Stress

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).

Graig's (1993) concept of urban press illustrates how ever-present environmental stressors (e.g., 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. Graphic © Wachiwit/Shutterstock.com.





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. Graphic © CNN.




The framework of intersectionality proposes that social identities (e.g., biological sex, class, gender identity, and race) interact to produce discrimination, disadvantage, or advantage. For example, a white woman with a disability may encounter sexism and ableism, while a Black transgender woman with the same disability may experience discrimination and transphobia. Their lived experiences will differ because their unique identities intersect, creating different patterns of discrimination and access barriers (Surrey Place-Staff, 2021). Graphic courtesy of Womankind Worldwide.

The hardiness concept emerged from a 12-year study of manager stress responses at the Illinois Bell Company (Maddi, 1987). Halfway through the study, their parent company's reorganization eliminated half their employees within a year. Two-thirds of the managers experienced severe stress reactions (e.g., heart attacks, depression, and suicide), and one-third thrived. The investigators concluded that the hardy managers were protected by attitudes of commitment (strong involvement), control (internal locus of control), and challenge (learning from experience and accepting change).

Hardiness involves biological (McVicar et al., 2014; Oken et al., 2015; Parkash et al., 2017) and social factors (Kuzman & Konopak, 2016; Zeer et al., 2016). Longitudinal studies suggest that infants' autonomic and emotional reactivity predicts later emotional reactivity (Berry et al., 2012; Cohen, 1989; Raby, 2016; Wagner et al., 2017). Less reactive infants may become more resilient. In addition, cohesiveness and social support (actual and perceived) may buffer hardy individuals against stressors. Graphic © Nina Buday/Shutterstock.com.

A single traumatic event can reshape synapses and increase electrical activity in the amygdala 10 days later. The N-methyl-D-aspartate receptor (NMDA-R) protein, which plays a central role in long-term memory, mediates these changes (Yasmin et al., 2016). Amygdala graphic © Kateryna Kon/ Shutterstock.com.





Children with depression experience trauma (35 percent) and bullying (29 percent) (Advokat, Comaty, & Julien, 2014). Graphic © fasphotographic/Shutterstock.com.





Intentional acts may produce more widespread distress than natural disasters because they threaten future and more devastating attacks. The impact of a catastrophic event depends on your distance from the event, the time interval since the event, and the perpetrators' perceived intentions (Brannon et al., 2022).

PTSD can permanently damage the systems that regulate our stress response, particularly the amygdala and hypothalamic-pituitary-adrenal (HPA) axis. Patients experience increased cortisol level fluctuation and persistent epinephrine, norepinephrine, testosterone, and thyroxin elevation (Taylor, 2006).

PTSD may promote medical illness through persistent immunosuppression (Kawamura et al., 2001). Military veterans diagnosed with PTSD have a greater risk of developing severe diseases following discharge than veterans without PTSD (Deykin et al., 2001). PTSD may also exacerbate pre-existing health problems. PTSD resulting from the September 11, 2001, World Trade Center attacks may have helped worsen asthmatic symptoms in New York residents (Fagan et al., 2003).

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). Five-Factor Model of Personality adapted from Sarafino et al. (2020).



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.

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. Graphic © MeganAlter/Shutterstock.com.

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

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.

The catecholamines epinephrine and norepinephrine mobilize blood glucose and fatty acids to provide energy for skeletal muscle contraction. They increase blood flow to the muscles by increasing cardiac output and blood pressure. They dilate coronary blood vessels and the bronchioles of the lungs and increase respiratory rate. Increased delivery of oxygen to the brain heightens alertness. As part of fight or flight, they increase metabolic rate, activate fibrinogen to accelerate clotting, constrict skin blood vessels to reduce blood loss, and release endorphins to suppress pain (McEwen, 2002). Epinephrine levels are higher when we are fearful, and norepinephrine levels are higher when angry (Ward et al., 1983).

SAM activation is adaptive when its intensity and duration enable us to cope with an external threat. Low SAM activation facilitates athletic and cognitive performance, while intense SAM activation allows us to overcome physical threats. However, intense SAM activation is maladaptive in panic attacks or anticipatory anxiety, where there is neither an external threat nor active coping. 

Intense SAM activation can threaten health and produce medical complaints.




Listen to a mini-lecture on the Effects of Intense SAM Activation © BioSource Software.

Anger can constrict coronary arteries, reduce cardiac output in cardiac patients (Committee on Health and Behavior, 2001), and are a risk factor for heart attacks and sudden cardiac death (Williams et al., 2000). Anxiety and acute grief, which can also produce intense SAM activation, are risk factors for sudden cardiac death (Engel, 1971; Kawachi et al., 1994). SAM activation also underlies common symptoms of chest pain, dizziness, and shortness of breath that can be confused with coronary insufficiency (Crider, 2004).

While Cannon emphasized sympathetic activation, stressors can also suppress parasympathetic activation and reduce HRV, consisting of changes in the time intervals between consecutive heartbeats (Task Force, 1996). Reduced parasympathetic tone can decrease restorative stage 3 sleep, contribute to illness, and increase mortality (Hall et al., 2004).

This pathway is regulated by negative feedback as rising cortisol levels inhibit hormone secretion by the hypothalamus and anterior pituitary. Graphic © Designua/Shutterstock.com.
Sustained elevated cortisol levels can affect mood and produce system-wide damage. Graphic © medicalstocks/Shutterstock.com.

CRH

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

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

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).




Listen to a mini-lecture on Cortisol © BioSource Software LLC.

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, or 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. Researchers have associated oxytocin, which is affected by estrogen, with social bonding.

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. Graphic © YAKOBCHUK VIACHESLAV/Shutterstock.com.

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).

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 animation below is courtesy of Wikipedia.

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 animation below is courtesy of Wikipedia.

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). Graphic © Alila Medical Media/Shutterstock.com.





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. Graphic © decade3d - anatomy online/Shutterstock.com.






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. Graphic © 2003 by Josephine F. Wilson.

Psychoneuroimmunology (PNI)

We develop specific immunity after birth through exposure to microorganisms and vaccinations, and it employs an antigen-antibody reaction to protect us against specific microorganisms and their toxins. Antigens are foreign molecules (proteins or polysaccharides) that stimulate antibody production. Antibodies are cellular proteins that combine with antigens to neutralize them.

Humoral and cell-mediated immunity are two types of specific immune responses. In humoral immunity, B lymphocytes rapidly produce antibodies that counter bacteria into the blood, neutralize toxins, and prevent reinfection by viruses. The illustration below shows lymphocytes (white) attacking bacteria. Graphic © dreamerb/Shutterstock.com.






Activated B cells differentiate into plasma cells, which secrete antibodies (immunoglobulins), and memory B cells, which are transformed into antigen-specific plasma cells when they reencounter the original antigen. Humoral immunity is most effective in countering bacterial infections and preventing new viral infections. The illustration below shows lymphocytes (white) attacking bacteria. Graphic © Designua/Shutterstock.com.





Cell-mediated immunity provides a slower cellular response that utilizes cytotoxic and helper T cells from T lymphocytes provided by the thymus gland. Cytotoxic T (TC) cells release toxins to destroy specific virally infected cells. Helper T (TH) cells release cytokines like interleukin-2 to aid TC and B cells' action and macrophages. TH cell cytokines can also suppress immune responses. Cell-mediated immunity is most effective in controlling cancer, foreign tissue, fungal and viral infections, and parasites.

Two-Way Brain-Immune System Communication

Nervous and immune system communication is bidirectional. From the nervous system side, the adrenal cortical release of glucocorticoids suppresses immunity, including cell-mediated mechanisms like phagocytosis. At the start of the COVID-19 pandemic, admitted patients with higher cortisol levels were more likely to die from this infection (Tan et al., 2020).

From the immune system side, increased proinflammatory cytokine release can signal the nervous system, resulting in feelings of depression, fatigue, loss of energy, and reduced pleasure (Anisman et al., 2005; Brannon et al., 2022; Dantzer et al., 2008). Acute and prolonged brain fog due to COVID-19 has been attributed to elevated cytokine levels (Theoharides et al., 2021). Graphic © Designua/Shutterstock.com.






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).

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, 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. The diagram below was adapted from Crider (2004).

Evaluation

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).  

Mastery

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. Graphic © pamspix/iStockphoto.com.






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

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






Examples include binge drinking, suspending medication and physical exercise, consuming unhealthy meals, and defaulting on responsibilities like attending class or work. Substance abuse may reduce an individual's motivation and capacity to meet their commitments.

Hopelessness

Hopelessness is a depressive symptom that might be an independent heart attack risk factor. Compared with middle-aged Finnish men scoring low in hopelessness, those scoring high were two to three times more vulnerable to a heart attack over the ensuing 6 years and three to four times more likely to die (Everson et al., 1996). Graphic © microcosmos/Shutterstock.

Optimism

Optimism is a generalized expectancy of positive future outcomes. Optimists focus on a situation's positive dimensions, minimizing daily hassles (Nelson et al., 1995). Graphic © hidesy/iStockphoto.com.






Optimism aids health by encouraging more effective problem-focused coping strategies instead of avoidant coping strategies. These strategies result in better stress management and practice of health-promoting behaviors like barrier protection during sex. Optimists show good psychological health, effective natural killer (NK) cell response during stress, and slower AIDS progression. In the context of the Transactional Model of Stress, optimists diverge from pessimists in secondary appraisal, actions, and personal adjustment (Gurung, 2019).

A prospective study showed that the 25 percent most optimistic women had about a 30 percent lower mortality risk than the 25 percent least optimistic women. Dispositional optimism was associated with reduced mortality due to cancer, heart disease, infection, respiratory disease, and stroke. While attenuated, these results held up after controlling socioeconomic status, depression, health conditions, and health-related behaviors (Kim et al., 2016).

Pessimism

Pessimism, a generalized expectancy of future adverse outcomes, is also 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

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.

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). Graphic © Ljupco Smokovski/Shutterstock.com.






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).




Listen to a mini-lecture on the importance of social contact © BioSource Software LLC. Graphic © Ljupco Smokovski/Shutterstock.com.



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 (e.g., 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.

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).

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).