonigal proposes that we train clients to reframe sympathetic activation as evidence of our courage to rise to a challenge instead of the body injuring itself.
Prosocial Behavior Buffers Stress Effects
A prospective study of 846 adults by Poulin et al. (2013) showed that providing tangible assistance to friends or family members in the previous year buffered the effects of stress on mortality over 5 years. In contrast, stress predicted mortality for participants who did not help others. Graphic © Ljupco Smokovski/Shutterstock.com.
Follow-up data from the longitudinal National Survey of Midlife Development in the U.S. (MIDUS II) of 1054 middle-aged adults found that women who perceived that they supported others in positive social relationships had lower IL-6 levels, which is a marker for inflammation (Jiang et al., 2021). Elevated IL-6 levels are linked to an increased risk for serious diseases.
Hardiness: Thriving in the Face of Adversity
Some individuals do not experience illness or psychological distress when exposed to adverse life events and hassles. Although they may experience brief distress, they generally recover (Lehrer, 2021). Researchers use the concept of hardiness to explain these outliers (Maddi, 2017; Maddi et al., 2017; Pitts et al., 2016; Stoppelbein et al., 2017). Graphic © lassedesignen/Shutterstock.com.
The hardiness concept emerged from a 12-year study of manager stress responses at the Illinois Bell Company (Maddi, 1987). Halfway through the study, their parent company's reorganization eliminated half their employees within a year. Two-thirds of the managers experienced severe stress reactions (e.g., heart attacks, depression, and suicide), and one-third thrived. The investigators concluded that the hardy managers were protected by attitudes of commitment (strong involvement), control (internal locus of control), and challenge (learning from experience and accepting change).
Hardiness involves biological (McVicar et al., 2014; Parkash et al., 2017) and social factors (Kuzman & Konopak, 2016). Longitudinal studies suggest that infants' autonomic and emotional reactivity predicts later emotional reactivity (Berry et al., 2012; Wagner et al., 2017). Less reactive infants may become more resilient. In addition, cohesiveness and social support (actual and perceived) may buffer hardy individuals against stressors. Graphic © Nina Buday/Shutterstock.com.
Dr. Inna Khazan's Mindfulness Perspective
Brooks (2014) showed that attempts to calm oneself before stressful performances failed to reduce physiological arousal and were unnecessary. In several studies, arousal was associated with better math, public speaking, and singing performance. We do not need to calm ourselves; we need to reframe our arousal as excitement instead of anxiety.
Mindfulness involves "paying attention in a particular way: on purpose, in the present moment, and nonjudgmentally" (Kabat-Zinn, 1994). Mindfulness teaches clients to focus on their immediate feelings, cognitions, and sensations in an accepting and nonjudgmental way.
Clients learn to distinguish between what they can and cannot change and to change the things they can (Khazan, 2013). The key to escaping quicksand is not to struggle.
Quicksand graphic © Cory Thoman/Dreamstime.com.
Dr. Khazan proposes that we reframe "threats" as "challenges." This avoids the "futile effort to control the uncontrollable" (Khazan, 2019, p. 217).
Reframing improves performance and produces a healthier cardiovascular response to stressors, increasing cardiac performance while reducing peripheral resistance (Jamieson et al., 2010).
The Yerkes-Dodson curve graphs the relationship between stressors and performance. Reframing can reduce perceived pressure and energize performance.
The left side of the inverted U-curve depicts an underload where an individual is insufficiently challenged and bored. This phenomenon of low motivation and performance has been termed rust out and reminds us that we require stressors for motivation and creativity (O'Dowd, 1987). The middle region that ends with peak performance corresponds to eustress. An optimal level of challenge promotes focus, motivation, and creativity. The right side of the curve represents the worsening effects of excessive pressure, overload, and burn-out with anxiety, panic, and anger. Graphic © Olivier Le Moal/Shutterstock.com.
Reinterpreting physiological activation as adaptive increases the dehydroepiandrosterone (DHEA) to cortisol ratio (Morgan et al., 2004). This is beneficial for several reasons. DHEA and cortisol are steroid hormones produced by the adrenal glands but have different bodily functions.
Balancing effects: DHEA and cortisol have opposing effects on the body. While cortisol is a catabolic hormone that breaks down tissues, increases inflammation, and suppresses the immune system, DHEA is anabolic, promoting tissue growth, repair, and a healthy immune response. A higher DHEA-to-cortisol ratio signifies that the body is more balanced, with adequate resources for growth and repair.
Stress response: Cortisol is a stress hormone that increases in response to physical, emotional, or psychological stressors. Chronic stress can lead to persistently elevated cortisol levels, negatively impacting health by promoting inflammation, impairing immune function, and increasing the risk of chronic diseases. A higher DHEA-to-cortisol ratio suggests that the body can better cope with stress and maintain a healthier stress response.
Aging and cognitive function: DHEA levels decline with age, and lower levels have been associated with cognitive decline, mood disorders, and other age-related health issues. A higher DHEA-to-cortisol ratio may indicate better overall cognitive function and reduced risk of age-related diseases.
Cardiovascular health: A higher DHEA-to-cortisol ratio has been linked to better cardiovascular health. Elevated cortisol levels can contribute to high blood pressure, arterial stiffness, and other risk factors for heart disease, while DHEA has been shown to have cardioprotective effects.
Conclusion
We do not need to purposefully change our physiological response to stress. We do not need to calm down in order to do our best. All we need to do is interpret the sensations of activation in a more helpful way (Khazan, 2019, p. 217).
Quiz
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Glossary
amygdala: a limbic system structure that plays a crucial role in learning about the consequences of our actions and creating declarative memories for events with emotional significance.
B lymphocytes: the immune cells central to humoral immunity that rapidly produce antibodies that counter bacteria in the blood, neutralize toxins, and prevent reinfection by viruses.
Biopsychosocial (BPS) Model of Challenge and Threat: a theoretical framework explaining how individuals respond physiologically and psychologically to stress, based on their appraisals of the situation and available resources.
cataclysmic event: a sudden, large-scale, and often destructive natural or man-made occurrence that results in significant changes to the environment, ecosystems, and human societies.
childhood trauma: experiencing harm or threat of harm to oneself or others.
corticotropin-releasing hormone (CRH): hormone released by the hypothalamus that triggers ACTH release by the pituitary gland.
cortisol: a catabolic steroid hormone that catabolic hormone that breaks down tissues, increases inflammation, and suppresses the immune system.
cytotoxic T (Tc) cells: immune cells that release toxins to destroy specific virally infected cells.
dehydroepiandrosterone (DHEA): a steroid hormone that promotes tissue growth, repair, and healthy immune response.
functional near-infrared spectroscopy (fNIRS): non-invasive imaging technique used to monitor brain activity by measuring changes in oxygenated (HbO) and deoxygenated hemoglobin (HbR).
hardiness: the ability to thrive under stressful conditions.
lymphocytes: white blood cells, including T cells, B cells, and natural killer (Nk) cells, that play a crucial role in immune defenses. microbiome: the collection of microorganisms that reside in the human body.
pituitary gland: the endocrine gland found at the base of the skull that is divided into the anterior pituitary, which secretes the tropic hormones adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin, and growth hormone (GH), and the posterior pituitary that releases oxytocin and vasopressin produced by the hypothalamus.
post-traumatic stress disorder (PTSD): a severe and long-lasting trauma and stressor-related disorder that often develops within three months of a traumatic event and may include re-experiencing a traumatic event, avoidance of stimuli associated with the trauma, numbing of responsiveness, and hyperarousal.
social support: received (support provided) and perceived support (expected support) from individuals and organizations.
traumatic stress: stress produced by a highly intense stressor that disrupts coping and endangers ourselves or others.
References
Al-Shargie, F. (2021). Prefrontal cortex functional connectivity based on simultaneous record of electrical and hemodynamic responses associated with mental stress. arXiv. https://arxiv.org/abs/2103.04636
American Psychiatric Association (APA). (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Author. Berry, D., Blair, C., Willoughby, M., & Granger, D. A. (2012). Salivary alpha-amylase and cortisol in infancy and toddlerhood: Direct and indirect relations with executive functioning and academic ability in childhood. Psychoneuroendocrinology, 37(10), 1700–1711. https://doi.org/10.1016/j.psyneuen.2012.03.002 Birnie, M. T., Short, A. K., de Carvalho, G. B., Taniguchi, L., Gunn, B. G., Pham, A. L., Itoga, C. A., Xu, X., Chen, L. Y., Mahler, S. V., Chen, Y., & Baram, T. Z. (2023). Stress-induced plasticity of a CRH/GABA projection disrupts reward behaviors in mice. Nature communications, 14(1), 1088. https://doi.org/10.1038/s41467-023-36780-x Brannon, L., Feist, J., & Updegraff, J. A. (2022). Health psychology (10th ed.). Cengage Learning. Brooks A. W. (2014). Get excited: reappraising pre-performance anxiety as excitement. Journal of experimental psychology. General, 143(3), 1144–1158. https://doi.org/10.1037/a0035325 Cannon, W. (1942). Voodoo death. American Anthropologist, 44, 169–181. https://doi.org/10.1525/aa.1942.44.2.02a00010 Carpenter, S. (2012). That gut feeling. Monitor on Psychology, 43(8), 50.
Crider, A. (2004). Module 2: Stress and illness. In A. Crider & D. D. Montgomery (Eds.). Introduction to biofeedback. Association for Applied Psychophysiology and Biofeedback.
Daviu, N., Bruchas, M., Moghaddam, B., Sandi, C., & Beyeler, A. (2019). Neurobiological links between stress and anxiety. Neurobiology of Stress, 11. https://doi.org/10.1016/j.ynstr.2019.100191
Dhabhar, F. S. (2018). The short-term stress response: Mother nature’s mechanism for enhancing protection and performance under conditions of threat, challenge, and opportunity. Front. Neuroendocrinol., 49, 175–192.
Deykin, E. Y., Keane, T. M., Kaloupek, D., Findke, G., Rothendler, J., Siegfried, M., & Creamer, K. (2001). Posttraumatic stress disorder and the use of health services. Psychosomatic Medicine, 63, 835-841. https://doi.org/10.1097/00006842-200109000-00018
Fagan, J., Galea, S., Ahern, J., Bonner, S., & Vlahov, D. (2003). Relationship of self-reported asthma severity and urgent health care utilization to psychological sequelae of the September 11, 2001, terrorist attacks on the World Trade Center among New York City area residents. Psychosomatic Medicine, 65, 993-996. https://doi.org/10.1097/01.psy.0000097334.48556.5f
Jamieson, J. P., Nock, M. K., & Mendes, W. B. (2012). Mind over matter: Reappraising arousal improves cardiovascular and cognitive responses to stress. Journal of Experimental Psychology. General, 141(3), 417–422. https://doi.org/10.1037/a0025719
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. Healthy Psychology, 31(5), 677-684. https://doi.org/10.1037/a0026743
Kessler, R. C., Berglund, P., Delmer, O., Jin, R., Merikangas, K. R., & Walters, E. E. (2005). Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Archives of General Psychiatry, 62(6), 593-602. https://doi.org/10.1001/archpsyc.62.6.593
Khazan, I. (2013). The clinical handbook of biofeedback: A step-by-step guide for training and practice with mindfulness. John Wiley & Sons, Ltd.
Khazan, I. (2019). Biofeedback and mindfulness in everyday life. W. W. Norton & Company.
Klopack, E. T., Crimmins, E. M., Cole, S. W., Seeman, T. E., & Carroll, J. E. (2022). Social stressors associated with age-related T lymphocyte percentages in older US adults: Evidence from the US Health and Retirement Study. Proceedings of the National Academy of Sciences of the United States of America, 119(25), e2202780119. https://doi.org/10.1073/pnas.2202780119
Kogler, L., Müller, V., Chang, A., Eickhoff, S., Fox, P., Gur, R., & Derntl, B. (2015). Psychosocial versus physiological stress — Meta-analyses on deactivations and activations of the neural correlates of stress reactions. NeuroImage, 119, 235-251. https://doi.org/10.1016/j.neuroimage.2015.06.059
Kuzmin, M. Y., & Konopak, I. A. (2016). Distinctive features of adolescent hardiness in families of different composition. Psychology in Russia: State of the Art, 9(3), 95–10. https://doi.org/10.11621/pir.2016.0306
Lamprecht, F., & Sack, M. (2002). Posttraumatic stress disorder revisited. Psychosomatic Medicine, 64, 222-237. https://doi.org/10.1097/00006842-200203000-00005 Lehrer, P. M. (2021). Psychophysiological and systems perspective. In P. M. Lehrer & R. L. Woolfolk (Eds.), Principles and practice of stress management (4th ed.). The Guilford Press. Maddi, S. R. (1987). Hardiness training at Illinois Bell Telephone. In J. P. Opatz (Ed.), Health promotion evaluation, pp. 101-1115. National Wellness Institute. Maddi, S. R. (2017). Hardiness as a pathway to resilience under stress. In U. Kumar (Ed.), The Routledge international handbook of psychosocial resilience (pp. 104–110). Routledge/Taylor & Francis. Maddi, S. R., Matthews, M. D., Kelly, D. R., Villarreal, B. J., Gundersen, K. K., & Savino, S. C. (2017). The continuing role of hardiness and grit on performance and retention in West Point cadets. Military Psychology, 29(5), 355–358. https://doi.org/10.1037/mil0000145
McVicar, A., Ravalier, J. M., & Greenwood, C. (2014). Biology of stress revisited: Intracellular mechanisms and the conceptualization of stress. Stress and Health, 30(4), 272–279. https://doi.org/10.1002/smi.2508 Morgan, C. A., 3rd, Southwick, S., Hazlett, G., Rasmusson, A., Hoyt, G., Zimolo, Z., & Charney, D. (2004). Relationships among plasma dehydroepiandrosterone sulfate and cortisol levels, symptoms of dissociation, and objective performance in humans exposed to acute stress. Archives of general psychiatry, 61(8), 819–825. https://doi.org/10.1001/archpsyc.61.8.819 Muscatell, K., & Eisenberger, N. (2012). A social neuroscience perspective on stress and health. Social and Personality Psychology Compass, 6(12), 890-904. https://doi.org/10.1111/J.1751-9004.2012.00467.X O'Dowd, T. C. (1987). To burn out or to rust out in general practice. J R Coll Gen Pract, 37(300), 290-291. PMID: 3449629 Parkash, V., Archana, & Kumar, U. (2017). Role of genetics and temperament in resilience. In U. Kumar (Ed.), The Routledge international handbook of psychosocial resilience (pp. 75–87). Routledge/Taylor & Francis. Pitts, B. L., Safer, M. A., Russell, D. W., & Castro-Chapman, P. L. (2016). Effects of hardiness and years of military service on post-traumatic stress symptoms in U.S. Army medics. Military Psychology, 28(4), 278–284. https://doi.org/10.1037/mil0000106
Saey, T. H. (2016). Body's bacteria don't outnumber human cells so much after all: New calculations suggest roughly equal populations, not 10-to-1 ratio. Science News. Retrieved from https://www.sciencenews.org
Substance Abuse and Mental Health Services Administration. (2022, September 27). Understanding child trauma. SAMHSA. Retrieved January 23, 2023, from https://www.samhsa.gov/child-trauma/understanding-child-trauma
Sender, R., Fuchs, S., & Milo, R. (2016), Revised estimates for the number of human and bacteria cells in the body. BioRxiv. Posted online January 6, 2016.
Silva, R. P., Alpert, M., Munoz, D. M., Singh, S., Matzner, F., & Dummit, S. (2000). Stress and vulnerability to posttraumatic stress disorder in children and adolescents. Journal of Psychiatry, 157, 1229-1235. https://doi.org/10.1176/appi.ajp.157.8.1229
Stein, M. B., Walker, J. R., & Forde, D. R. (2000). Gender differences in susceptibility to posttraumatic stress disorder. Behavior Research and Therapy, 38, 619-628. https://doi.org/10.1016/s0005-7967(99)00098-4
Stoppelbein, L., McRae, E., & Greening, L. (2017). A longitudinal study of hardiness as a buffer for posttraumatic stress symptoms in mothers of children with cancer. Clinical Practice in Pediatric Psychology, 5(2), 149–160. Taylor, S. E., Gonzaga, G., Klein, L. C., Hu, P., Greendale, G. A., & Seeman, T. E. (2006). Relation of oxytocin to psychological and biological stress responses in women. Psychosomatic Medicine, 68, 238–245. https://doi.org/10.1097/01.psy.0000203242.95990.74 Wagner, N., Mills-Koonce, R., Willoughby, M., Propper, C., Rehder, P., & Gueron-Sela, N. (2017). Respiratory sinus arrhythmia and heart period in infancy as correlates of later oppositional defiant and callous–unemotional behaviors. International Journal of Behavioral Development, 41(1), 12. https://doi.org/10.1177%2F0165025415605391
Yasmin, F., Saxena, K., McEwen, B. S., & Chattarji, S. (2016). The delayed strengthening of synaptic connectivity in the amygdala depends on NMDA receptor activation during acute stress. Physiol Rep, 4(20), pii: e13002. https://doi.org/10.14814/phy2.13002
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