Assumptions

Biofeedback is a learning process much like mastering a musical instrument or a videogame. During biofeedback, an individual interacts with a device, usually electronic, that monitors and feeds back information about physiological activity. For example, a child uses a strategy (instructing the body to remain still), observes the results (SMR increases and high beta decreases), and repeats this cycle throughout the day. Graphic © Pepermpron/Shutterstock.com.

Think of biofeedback as a "psychophysiological mirror" that teaches individuals to monitor, understand, and change their physiology (Peper, Shumay, & Moss, 2012). Just as a mirror reveals posture you cannot otherwise see, biofeedback reveals internal physiological processes that typically escape awareness.

Biofeedback training aims to teach self-regulation, which is control of behavior without feedback.

Consider a client who uses a mirror or a position sensor on the back (e.g., biofeedback) to practice keeping the chin level. When the client has practiced sufficiently to achieve good posture without reminders, this demonstrates self-regulation, the ability to maintain a desired physiological state without external feedback. Biofeedback training is a bridge to self-regulation. Graphic © fizkes/Shutterstock.com.

Biofeedback is information that can be used to guide and improve performance.

While biofeedback training is a powerful intervention for clinical disorders, it is increasingly used to promote optimal performance in settings ranging from athletics to military operations. Graphic © LDprod/Shutterstock.com.

Biofeedback training may be more effective when it promotes mindfulness, the practice of "paying attention in a particular way: on purpose, in the present moment, and nonjudgmentally" (Kabat-Zinn, 1994). A mindfulness approach teaches clients to focus on their immediate feelings, cognitions, and sensations in an accepting and non-judgmental way, to distinguish between what can and cannot be changed, and to change the things they can (Khazan, 2013). In biofeedback practice, mindfulness can focus on interoceptive feedback. Mindfulness of our physiology can guide the trial-and-error process underlying self-regulation by helping clients draw connections between their actions, internal feedback, and results. Graphic © fizkes/Shutterstock.com.

Clients can become stuck when they focus on outcomes they cannot immediately control. For example, Jane was diagnosed with elevated blood pressure. When she measured her pressure several times a day, her anxious attention increased these values and amplified her anxiety, which in turn interfered with her practice of slow-paced breathing. Her blood pressure gradually decreased when Jane learned to accept her high blood pressure without fear, reduce her measurement frequency to once a day, and focus entirely on healthy breathing, changing what she could control: her breathing pattern. Graphic © Ivelin Radkov/Shutterstock.com.

A comprehensive view of health and optimal performance recognizes the importance of the interconnected domains of body, mind, and spirit. In this context, spirit can mean philosophical beliefs or soul. Graphic © Gustavo Frazao/Shutterstock.com.

Neurofeedback, also called EEG biofeedback, is a specialized form of biofeedback in which an individual interacts with an electronic device that measures and feeds back information about brain electrical activity via brainwave displays. The process aims to promote effective regulation by the brain's neuromodulating systems, encourage global neurophysiological change, and correct specific, identifiable disorders arising from underlying dysregulation.

What does neurofeedback do? Neurofeedback provides accurate, timely, and useful information to the client through visual, auditory, or tactile feedback that corresponds to meaningful changes in the monitored systems. By making brain activity observable in real time, neurofeedback training encourages flexibility, resilience, and choice in how the brain responds to challenges.

Neuroplasticity, the ability of neurons and their networks to remodel themselves in response to experience, makes neurofeedback training possible (Breedlove & Watson, 2023). The learning mechanisms that underlie neurofeedback depend on interrelated structural and functional changes, including alterations in transmitter release and binding, modulation of transmitter release by interneurons, the formation and elimination of synapses, selection among competing neural pathways, and strengthening or weakening the connectivity between brain regions.

BCIA Blueprint Coverage

This unit addresses I. Orientation to Neurofeedback - D. Assumptions underlying neurofeedback.

This unit covers Concepts of Feedback and Control, Basic Psychophysiology of Stress, and Basic Physiology of Attention.

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Concepts of Feedback and Control

This section introduces the cybernetic foundations of biofeedback and neurofeedback, including feedback loops, homeostasis, and the thermostat analogy that shaped the field. These concepts explain why accurate physiological feedback is essential for self-regulation.

Both biofeedback and neurofeedback are grounded in concepts of feedback and control from cybernetic theory, the study of how systems use information to regulate themselves. Two everyday examples illustrate these principles: radar speed displays and handheld thermometers.

Continuous glucose monitoring (CGM) shows patients how closely their glucose level tracks their target range, illustrating the core concept of biofeedback. The device displays information about a physiological signal (glucose) back to an individual (a person managing their metabolic health) to change behaviors that drive glucose out of range, such as food choices, meal timing, and activity. A reward occurs when the high-glucose alert silences, the trend arrow flattens, and the reading settles back within the target range.

Cybernetic Model

The cybernetic model proposes that "biofeedback is like a thermostat." In fact, the term biofeedback originated in cybernetic theory, reflecting the principle that learning self-regulation requires accurate feedback about our physiology (Annett, 1969). Graphic © Maridav/Shutterstock.com.

The components of a thermostat system include a setpoint or goal (75° F/ 23.9° C), a system variable or what is controlled (room temperature), negative feedback or corrective instructions (commands to change furnace output), and positive feedback or instructions to continue action (orders to maintain furnace output). These same elements apply to biofeedback: the setpoint is the target physiological value, the system variable is the client's physiology, and the feedback display provides corrective information.

The internal environment fluctuates around a setpoint and is never stationary, which allows rapid adaptation to changing activity levels and environmental conditions. Homeostasis is a state of dynamic constancy achieved by stabilizing conditions above and below a setpoint, which may itself shift over time. From the perspective of the cybernetic model, biofeedback training supplements a client's proprioception to bring a malfunctioning biological system variable (such as blood pressure) under better control (Fox & Rompolski, 2021).

Homeostasis depends on three components: sensory systems (networks that monitor system variables) to detect an actual or anticipated change in physiological processes like temperature, an integrating center that receives input from many sensors, and multiple effector systems (control systems) that adjust physiological processes. This architecture mirrors the biofeedback clinic, where sensors monitor the client, biofeedback software integrates these signals, and the client's voluntary responses serve as effectors.

The body maintains dynamic constancy through continuous negative feedback loops amplified by positive feedback and antagonistic effectors.

Negative feedback loops produce corrective changes when a physiological variable is outside an acceptable range. For example, we initiate clotting to stop blood loss from a wound.

Positive feedback loops amplify the changes produced by negative feedback. For example, activating one clotting factor activates others to create a blood clot.

Push-pull control by effectors that produce antagonistic effects achieves more precise control than turning a single effector on or off. For example, the sympathetic nervous system accelerates the heart while the parasympathetic vagus nerve slows it, a principle directly relevant to heart rate variability biofeedback.

In summary, cybernetic theory provides the conceptual backbone of biofeedback and neurofeedback. The thermostat analogy illustrates how setpoints, system variables, and feedback loops work together to maintain homeostasis, and how biofeedback training leverages these principles to restore self-regulation.

Basic Psychophysiology of Stress

Let us be honest: the word stress can be confusing because it refers to a stimulus, a response, or a transaction between a person and their environment. The stress response is multidimensional, meaning multiple systems respond in complex ways. Additionally, individuals often show characteristic response patterns. The old idea that the stress response is "nonspecific" is misleading because clients may have unique stress triggers (like time pressure) and specific psychophysiological changes (like blood pressure spikes).

While early theories of stress emphasized the role of stimuli, more recent theories focus on our cognitive appraisal of events and our coping resources. The biopsychosocial model has replaced the aging biomedical model due to its greater comprehensiveness and support for interdisciplinary treatment of disorders. Likewise, the allostatic load model has replaced Selye's General Adaptation Syndrome framework for understanding the role of stress in disease.

Chronic stress reduces heart rate variability (HRV), which is the organized fluctuation of time intervals (measured in milliseconds) between successive heartbeats. HRV is crucial to health, performance, and resilience because it reflects the nervous system’s ability to flexibly control the heart in real time, adapting to changing demands and recovering from stress efficiently.

Low HRV is a marker for cardiovascular disorders, including hypertension (especially with left ventricular hypertrophy), ventricular arrhythmia, chronic heart failure, and ischemic heart disease (Bigger et al., 1995; Casolo et al., 1989; Maver et al., 2004; Nolan et al., 1992; Roach et al., 2004). Low HRV predicts sudden cardiac death, particularly due to arrhythmia following myocardial infarction and post-heart attack survival (Bigger et al., 1993; Bigger et al., 1992; Kleiger et al., 1987).

Reduced HRV may predict disease and mortality because it indexes reduced regulatory capacity, which is the ability to surmount challenges like exercise and stressors. Patient age may be an essential link between reduced HRV and regulatory capacity since HRV and nervous system function decline with age (Shaffer, McCraty, & Zerr, 2014).

A 2023 scoping review confirmed that HRV serves as a valid biomarker for psychological stress, with the root mean square of successive differences (RMSSD) emerging as the most frequently reported metric significantly associated with stress across both experimental and real-life conditions (Immanuel, Teferra, Baumert, & Bidargaddi, 2023). The reviewers found consistent evidence that stress decreases parasympathetic activity.

Neuroimaging research has further strengthened the connection between HRV and stress by demonstrating that HRV correlates with activity in brain regions involved in emotional regulation, particularly the ventromedial prefrontal cortex (Kim, Cheon, Bai, Lee, & Koo, 2018).

Even more encouraging, a 2024 meta-analysis found that stress-reducing interventions such as relaxation training and mindfulness increased HRV in cardiovascular disease patients (El-Malahi et al., 2024). These findings suggest that HRV can serve both as an objective marker for assessing stress and as a target for therapeutic intervention.

Stress Resilience and Common Myths About Stress

Before we examine how stress harms the body, it helps to reframe what stress is and what we should do about it. Stress is unavoidable, and it is also costly, with researchers estimating that roughly 75% of physician visits stem at least partly from stress-related symptoms and complaints (Nerurkar et al., 2013). People want help coping, yet the flood of conflicting stress-management advice can leave them more confused than before. For that reason, Steffen and Bartlett (2022) argue for grounding practice in evidence rather than fashion. The central message of this unit is that the goal of biofeedback is balanced self-regulation, not the elimination of stress.

Stress resilience is positive adaptation in the face of significant stress (Steffen & Bartlett, 2022; Steffen, 2026). It is not a fixed trait people are born with; it develops over time through balance, flexibility, adaptive coping, and emotional stability. Steffen (2026) describes its opposite as fragility, a pattern of negative adaptation marked by inflexibility, maladaptive coping, and emotional instability. Resilient people tend to show improved energy, focus, and mood, while fragile people show the reverse. Because resilience is learned, your clients can build it deliberately, much as they would strengthen a muscle.

Four Myths About Stress and Stress Hormones

Several widely held beliefs about stress are mistaken, and correcting them changes how clinicians frame treatment (Steffen, 2026).

The first myth is that the body releases cortisol and adrenaline only during stress. In reality, we carry these hormones in our blood even on our most relaxing days, because they regulate energy and metabolism around the clock (Steffen & Bartlett, 2022). Thinking of them as energy hormones rather than narrowly as stress hormones is both more accurate and more useful. If these hormones fell too low, people would feel tired and lethargic, so the goal is balanced hormonal functioning that supports healthy energy and focus.

A second myth holds that the stress response is primarily a negative thing to be avoided. The stress response actually evolved to support healthy adaptation, supplying the energy we need to act, so the aim is to harness that energy rather than escape it (Steffen, 2026).

A third myth treats the stress response as a switch that is either on or off, when it behaves far more like a dial with many settings that allow graded levels of activation suited to the moment.

A fourth myth urges us to turn the stress response off entirely, when the realistic goal is to regulate it to a healthy level. These corrections matter clinically, because a client who believes that adrenaline and cortisol are toxins to be purged will chase an impossible target.

Moderate Stress Builds Resilience

Because stress is unavoidable, it helps to know that the right amount of it is good for us. Moderate stress exposure across the lifespan is associated with greater psychological resilience (Dooley et al., 2017; Seery et al., 2010). As people engage manageable challenges, their coping abilities grow, much as muscles grow under load (Steffen & Bartlett, 2022). The goal is therefore not to eliminate stress but to experience a healthy, balanced amount of it.

How a person perceives stress also shapes its biological impact. As Keller et al. (2012) found, high stress predicted earlier death mainly among people who also believed they could not cope, while those confident in their coping showed no such penalty. Helping clients reappraise stress as a challenge they can meet is therefore part of building resilience, not a distraction from it (Steffen & Bartlett, 2022).

Three Practices That Build Stress Resilience

Steffen and Bartlett (2022) distilled the integration of biofeedback and psychotherapy into three learnable practices: balancing life demands with equanimity, becoming more aware but less worried, and engaging in flexible coping. Equanimity is mental and emotional stability and calmness, the ability to experience difficult emotions in a balanced way even under strain (Desbordes et al., 2015). It is not the same as indifference or emotional suppression, because a person with equanimity accepts the present moment rather than avoiding it or dwelling on past distress. Biofeedback supports equanimity directly, since learning to steady one's physiology makes a steady mind easier to reach.

Awareness is the second practice. Avoidance reduces pain in the short term but erodes resilience over time, because it prevents us from understanding what the stress is about (Steffen & Bartlett, 2022). Approached with curiosity instead of dread, awareness of stress is associated with reduced stress, since understanding a problem is the first step toward coping with it. This is precisely what biofeedback trains, as clients watch their physiology on a screen and learn to recognize and regulate it.

Flexible coping is the third practice, meaning that people adapt their coping responses to the demands of the current situation rather than applying one rigid strategy to everything (Steffen & Bartlett, 2022). When the first approach does not work, it is not only acceptable but beneficial to try another. Rigid, inflexible behavior is a hallmark of many mood and anxiety disorders, whereas flexibility is a hallmark of resilience.

This flexibility has a physiological signature. Heart rate variability is a measure of autonomic flexibility and adaptability, and it is often reduced in people with mood and anxiety disorders (Steffen & Bartlett, 2022). A person with lower HRV is, in a real sense, physiologically less adaptable and will face greater difficulty responding to stress. This is why HRV biofeedback, which teaches slow resonance breathing at roughly six breaths per minute, offers a practical route to building resilient self-regulation (Khazan, 2013; Steffen & Bartlett, 2022).

Finally, resilience draws on what Steffen (2026) calls resilient capacity, the physiological, psychological, social, and material resources we can bring to bear on stress, summarized as the health of our body, mind, relationships, and resources. This capacity is neither innate nor fixed; it grows or shrinks with our daily life habits, including sleep, enjoyable physical activity, nourishing relationships, and continued learning. The protective factors covered later in this unit, such as social support and aerobic exercise, are precisely the deposits that keep this reservoir full.

How We Define and Measure Stressors

Cannon (1939) studied how environmental stressors like cold temperatures and loss of oxygen trigger a fight-or-flight response. He conceptualized stress as the disruption of homeostasis when the body mobilizes the sympathetic and endocrine systems to deal with external threats.

Selye (1956) also studied environmental challenges to homeostasis. He referred to stress (and strain) as emotional and physiological responses to stimuli called stressors.

Selye's Nonspecific Response Theory and Its Limitations

Selye conceptualized stress responses as nonspecific since many stimuli can produce the same physiological changes. He theorized that both negative and positive stimuli could provoke stress responses requiring coping resources. He termed stress due to aversive stimuli distress and stress due to positive events eustress (Moksnes & Espnes, 2016).

The Yerkes-Dodson curve graphs the relationship between stressors and performance. Think of it like a hill: 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 burnout with anxiety, panic, and anger.

Why Selye's Model Needed Updating

Selye's model excluded psychological factors like appraisal. His assumption that stress involves nonspecific physiological changes is incorrect. All stressors do not produce a uniform endocrine stress response. Instead, stressors can change multiple body systems in response to stressor intensity, biological predisposition, cognitive appraisal, perceived support, and emotional response (Mason, 1971, 1975; McEwen, 2005; Taylor, 2021). Finally, whereas Selye proposed that our stress responses attempt to maintain physiological processes within a narrow optimal range, current research focuses on adaptation (such as the allostatic load model) instead of set points (Brannon et al., 2022).

The Stress Response Is Multidimensional

The human stress response is multidimensional and involves diverse systems, from the central nervous system to the immune system. Each person uniquely responds to stressors. This individualized pattern is called response stereotypy. Individuals differ in the systems impacted, their activation or suppression, and how these changes affect health. While stressors can produce system-wide macroscopic changes like increased blood pressure, they can also cause epigenetic changes that alter DNA expression.

Sympathetic and Parasympathetic Responders Show Different Patterns

Two modal patterns of autonomic response to stressors have been observed. A sympathetic responder may increase blood pressure, heart rate, and sweat gland activity and decrease heart rate variability and peripheral blood flow. These changes may result from increased sympathetic activation, decreased parasympathetic activation called parasympathetic withdrawal, or a combination of both.

In contrast, a parasympathetic responder may increase digestive activity, constrict the lungs' alveoli, and faint from low blood pressure.

Individuals can react to stressors with elements of both autonomic patterns. For example, consider a client named Marcus who comes to you for stress management. During his assessment, you notice that he increases his heart rate and blood pressure (sympathetic) while simultaneously experiencing gastrointestinal symptoms of diarrhea and gas (parasympathetic). Understanding his unique pattern is essential for effective treatment.

The Biopsychosocial Model Has Replaced the Biomedical Model

Engel (1977) proposed the biopsychosocial model to replace the biomedical model. While the biomedical model holds that abnormal biological processes cause illness, the biopsychosocial model argues that biological, psychological, and social factors all contribute to the development of disease and maintenance of health.

Think of it this way: the biomedical model treats the body like a car that breaks down due to mechanical problems. The biopsychosocial model recognizes that humans are far more complex; how you think, how you feel, and the social world you live in all shape your health.

The Allostatic Load Model Explains Wear and Tear

McEwen and Stellar (1993) introduced the allostatic load model to capture the price our bodies pay for adapting to stressors. Allostasis refers to maintaining stability through change by mechanisms that anticipate challenges and adapt through behavior and physiological change.

Allostatic load is the wear and tear on the body from chronic overactivity or underactivity of allostatic systems. Imagine your stress response as a fire alarm: helpful when there is a real fire, but damaging if it keeps going off for no reason. Over time, this constant activation exhausts your body's resources and damages organs.

A 2021 systematic review by Guidi and colleagues confirmed the clinical utility of the allostatic load concept, demonstrating consistent associations between elevated allostatic load scores and adverse health outcomes across diverse populations.

A 2025 systematic review examining the relationship between allostatic load and cardiovascular disease analyzed 22 studies and found that allostatic load was significantly associated with incident cardiovascular disease at baseline, though fewer significant relationships emerged for longitudinal changes (Colvin & Glover, 2025). The researchers noted that allostatic load may serve as a useful indicator of cardiovascular disease risk but may not as accurately predict cardiovascular outcomes such as mortality. This distinction has important implications for clinicians using allostatic load as a clinical marker.

Newer research has extended the allostatic load framework to cancer outcomes. Stabellini and colleagues (2025) examined allostatic load in patients diagnosed with breast, lung, or colorectal cancer and found that higher allostatic load scores were associated with increased risk of major cardiac events following cancer diagnosis.

A one-point increase in allostatic load was linked to up to a 21% increased risk of major adverse cardiac events, with heart failure showing the highest associated risk at 23%. The association was particularly strong during the 6 to 12 months following cancer diagnosis, a period marked by intense psychological and physiological stress from both the diagnosis and treatment.

These findings highlight the importance of addressing chronic stress during cancer care to reduce cardiovascular complications.

The Stress-Diathesis Model Explains Individual Vulnerability

The stress-diathesis model proposes that stressors interact with our inherited or acquired biological vulnerabilities, called diatheses, producing medical and psychological symptoms. For example, obesity is a diathesis for diabetes; when combined with chronic stress, the risk of developing diabetes increases significantly.

System-Wide Effects of Stress

The Microbiome and Stress

Your gut contains trillions of microorganisms collectively called the microbiome. These beneficial bacteria play a role in digestion, synthesize neurotransmitters and vitamins, modulate immunity, and influence nervous system function. The microbiome's role in health and disease is the subject of extensive current research.

The Microbiome Modulates Neurotransmitters

The gut microbiota communicates with the brain through the microbiota-gut-brain axis, influencing neurotransmitter production, transportation, and function, which in turn affects cognitive functions and brain activity (Chen, Xu, & Chen, 2021; Lynch & Hsiao, 2023).

Key neurotransmitters such as dopamine, serotonin, and gamma-aminobutyric acid (GABA) are modulated by gut bacteria, which can produce or alter these neuroactive compounds, impacting host physiology and potentially contributing to conditions like Parkinson's disease, anxiety, and depression (Foster & Neufeld, 2013; Hamamah et al., 2022; Strandwitz, 2022).

The microbiome's ability to produce neurotransmitters and interact with host receptors underscores its potential as a therapeutic target, with emerging research focusing on psychobiotics, probiotics, and prebiotics that influence mental health (LaGreca, Skehan, & Hutchinson, 2022). Additionally, microbial metabolites such as short-chain fatty acids and bile acids play a role in signaling pathways that affect brain function and behavior (Caspani & Swann, 2019; Foster, 2022).

The Gut-Brain Axis and Disease

The gut-brain axis refers to the bidirectional communication network linking the gastrointestinal tract and the central nervous system, encompassing neural, hormonal, and immunological pathways. The gut microbiota significantly influences this axis by producing neurotransmitters (such as serotonin and gamma-aminobutyric acid) and metabolites like short-chain fatty acids, which can affect brain function and behavior.

Alterations in gut microbiota composition, known as dysbiosis, have been associated with various neurological and psychiatric disorders, including depression, anxiety, and autism spectrum disorders. For instance, studies have demonstrated that germ-free mice exhibit altered stress responses and anxiety-like behaviors, which can be mitigated by introducing specific microbial species, highlighting the microbiota's role in modulating the gut-brain axis (Schächtle & Rosshart, 2021).

Furthermore, systemic inflammation resulting from gut dysbiosis may compromise the integrity of the blood-brain barrier, facilitating the entry of neurotoxic substances and contributing to neuroinflammation. This mechanism has been implicated in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease.

How Stress Affects the Microbiome

Stress, whether psychological, environmental, or physical, can significantly alter the composition and function of gut microbiota, which in turn affects the host's stress response and overall health (Karl et al., 2018). The gut-brain axis, a complex communication network involving the gut microbiota, plays a crucial role in regulating stress-related responses, with diet being a significant modifying factor (Foster, Rinaman, & Cryan, 2017). Stress-induced changes in the gut microbiota can lead to immune system activation and inflammation, which are linked to various stress-related conditions such as anxiety, depression, and irritable bowel syndrome (Buerel, 2024).

Moreover, early life stress has been shown to impact the gut microbiome, although consistent microbiome signatures associated with stress are yet to be identified (Agusti et al., 2023). Chronic stress can exacerbate conditions like inflammatory bowel disease by disturbing the gut microbiota and triggering immune responses (Gao et al., 2018).

Groundbreaking research in 2024 revealed that the microbiome may help explain why some people bounce back from stress while others struggle.

An and colleagues (2024) studied 116 healthy adults and discovered distinct biological signatures in the gut microbiomes of highly resilient individuals. Using brain imaging and stool samples, the researchers found that people with high psychological resilience showed microbiome activity associated with lower inflammation, better gut barrier integrity, and increased production of beneficial metabolites like N-acetylglutamate and dimethylglycine. Their brains also displayed enhanced functional connectivity between reward circuits and sensorimotor networks, suggesting better emotion regulation.

This study represents the first evidence linking resilience, brain activity, and the gut microbiome in a comprehensive model. The findings raise exciting possibilities for future interventions, with researchers suggesting that engineered probiotic blends might someday help people cope with stress and prevent stress-related diseases (An et al., 2024).

A 2025 systematic review synthesized findings from studies on gut microbiota and mental health disorders, reporting that depression was consistently associated with reduced microbial diversity and elevated levels of Firmicutes bacteria, while anxiety was linked to lower levels of short-chain fatty acid-producing bacteria and higher levels of inflammatory Proteobacteria (Shaikh et al., 2025). The review noted that probiotics and dietary interventions showed promise in alleviating symptoms for many patients, sometimes matching the effectiveness of pharmaceutical treatments.

These findings underscore the growing recognition that the gut microbiome represents a viable therapeutic target for stress-related mental health conditions.

Protein Kinase C and Stress-Induced Cognitive Impairment

Birnbaum and colleagues (2004) reported that uncontrollable stressful situations activate the enzyme protein kinase C (PKC), interfering with prefrontal cortical functions like working memory. Elevated PKC levels may result in symptoms of distractibility, impulsiveness, and poor judgment seen in bipolar disorder and schizophrenia. Initial psychotic episodes often follow stressors like leaving home for college or the military. Very low levels of lead exposure can elevate PKC levels in children, possibly impairing their regulation of behavior and producing distractibility and impulsivity.

More recent research has expanded our understanding of how stress damages prefrontal networks. Joyce, Uchendu, and Arnsten (2025) explained that stress and neuroinflammation, the activation of immune responses within the brain, work together to weaken the dorsolateral prefrontal cortex (dlPFC), a brain region essential for working memory and the top-down regulation of attention, action, and emotion.

When we encounter uncontrollable stress, catecholamines like norepinephrine flood the prefrontal cortex and activate feedforward PKC and cAMP-protein kinase A signaling pathways. These molecular events open potassium channels on dendritic spines, weakening synaptic connections and reducing the persistent neuronal firing that supports higher cognition.

Essentially, stress flips a neurochemical switch that shifts control of behavior from the thoughtful prefrontal cortex to more primitive brain regions like the amygdala and striatum. Chronic stress makes matters worse by causing architectural changes, including the loss of dendritic spines from prefrontal neurons, leading to lasting cognitive impairments (Joyce et al., 2025).

The connection between stress and brain inflammation has emerged as a critical research frontier. When chronic stress activates microglia, the brain's resident immune cells, these cells release pro-inflammatory cytokines that can damage neural tissue and disrupt neurotransmitter function.

Joyce and colleagues (2025) noted that neuroinflammation and stress hormones create a destructive cycle: inflammation sensitizes prefrontal circuits to the harmful effects of catecholamines, while stress-induced catecholamine release promotes further inflammation. This bidirectional relationship helps explain why people under chronic stress often experience cognitive symptoms like difficulty concentrating, poor decision-making, and memory problems.

The findings have significant implications for treatment, suggesting that anti-inflammatory strategies combined with stress reduction techniques may help protect and restore prefrontal cortex function in people experiencing chronic stress.

Stress Accelerates Aging at the Cellular Level

Epel and colleagues (2004) studied 58 healthy women who cared for either healthy or chronically ill children. The researchers administered a brief questionnaire that assessed chronic stress during the previous month and obtained a blood sample to measure telomere (DNA and protein that cover the ends of chromosomes) length and levels of telomerase (an enzyme that adds DNA to telomeres).

With repeated cell division, telomere DNA is lost, the telomere shortens, and eventually, cell division stops. When cells age, telomerase activity declines, and the telomere shortens.

The researchers found that the mothers of chronically ill children reported higher chronic stress levels than mothers of healthy children. More years of caring for chronically ill children were correlated with shorter telomeres and lower telomerase levels. Perceived levels of chronic stress, and not a child's actual health status, predicted telomere length. The researchers calculated that the cells of high-stress mothers had aged 9 to 17 more years than those of the low-stress mothers.

Building on these findings, Guillen-Parra and colleagues (2024) examined how chronic stress affects the cellular machinery that maintains telomeres. Their longitudinal study followed mothers caring for children with autism spectrum disorder and compared them to mothers of neurotypical children.

They measured Mitochondrial Health Index (MHI), a composite measure that reflects how well mitochondria produce cellular energy. The researchers discovered that both chronic stress exposure and lower MHI independently predicted decreases in telomerase activity over a nine-month period. Since telomerase is the enzyme that maintains telomere length, reduced telomerase activity leads to accelerated telomere shortening.

The study revealed that changes in telomere length were directly related to changes in telomerase activity and indirectly linked to both MHI and chronic stress, suggesting that stress may accelerate cellular aging partly through its effects on mitochondrial function (Guillen-Parra et al., 2024).

A comprehensive 2021 review by Chae and colleagues detailed the biological pathways through which psychological stress damages telomeres. The researchers identified three interconnected mediators: glucocorticoids like cortisol, reactive oxygen species and mitochondrial dysfunction, and chronic inflammation.

These mediators operate in positive feedback loops, meaning each one amplifies the effects of the others. For example, chronic cortisol exposure increases oxidative stress, which damages both mitochondria and telomeres, while also promoting inflammation that further accelerates telomere shortening.

The review emphasized that the duration of stress exposure matters critically: acute stress may temporarily increase telomerase activity as a protective response, but chronic stress suppresses telomerase and accelerates cellular aging. The authors also highlighted intergenerational effects, noting that parental stress can influence telomere length in offspring through both prenatal stress exposure and direct inheritance of shortened telomeres (Chae, Lin, & Blackburn, 2021).

Stress May Contribute to Mild Cognitive Impairment

Older adults enrolled in the Einstein Aging Study who reported high stress levels were twice as likely to exhibit the memory deficits associated with mild cognitive impairment (MCI), which may precede Alzheimer's disease (Katz et al., 2015).

A landmark 2023 Swedish cohort study provided compelling evidence that chronic stress may increase dementia risk. Wallensten and colleagues (2023) analyzed healthcare records from over 1.3 million adults aged 18 to 65 in the Stockholm region. They tracked participants diagnosed with chronic stress or depression between 2012 and 2013.

Over an 8-year follow-up period, individuals with a history of chronic stress were nearly twice as likely to develop MCI compared to those without such diagnoses. The risk of Alzheimer's disease was similarly elevated.

Perhaps most striking, participants diagnosed with both chronic stress and depression faced up to four times the risk of developing Alzheimer's disease compared to those without either condition.

Although the researchers cautioned that causality remains uncertain, these findings underscore the importance of stress management as a potential strategy for reducing dementia risk (Wallensten et al., 2023).

Stressful Life Events

Cataclysmic Events Can Overwhelm Coping Resources

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 (such as mass shootings), geographic regions (such as earthquakes, fires, hurricanes, and tsunamis), and the entire planet (such as the COVID-19 pandemic). These catastrophes can produce death, dislocation, fear, grief, trauma, and Post-Traumatic Stress Disorder.

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).

Life Events Require Adjustment

Cataclysmic events like a pandemic are so disruptive because they change our lives in various ways: education, employment, exercise, personal and family member illness, routines, sleep, social interaction, and working conditions.

Life events differ from cataclysmic events in three ways. They affect fewer individuals. They require adjustment, whether positive (such as the birth of a child) or negative (such as the death of a loved one). Last, they can develop more slowly (such as divorce) or suddenly (such as injury in a car crash).

Holmes and Rahe (1967) measured major positive and negative life changes using their Social Readjustment Rating Scale (SRRS). The scale lists 43 events, each assigned a different Life Change Unit (LCU) value. They arranged these events in descending order from the death of a spouse (100 LCUs) to minor law violations (11 LCUs). Individuals select the events they have experienced within the last 6 to 24 months. Researchers calculate a stress score by summing the LCU value of the checked events.

Studies that combine prospective (participants report current events) and retrospective methods (researchers examine subsequent health records) have reported increased illness and accidents following increased stressful events (Johnson, 1986; Rahe & Arthur, 1978). However, the correlation between SRRS scores and disease is around +0.30 (Dohrenwend & Dohrenwend, 1984), which means that the SRRS accounts for only 9% of the variance in disease.

The SRRS has received severe criticism, and its popularity has declined. Critics have argued that its positive events can reduce the risk of illness (Ray, Jefferies, & Weir, 1995). Many individuals who exceed 300 points in a year remain healthy. Scales like the SRRS underestimate African-American life stress (Turner & Avison, 2003). The SRRS assumes that an event impacts all people equally. The wording of some items is vague (such as "change in responsibilities at work"). Pessimism can distort recollections of life events (Brett et al., 1990). Finally, the scale does not consider whether an event has been resolved (Turner & Avison, 1992) or an event's controllability or probability (Gump & Matthews, 2000).

The Undergraduate Stress Questionnaire (USQ) developed by Crandall and colleagues (1992) instructs students to select events, mostly hassles, they have experienced during the past two weeks. Higher USQ scores are associated with increased use of health services.

The Perceived Stress Scale (PSS) developed by Cohen and colleagues (1983) measures perceived hassles, major life changes, and shifts in coping resources during the previous month using a 14-item scale. PSS items assess the degree to which respondents rate their lives as unpredictable, uncontrollable, and overloaded (p. 387). The PSS achieves good reliability and validity (Brannon, Feist, & Updegraff, 2022). PSS scores predict cortisol levels (Harrell et al., 1996), fatigue, headache, sore throat (Lacey et al., 2000), and immune changes (Maes et al., 1997).

Hassles and Uplifts: The Small Stuff Matters

A hassle is a minor stressful event like waiting in a checkout line or experiencing a traffic jam. Hassles can produce illness via several pathways. First, hassles can cause accumulating allostatic load. Second, hassles can amplify the effects of adverse life events and chronic stress (Marin et al., 2007; Serido et al., 2004; Taylor, 2021).

Graig's (1993) concept of urban press illustrates how ever-present environmental stressors (such as alienation, crowding, fear of crime, noise, and pollution) acting in concert as daily hassles can increase death from heart attacks (Christenfeld et al., 1999). As with stressors in general, an individual's perception of daily hassles like noise and population density determines their effects on behavior, health, and performance (Brannon et al., 2022; Evans & Stecker, 2004; Schell & Denham, 2003). For example, crowding is our perception of density, influenced by our perceived degree of control.

Discrimination experienced in the classroom, community, family, media, and workplace is another source of daily hassles. Discrimination based on age, biological sex, ethnicity, gender identity, and religion can disadvantage and physically endanger individuals and threaten their mental and physical health (Brannon et al., 2022; Pascoe & Richman, 2009; Troxel et al., 2003). Discrimination has elevated the risk of suicide in the bisexual, gay, lesbian, and transgender communities (Haas et al., 2011). Further, Anti-Asian hate has resulted in a wave of attacks against Asian Americans.

Social identities (such as biological sex, class, gender identity, and race) can interact with stressors and the environment to produce diseases like cancer. For example, a low-income Black woman living in a neighborhood with industrial pollution might face a perfect storm of risk factors: chronic stress from financial strain and racial discrimination, limited access to preventive healthcare, greater environmental toxin exposure, and fewer resources for healthy food or safe spaces to exercise. The persistent activation of her stress response system elevates cortisol and inflammatory markers, which over time can suppress immune surveillance and create conditions favorable to tumor development.

Her cancer risk emerges not from any single factor but from the cumulative biological toll of navigating intersecting systems of disadvantage that simultaneously assault her body through multiple pathways.

An uplift is a minor positive event like receiving an unexpected call from a friend or playing with new puppies.

Kanner and colleagues (1981) developed a 117-item Hassles Scale and 138-item Uplifts Scale to measure negative and positive daily experiences. Respondents selected the hassles and uplifts they experienced during the previous month. Next, they rated the degree to which they experienced each selected item on a 3-point scale to assess their perception of each stressor. They found a moderate correlation between hassles and major life changes. Lazarus (1984) reported that the Hassles Scale better predicted health outcomes than the SRRS.

Psychological Factors in Stress

Affective States and the Circumplex Model

Barrett and Russell (1999) proposed a structural model that organizes affective states within a circumplex (circular structure) based on its degrees of affective valence (unpleasant to pleasant) and affective intensity (activation to deactivation). Specific affective states fall inside or along the surface of this circular structure.

Negative states (sad) are located in the left hemisphere and positive states (contented) are located in the right hemisphere. Activated states (tense) are placed in the top hemisphere, and deactivated states (fatigued) are placed in the bottom hemisphere. While adjacent affective states (stressed and nervous) most resemble each other, those 180° apart (stressed and relaxed) are opposites. After clinicians identify their clients' position within the circumplex, they may intervene to shift them to a more appropriate affective state, like relaxed instead of nervous.

Researchers have reported psychophysiological correlates of the affective valence and activation dimensions. Surface EMG (SEMG) and EEG can help assess affective valence. SEMG measurements of the zygomatic (smiling) and corrugator (frowning) muscles are correlated with positive and negative affect (Lang et al., 1993). Higher left/right prefrontal cortex activation ratios are correlated with positive affect, while reverse ratios are correlated with negative affect (Sutton & Davidson, 1997). Sympathetic nervous system modalities like electrodermal activity are associated with affective intensity (Crider, 2004; Lang et al., 1993).

Negative affectivity (neuroticism) is a predisposition toward distress and dissatisfaction. Individuals rated high on this trait negatively perceive themselves, others, and the environment and have a pessimistic perspective. They rank more events as stressful, report more intense stress, complain more frequently about health problems, and report more severe symptoms when physically ill than those with lower negative affectivity (Cohen et al., 1995; Gunthert et al., 1999). Negative affectivity may increase vulnerability to stressors and health conditions like anxiety and depressive disorders they exacerbate (Brannon et al., 2022).

The Type D (distressed) personality combines high negative affectivity and social inhibition levels. Individuals rated high on this dimension cannot communicate their distress with others. Researchers have studied the relationship between negative emotionality and social inhibition and the Five-Factor Model of Personality. Negative emotionality is positively correlated with Neuroticism, whereas social inhibition is negatively correlated with Conscientiousness and Agreeableness (De Fruyt & Denollet, 2002).

The Type D personality better predicted the buildup of arterial plaque than the Type A behavior pattern (Lin et al., 2018). However, although initial studies suggested that Type-D coronary artery disease patients have poorer prognoses, later studies (Bishop, 2016; Meyer et al., 2014) have not consistently supported this association.

Anxiety and Heart Disease

A Framingham study report by Markovitz et al. (1993) showed that men with elevated anxiety had twice the risk of middle-age hypertension as men with lower anxiety. This increased risk was not found for women. A prospective study by Kawachi et al. (1994) revealed that men diagnosed with phobic anxiety had a three times greater risk of sudden cardiac death. Albert et al. (2005) found that women diagnosed with phobic anxiety had a 59% greater risk of sudden cardiac death and a 31% greater risk of fatal coronary heart disease than women who scored low. These increased risks were associated with risk factors such as diabetes, hypertension, and high cholesterol.

Depression and Cardiovascular Risk

Pratt et al. (1996) reported that depressed individuals had a four times greater risk of a heart attack in the next 14 years than non-depressed individuals. Frasure-Smith et al. (1995) found that depressed heart attack patients had a four times greater risk of another heart attack in the next 18 months than non-depressed heart attack patients. Carney et al. (2005) discovered that depressed heart attack patients were almost three times more likely to die over 30 months than non-depressed heart patients. Decreased heart rate variability accounted for a significant share of the increased risk of death.

Jonas and Mussolino (2000) found in a 16-year longitudinal study that participants diagnosed with depression had a 70% greater risk of stroke mediated by ethnicity. Stroke risk was higher for depressed European American men than women and depressed African Americans than European Americans. Everson et al. (1998) reported that depressed individuals had a greater risk of death from stroke than nondepressed participants.

A landmark 2025 meta-analysis and Mendelian randomization study by Liu and colleagues provided the most comprehensive examination to date of the depression-cardiovascular disease relationship. Analyzing 39 studies involving 63,444 cardiovascular patients, the researchers found an estimated overall prevalence of depression of 20.8% among those with cardiovascular disease, with heart failure patients showing the highest rates at 24.7%.

Depressive symptoms were associated with more than double the unadjusted all-cause mortality rate compared to non-depressed patients. The Mendelian randomization analysis, which uses genetic variants to test for causal relationships, provided the first genetically-informed evidence that depression plays a critical role in both the development and progression of certain cardiovascular conditions. Specifically, the analysis revealed significant causal associations between major depressive disorder and coronary artery disease, myocardial infarction, heart failure, and hypertension (Liu et al., 2025).

A 2024 review in Frontiers in Psychiatry summarized the bidirectional relationship between depression and coronary heart disease. The authors reported that even after accounting for traditional risk factors such as hypertension and obesity, the incidence of coronary heart disease was three times higher in individuals with depression (Xu, Zhai, Shi, & Zhang, 2024).

Depression constituted a significant independent risk factor for mortality in coronary heart disease patients, with one study showing a hazard ratio of 3.19 and demonstrating that depression severity correlated with worse prognosis and higher incidence of adverse cardiovascular outcomes.

Type A-B Continuum and Heart Disease

Friedman and Rosenman (1974) proposed the Type A-B continuum of risk for coronary artery disease. They described extreme Type A's as competitive, concerned with numbers and acquisition, hostile, and time-pressured. In contrast, Type B's are less motivated and do not usually exhibit Type A behaviors. Their study of 3,000 men over 8.5 years showed that Type A behavior doubled the risk of a heart attack. The National Heart Lung and Blood Institute (1981) concluded that Type A behavior is an independent risk for heart disease.

Despite early hopes that the global Type A behavior pattern could independently predict heart disease, current research has not consistently supported this association (Brannon et al., 2022; Espnes & Byrne, 2016).

Hostility: The Toxic Component of Type A

Hostility is a negative attitude about others, not an emotion. Hostility is the toxic component of the Type A behavior pattern. In contrast, anger is a difficult emotion associated with physiological arousal. Longitudinal studies suggest a modest predictive relationship between hostility, hypertension (Yan et al., 2003), and cardiovascular disease (Chida & Steptoe, 2009).

Anger and Cardiovascular Reactivity

Taylor (2012) proposed that cardiovascular reactivity (changes in cardiovascular function due to physical or psychological challenge) and hostility in conflict situations might promote heart disease. The disease pathways may involve changes in blood vessels and catecholamine levels, sympathetic nervous system release of lipids into circulating blood, and blood platelet activation.

Anger is a difficult emotion that involves physiological arousal and persists for a brief period. Siegman and colleagues (1987) proposed that the expression of anger, and not our experience of it, could result in heart disease. Examples of expressed anger include raising your voice during arguments and temper tantrums (Brannon et al., 2022).

Jain and colleagues (1995) monitored patients using an electronic stethoscope. When patients were angry, the researchers observed declines in the heart's ejection fraction (the ratio of blood pumped by the left ventricle during a contraction compared to its total filling volume). Bhat and Bhat (1999) demonstrated that an intervention to manage anger using biofeedback significantly increased their patients' ejection fraction.

Expressed anger may contribute to heart disease by increasing cardiovascular reactivity (CVR), often revealed as increased blood pressure and heart rate in response to social stressors like a provocation.

Dujovne and Houston (1991) linked expressed hostility with increased total cholesterol and low-density lipoprotein (LDL) in men and women. Goldman (1996) reported that individuals classified with high anger had a 2.5 times greater chance of re-clogging arteries after angioplasty. Siegman and colleagues (1992) found that training to slow speech rate and lower speech volume reduced CVR.

Researchers have shown that provocation can increase cardiovascular reactivity. Smith and Brown (1991) found that when provoked, women showed less CVR than men. While husbands increased their heart rate and systolic blood pressure while trying to control their wives, they did not experience these changes when trying to control their husbands. The wives' systolic blood pressure only increased when their husbands expressed cynical hostility.

After provoking male undergraduates, Siegman, Anderson, Herbst, Boyle, and Wilkinson (1992) observed increased heart rate and blood pressure (diastolic and systolic). The subjects reported experiencing considerable anger following their provocation.

Fredrickson et al. (2000) asked adult men and women to re-experience earlier anger experiences. More hostile participants produced larger and longer-duration blood pressure increases than less hostile individuals. Also, African Americans showed greater CVR than European Americans.

Bishop and Robinson (2000) studied Chinese and Indian men in Singapore who performed a difficult task either with or without harassment. The harassed participants showed greater CVR than those who were not provoked.

Smith et al. (2004) reported that high-hostile husbands experienced greater cardiovascular reactivity during stressful interactions with their wives than low-hostile husbands.

Suppressed Anger Can Also Be Harmful

Diamond (1982) hypothesized an anger-in dimension, which is the tendency to withhold the expression of anger, even when anger is warranted. Dembroski and colleagues (1985) reported that anger suppression could contribute to heart disease. Siegman (1994) recommended that patients develop an awareness of their anger but express it using a quiet, slow voice.

Acute and Chronic Stress Responses

Acute Stress Activates the Fight-or-Flight Response

Cannon's fight-or-flight response focuses on sympathetic nervous system responses to an acute stressor and describes the sympathetic-adrenomedullary (SAM) pathway that releases the hormones epinephrine and norepinephrine. Selye's General Adaptation Syndrome (GAS) describes our prolonged response to a chronic stressor across three stages. The GAS summarizes changes in the hypothalamic-pituitary-adrenal (HPA) axis, which releases the hormones CRH, ACTH, and cortisol, and explains how chronic stress can produce disease and death.

The Fight-or-Flight Response in Detail

Cannon (1932) described the fight-or-flight response, in which an individual confronts or flees a stressor. During an acute stress response, which corresponds to the end of Selye's alarm stage, we activate the sympathetic nervous system (SNS), increasing respiration, cardiac output, blood flow to skeletal muscles, and metabolism while decreasing digestion and reproductive system activity. The SNS, in turn, activates the hard-wired sympathetic-adrenomedullary (SAM) pathway, resulting in the release of the hormones epinephrine and norepinephrine by the adrenal medulla (inner adrenal gland).

The adrenal medulla releases epinephrine and norepinephrine in a 4:1 ratio (Fox, 2019). The adrenal medulla is the inner region of the adrenal glands located at the top of each kidney.

The Challenge Response: A Healthier Alternative

While the fight-or-flight response evolved to help us escape predators, not all stressors require such an extreme reaction. The Biopsychosocial Model (BPS) of Challenge and Threat proposes that how we appraise a stressor determines whether we mount a healthy challenge response or a potentially harmful threat response (Blascovich & Tomaka, 1996; Seery, 2013). When we evaluate our coping resources as sufficient to meet situational demands, we experience a challenge response. When demands seem to exceed our resources, we experience a threat response that resembles the classic fight-or-flight pattern.

These two stress responses differ in their hormonal signatures. Both activate the sympathetic-adrenomedullary (SAM) axis, releasing catecholamines that increase heart rate and mobilize energy. However, the threat response additionally activates the hypothalamic-pituitary-adrenal (HPA) axis, producing elevated cortisol levels (Hase et al., 2025). Research has identified the cortisol-to-DHEA ratio as a key biomarker distinguishing these responses. Dehydroepiandrosterone (DHEA) is an adrenal hormone with anti-glucocorticoid properties that can buffer the harmful effects of cortisol (van Honk et al., 2024). A challenge state is marked by increased DHEA relative to cortisol, while a threat state shows elevated cortisol relative to DHEA (Crum et al., 2017; Yeager et al., 2016).

The cardiovascular consequences of these responses differ dramatically. During a challenge response, blood vessels dilate, cardiac output increases, and total peripheral resistance decreases, efficiently delivering oxygenated blood to the brain and muscles (Seery, 2013). During a threat response, blood vessels constrict while the heart pumps harder, creating an inefficient pattern where the cardiovascular system works against itself (Blascovich, 2008). In healthy coronary arteries, mental stress typically produces dilation or no change. However, in atherosclerotic arteries, mental stress causes paradoxical constriction, particularly at stenotic sites (Yeung et al., 1991). This explains why psychological stress can trigger angina and cardiac events in people with coronary artery disease.

A 2025 meta-analysis of 62 studies confirmed that individuals in a challenge state achieve better performance outcomes than those in a threat state across multiple domains including sports, education, and healthcare (Hase et al., 2025). While the long-term health implications continue to be studied, repeated threat responses are associated with accelerated cognitive decline and increased cardiovascular disease risk (McLoughlin et al., 2024). These findings suggest that learning to appraise stressors as challenges rather than threats may protect both performance and health.

The HPA Axis Responds to Chronic Stress

Sustained elevated cortisol levels can affect mood and produce system-wide damage.

CRH: The First Signal in the HPA Axis

In response to stressful stimuli, the amygdala's central nucleus activates the hypothalamus' paraventricular nucleus (PVN), resulting in increased CRH release to the pituitary gland.

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.

ACTH Triggers Cortisol Release

When CRH binds to the pituitary gland, it releases corticotropin (ACTH). ACTH triggers cortisol release by the adrenal cortex (outer part) and helps resist infection.

Cortisol Has Widespread Effects

Cortisol exerts widespread effects on critical body organs (Kemeny, 2003) and cortisol levels in the blood index stress, peaking 20 to 40 minutes following a stressor (Brannon et al., 2022).

It is worth pausing on what cortisol is for. Although the rest of this section details the damage that chronically elevated cortisol can cause, cortisol and adrenaline are fundamentally energy hormones rather than mere stress hormones, and we carry them in our blood even at rest (Steffen & Bartlett, 2022; Steffen, 2026). As discussed earlier in this unit, the clinical goal is to regulate these hormones to a healthy level rather than to eliminate them.

Cortisol increases our activity and appetite. It helps convert fat and protein to glucose. Cortisol has short-term and long-term effects on immunity. At first, cortisol directs white blood cells to sites of infection or wounds, increases their stickiness and adherence to blood vessels and damaged tissue, and communicates when immune activity is sufficient. Cortisol's long-term effect, however, is impaired immune function (McEwen, 2002).

In healthy individuals, cortisol levels are highest in the early morning, when they help wake us up, and are lowest at night. In severely depressed individuals, the cortisol rhythm is suppressed, and its levels remain moderately high over 24 hours. Chronically elevated cortisol levels in the bloodstream adversely affect many organs, including the brain.

Allostatic load can result in hyperglycemia (elevated blood sugar), insulin insensitivity (prevents insulin from transporting glucose into skeletal muscles), increased gastric acid secretion, and ulcers. Muscle protein is converted to fat. Fat storage in the abdomen increases, which endangers health more than storage in the hips and thighs. Bone mass is reduced due to the loss of minerals (McEwen, 2002).

Cortisol release can affect gene transcription, thus producing long-term and immediate effects on the body and setting the stage for several physical and psychological disorders (panic, PTSD, and somatization).

While we've seen how allostatic load can result in chronically elevated HPA axis release of cortisol, the opposite pattern, underproduction of cortisol, also occurs. Cortisol suppresses the immune system, which reduces inflammation and swelling, and moderates chronic pain. Low cortisol levels can result in allergies, asthma, autoimmune disorders like rheumatoid arthritis and multiple sclerosis, and chronic pain syndromes like fibromyalgia (McEwen, 2002).

Cortisol binding to the amygdala increases CRH and ACTH. Cortisol release amplifies the fear response, increases our ability to store implicit memories about stressful stimuli, and increases the amygdala's ability to escape the prefrontal cortex's regulation of emotional behavior.

Cortisol binding to the hippocampal formation disrupts the medial temporal lobe memory system's creation of explicit (conscious) memories. Cortisol interferes with hippocampal regulation of the PVN of the hypothalamus. Chronically elevated cortisol levels harm and kill hippocampal neurons. Cortisol suppresses neuronal repair by BDNF and interferes with creating new neurons. The elderly are more vulnerable to cortisol's harmful effects because they more slowly shut down their stress response. Their cortisol negative feedback loop functions less efficiently than in younger individuals (McEwen, 2002).

Two pathways from the raphe system terminate in the hippocampus: an anxiogenic (anxiety-producing) pathway, and an anxiolytic (anxiety-reducing) pathway. Elevated cortisol levels suppress the anxiolytic pathway and facilitate the anxiogenic pathway. These changes heighten anxiety in a chronically stressed individual.

Cortisol binding to the dorsolateral and ventromedial prefrontal cortex injures and kills neurons as in the hippocampus. Cortisol disrupts executive functions like attention and decision-making, increasing anxiety and fear.

Men and Women Respond Differently to Stressors

Taylor and colleagues argue that men's and women's behavioral and neuroendocrine responses to stressors differ, largely because of oxytocin. The posterior pituitary releases oxytocin when we encounter stressors. While traditionally known for its role in childbirth and breastfeeding, oxytocin is now recognized as a stress hormone that promotes social engagement and may protect cardiovascular health (Quintana et al., 2013).

Although they share the same nervous system reactions to stressors, men tend to react with fight-or-flight while women respond with tend-and-befriend. Taylor and colleagues (2000) theorize that a tend-and-befriend response is an alternative reaction to stressors. They believe tending (nurturing behavior) and befriending (seeking and providing social support) may characterize women better. The tend-and-befriend response may protect their safety and the lives of their offspring.

Their higher oxytocin levels cause women to seek and provide greater support when distressed than men (Bodenmann et al., 2015; Tamres et al., 2002; Taylor et al., 2000). Supporting this view, women reporting relationship stress have higher blood oxytocin levels (Taylor et al., 2006; Taylor, Saphire-Bernstein, & Seeman, 2010). An interaction may mediate this response between oxytocin and estrogen and endogenous opioids.

Oxytocin as a Cardiovascular Protector

Research has revealed that oxytocin does far more than promote social bonding; it actively modulates cardiovascular responses to stress. In a placebo-controlled experiment, Norman and colleagues (2012) found that participants given intranasal oxytocin responded to social stress with a challenge-oriented cardiovascular pattern, characterized by increased cardiac output and reduced total peripheral resistance. This efficient pattern contrasts sharply with the threat response, where the heart and blood vessels work against each other. Oxytocin administration also increased vagal tone, suggesting enhanced parasympathetic activity that could protect heart health over time.

Animal research has demonstrated that oxytocin in the hypothalamus mediates social buffering, the phenomenon whereby social contact reduces stress responses (Smith & Wang, 2014). When prairie voles were exposed to immobilization stress, those who recovered with their partner showed lower corticosterone levels and reduced anxiety-like behaviors compared to those recovering alone. Blocking oxytocin receptors eliminated these social buffering effects. Oxytocin also increases heart rate variability and may contribute to resilience by helping individuals return to homeostasis more quickly after stressful events (Quintana et al., 2013; Onaka & Takayanagi, 2021).

Chronic Stress and the General Adaptation Syndrome

Selye's Three-Stage Model

The General Adaptation Syndrome (GAS) was Selye's (1956) three-stage model of chronic autonomic and endocrine system responses to stressors.

Selye argued that diverse stressors produce a three-stage response (alarm, resistance, and exhaustion) in all subjects. In this model, a cold stressor is interchangeable with a shock stressor because they produce the same autonomic and endocrine responses. Whereas Cannon showed that acute stress could change the functions of our internal organs, Selye mainly demonstrated using animal models that chronic stress can change their structure (Crider, 2004).

Alarm is the first stage of Selye's GAS and consists of shock and countershock phases. The shock phase includes reduced body stress resistance and increased autonomic arousal and hormone release (ACTH, cortisol, epinephrine, and norepinephrine) that comprise the fight-or-flight response. In the countershock phase, resistance increases due to local defenses.

Resistance is the second stage of Selye's General Adaptation Syndrome. Local defenses have made the generalized stress response unnecessary. Both cortisol output and stress symptoms, like adrenal gland enlargement, decline. While the person appears normal, adaptation to the stressor places mounting demands on the body, leading to diseases of adaptation like hypertension as adaptation energy is depleted. Local defenses will break down if stressors persist. McEwen calls these adjustments allostatic load.

Recovery or Exhaustion is the third stage of Selye's General Adaptation Syndrome. We recover when a stressor has ended, and we can restore homeostasis. In exhaustion, increased endocrine activity depletes body resources and raises cortisol levels, resulting in suppressed immunity and stress syndrome symptoms. Selye believed these changes could cripple immunity and cause bronchial asthma, cardiovascular disease, depression, hypertension, hyperthyroidism, peptic ulcer, ulcerative colitis, and possibly death (Brannon et al., 2022).

While Selye conceptualized stress as the outcome of the three-stage GAS, stress may occur at any time. Individuals may experience stress-related changes in anticipation of an event or after it has ended. Chronic resistance may produce more significant harm than exhaustion (Taylor, 2021).

While Selye made a landmark contribution to our understanding of the role of chronic stress and glucocorticoid-mediated damage in disease, critics have challenged his characterization of the stress response as nonspecific and his conceptualization of stressors. Critics have questioned the GAS on four issues.

First, since most of Selye's research subjects were nonhuman animals, this may have caused him to overlook the role of human emotion and cognitive appraisal in the chronic stress response.

Second, since Selye focused on stressors instead of human characteristics like biological predispositions and personality, he mistakenly assumed a uniform response to stressors. Stressors can produce different hormonal responses (Kemeny, 2003).

Third, while Selye emphasized the role of exhaustion in disease, there is more evidence that chronic resistance may produce more significant harm (Taylor, 2012).

Fourth, while Selye conceptualized stress as the outcome of the GAS, both the anticipation of an event and coping with it during the resistance stage can disrupt performance and produce suffering (Taylor, 2012).

Brain Structures Involved in Stress

The four brain structures most important to the stress response are the amygdala, hypothalamus, hippocampus, and prefrontal cortex.

The amygdala is part of the limbic system and evaluates whether stimuli are threatening, establishing unconscious emotional memories, learning conditioned emotional responses, and producing anxiety and fear responses.

The hypothalamus lies beneath the thalamus in the forebrain. It helps the body maintain a dynamic homeostatic balance by controlling the autonomic nervous system, endocrine system, survival behaviors (four F's), and interconnections with the immune system.

The Hypothalamus Receives Information About Stressors

Much of the information about stressors is relayed to the PVN. This hypothalamic nucleus organizes behavior to respond to changes in internal body states. The PVN receives input from the limbic system, cerebral cortex, hypothalamus, and brainstem structures (nucleus of the solitary tract, tegmentum and reticular formation, periaqueductal gray, locus coeruleus, and raphe system).

When the PVN is excited, it releases several chemical substances, including CRH, oxytocin, arginine-vasopressin, thyrotropin-releasing hormone, growth hormone-releasing hormone, somatostatin, dopamine, enkephalin, cholecystokinin, and angiotensin.

This large variety of hormones enables the individual to respond to a wide range of stressors. Since stressful events may simultaneously present many stressors, these chemical substances allow the individual to respond completely and appropriately.

The hippocampus is part of the medial temporal lobe memory system and helps form declarative memories, allows us to navigate our environment, and prevents excessive hypothalamic CRH release.

The prefrontal cortex (PFC) is the most anterior region of the frontal lobes. The PFC contains the orbitofrontal and ventromedial, dorsolateral prefrontal cortex, and anterior and ventral cingulate cortex. The PFC is responsible for the brain's executive functions, including planning, guiding decisions using emotional intelligence, working memory, allocation of attention, and emotional experience. The PFC inhibits emotional behavior triggered by the amygdala.

Psychoneuroimmunology (PNI)

Nonspecific and Specific Immune Mechanisms

The human body utilizes nonspecific and specific immune mechanisms to protect itself against invading organisms, damaged cells, and cancer.

The main nonspecific, or innate, mechanisms are relatively rapid in response and include anatomical barriers (skin and mucous membranes) and phagocytosis (ingestion of microorganisms) by macrophages and neutrophils. Natural killer cells and neutrophils destroy infectious agents. Nonspecific mechanisms release antimicrobial agents (hydrochloric acid, interferons, and lysozymes) and signal to other immune responders. Local inflammatory responses confine microbes, allowing white blood cells and other immune cells to attack them.

Check out Professor Gillian Griffiths' video Killer T Cell: The Cancer Assassin.

The Immune System Is Interconnected with the Nervous System

The classical model of the immune system is that it operates independently of the nervous system and psychological processes. However, researchers have demonstrated complex interactions among the nervous, endocrine, and immune systems, consistent with Green and Green's psychophysiological principle. Psychological processes like expectancies (placebo effect) and learning (classical conditioning) can affect all three systems, and the immune system can affect psychological functioning (drowsiness from a fever).

Psychoneuroimmunology is a multidisciplinary field that studies the interactions between behavior and these three systems.

After Solomon and Moos (1964) introduced the term psychoneuroimmunology in a journal article, Ader and Cohen's (1975) demonstration of classical conditioning in a rat's immune system helped establish this field's scientific legitimacy.

Ader and Cohen trained rats to associate a conditioned stimulus (a saccharine and water solution) with an unconditioned stimulus (the immunosuppressive drug cyclophosphamide). This resulted in a conditioned response (CR) of immune suppression, which resulted in rat fatalities. Following conditioning, rats who drank only sweetened water (CS) died due to conditioned immunosuppression. Successful replication of these findings helped overcome resistance to the controversial view that the nervous and immune systems interact.

The mechanisms underlying these complex interactions include HPA axis hormones (ACTH, cortisol, CRH, epinephrine, and norepinephrine), immune cell chemical messengers called cytokines (interleukins), additional hormones (androgens, estrogens, progesterone, and growth hormone), and neuropeptides. Neuropeptides are chains of amino acids, like beta-endorphins, that neurons use for communication.

Stress and Immunity

There is persuasive evidence that stressful life events can reduce immunity and that behavioral interventions can enhance or maintain it. Bereavement can reduce lymphocyte (lymphatic white blood cell) proliferation (Schleifer et al., 1983). Academic exams, marital conflict, negative affect associated with stress, clinical and subclinical depression, and negative daily mood can suppress immunity (Herbert & Cohen, 1993; Kiecolt-Glaser et al., 2002; Stone et al., 1994).

The stress of living near the Three Mile Island nuclear plant when it experienced a significant accident reduced residents' B cell, T cell, and natural killer cell counts compared with control subjects (McKinnon et al., 1989).

A study of Alzheimer's caregivers showed lowered immunity and longer wound healing times, and worse psychological and physical health than controls who were not caregivers (Kiecolt-Glaser, 1999). The Alzheimer's patients' deaths did not improve caregiver immunity or psychological functioning (Robinson-Whelen et al., 2001).

Finally, laboratory stressors produced more significant discomfort and immunosuppression in chronically-stressed young males than in those not chronically stressed (Pike et al., 1994). Exposure to chronic stress may have intensified their subjects' response to acute laboratory stressors.

Behavioral Interventions Can Strengthen Immunity

Behavioral interventions can increase immunocompetence. Miller and Cohen's (2001) meta-analytical study of behavioral interventions showed modest increases in immunity. Hypnosis increased immune function more than relaxation and stress management.

A stress management program incorporating relaxation training reduced symptoms and increased salivary antibodies and psychological functioning in children diagnosed with frequent upper respiratory infections (Hewson-Bower & Drummond, 2001).

College students who wrote journal entries about highly stressful experiences increased lymphocyte proliferation and made fewer health center visits (Pennebaker et al., 1988). Smyth et al. (1999) asked asthma and rheumatoid arthritis patients to write journal entries about highly stressful experiences or planned daily activities. At a 4-month follow-up, 50% of the Pennebaker journal group who wrote about stressful experiences and 25% of the control group achieved clinically significant improvement in their immune-related disorders (Crider, 2004).

Dental and medical students who received hypnosis training maintained immune function, while a control group showed declines in immunity (Kiecolt-Glaser et al., 2001). This finding suggests that behavioral interventions may be more effective in maintaining normal immunity than boosting immunity (Brannon et al., 2022).

Cognitive Appraisal of Stressors and Coping

Lazarus and Folkman's (1984) Transactional Model of Stress has more strongly influenced psychologists than Selye's General Adaptation Syndrome.

Whereas Selye's stimulus model theorized that events determine stress, Lazarus' cognitive model proposed that stress is determined by our perception of the situation and emphasizes person-environment fit (Taylor, 2012).

Coping is central to the Transactional Model of Stress. Lazarus and Folkman defined it as "constantly changing cognitive and behavioral efforts to manage specific external and/or internal demands that are appraised as taxing or exceeding the resources of the person" (1984, p. 141). Coping is an effortful learned process whose goal is to manage a situation (Brannon et al., 2022).

In primary appraisal, we categorize the consequences of events as positive, neutral, or negative and determine whether an event is relevant, negative, or potentially negative. We evaluate these events for their possible harm, threat, or challenge.

Harm is damage that has already occurred. For example, a person who experiences a heart attack may perceive harm as damage to the heart muscle. Threat means damage that could arise in the future. The heart attack survivor may anticipate restricted physical activity and reduced income. The perception of an event as a threat has physiological consequences and can result in elevated blood pressure. Challenge is the potential to cope with the event and gain from this opportunity. The heart attack survivor may reframe this health crisis as an opportunity to make a career change. The perception of an event as a challenge can increase perceived self-efficacy and positive emotion while lowering blood pressure (Maier et al., 2003).

The Chinese pictogram wei ji (pronounced way jee), representing danger and opportunity, illustrates the negative and positive possibilities considered during primary appraisal.

During secondary appraisal, we evaluate whether our coping abilities and resources can surmount an event's harm, threat, or challenge. Lazarus and Folkman (1984) listed health and energy, positive belief, problem-solving skills, social skills, social support, and material resources as necessary coping resources. Again, perception of our coping abilities and resources is more important than their actual existence.

The balance between primary and secondary appraisal determines how we subjectively experience the event. We experience the most stress when perceived harm or threat is high and perceived coping skills and resources are low. Stress is reduced when we perceive that our coping abilities and resources are high (Taylor, 2012).

Secondary appraisal can lead to our use of direct action, reappraisal, and palliation.

Direct action can take different forms depending on the nature of the threat. We may use aggression and escape behaviors from Cannon's fight-or-flight response for violent threats to our survival. We may use problem-solving for medical or psychological threats, define the problem, identify options, and test these options until we succeed. A cardiac patient may enroll in a cardiac rehabilitation program to increase exercise tolerance and reduce the risk of artery narrowing.

Reappraisal may reduce stress when direct action is impractical or unsuccessful. Reappraisal modifies our perception of a threat. When overwhelmed by traumatic stress, individuals may initially use ineffective strategies like denial and rationalization. As they cope with the crisis, they may progress with more successful strategies like reframing in which they place the stressful situation in perspective and focus on available opportunities. For example, a cardiac patient may decide that his heart attack allowed him to spend more time with his grandchildren.

Palliation consists of efforts to reduce our stress response rather than attack the stressor. Clinicians may use biofeedback and adjunctive techniques like effortless breathing to teach cardiac patients to control their anxiety. While this does not correct the cause of the stress response, it is often superior to medications like anxiolytics that risk side effects, tolerance, physical dependence, and withdrawal effects. Successful clinical interventions for chronic problems like anxiety, depression, and pain incorporate effective palliation since complete remission may be unlikely.

Evaluating the Transactional Model

The Transactional Model of Stress encompasses cognitive appraisal, missing from the General Adaptation Syndrome. Research supports this model. For example, performance is better when we perceive an event as challenging instead of threatening (Moore et al., 2012).

Lazarus and Folkman's model recognizes that we constantly change as we cope with stressors and that our coping successes and failures influence our appraisals of future events (Brannon et al., 2022).

Primary Appraisal Is Affective, Not Cognitive

Steffen and Anderson (2025) proposed a significant revision to the Transactional Model based on current neuroscience research. Their central argument challenges a long-held assumption: primary appraisal is not primarily a cognitive process but an affective one. When you encounter a potential stressor, your body does not wait for your thinking brain to analyze the situation before responding. Instead, your affective primary appraisal, which is the initial emotional and bodily response that occurs before conscious thought, kicks in first. This gut-level reaction, which researchers call core affect, represents how your body continuously evaluates its relationship to the environment over time. Think of core affect as your internal compass that constantly registers whether things feel good, bad, or neutral, long before you consciously think about them. This body-based knowing forms the foundation for all emotional experience and conscious awareness.

The idea that cognition and emotion operate as separate systems, which traces back to philosophers like Plato and Descartes, turns out to be neurobiologically incorrect. Brain imaging studies confirm that there are no purely emotional or purely cognitive circuits in the brain; instead, these processes are anatomically and functionally intertwined (Steffen & Anderson, 2025).

This revised model has important implications for how clinicians help people manage stress. If the body's affective response comes first and cognition follows, then therapeutic approaches that start by trying to change thoughts may be working backward.

Steffen and Anderson (2025) suggest three alternative strategies. First, affective focus involves targeting emotional experience directly rather than beginning with cognitive interpretation. A therapist might help a client notice and work with bodily sensations of anxiety before analyzing the thoughts that accompany them.

Second, behavioral activation uses lifestyle modifications such as improved sleep, nutrition, and physical activity to enhance physiological resources and mood. These behavioral changes can shift core affect in positive directions, making cognitive reappraisal easier.

Third, environmental support involves accessing external resources, whether social connections, material stability, or safe physical surroundings, that promote wellbeing and stress management. These factors directly influence core affective attunement, which is the body's ongoing evaluation of its internal state in relation to current circumstances.

By recognizing that the body frames our understanding of the world through affect, clinicians can ground their most abstract cognitive interventions in the reality of bodily experience (Steffen & Anderson, 2025).

The Perception That Stress Impacts Health Matters

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.

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, subjects who reported high levels of stress and the perception that stress impacts health experienced a 43% greater risk of early death.

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.

Personality Dimensions That Influence Stress Responses

The personality dimensions of mastery, impulsiveness, hopelessness, optimism, and pessimism, and constructs like alexithymia and reactivity are important to understanding stress responses.

Mastery and Perceived Control

Mastery overlaps with the concepts of locus of control, perceived control, and self-efficacy. Mastery is the relatively stable expectancy that we can control personal outcomes.

Mastery affects our appraisal and coping with stressors. Individuals with high levels of mastery expect to succeed when challenged by stressors, cope more effectively, and report lower levels of depression and stress than people with low levels of mastery (Gurung, 2019).

In Weiss's (1977) replication of the Brady "executive monkey" study, the "executive" rat could switch off the tail shock by turning the wheel. Because it had control over the shock, it was no more likely to develop ulcers than an unshocked control rat. The "subordinate" rat received the same shocks as the "executive" rat. Because the "subordinate" rat had no control over the shocks, it was more likely to develop ulcers than the "executive" rat.

Impulsiveness and Stress

Distress can increase impulsive behavior that produces immediate relief or pleasure, sometimes at the cost of personal health (Tice et al., 2001).

Optimism and Pessimism

Pessimism is a generalized expectancy of future adverse outcomes and is a heart attack risk factor. A Harvard School of Public Health team found pessimistic adult men had a doubled risk of developing heart disease over 10 years (Kubzansky et al., 2001).

Alexithymia

Wickramasekera (1988) described alexithymics as low in hypnotic ability and awareness of internal cues and feelings associated with illness. Alexithymia is prevalent in patients with multiple psychosomatic complaints and may delay seeking and receiving medical attention.

Reactivity: Hot Reactors

Eliot's (1992) hot reactors cannot be identified by their overt behavior but risk sudden death due to pathological acute and chronic responses to stressors. Hot reactors show an acute increase in catecholamine secretion, which increases the risk of cardiac arrhythmia due to excessive myocardial fiber contraction and clot formation. When challenged by long-term stressors and experience fear, uncertainty, and loss of control, they also show a chronic increase in glucocorticoid secretion, which raises total cholesterol while lowering protective HDL-C.

African Americans start to show greater reactivity than their European American counterparts by childhood (Murphy et al., 1995), perhaps due to stressors associated with their ethnicity. This difference may help explain their higher prevalence of cardiovascular disease.

Everson et al. (2001) discovered that the risk of stroke was more significant for men with higher systolic blood pressure reactivity.

Resources to Buffer Stress

Social Support Protects Health

Social support consists of received support (support provided) and perceived support (expected support) from individuals and organizations. Both forms of social support include informational, material, and psychological assistance from others. The value of each kind of social support depends on an individual's specific needs.

Social networks and social contacts both concern the number and kinds of an individual's interpersonal relationships. A social network is a social structure consisting of nodes (individuals or organizations) tied together. Social contacts are the nodes (individuals or organizations) comprising a person's social network.

Patients with a high level of social support participate in an extensive social network consisting of numerous social contacts. Those with low social support have a limited social network with few social connections.

High levels of social support are associated with better health, faster recuperation, less psychological distress, lower depression risk, and lower mortality than low levels of social support (Gurung, 2019).

The Alameda County Study (Berkman & Syme, 1979) documented a relationship between social contacts and longevity. Adults with the fewest social connections had 2-4 times the risk of death than those with the most social contacts. Gender and age moderated the effect of social connection. Males' highest relative risk of death (3.2) was from age 50-59, whereas women's highest relative risk (4.6) was from age 30-49 (Brannon et al., 2022).

A massive 2023 meta-analysis by Wang and colleagues analyzed 90 prospective cohort studies involving over 2.2 million individuals and provided compelling evidence for the mortality risks of social disconnection.

The researchers found that social isolation was associated with a 32% increased risk of all-cause mortality, while loneliness was associated with a 14% increased risk (Wang et al., 2023).

Both social isolation and loneliness were also significantly associated with increased cancer mortality. The findings held true for the general population and for individuals with existing cardiovascular disease or cancer.

A 2025 systematic review and meta-analysis focusing specifically on older adults confirmed these patterns, finding that social isolation had the strongest association with mortality (hazard ratio of 1.35), followed by living alone (1.21) and loneliness (1.14).

The researchers noted that loneliness, social isolation, and living alone each independently increased the risk of cardiovascular mortality, underscoring the importance of social connectedness for heart health (Savas et al., 2025).

The health consequences of social disconnection are now recognized as a public health priority. Researchers have identified multiple biological pathways through which loneliness and social isolation affect health, including elevated cortisol, increased inflammation, reduced immune function, and disrupted sleep. The U.S. Surgeon General declared loneliness an epidemic in 2023, noting that the mortality risk associated with loneliness rivals that of smoking 15 cigarettes a day (Holt-Lunstad, Smith, & Layton, 2010).

These findings have prompted calls for healthcare providers to screen for social isolation and loneliness as part of routine health assessments and for communities to develop interventions that strengthen social connections.

Hawkley and colleagues (2006) reported that loneliness is an independent risk factor for hypertension comparable to obesity and a sedentary lifestyle. They studied 229 participants aged 50 to 68 years and measured their perceived degree of loneliness and previously established cardiovascular and psychosocial risk factors. Even after statistically controlling for other negative emotional states (such as depression, hostility, or stress), lonely older participants had systolic blood pressures up to 30 mmHg higher than their non-lonely counterparts. They discovered that loneliness and stress raised blood pressure via different mechanisms and produced an additive effect. Furthermore, the impact of loneliness on blood pressure increased with age.

Prosocial Behavior Buffers Stress

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.

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.

Aerobic Exercise Reduces Stress Effects

A sedentary lifestyle marked by prolonged sitting and TV-viewing time was linked to chronic health conditions and all-cause mortality in a meta-analysis of data from over 1 million middle-aged men and women. Individuals who engaged in moderate-intensity exercise for 60-75 minutes per day eliminated the increased risk of death due to sitting but only attenuated the risk associated with TV-viewing time (Ekelund et al., 2016).

Mildly depressed college women who participated in an aerobic exercise program showed markedly reduced depression compared with those who did relaxation exercises or received no treatment (McCann & Holmes, 1984).

A study that compared exercise with drug treatment or a combination of exercise and drug treatment found that exercise improved mood and the other two conditions. When treatment was discontinued, participants who continued to exercise were less likely to relapse than those who had received drug treatment (Babyak et al., 2000).

A landmark 2024 network meta-analysis published in the British Medical Journal examined 218 randomized controlled trials involving 14,170 participants with major depressive disorder to determine the optimal exercise prescription for depression (Noetel et al., 2024).

The researchers found that exercise was as effective as antidepressants and psychotherapy for treating depression, with walking or jogging, yoga, strength training, and dancing all showing strong evidence of benefit. Higher intensity exercise produced greater symptom reductions, though even moderate activity was helpful.

The most effective exercise programs involved supervised sessions and group formats, suggesting that social interaction may contribute to the mental health benefits of physical activity. These findings led experts to conclude that exercise should be considered a "mainstay approach" in managing depression alongside traditional treatments.

A 2022 dose-response meta-analysis in JAMA Psychiatry analyzed 15 prospective studies with over 191,000 participants and found that even modest amounts of physical activity were associated with substantial reductions in depression risk (Pearce et al., 2022).

Adults who accumulated half the recommended amount of physical activity, equivalent to 1.25 hours per week of brisk walking, had an 18% lower risk of depression compared to inactive adults. Meeting the full recommended target of 2.5 hours per week was associated with a 25% risk reduction.

The researchers calculated that if less active adults had reached the recommended physical activity level, 11.5% of depression cases could have been prevented. These findings suggest that clinicians should encourage any increase in physical activity, even below recommended levels, as a strategy for improving mental health.

The positive impact of exercise on mood may be mediated by reduced cardiovascular reactivity (Perkins et al., 1986), social involvement (Estabrooks & Carron, 1999), and increased self-efficacy (McAuley et al., 2003), and self-esteem (Sonstroem, 1997).

Religious and Spiritual Activity

In a national health survey financed by the U.S. Centers for Disease Control and Prevention, religiously active people had longer life expectancies (Hummer et al., 1999). McCullough and colleagues (2000) performed a meta-analysis that assigned greater weights to studies that controlled confounding variables like age, gender, health, and social support. They found that religious involvement was linked to a slightly lower mortality rate and was not due to social support.

Taken together, these protective factors are deposits in what Steffen (2026) calls our resilient capacity, the reservoir of physiological, psychological, social, and material resources we draw on to meet stress. Sleep, enjoyable exercise, supportive relationships, and meaningful activity replenish this reservoir, while chronic stress without recovery drains it. Helping clients build these habits is therefore a direct way to strengthen stress resilience.

Basic Physiology of Attention

A Neurofeedback Paradigm Shift

With neurofeedback, we want to know where to place active electrodes and what brain activity to train. It is natural to assume that the sensor should sit over the part of the brain corresponding to a Brodmann area that needs to be up-trained or down-trained. That approach can work for some conditions that respond to single-channel training. However, one site connects to another, and so on, within networks.

Networks, which can be functional or structural, mediate connectivity. In functional networks, regions show correlated activity over time. Structural networks consist of axonal projections and pathways. Functional and structural networks can overlap, but functional connectivity does not automatically imply an underlying anatomical connection.

Fornito et al. (2016) emphasized the role of time scale in their convergence. As functional connectivity is averaged over longer periods, it may converge onto structural connectivity, although the two remain different measures that can yield connectomes with different topological values (p. 25).

Interventions as different as immobilizing a limb and neurofeedback can change functional connectivity. Newbold and Dosenbach (2021) placed a cast on the intact dominant hand of participants for several weeks and ran repeated fMRI scans to observe the effect on motor cortex connectivity. Within a day or two, functional connectivity between the left and right motor cortices had nearly disappeared, a faster timescale than many had predicted. Recovery was also rapid in two of the three participants.

The premise of connectivity training is that neurofeedback, using EEG and functional MRI, can increase or decrease functional connectivity to improve performance.

Commonsense About Functional Brain Areas

Petersen and Fiez (1993) observed that a functional area of the brain is not a task area. There is no "tennis forehand area" waiting to be discovered, and no single area is devoted to a complex function, so attention and language are not localized to one Brodmann area or lobe. Any task or function draws on a complex, distributed set of brain areas.

The areas that perform a task are distributed across different locations, yet the processing is not diffusely spread among them. Each area makes a specific contribution that is determined by where it sits within its richly connected, parallel, distributed hierarchy.

Key Anatomical Terms

Long brain region names can be intimidating, and six descriptions can serve as a decoder ring. Anterior or rostral refers to toward the head end, whereas posterior or caudal means toward the tail. Dorsal means toward the top of the brain, while ventral means toward the bottom. A gyrus is a ridge of convoluted brain tissue, whereas a sulcus is a furrow (Breedlove & Watson, 2023).

Networks carry both functional and anatomical names. For example, the dorsal attention network (DAN) corresponds to the dorsal frontoparietal network (D-FPN).

Brodmann Areas

The original Brodmann areas consisted of 47 numbered cytoarchitectural zones of the cerebral cortex based on Nissl staining. They require subdividing certain areas, and they vary in size and shape across individuals.

Gordon et al. (2016) compared the original Brodmann areas with several other brain atlases using fMRI. They concluded that Brodmann's parcellation captures real structure in the data but is too coarse to represent true cortical areas. Modern attempts to parcellate the cortex frequently reveal finer architectonic divisions than Brodmann reported. The more than 100-year-old Brodmann areas therefore lack some of the specificity needed for in vivo and functional studies.

Revised Brodmann maps reveal 180 regions, 100 of which were not previously identified (Glasser et al., 2016). Cognitive neuroscience tends to use modern brain atlases of defined regions (e.g., Yeo et al., 2011) and exact coordinates such as Montreal Neurological Institute (MNI) space and Talairach space (Chau & McIntosh, 2005). Researchers sometimes convert these coordinates to corresponding Brodmann areas because the areas are well known.

Brodmann areas participate in networks. They matter for neurofeedback because they help us target functional and structural networks rather than discrete, disconnected scalp sites. Neuroscience reveals the connections between Brodmann areas and how different networks become active or quiet together across diverse conditions.

For example, attention to an object's location activates four main areas of the dorsal attention network (dorsal frontoparietal network), while five areas of the ventral attention network (ventral frontoparietal network) automatically process unanticipated events. Flexible attention control involves the dynamic interaction of these top-down and bottom-up systems (Vossel et al., 2014).

Psychological disorders can be associated with shifts from normal activity in particular brain areas and their connections. After traumatic brain injury (TBI), neuronal connections change across the entire brain, and surviving long axonal projections no longer target inhibitory neurons (Frankowski et al., 2022).

Current neurofeedback protocols allow us to train networks involved in cognitive functions like attention or psychological disorders like depression using multiple electrodes simultaneously. Connectivity training enables us to increase or decrease communication between brain locations to treat symptoms and improve performance, and both activations and deactivations matter. Quantitative EEG (qEEG) normative databases can reveal the key parts of a network that need training and the required direction.

Brain Organization and Dynamics

This section introduces the brain's network architecture, from large-scale systems to specific cortical regions. Understanding these systems is essential for neurofeedback practitioners, since many protocols target the networks described here.

The brain is organized into interactive, functional, distributed networks with spatial, temporal, and content-based relationships. These networks interact through feedback loops and transiently organized aggregates of neurons, all mediated by rhythmic, oscillatory electrical discharges that ultimately produce the EEG. This process is further shaped by selective attention to specific categories of interest.

Graphic uploaded to ResearchGate by Maurizio Corbetta from The dynamical balance of the brain at rest.

Each type of local cognitive, sensory processing, or emotional network produces oscillatory activity and contains internal stabilizing characteristics. These local networks exist within a global dynamic network system that links and provides interactive capacity to the smaller networks, also operating within an oscillatory framework.

A densely connected lateral prefrontal and posterior parietal cortical network orchestrates responses to novel cognitive tasks using flexible hubs. This frontoparietal network assigns tasks to the most appropriate brain regions and shares information among them to master new skills (Cole et al., 2013).

The central nervous system processes incoming content through separate regions that handle specialized input (e.g., auditory, kinesthetic, tactile, visual). Content is shared, integrated, compared to previous content, and analyzed, and decisions are made about memory and responses. All of this activity occurs within interacting networks linked by electrical and chemical signals, and the electrical discharges from this activity are recorded from the scalp surface as the EEG.

Network Overview

The networks most relevant to attention include the oculomotor, motor, affective, central autonomic, social, and executive circuits. Each plays a distinct role in how we focus, respond, and regulate behavior.

Oculomotor Network

The frontal eye field (FEF), in concert with the dorsolateral prefrontal cortex, posterior parietal cortex, basal ganglia, and thalamus, programs and initiates voluntary eye movements, inhibits eye movements toward distracting stimuli, and allows us to return our focus to locations we have previously attended (Thompson & Thompson, 2015).

Motor Network

The supplementary motor area (SMA), in concert with the premotor cortex, primary motor cortex, sensorimotor cortex, and cerebellum, plans, initiates, and inhibits voluntary movements and muscle contractions (Breedlove & Watson, 2023; Thompson & Thompson, 2015). Understanding the motor network helps clinicians appreciate why SEMG biofeedback can influence broader neural circuits.

Somato-Cognitive Action Network (SCAN)

Gordon and colleagues (2023) used precision fMRI from seven participants together with datasets from the Adolescent Brain Cognitive Development Study, the Human Connectome Project, and the UK Biobank, drawing on roughly 50,000 individuals. They identified three interconnected primary motor cortex (M1) regions that participate in the integrated movement of multiple body parts.

The somato-cognitive action network (SCAN) consists of M1, the SMA, the centromedian and ventral intermediate nuclei of the thalamus, the posterior putamen, and the vermis and flocculonodular lobe of the cerebellum, which mediate posture and balance. Connectivity analysis showed that the SCAN communicates with the cingulo-opercular network, or salience network, which supports cognitive control and sustains task focus over extended periods.

M1's two interlacing systems establish a pattern of integration and isolation. Effector-specific regions for the foot, hand, and mouth support the isolation of fine motor control, while the SCAN integrates goals, body movement, and physiology.

The relative expansion of SCAN regions in humans may support uniquely human integrated actions, such as coordinating breathing for speech and combining hand, body, and eye movement for tool use. By enabling anticipatory postural, respiratory, cardiovascular, and arousal adjustments before action, such as shoulder tension, increased heart rate, or butterflies in the stomach, the SCAN provides a substrate that may help explain why mental and bodily states so often interact.

Mesa (2023) placed these findings in context. The dominant paradigm has treated the motor cortex as a simple relay that passes movement commands to muscles, with planning, cognition, and conscious initiation of movement occurring elsewhere in the brain.

The SCAN, in concert with the salience network, supports complex adaptations such as allostasis. These findings agree with primate studies showing that more M1 neurons govern movements independent of the specific muscles used than govern the contraction of particular muscles (Griffin et al., 2015; Kaufman et al., 2014). Together they challenge the 1870 cortical homunculus model, the distorted human figure whose body parts are sized by the amount of cortical area dedicated to them.

Affective Network

The pre- and subgenual areas of the anterior cingulate cortex (ACC) participate in affective circuits triggered when we make mistakes (Arnsten, 2009). The dorsal rostral cingulate zone monitors cognitive activity to predict when errors are likely and greater executive control may be needed (Thompson & Thompson, 2015). The ventromedial prefrontal cortex projects to the amygdala, basal ganglia, hypothalamus, and brainstem arousal and reward pathways. This network is relevant to neurofeedback for anxiety and mood disorders.

Central Autonomic Network

The central autonomic network (CAN) consists of forebrain, limbic, and brainstem regions (Benarroch, 1993). Neuroimaging studies reveal a cortico-limbic network for autonomic control that includes the ventromedial prefrontal cortex, cingulate cortex, insula, mediodorsal thalamus, hypothalamus, and amygdala (Beissner et al., 2013; Shoemaker et al., 2015; Schumann et al., 2021).

Thayer and Lane (2000) proposed a neurovisceral integration model that places the prefrontal cortex at the top of a hierarchy, with direct functional links to the insula and cingulate. The limbic system extends these connections through the amygdala to downstream subcortical regions, such as the hypothalamus and brainstem nuclei, that drive parasympathetic and sympathetic heart rate modulation. The model highlights how prefrontal control over subcortical structures links sympathovagal balance with cognitive and emotional processes. This framework is central to HRV biofeedback, which trains the prefrontal and autonomic circuitry that governs heart rate regulation.

Magnetic resonance imaging (MRI) and resting-state functional connectivity (RSFC) studies have reinforced the role of medial prefrontal and limbic interplay in heart rate control (Kumral et al., 2019; Sakaki et al., 2016). Individuals with slower heart rates show heightened RSFC within a network of central autonomic and sensorimotor regions compared with those who have faster heart rates (de la Cruz et al., 2019). Slower heart rates were associated with elevated RSFC between the ventromedial prefrontal cortex and the anterior insula.

Social Network

The orbitofrontal cortex (OFC), along with the basal ganglia and thalamus, orchestrates the highest level of emotional processing in the nervous system. The social network is responsible for socially responsible behavior, empathy, behavioral inhibition, emotional regulation, and sound judgment (Thompson & Thompson, 2015). Graphic courtesy of Han and colleagues (2021).

A mentalizing network that includes the ventromedial, orbitofrontal, dorsolateral, and dorsomedial prefrontal cortices lets us reason about our own and others' mental states (Hoskinson et al., 2019). A mirror network centered on the superior temporal sulcus is active during our own actions and our observation of others' actions, supporting observational learning and social cognition (Sadeghi et al., 2022). The amygdala detects salient stimuli, while the entorhinal cortex and anterior insular cortex contribute to this social circuitry.

Executive Network

The dorsolateral prefrontal cortex plays a critical role in executive functions, which Kropotov (2009) described as the coordination and control of motor and cognitive actions to attain specific goals. Executive functions include allocation of attention, cognitive inhibition, behavioral inhibition, working memory, and cognitive flexibility. The executive network focuses and maintains continuous attention (Faraone et al., 2006) and shows reduced activation and connectivity in ADHD, making it a primary target of neurofeedback protocols for ADHD and other attention-related conditions. The diagrams below were adapted from Alexander et al. (1986) and Thompson and Thompson (2015).

Attentional Processes

Attention is the selection of sensory information or cognition for enhanced processing. We can overtly or covertly attend to stimuli. In overt attention, our attentional focus and sensory orientation coincide. For example, you parse this sentence as you focus your gaze on it. In covert attention, we shift our attentional focus from our sensory orientation. For example, you attend to a reminder on the corner of your screen while gazing at this sentence. While the midbrain superior colliculus is mainly implicated in overt attention, it may also regulate covert attention (Breedlove & Watson, 2023).

Attention is more selective than arousal, which is our overall level of alertness (Breedlove & Watson, 2023).

Research using divided attention tasks, where subjects simultaneously process multiple stimuli, shows that attentional resources are finite. The challenge of attending to more than one target increases when targets occupy different spatial locations. When we attend to a stimulus, we shift our attentional spotlight (focus) to select that stimulus for enhanced analysis (Bee & Micheyl, 2008).

Perceptual load (stimulus processing demands) determines the level at which an attentional bottleneck (stimulus selection) occurs. Complex stimuli involving a high perceptual load monopolize processing resources, resulting in early selection, where we filter out lower-priority competing stimuli before preliminary perceptual and semantic analysis. Conversely, simple stimuli involving a low perceptual load leave free processing resources, resulting in late selection, where we filter out competing stimuli after performing extensive analysis (Lavie et al., 2004). This distinction has practical implications for neurofeedback, since training in high-demand environments may engage different attentional mechanisms than training in quiet clinical settings.

Cortical Regions That Guide Attention

The dorsal frontoparietal system, comprising the intraparietal sulcus and frontal eye field, is responsible for the top-down direction of attention (Breedlove & Watson, 2023). The intraparietal sulcus (IPS), located in the parietal lobe, provides voluntary top-down steering of attention (Corbetta & Shulman, 1998). The frontal eye field (FEF), found in the premotor region of the frontal lobes, directs gaze toward targets selected by the IPS (Paus et al., 1991). Target selection is guided by cognitive goals (top-down processing) rather than stimulus characteristics (bottom-up processing).

In contrast, the temporoparietal junction (TPJ), where the superior temporal gyrus and inferior parietal lobe intersect, mediates bottom-up shifts in attention in response to stimulus attributes (Corbetta & Shulman, 2002). The TPJ functions like a circuit breaker, overruling immediate attentional priorities and reallocating attentional resources to a new target (Breedlove & Watson, 2023).

Two Cortical Networks Regulate Attention

Two cortical networks cooperatively regulate subcortical and cortical systems to produce a coherent perceptual experience (Breedlove & Watson, 2023). A dorsal frontoparietal system provides top-down control of endogenous attention (voluntary attention), directing the attentional spotlight to support cognitive system priorities.

Extensive interconnections between the two networks allow us to fluidly redirect attention from stimuli that are forebrain priorities (IPS) to those that are unexpected. This balance between top-down and bottom-up attention is a key consideration in neurofeedback training for attention disorders.

Salience Network

The salience network comprises structures that monitor our external and internal environments to determine which inputs are essential and require further processing and attention. The insula, primarily the anterior insula, is a crucial component because it facilitates bottom-up access to the brain's attentional and working memory resources (Menon & Uddin, 2010). The cingulate gyrus, particularly the right dorsal anterior cingulate cortex, is another crucial component (Thompson & Thompson, 2015). Graphic shared by Nekovarova, Fajnerova, Horacek, and Spaniel under the Creative Commons Attribution 3.0.

The clinical literature on ADHD, depression, and schizophrenia has explored the role of the anterior cingulate cortex in these disorders. Deep brain stimulation of this region has successfully improved treatment-resistant depression (Mayberg et al., 2005).

The insula, a cortical region located within the lateral sulcus, functions as an integrative hub for the salience network. The insula integrates interoceptive awareness (perception of internal body signals), emotional experience, and external perception to facilitate an individual's global perception of the world. It directs specific networks in processing salient stimuli and generating appropriate responses (Wiebking & Northoff, 2014). For biofeedback practitioners, the insula's role in interoceptive awareness is particularly relevant, since biofeedback training fundamentally depends on clients learning to detect and interpret internal signals.

The insula appears to provide an interface between the brain's cognitive, homeostatic, and affective systems, linking the areas involved in monitoring internal signals with those engaged in processing incoming external sensory streams. The insula detects salient events via afferent pathways and switches between other large-scale networks when these events are recognized, thereby guiding attention and working memory.

The anterior and posterior insula interact to regulate autonomic responses to salient stimuli. Interactive communication between the insula and anterior cingulate cortex facilitates access to the motor system (Menon & Uddin, 2010).

This network appears to help us switch between task-oriented (executive) and default mode (attention) networks (Seeley et al., 2007; Shirer et al., 2012).

Default Mode Network (DMN)

Brain regions are selectively active when we are conscious (Breedlove & Watson, 2023). The default mode network (DMN) consists of frontal, temporal, and parietal lobe circuits active during spontaneous cognition like introspection, daydreaming, and streams of consciousness. The DMN appears to contribute flexible memory retrieval and idea generation, critical elements of creativity, and is relatively inactive when pursuing external goals (Andrews-Hanna et al., 2010). In neurofeedback practice, understanding the DMN helps explain why some clients need to learn to suppress mind-wandering, as in ADHD, while others may benefit from cultivating it, as in creative performance training.

ADHD has been linked to irregular connectivity among brain regions, including within the DMN (Cao et al., 2014). The strength of specific brain connections can forecast variations in a person's capacity to sustain attention, and this holds true even at rest when the individual is not engaged in a specific task (Rosenberg et al., 2016, 2017).

There has been increasing discussion about whether some DMN regions belong to a distinct Parietal Memory Network that includes the precuneus, the mid-cingulate cortex, and the posterior inferior parietal lobule and dorsal angular gyrus (Gilmore et al., 2015; Hu et al., 2016).

Deactivations can be as important as activations. The degree of DMN deactivation appears critical for attentional control, since people who suppress it more readily can learn new material more easily (Nelson et al., 2016; Zerr et al., 2018). The DMN also helps synthesize details into single coherent events and supports envisioning the future (Gilmore et al., 2018).

The DMN may contribute to creative fluency, the ability to generate innovative ideas like alternative uses for everyday objects. A study of neurosurgical patients showed that left DMN stimulation reduced the number of uses generated but not their originality (Shofty et al., 2022).

The DMN graphic shows default mode and task-related maps for healthy subjects. On a green background, the default mode network is highlighted in warm colors (red and yellow) and the task-related network is highlighted in cold colors (blue and light blue) depending on the p-value of one sample t-test. Authors are Shim, G., Oh, J. S., Jung, W. H., et al., CC BY 3.0.

Understanding Ourselves

The posterior cingulate cortex (PCC) and precuneus combine bottom-up attention with information from memory and perception. The ventral (lower) part of the PCC activates in all tasks involving the DMN, including those related to the self or others, remembering the past, thinking about the future, processing concepts, and spatial navigation. The dorsal (upper) part of PCC mediates involuntary awareness and arousal. The precuneus is concerned with visual, sensorimotor, and attentional information.

The medial prefrontal cortex (mPFC) participates in decisions about the self, such as personal information, autobiographical memories, future goals and events, and decision-making regarding those close to us like family members. The ventral (lower) part is involved in positive emotional information and reward.

The angular gyrus connects perception, attention, spatial cognition, and action and helps us recall episodic memories.

Understanding Others

The major functional hubs include the PCC, mPFC, and angular gyrus. The dorsal medial prefrontal cortex (dmPFC) analyzes others' objectives. The temporoparietal junction (TPJ) constructs theories of mind, models of others' cognitive processes, emotions, knowledge, and motivation. The lateral temporal cortex is concerned with short-term verbal memory, naming, and reading. Finally, the anterior temporal pole is part of a bilateral semantic system representing object concepts and a left hemisphere-dominant network concerned with naming and understanding object names.

Autobiography and Future Simulations

The major functional hubs include the PCC, mPFC, and angular gyrus. The hippocampus forms new declarative memories. The parahippocampal cortex (PHC) mediates spatial memory, navigation, and high-level visual processing like facial recognition. The retrosplenial cortex (RSC) is involved in episodic memory, navigation, predicting future events, and analyzing visual scenes. Finally, the posterior inferior parietal lobe (pIPL) integrates sensory information and participates in top-down attentional orienting.

The Pulvinar Mediates Attentional Shifts

The pulvinar nucleus, comprising the posterior quarter of the human thalamus, processes visual information and directs attention. The pulvinar shares widespread connections with the cingulate, parietal cortex, and superior colliculus, and is crucial for orienting, shifting attention, and filtering out irrelevant stimuli. Tasks that present subjects with more distracting stimuli increase pulvinar activation, as shown by functional MRI (fMRI) (Buchsbaum et al., 2006). Graphic © Songkram Chotik-anuchit/Shutterstock.com.

Overall, the pulvinar guides the processing of relevant information across wide-ranging cortical networks based on dynamically changing attentional priorities (Breedlove & Watson, 2023; Saalmann et al., 2012).

Training Networks Summary

Neurofeedback training increasingly monitors and trains network activity using qEEG normative databases. To employ these protocols effectively, neurofeedback professionals must thoroughly understand Brodmann areas and the functional and structural networks in which they participate. The dorsal frontoparietal system provides top-down attentional control while the temporoparietal system enables bottom-up redirection, with the salience network serving as the switch between them. This network architecture provides the rationale for targeting specific networks and frequencies to address attention disorders, optimize performance, and restore healthy brain function.

Glossary

activated states: in Barrett and Russell's structural model, high-intensity affective states like tenseness and alertness are placed in the upper hemisphere.

acute stress response: autonomic changes that occur at the end of Selye’s alarm stage, for example, increased heart rate.

adaptation energy: in Selye’s General Adaptation Syndrome, the capacity of local organs to respond to the demands created by stressors. Depletion of adaptation energy theoretically results in local adaptation syndromes like muscle fatigue and tissue inflammation.

adrenal cortex: the outer region of the adrenal gland that produces the hormone cortisol.

adrenal medulla: the inner region of the adrenal gland that produces the hormones epinephrine and norepinephrine.

affective focus: a therapeutic approach that emphasizes targeting emotional experience rather than starting with cognitive interpretation.

affective intensity: in Barrett and Russell’s structural model, a dimension that ranges from activated to deactivated states.

affective network: a network that is triggered when we make mistakes and that monitors cognitive activity to predict when errors are likely, and greater executive control may be needed. The affective network includes the anterior cingulate cortex, hippocampal cortex, entorhinal cortex, superior temporal gyrus, inferior temporal gyrus, posterior parietal cortex, globus pallidus internal segment, substantia nigra, pars reticulata, and medial dorsal nucleus of the thalamus.

affective primary appraisal: in Steffen and Anderson's revised Transactional Model, the first stage in evaluating a situation where emotional and bodily responses occur before conscious thought.

affective valence: in Barrett and Russell’s structural model, a dimension that ranges from unpleasant to pleasant affective states.

alarm: the first stage of Selye’s General Adaptation Syndrome that consists of shock and countershock phases.

alexithymics: individuals who are low in hypnotic ability and awareness of internal cues and feelings associated with illness. Alexithymia is prevalent in patients with multiple psychosomatic complaints and may delay their seeking and receiving medical attention.

allostasis: the maintenance of stability through change by mechanisms that anticipate challenge and adapt through behavior and physiological change.

allostatic load model: McEwen and Seeman’s hypothesis that when stressors are acute or repeatedly occur, biological responses to stress can harm the body.

amygdala: limbic system structure that participates in evaluating whether stimuli are threatening, establishing unconscious emotional memories, learning conditioned emotional responses, and producing anxiety and fear responses.

anger-in dimension: Diamond's hypothesized tendency to withhold the expression of anger, even when anger is warranted.

antibodies: immune system proteins called immunoglobulins that recognize and neutralize bacteria and viruses.

antigen-antibody reaction: antibodies permanently bind to antigens and neutralize them.

antigens: foreign molecules (proteins or polysaccharides) that trigger an immune response.

anxiogenic: there is an anxiety-producing pathway from the raphe system to the hippocampus.

anxiolytic: there is an anxiety-reducing pathway from the raphe system to the hippocampus.

arousal: overall level of alertness.

attention: the selection of sensory information or cognition for enhanced processing.

attentional bottleneck: a filter that limits enhanced processing to only the highest priority stimuli.

attentional spotlight: a shift of selective attention to choose stimuli for enhanced processing.

avoidant coping strategies: coping by refusing to recognize potential problems.

B lymphocytes: the immune cells central to humoral immunity that rapidly produce antibodies that counter bacteria into the blood, neutralize toxins, and prevent reinfection by viruses.

behavioral activation: a therapeutic strategy that uses behavioral changes, especially lifestyle modifications like improved sleep, nutrition, and exercise, to improve mood and physiological resources.

biofeedback: (1) learning process that teaches an individual to control her physiological activity, (2) biofeedback training aims to improve health and performance, (3) instruments rapidly monitor an individual's performance and display it back to her, (4) the individual uses this feedback to produce physiological changes, (5) changes in thinking, emotions, and behavior often accompany and reinforce physiological changes, and (6) these changes become independent of external feedback from instruments. Information about psychophysiological performance is obtained by noninvasive monitoring and used to help individuals achieve self-regulation through a learning process that resembles motor skill learning.

biomedical model: the conventional view that illness is primarily due to biological abnormalities.

biopsychosocial model: Engel’s perspective that the complex interplay of psychological, biological, and sociological factors results in health or illness.

Biopsychosocial Model (BPS) of Challenge and Threat: a framework proposing that cognitive appraisals of demands and coping resources determine whether a stressor triggers a healthy challenge response or a harmful threat response, with distinct cardiovascular and hormonal signatures for each.

blood-brain barrier: a selective permeability barrier formed by specialized cells lining blood vessels in the brain that protects neural tissue from potentially harmful substances in the bloodstream while allowing essential nutrients to pass through.

cardiac output: the volume of blood pumped by the heart per minute, calculated as heart rate multiplied by stroke volume. During a challenge response, cardiac output increases to efficiently deliver oxygenated blood to the brain and muscles.

cardiovascular reactivity (CVR): changes in cardiovascular function due to physical or psychological challenges. For example, increased blood pressure and heart rate in response to social stressors like a provocation.

cataclysmic events: sudden, unique, and powerful single life-events requiring major adaptive responses from population groups sharing the experience.

catecholamines: chemical compounds containing catechol and amine groups, like dopamine, epinephrine, and norepinephrine, derived from the amino acid tyrosine.

cell-mediated immunity: the slower, cellular response that utilizes cytotoxic and helper T cells from T lymphocytes provided by the thymus gland and is most effective in controlling cancer, foreign tissue, fungal and viral infections, and parasites.

central autonomic network (CAN): a system of forebrain, limbic, and brainstem regions that regulates the autonomic nervous system. It includes the prefrontal cortex, anterior cingulate cortex, insula, amygdala, hypothalamus, periaqueductal gray, parabrachial complex, nucleus of the solitary tract, and medulla oblongata. These structures work together to regulate physiological states such as heart rate, blood pressure, respiration, digestion, and thermoregulation.

central executive network: structures including the dorsolateral prefrontal cortex, anterior cingulate cortex, and orbitofrontal cortex responsible for cognitive regulation of behavior.

central nucleus of the amygdala: the region of the amygdala that orchestrates the amygdala’s response to stressors. For example, it activates the paraventricular nucleus (PVN) of the hypothalamus, resulting in increased CRH release to the pituitary gland.

challenge: in Lazarus and Folkman’s Transactional Model of stress, an individual’s assessment during primary appraisal of her potential to cope with an event and gain from this opportunity.

challenge response: a stress response that occurs when an individual appraises their coping resources as sufficient to meet situational demands, characterized by increased cardiac output, decreased total peripheral resistance, and elevated DHEA relative to cortisol.

cingulate cortex: cortex which lies above the corpus callosum that is responsible for the motivation dimension of attention, like pain due to physical injury and social rejection.

conditioned immunosuppression: classically conditioned suppression of immunity. For example, in Ader and Cohen's research, rats conditioned with sweetened water and an immunosuppressive drug died after only drinking the water.

conditioned response (CR): in classical conditioning, a response (blood pressure rise) elicited by a conditioned stimulus (criticism).

conditioned stimulus: in classical conditioning, a stimulus (dentist's office), that in association with an unconditioned stimulus (pain), elicits an unconditioned response (anxiety) like the original unconditioned response.

continuous glucose monitoring: a method of tracking glucose levels in real time using a small sensor worn under the skin, which measures glucose in the interstitial fluid and reports readings and trends throughout the day and night.

coping: constantly changing cognitive and behavioral efforts to manage specific external and/or internal demands that are appraised as taxing or exceeding the resources of the person.

core affect: in Steffen and Anderson's revised Transactional Model, a fundamental, continuous bodily sense of one's relationship to the environment over time that underlies all emotional and conscious experiences.

core affective attunement: the body's ongoing evaluation of its internal state in relation to current circumstances, which shapes how we perceive and respond to stressors.

corrugator: the muscle used in frowning whose SEMG level is correlated with negative affect.

corticotropin (ACTH): the hormone released by the pituitary gland following CRH binding that triggers cortisol release by the adrenal cortex.

corticotropin releasing hormone (CRH): the hormone released by the hypothalamus that triggers ACTH release by the pituitary gland.

cortisol: a glucocorticoid produced by the adrenal cortex that helps convert fat and protein to glucose and reduces inflammation.

cortisol-to-DHEA ratio: a biomarker comparing levels of cortisol to dehydroepiandrosterone (DHEA) that distinguishes challenge from threat responses. A higher ratio indicates threat state dominance, while a lower ratio suggests a healthier challenge response.

countershock phase: the last part of Selye’s alarm stage of the General Adaptation Syndrome during which resistance increases due to increased activity by local defenses.

covert attention: an attentional focus independent of sensory orientation.

creative fluency: generating creative ideas like alternative uses for everyday objects.

critical ignoring: the deliberate practice of checking initial signals about an information source and then filtering out unreliable sources and low-quality data rather than engaging deeply with all available content (Mims, 2026).

crowding: our perception of density, influenced by our perceived degree of control.

cynical hostility: mistrust of humanity and those with whom they interact. This attitude is associated with alcohol consumption, obesity, and smoking, which affect the development of heart disease.

cytokines (interleukins): immune cell chemical messengers that can aid the action of cytotoxic T (Tc) and B cells and macrophages.

cytotoxic T (Tc) cells: immune cells that release toxins to destroy specific virally infected cells.

deactivated states: in Barrett and Russell's structural model, lower-intensity affective states like fatigue and calm are placed in the lower hemisphere.

default mode network: frontal, temporal, and parietal lobe circuits that are active during introspection and daydreaming and relatively inactive when we pursue external goals.

dehydroepiandrosterone (DHEA): an adrenal steroid hormone with anti-glucocorticoid properties that can buffer the harmful effects of cortisol. Higher DHEA levels relative to cortisol characterize challenge states and are associated with better stress outcomes.

diathesis: inherited or acquired biological vulnerability. For example, obesity is a diathesis for diabetes.

direct action: in Lazarus and Folkman's Transactional Model of Stress, this is an active attempt to resolve a threat that may follow secondary appraisal. For example, enrolling in a cardiac rehabilitation program following a diagnosis of coronary artery narrowing.

diseases of adaptation: in Selye’s General Adaptation Syndrome, depletion of adaptation energy theoretically results in adaptation syndromes like atrial tachycardia.

distress: Selye’s term for stress due to negative stimuli.

divided attention tasks: situations where subjects must simultaneously process two or more stimuli.

dorsal frontoparietal system: the network comprised of the intraparietal sulcus and frontal eye field responsible for the top-down direction of attention.

dorsolateral prefrontal cortex: the left dorsolateral prefrontal cortex is concerned with approach behavior and positive affect. It helps us select positive goals and organizes and implements behavior to achieve these goals. The right dorsolateral prefrontal cortex organizes withdrawal-related behavior and negative affect and mediates threat-related vigilance. It plays a role in working memory for object location.

dove strategy: passive, reactive, nonaggressive, and cautious response to stressors.

dysbiosis: an imbalance in the composition or function of the gut microbiota, often linked to health issues.

early selection: filtering out lower-priority competing stimuli before preliminary perceptual and semantic analysis.

ejection fraction: the ratio of blood pumped by the left ventricle during a contraction compared to its total filling volume.

electronic skin: a thin, flexible wearable sensor patch that adheres to the skin and continuously monitors multiple physiological and biochemical stress biomarkers, including vital signs and sweat-based molecular markers.

endogenous attention: voluntary attention that directs the attentional spotlight to support cognitive system priorities.

energy hormones: a reframing of adrenaline (epinephrine) and cortisol that emphasizes their everyday role in regulating energy and metabolism. These hormones circulate even at rest, so the clinical goal is balanced functioning rather than their elimination (Steffen & Bartlett, 2022).

environmental support: therapeutic efforts to help individuals access external resources, such as social connections, material stability, and safe physical surroundings, that promote wellbeing and stress management.

epigenetic: the modification of gene expression due to environmental influences.

epinephrine: adrenal medulla hormone that increases muscle blood flow, converts stored nutrients into glucose for use by skeletal muscles, and initiates cardiac muscle contraction when it binds to β1 receptors.

equanimity: mental and emotional stability and calmness; the ability to experience difficult emotions in a balanced way, even under strain, without indifference or emotional suppression (Desbordes et al., 2015).

eustress: Selye’s term for stress due to positive stimuli.

executive network: a network responsible for allocating attention, cognitive inhibition, behavioral inhibition, working memory, and cognitive flexibility. The executive network includes the dorsolateral prefrontal cortex, posterior parietal cortex, arcuate premotor area, globus pallidus internal segment, substantia nigra, pars reticulata, ventral anterior nucleus of the thalamus, and medial dorsal nucleus of the thalamus.

exhaustion: the third stage of Selye’s General Adaptation Syndrome during which increased endocrine activity depletes body resources and raises cortisol levels resulting in suppressed immunity, stress syndrome symptoms, and possible hospitalization and death.

exogenous attention: involuntary reflexive attention that redirects attention based on the novelty or importance of incoming stimuli.

expressed anger: a component of hostility involving direct communication of anger. For example, raising your voice during an argument.

fight-or-flight response: Cannon’s response of confronting or fleeing a threat that occurs at the end of Selye’s alarm stage.

flexible coping: adapting one’s coping responses to the demands of the current situation rather than applying one rigid strategy to every stressor (Steffen & Bartlett, 2022).

fragility: negative adaptation in the face of stress, marked by inflexibility, maladaptive coping, and emotional instability; the opposite of stress resilience (Steffen & Bartlett, 2022).

frontal eye field (FEF): region of the premotor cortex that directs gaze towards targets selected by the IPS.

functional networks: regions that show correlated activity over time.

General Adaptation Syndrome (GAS): Selye proposed that diverse stressors produce a three-stage (alarm, resistance, and exhaustion) autonomic and endocrine response in all subjects.

gut-brain axis: the bidirectional communication network between the gastrointestinal system and the central nervous system, involving neural, hormonal, and immune pathways.

hardiness: the ability to thrive under stressful conditions.

harm: in Lazarus and Folkman's Transactional Model of Stress, damage that has already occurred. For example, a heart attack survivor may perceive harm as damage to the heart muscle.

hassle: minor stressful event, for example, waiting in a checkout line.

Hassles and Uplifts Scale: DeLongis, Folkman, and Lazarus’s revised 53-item scale measured hassle frequency and intensity. This scale better predicted headache frequency and intensity and inflammatory bowel disease frequency than the Social Readjustment Rating Scale (SRRS).

Hassles Scale: Kanner and colleagues’ 117-item scale that measures negative daily experiences.

hawk strategy: a proactive and bold response to stressors.

heart rate variability (HRV): beat-to-beat changes in heart rate, including changes in the RR intervals between consecutive heartbeats.

hippocampal formation: the limbic structure involved in controlling the endocrine system’s response to stressors, formation of explicit memories, and navigation. Cortisol binding to this structure disrupts these functions, interferes with creating new neurons, and harms and kills hippocampal neurons.

hippocampus: part of the medial temporal lobe memory system that helps form declarative memories, allows us to navigate our environment, and prevents excessive hypothalamic CRH release.

hostility: a negative attitude about others, not an emotion. Hostility is the toxic component of the Type A behavior pattern.

hot reactors: individuals who cannot be identified by their overt behavior but risk sudden death due to pathological acute and chronic responses to stressors.

hyperglycemia: elevated blood sugar.

hypothalamic-pituitary-adrenal (HPA) axis: the hormonal cascade that starts with signals from the amygdala to the hypothalamus and ultimately targets the adrenal glands, releasing the hormones CRH, ACTH (corticotropin), and cortisol.

hypothalamus: a forebrain structure located below the thalamus that dynamically maintains homeostasis by controlling the autonomic nervous system, endocrine system, survival behaviors, and interconnections with the immune system.

insula: the cortical region located within the lateral sulcus of the frontal, parietal, and temporal lobes that functions as an the information the nervous system receives about the internal state of the body, such as heartbeat, breathing, hunger, temperature, and visceral sensations, allowing a person to perceive and respond to their own physiological condition.

interoceptive feedback: the information the nervous system receives about the internal state of the body, such as heartbeat, breathing, hunger, temperature, and visceral sensations, allowing a person to perceive and respond to their own physiological condition.

intraparietal sulcus (IPS): the region of the parietal lobe that provides voluntary top-down steering of attention.

late selection: filtering out competing stimuli after performing extensive analysis.

lateral reading: a fact-checking strategy in which a person steps away from an unfamiliar claim or source and opens a new search to discover what credible sources say about it, rather than engaging deeply with the original content (Mims, 2026).

life events: events that affect fewer individuals than cataclysmic events, require adjustment whether positive or negative, and can develop slowly or suddenly.

locus of control: Rotter’s concept of a continuum of control of outcomes where internals attribute outcomes to their efforts and externals attribute them to external events. This concept overlaps with the concepts of mastery, perceived control, and self-efficacy.

machine learning: a branch of artificial intelligence that uses computational algorithms to enable computers to learn patterns from data and make predictions without being explicitly programmed for each task.

magnetic resonance imaging (MRI): a noninvasive imaging technology that uses a strong magnetic field and radio waves to produce detailed, high-resolution, three-dimensional images of the body. It is especially useful for imaging soft tissues and organs such as the brain, spinal cord, muscles, and heart.

mastery: the relatively stable expectancy that we can control our personal outcomes. This concept overlaps with the concepts of locus of control, perceived control, and self-efficacy.

microbiome: the collection of the microorganisms that reside in the human body.

Mitochondrial Health Index (MHI): a composite measure that integrates mitochondrial energy-transformation capacity and content, reflecting how well mitochondria produce cellular energy.

motor network: the network that plans, initiates and inhibits voluntary movements and muscle contractions. The motor network includes the supplementary motor area, premotor cortex, primary motor cortex, primary somatosensory cortex, cerebellum, arcuate premotor area, globus pallidus internal segment, substantia nigra, pars reticulata, and ventral lateral nucleus of the thalamus.

myelinated vagus: in Porges' polyvagal theory, the phylogenetically newer ventral vagal complex that rapidly adjusts cardiac output and promotes social engagement.

negative affective states: in Barrett and Russell’s structural model, unpleasant states like sadness are located in the left hemisphere.

negative affectivity: a predisposition toward distress and dissatisfaction. Individuals who are rated high on this trait negatively perceive themselves, others, and the environment and have a pessimistic perspective.

negative states: in Barrett and Russell's structural model, unpleasant affective states like sadness are located in the left hemisphere.

neurofeedback: information about EEG activity obtained by noninvasive monitoring and used to help individuals achieve self-regulation through a learning process that resembles motor skill learning.

neuroinflammation: the activation of immune responses within the brain, which can impair cognitive function and contribute to neurodegenerative conditions when chronic.

neuropeptides: chains of amino acids, like beta-endorphins, that neurons use for communication.

neuroplasticity: the ability of neurons and their networks to remodel themselves in response to experience.

neurovisceral integration model: a framework proposing that the heart, brain, and other bodily systems communicate to maintain overall health and well-being. It posits that autonomic, attentional, and affective systems are integrated within the central autonomic network and that imbalances in this network may underlie associations among stress, disease, and cognitive function.

nonspecific: Selye's characterization of stress responses as the same regardless of the stressor.

norepinephrine: an adrenal medullary hormone that increases muscle blood flow and converts stored nutrients into glucose for skeletal muscles.

nucleus (PVN) of the hypothalamus: when activated by the central nucleus of the amygdala, this nucleus releases CRH to the pituitary gland.

oculomotor network: a network that programs and initiates voluntary eye movements, inhibits eye movements toward distracting stimuli, and allows us to return our focus to locations we've experienced in the past. The oculomotor network includes the frontal eye field, dorsolateral prefrontal cortex, posterior parietal cortex, caudate, globus pallidus internal segment, substantia nigra, pars reticulata, ventral anterior nucleus of the thalamus, and medial dorsal nucleus of the thalamus.

overt attention: the agreement between attentional focus and sensory orientation.

oxytocin: a hormone and neurotransmitter that may contribute to social bonding, anxiety following exposure to stressors, and the milk letdown reflex.

palliation: in Lazarus and Folkman’s Transactional Model of Stress, secondary appraisal can lead to efforts to reduce our stress response rather than attack the stressor.

parasympathetic responder: a response stereotypy in which an individual may increase digestive activity, constrict the lungs' alveoli, and faint from low blood pressure when challenged by stressors.

parasympathetic withdrawal: decreased parasympathetic activation in response to stressors.

perceived control: an individual’s expectancy that she can influence her outcomes. This concept overlaps with the concepts of locus of control, mastery, and self-efficacy.

Perceived Stress Scale (PSS): Cohen and colleagues’ scale that measures perceived hassles, major life changes, and shifts in coping resources during the previous month using a 14-item scale. PSS items assess the degree to which respondents rate their lives as unpredictable, uncontrollable, and overloaded.

perceived support: expected social support.

perceptual load: stimulus processing demands.

person-environment fit: Lazarus' emphasis on how the match between a person and their environment determines stress.

pessimism: generalized expectancy of future adverse outcomes, a heart attack risk factor.

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 or vasopressin produced by the hypothalamus.

polyvagal theory: Porges' theory that the unmyelinated vagus (dorsal vagus complex) and newer myelinated vagus (ventral vagal complex) mediate competing adaptive responses.

positive states: in Barrett and Russell’s structural model, pleasant states like contentment are located in the right hemisphere.

posttraumatic stress disorder (PTSD): 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.

prefrontal cortex (PFC): the most anterior region of the frontal lobes divided into orbitofrontal and ventromedial, dorsolateral prefrontal cortex, and anterior and ventral cingulate cortex subdivisions, and is responsible for the brain's executive functions.

primary appraisal: in Lazarus and Folkman’s Transactional Model of Stress, the first stage of our response to an event during which we categorize the consequences of events as positive, neutral, or negative and determine whether an event is relevant and negative, or potentially harmful. We evaluate these events for their possible harm, threat, or challenge.

protein kinase C (PKC): an enzyme activated by uncontrollable stressful situations that interferes with PFC functions and may result in symptoms of distractibility, impulsiveness, and poor judgment.

psychobiotics: a class of probiotics specifically formulated to influence mental health and brain function through the gut-brain axis, potentially reducing symptoms of anxiety and depression.

psychoneuroimmunology: Solomon and Moos’ term for a multidisciplinary field that studies the interactions between behavior and the nervous system, endocrine system, and immune system.

pulvinar nucleus: the posterior region of the thalamus that processes visual information and directs attention.

raphe system: a network of serotonergic neurons located in the brainstem that includes anxiety-producing and anxiety-reducing pathways that terminate on the hippocampus.

reappraisal: in Lazarus and Folkman’s Transactional Model of Stress, secondary appraisal can modify our perception of a threat when direct action is impractical or unsuccessful.

received support: support provided.

reframing: a reappraisal strategy in which they place the stressful situation in perspective and focus on available opportunities.

regulatory capacity: the ability to surmount challenges like exercise and stressors.

reserve capacity: the set of physiological, psychological, social, and material resources we draw upon to respond to stress; also called resilient capacity, it is not fixed and can be replenished through healthy habits (Gallo et al., 2009; Steffen & Bartlett, 2022).

resilience: the capacity to adapt successfully to stress, adversity, or significant challenges while maintaining psychological and physical well-being.

resilient capacity: the physiological, psychological, social, and material resources a person can draw on to adapt to stress, summarized as the health of body, mind, relationships, and resources.

resistance: the second stage of Selye’s General Adaptation Syndrome where local defenses have made the generalized stress response unnecessary. Both cortisol output and stress symptoms, like adrenal gland enlargement, decline.

response stereotypy: a person’s unique response pattern to stressors of identical intensity.

resting-state functional connectivity (RSFC): a neuroimaging method that investigates brain networks active when a person is at rest and not focused on the outside world. These networks show synchronous activity during functional magnetic resonance imaging when the person is not performing an explicit task, helping reveal brain organization and baseline neural activity.

RMSSD: the root mean square of successive differences, a time-domain measure of heart rate variability that reflects parasympathetic nervous system activity and is frequently used as a biomarker for stress.

rust out: the phenomenon of low motivation and performance due to insufficient challenge.

salience network: structures including the insula and anterior cingulate cortex that seek to monitor our external and internal environments to determine which of these inputs are salient and require further processing and attention.

secondary appraisal: in Lazarus and Folkman’s Transaction Model of Stress, the second stage of our response to an event during which we evaluate whether our coping abilities and resources can surmount an event's harm, threat, or challenge.

self-efficacy: an individual’s expectancy that they can influence her outcomes. This concept overlaps with the concepts of locus of control, mastery, and perceived control.

self-nudging: the deliberate restructuring of one's own media habits and scrolling practices to reduce exposure to low-quality information and mental fatigue, for example by setting a timer before picking up a phone (Mims, 2026).

shock phase: the first part of Selye’s alarm stage of the General Adaptation Syndrome that includes the reduced body stress resistance and increased autonomic arousal and hormone release (ACTH, cortisol, epinephrine, and norepinephrine) that comprise the “fight-or-flight” response.

social buffering: the phenomenon whereby social contact reduces physiological and behavioral stress responses, mediated in part by oxytocin release in the hypothalamus.

social contacts: the nodes (individuals or organizations) comprising a person's social network.

social network: the network that mediates socially responsible behavior, empathy, behavioral inhibition, emotional regulation, and sound judgment. The social network includes the orbitofrontal cortex, superior temporal gyrus, inferior temporal gyrus, anterior cingulate cortex, caudate, globus pallidus internal segment, substantia nigra, pars reticulata, ventral anterior nucleus of the thalamus, and medial dorsal nucleus of the thalamus.

Social Readjustment Rating Scale (SRRS): Holmes and Rahe measured major positive and negative life changes using their Social Readjustment Rating Scale (SRRS), which lists 43 events, each assigned a different Life Change Unit (LCU) value.

Social Safety Theory: a biologically-based theory proposing that developing and maintaining friendly social bonds is a fundamental organizing principle of human behavior, and that threats to social safety are critical features of psychological stressors that increase disease risk.

social support: received (support provided) and perceived support (expected support) from individuals and organizations.

specific immunity: humoral and cell-mediated immune responses that protect us against specific microorganisms and their toxins developed after birth through exposure to microorganisms and vaccinations.

stress: Selye’s term for a nonspecific response to stimuli called stressors.

stress resilience: positive adaptation in the face of significant stress; a learned capacity involving balance, flexibility, adaptive coping, and emotional stability (Steffen & Bartlett, 2022).

stress-diathesis model: the view that stressors interact with our inherited or acquired biological vulnerabilities, diatheses, to produce medical and psychological symptoms.

stressors: Selye’s term for stimuli that elicit the stress response.

structural model: Barrett and Russell's representation of affective states within a circumplex (circular structure) based on its degrees of affective valence (unpleasant to pleasant) and affective intensity (activation to deactivation).

structural networks: axonal projections and pathways.

superior colliculus: the dorsal midbrain structure composed of gray matter that processes visual information, directs visual gaze and visual attention to selected stimuli, and participates in overt and covert attention.

sympathetic nervous system (SNS): autonomic nervous system branch that regulates activities that expend stored energy, such as when we are excited.

sympathetic responder: a response stereotypy in which an individual may increase blood pressure, heart rate, and sweat gland activity and decrease heart rate variability and peripheral blood flow pressure when challenged by stressors.

sympathetic-adrenomedullary (SAM) pathway: during an acute stress response, the sympathetic nervous system directs the adrenal medulla release of epinephrine and norepinephrine.

telomerase: an enzyme that adds DNA to telomeres. Telomerase levels decline with chronic stress and cellular aging.

telomere: DNA and protein that cover the ends of chromosomes. Telomeres shorten with chronic stress and cellular aging.

temporoparietal junction (TPJ): the intersection of the superior temporal gyrus and inferior parietal lobe that mediates bottom-up shifts in attention in response to stimulus attributes.

tend-and-befriend response: Taylor and colleagues’ proposition that women may tend (nurture others) and befriend (seek and provide social support) in response to stressors.

threat: in Lazarus and Folkman’s Transactional Model of Stress, we evaluate events for the damage they could inflict in the future during primary appraisal.

threat response: a stress response that occurs when an individual appraises situational demands as exceeding their coping resources, characterized by increased total peripheral resistance, reduced cardiac output efficiency, elevated cortisol relative to DHEA, and coronary artery constriction in those with atherosclerosis.

total peripheral resistance: the total resistance to blood flow through the systemic vasculature. During a threat response, total peripheral resistance increases due to vasoconstriction, while during a challenge response it decreases due to vasodilation.

Transactional Model of Stress: Lazarus and Folkman’s cognitive model proposed that stress is determined by our perception of the situation.

traumatic stress: stress produced by a highly intense stressor that disrupts coping and endangers ourselves or others.

Type A-B continuum: Friedman and Rosenman's continuum for behavioral risk of coronary artery disease.

Type A's: Friedman and Rosenman's competitive, concerned with numbers and acquisition, hostile, and time-pressured individuals who they showed had a doubled risk of a heart attack.

Type B's: Friedman and Rosenman's less-motivated individuals who do not usually exhibit Type A behaviors and have a reduced risk of a heart attack than extreme Type A's.

Type D (distressed) personality: individuals who combine high levels of negative affectivity and social inhibition.

Undergraduate Stress Questionnaire (USQ): Crandall and colleagues' scale identifies events, mostly hassles, experienced during the past two weeks. Higher USQ scores are associated with increased use of health services.

unmyelinated vagus: in Porges' polyvagal theory, the phylogenetically older dorsal vagus complex that responds to threats through immobilization, feigning death, passive avoidance, and shutdown.

uplift: a minor positive event like receiving an unexpected call from a friend.

Uplifts Scale: Kanner and colleagues' 138-item scale that measures positive daily experiences.

urban press: Graig's concept that ever-present environmental stressors (such as alienation, crowding, fear of crime, noise, and pollution) can act in concert as daily hassles, harming physical and psychological health.

vagal withdrawal: the inhibition of the myelinated vagus, often by daily stressors.

ventromedial prefrontal cortex: region of the prefrontal cortex may play a role in calculating risk and the emotional responses of anxiety and fear. Cortisol binding to this structure increases anxiety and fear and disrupts and kills neurons.

wearable sensors: electronic devices worn on the body that continuously measure physiological signals related to stress, such as heart rate variability, skin conductance, temperature, and biochemical markers in sweat.

wei ji: Chinese pictogram representing danger and opportunity and illustrates the negative and positive possibilities considered during primary appraisal.

Yerkes-Dodson curve: an inverted U-curve that illustrates the relationship between pressure and performance.

zygomatic muscle: the muscle contracted during smiling.

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Assignment

Now that you have completed this module, how has it changed your understanding of stress? Explain how the top-down and bottom-up attentional systems work together to direct our focus.

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