Which of the following terms is best defined as a state of physical and/or psychological arousal to a stimulus?

Psychological stress is a popular term denoting processes believed to contribute to a variety of mental and physical conditions. Despite widespread interest in the construct and its consequences for health and well-being, there is little consensus on definitions for psychological stress. Three perspectives for defining and studying psychological stress are reviewed with respect to their history, development, and current status. The three perspectives on psychological stress differ in terms of the relative emphasis each places on the environment, the organism, and the interaction between organism and environment over time. Conceptual and methodological considerations and implications of the three perspectives are reviewed. Promising leads for future inquiry are addressed.

Abstract

Psychological stress is a popular term denoting processes believed to contribute to the onset and maintenance of a variety of mental and physical conditions. Despite widespread interest in psychological stress and its consequences for health and well-being, debate remains about how to best define the term. Three perspectives for defining and studying psychological stress are reviewed with respect to their history, development, and current status. These three perspectives on psychological stress differ in terms of the relative emphasis each places on the environment, the organism, and the interaction between the organism and environment over time. Conceptual and methodological considerations and implications of the three perspectives are reviewed. Recent elaborations of the concept of stress that attempt to expand its biological consequences over time are also discussed. Finally, promising topics for future inquiry on psychological stress are addressed.

Key Issues

Psychological Stress and Correctional Work

The prevalence and nature of psychological stress among correctional officers

Correlates of stress in correctional settings

Programs intended to help alleviate officers’ stress

Intellectually Disabled Inmates

Prevalence of intellectually disabled offenders and their characteristics

Methods of identifying and treating intellectually disabled inmates

Society’s Reaction to Sex Offenders

The number of convicted sex offenders has tripled since 1996

Megan’s Law: Why federal legislation passed the law, and what it means for society

What it means for sex offenders who reenter society, how they are stigmatized and how it affects recidivism rates

How society chooses to handle sex offenders in society

Women Working in Male Prisons

A look at how women are accepted by male colleagues, inmates, and society when working in a correctional setting

“Make Believe” Families

Brief history at the familial support female inmates create while incarcerated

This section looks at the reasons why these familial support groups are created, and how the families are viewed by correctional officers

Women in Prison and Mother–Child Separation

A brief look at the psychological implications of programs that allow women in prison to have their child to live with them for a length of time

Community Reentry Programs and Family Reunification

This section will briefly review the history of reentry and reunification programs, and then discuss current programs, including literature regarding their effectiveness, as well as barriers to the effective implementation of reentry and reunification programs

C. Potential Mediating Pathways

Psychological stress activates the sympathetic nervous system (SNS), which regulates blood pressure, heart rate, and release of catecholamines; and the hypothalamic-pituitary-adrenal (HPA) axis, which regulates release of corticosteroids. Immune cells possess receptors for both catecholamines and glucocorticoids, and there is substantial evidence that these hormones modulate immune function, as noted elsewhere in this volume.

Supporting a role for the SNS, the effects of acute stress on leukocytosis, adhesion molecule expression, inflammatory cytokines, and platelets can be mimicked by infusion of β-adrenergic agonists, whereas infusion of β-blockers inhibits many of these effects (Benschop et al., 1996; Mills et al., 2000; von Kanel and Dimsdale, 2000). Furthermore, stress-induced increases in leukocytosis, inflammatory cytokines, and platelet-leukocyte aggregates were found to correlate with blood pressure and/or heart rate stress responses, and stress-induced alterations in hemostatic factors and lymphocyte adhesion molecule expression are positively correlated with increases in catecholamines (Brydon et al., 2005a; Redwine et al., 2003; Steptoe et al., 2003c; von Kanel et al., 2001).

Glucocorticoids are best known for their anti-inflammatory and immunosuppressive effects, and several studies in humans and animals have shown an inhibitory effect of glucocorticoids on the synthesis of inflammatory cytokines (Black and Garbutt, 2002). Accordingly, a recent investigation of healthy middle-aged men and women showed that people with large cortisol responses to an acute stressor had lower plasma levels of inflammatory cytokines as well as smaller cytokine responses to acute stress than people with small cortisol responses (Kunz-Ebrecht et al., 2003). However, glucocorticoids may also have permissive effects. For example, while they inhibit the synthesis of inflammatory cytokines, glucocorticoids also increase the expression of certain cytokine receptors (i.e., IFN-γ, IL-1, and IL-6 receptors). Increases in plasma fibrin following the Trier Social Stress Test in healthy middle-aged men were positively associated with stress-induced elevations in cortisol, indicating that activation of the HPA axis contributes to hemostatic stress responses (von Kanel et al., 2005a). Similarly, stress-related endothelial dysfunction and impaired baroreflex sensitivity in healthy volunteers can be prevented by blocking cortisol production with metyrapone, demonstrating a direct or facilitative role for cortisol in these phenomena (Broadley et al., 2005). Stress-induced hypercortisolemia in mice causes a redistribution of leukocytes, with a reduction in the number of circulating monocytes and lymphocytes, and similar effects were observed following the awakening cortisol rise in humans. Leukocytes are thought to exit the peripheral blood to enter sites of injury and inflammation. Relevant to this, glucocorticoids stimulate vascular cell adhesion molecule expression, thereby promoting leukocyte adhesion to inflamed endothelium (Black and Garbutt, 2002). Variations in glucocorticoid responses are thought to depend on their concentration, their physiological context (healthy or disease state), and whether they are activated on an acute or chronic basis.

A further mechanism thought to be involved in inflammatory stress responses is the activation of nuclear factor-κB (NF-κB). NF-κB is a transcription factor which upregulates the expression of a number of inflammatory molecules, including cytokines. Acute psychological stress upregulates NF-κB expression in peripheral blood mononuclear cells of healthy volunteers. Increases in NF-κB expression paralleled stress-induced increases in catecholamines and cortisol, suggesting that both sympathetic and HPA pathways were involved in this response (Bierhaus et al., 2003).

Lastly, a novel pathway that inhibits macrophage production of inflammatory cytokines, termed the cholinergic anti-inflammatory pathway, has been recently identified (Czura and Tracey, 2005). The central nervous system receives sensory input from the immune system via the vagus nerve, which innervates a number of organs that act as entry routes or filters for pathogens. Efferent vagal activity leads to release of acetylcholine (ACh), which specifically binds to α7 subunits of nicotinic ACh receptors on macrophages and inhibits NF-κB signaling and inflammatory cytokine release. Notably, human vascular endothelial cells also surface express the α7 subunit of nicotinic ACh receptors, and ACh was shown to inhibit cytokine-induced adhesion molecule expression and chemokine release by these cells.

V. STRESS AND WOUND HEALING

Psychological stress has been shown to impair human wound healing in a number of well-controlled studies. Kiecolt-Glaser, Marucha et al. (1995) placed 3.5 mm punch biopsy experimental wounds on the arms of 13 chronically stressed Alzheimer caregivers and 13 well-matched controls to study dermal wound healing. Chronically stressed Alzheimer caregivers took an average of 9 days more than controls (over a 4–7 week period), or 24% longer to heal standardized wounds. Group differences in wound size appeared within the first week of healing, reaching statistical significance within the second week. Furthermore, the ability to mount an inflammatory response was tested using an ex vivo endotoxin-stimulated IL-1β gene expression assay in whole blood. Alzheimer caregivers produced significantly less IL-1β than controls. These results suggest that stress begins to have an impact in the early phases of wound repair, specifically the inflammatory phase, resulting in delayed wound closure. In an oral wound model, with wounds placed 3 days before examinations, dental students healed an average of 40% slower than wounds made in the same students during summer vacation, and the differences were quite reliable. No student healed as rapidly during examinations as during vacation (Marucha et al., 1998). These data show that something as transient, predictable, and relatively benign as examination stress may have significant consequences for wound healing, even in young adults. A third experimental study used a cross-sectional approach to further generalize the effects of stress on healing. Ebrecht et al. (2003) demonstrated that perceived stress and cortisol predicted the rate of healing in a cross-sectional study of healthy young males. The subjects had 4 mm punch biopsies placed and healing was assessed using a novel ultrasound scanning method. Salivary cortisol was measured 2 weeks prior, directly after, and 2 weeks after wounding. A strong negative correlation (r = –.59) was found between the Perceived Stress Score (Cohen, 1988) and wound closure. Furthermore, when a median split was done between slow healers and fast healers, slow healers had significantly higher stress levels, lower trait optimism, and higher cortisol during awakening. This study further confirms links among stress, stress hormones known to suppress the inflammatory response, and impaired healing. All three of these studies used experimental wounds, and great care was taken to account for potential confounding effects, e.g., alterations in health behaviors or compliance with post-operative care. Furthermore, the wounds were small, and pain was not a likely confound. In fact, in the first two studies, no significant pain was reported by the subjects. Therefore, these studies indicate a strong effect of stressors activating neuroendocrine pathways that impact on physiologic outcomes.

Several studies have investigated the role of stress in altering cytokines in wound fluids. Glaser et al. (1999) used an experimental blister model to investigate the role of stress in the development of an inflammatory exudate in wounded skin. They found that women with higher perceived stress scores had lower levels of IL-1α and IL-β in the experimental blisters 5 hours after blister induction. After 24 hours, subjects with lower levels of both cytokines reported more stress and negative affect at the wound sites. They also had higher levels of salivary cortisol compared to those subjects that had high levels of the cytokines. Broadbent et al. (2003) investigated the role of pre-operative stress on IL-1 and MMP-9 in wound fluid from 36 inguinal surgery patients. Both IL-1 and MMP-9 were negatively correlated with stress; i.e., stress was again associated with decreased cytokine and inflammatory protease production in early wounds, suggesting immunosuppression. This is consistent with human and animal experimental studies suggesting links among stress, immunosuppressive hormones, pro-inflammatory cytokine responses, and impaired healing.

Since stress impairs wound healing, an essential issue is whether interventions that reduce stress also ameliorate wound healing. Devine (1992) used a meta analysis to show that a variety of interventions, including providing education to the patient, can reduce anxiety and stress to patients, ultimately leading to reduced pain and hospital stays. In a recent study, Holden-Lund (1998) showed that patients undergoing cholecystectomy and utilizing Relaxation with Guided Imagery had lower state anxiety, lower urinary cortisol, and less wound erythema as compared to randomly selected controls. Field et al. (1998) also demonstrated that burn patients undergoing debridement and receiving massage therapy had decreased anxiety, pain, depression, and cortisol. Two biological interventions have been used in a murine model of stress-impaired healing. Blockade of the GC pathway with RU486 (Padgett et al., 1998) restores wound closure to near control levels, but only partially restores microbial clearance. Hyperbaric oxygen therapy (Gajendrareddy et al., 2005) also ameliorates wound closure, suggesting oxygen as an important mediator of stress-impaired healing. Interventions have the potential for a high impact on surgical outcomes, and additional research on effective interventions are warranted.

Emergency Social Services

The psychological stresses that disaster victims face are extreme. (See exhibit 6.12.) In an instant, often with little or no warning, people’s entire lives are uprooted. They may have lost spouses, children, parents, or other family members or friends. They may have just found themselves homeless and jobless, with no apparent means to support their families. Without proper psychological care, victims may slip into depression.

Exhibit 6.12

Possible Reactions to the Trauma of a Disaster Situation, Considered Normal

Emotional Effects

Shock

Terror

Irritability

Blame

Anger

Guilt

Grief or sadness

Emotional numbing

Helplessness

Loss of pleasure derived from familiar activities

Difficulty feeling happy

Difficulty experiencing loving feelings

Cognitive Effects

Impaired concentration

Impaired decision-making ability

Memory impairment

Disbelief

Confusion

Nightmares

Decreased self-esteem

Decreased self-efficacy

Self-blame

Intrusive thoughts/memories

Worry

Dissociation (e.g., tunnel vision, dreamlike or “spacey” feeling)

Physical Effects

Fatigue, exhaustion

Insomnia

Cardiovascular strain

Startle response

Hyperarousal

Increased physical pain

Reduced immune response

Headaches

Gastrointestinal upset

Decreased appetite

Decreased libido

Vulnerability to illness

Interpersonal Effects

Increased relational conflict

Social withdrawal

Reduced relational intimacy

Alienation

Impaired work performance

Impaired school performance

Decreased satisfaction

Distrust

Externalization of blame

Externalization of vulnerability

Feeling abandoned/rejected

Over-protectiveness

If severe, depression can have extreme consequences for disaster victims. Rates of suicide and violence tend to rise many times over what is normal for the affected population. Depressed victims may begin to neglect the tasks they depend on to survive, such as cooking, acquiring food and water, bathing, and maintaining adequate health care. Proper counseling services can limit these effects.

Disaster responders also need counseling services. (See exhibit 6.13.) They are as exposed to the emotional pain and suffering associated with death, injury, and destruction as regular victims, and may even be victims themselves if they are from the affected area. Responders often have the added psychological pressure of feeling responsible for saving lives and protecting the community at a time when both tasks are extremely challenging.

Exhibit 6.13

Groups at Risk of Psychosocial Trauma

Anyone involved in a disaster is susceptible to some degree of emotional and psychological impact. This includes children, parents, adults, those with injuries, special needs populations, disaster workers and volunteers, community leaders, the elderly, and many others.

According to the National Child Traumatic Stress Network and National Center for

PTSD, not everyone in an emergency has or develops significant psychological problems. Many people show resilience, or the ability to cope relatively well in the adverse situation. There are numerous interacting social, psychological, and biological factors that influence whether people develop psychological problems or not.

Depending on the emergency context, particular groups of people are at increased risk of experiencing social and/or psychological problems. Although there are many response actions that can be taken to provide psychosocial support and many populations that need help, those at greatest overall risk need to be identified and assisted. The following are groups of people who have frequently been shown to be at increased risk of various problems after disasters:

Children, from newborn infants to young people 18 years of age:

who are separated from parents/caregivers (separated or unaccompanied children, including orphans)

whose parents/caregivers, family members, or friends have died

whose parents/caregivers were significantly injured or are missing

who are involved in the foster care system

who are recruited or used by armed forces or groups

who are trafficked

in conflict with the law

engaged in dangerous labor

who live or work on the streets

who are undernourished/under-stimulated

Those who have been injured

Those who have had multiple relocations and displacements

Medically frail children and adults

Those with serious mental illness

Those with physical disability, illness, or sensory deficit

Adolescents who may be risk-takers

Adolescents and adults with substance abuse problems

Women

Pregnant women

Mothers with babies and small children

Single mothers

Widows

In some cultures, unmarried adult women and teenage girls

Men

Ex-combatants

Idle men who have lost the means to take care of their families

Young men at risk of detention, abduction, or being targets of violence

Elderly people (especially when they have lost family members who were care-givers)

Disaster response personnel

Those with significant loss of possessions (e.g., home, pets, family memorabilia)

Those exposed first hand to grotesque scenes or extreme life threat

Extremely poor people

Refugees, internally displaced persons (IDPs), and migrants in irregular situations (especially trafficked women and children without identification papers)

People who have been exposed to extremely stressful events/trauma (e.g., people who have lost close family members or their entire livelihoods, rape and torture survivors, witnesses of atrocities, etc.)

People in the community with pre-existing, severe physical, neurological, or mental disabilities or disorders

People in institutions (orphans, elderly people, people with neurological/mental disabilities or disorders)

People experiencing severe social stigma (e.g., lower members of a social caste, commercial sex workers, people with severe mental disorders, survivors of sexual violence)

People at specific risk of human rights violations (e.g., political activists, ethnic or linguistic minorities, people in institutions or detention, people already exposed to human rights violations)

It is important to recognize that:

there is large diversity of risks, problems, and resources within and across each of the groups mentioned above.

some individuals within an at-risk group may fare relatively well.

some groups (e.g., combatants) may be simultaneously at increased risk of some problems (e.g., substance abuse) and at reduced risk of other problems (e.g. starvation).

some groups may be at risk in one emergency while being relatively privileged in another emergency.

Endocrine System and Stress

Physical and psychological stress is managed in part through the efforts of the endocrine system. When a stressor is perceived by the brain, two stress systems are activated. The first is the norepinephrine sympathetic adrenal medullary system (NE-SAM), and the second is the HPA-axis. The NE-SAM system has immediate results, known as the ‘flight or fight’ response. This includes increased heart rate, increased pupil dilation, and increased respiration. These effects are mediated by epinephrine and norepinephrine, both produced by the adrenal glands. Epinephrine and norepinephrine are also neurotransmitters produced by nonendocrine cells in the brain where they have a number of important effects.

The first response to stress by the NE-SAM system is metabolically costly, burning through reserve glucose stores. Thus, one of the main goals of the stress systems is to generate energy. The second stress system, the HPA-axis helps to generate energy. Once activated by a stressor, the HPA-axis works to replenish the glucose stores that were quickly depleted by the NE-SAM system in preparation for a response to a second stressor or to a prolonged response to the initial stressor. All three components of the HPA-axis are part of the endocrine system; however, it is the glucocorticoid hormone released by the adrenal gland which has effects throughout the body. This hormone is cortisol in humans and corticosterone in nonhuman animals.

8.02.2.1 Stress and Coping

The definition of psychological stress is an issue that has generated a great deal of discussion and dispute, reflected in the colorful title of the chapter by Engel (1985) Stress is a noun! No, a verb!, No, an adjective! It has been argued that stress is a term that is so misused and abused that it be jettisoned altogether as a construct of serious scientific value. Nevertheless, the term has proved difficult to discard, if only as a shorthand to help define a valid area of human experience and clinical importance.

Many of the problems surrounding the concept of stress have stemmed from the definition put forward by an early pioneer, Hans Selye. His definition of stress as the “nonspecific response of the body to any demand” gave rise to two major difficulties. First, the conditions eliciting stress responses were defined so widely (as “any demand”) as to be virtually meaningless. The second difficulty is that he introduced the idea of an undifferentiated biological stress response, characterized principally by release of the group of steroid hormones known as glucocorticoids from the adrenal glands. He failed to appreciate that the activation of neuroendocrine, autonomic, and immune pathways is delicately patterned, depending on the precise demands on the organism and the behavioral and cognitive coping responses that are mobilized.

Weiner (1992) has eloquently deconstructed the background to Selye's model, and argues that it arose from the type of animal experiment that was carried out in the middle decades of the century. These studies utilized a variety of intense aversive experiences such as anoxia, limb fracture, extreme cold, and exposure to X rays. They involved potentially life-threatening damage, isolated the organism from its social context, and the stimuli were typically painful, unavoidable, and uncontrollable. These intense experiences, which lacked ecological relevance, masked variations in biological response produced by different contingencies and patterns of coping. They also led to the belief that only very profound and overwhelming experiences were likely to generate damaging physiological change. The remnants of this concept persist in today's literature with the emphasis placed on the study of major life events at the expense of milder everyday aversive experiences that may be cumulatively more significant.

It is now recognized that stress is a biopsychosocial construct, and cannot be defined purely in terms of physiological response. The physiological responses are only part of the profile that include changes at the affective, behavioral, and cognitive levels as well. Nor can stress simply be defined as the response to aversive environmental stimulation or disturbing events. The same situation may produce quite different responses in two people, or in one individual on different occasions. Most frameworks of contemporary research and clinical practice therefore recognize that stress responses arise through interactions between demands on the one hand, and psychosocial resources on the other. Cohen et al. (1995a), for example, have defined stress as a process in which “environmental demands tax or exceed the adaptive capacity of an organism, resulting in psychological and biological changes that may place persons at risk for disease” (p. 3).

This process, and the physiological responses that may be elicited, is outlined schematically in Figure 1. The psychosocial demands (or stressors) can be defined as potential or actual threats or challenges to the integrity, survival, and reproduction of the organism (Weiner, 1992). They may be anticipated, and may be real or imaginary. In the field of health psychology, the main categories of psychosocial demand are acute life events, chronic stressors, and day-today hassles and irritations. The characteristics of these demands that make them particularly potent elicitors of psychophysiological responses are described in Section 8.02.4.2. Adaptive capacity is operationalized in terms of resistance and vulnerability factors, and aspects of people's psychological makeup and social world that may render them more or less susceptible. Personality, behavioral coping style, and social resources are among the major resistance and vulnerability factors, and their role is examined in Section 8.02.5. Of course, it must be recognized that although, for convenience, demands and adaptive resources are viewed as distinct categories, they are difficult to disentangle in practice. For example, social isolation can be conceptualized both as the absence of a social resource or as a chronic stressor, while close social contact may be supportive or the source of major interpersonal conflict.

Psychophysiological responses are elicited when the organism's adaptive capacity fails to match demands. Typically, this will be under conditions of over-stimulation, but it is conceivable that lack of stimulation may also lead to adverse physiological change. The physiological responses themselves include adjustment in a number of biological systems, but the most important for health risk are neuroendocrine, immunological and autonomically-mediated changes in physiological function.

3.1 Psychological Illness

Life stressors are associated with psychological stress reactions that involve depression and anxiety. For example, life stressors are linked both to the onset of depressive disorders and to relapse among individuals recovering from depressive disorders. Interpersonal problems and losses are especially likely to be associated with depressive reactions. Life stressors can also precipitate both onset and relapse of anxiety disorders such as generalized anxiety disorder, panic disorder, agoraphobia, and obsessive–compulsive disorder, and they can play a role in the development and progression of alcohol and drug abuse. Moreover, life stressors can trigger schizophrenic episodes among individuals who are vulnerable to this disorder. Trauma exposure produces a recognized pattern of PTSD symptoms, including reexperiencing the trauma psychologically through flashbacks and nightmares, emotional numbing, and experiencing heightened arousal and vigilance.

Exclusive of traumatic events, chronic stressors are more strongly linked to psychological distress than are acute events. Although chronic stressors generally are less severe than acute life events, their effects often last longer and are more pervasive (Fig. 1). Moreover, an event is more likely to have an adverse psychological outcome when it threatens or disrupts a domain in which a person has central commitments.

Psychological reactions themselves can exacerbate the stress process in two important ways. First, psychologically distressed individuals are more likely to perceive benign situations as threatening, and these perceptions of threat can trigger additional stress reactions. Second, persons who are psychologically distressed often create social conditions in their lives, such as conflictual family or work relationships, that are likely to produce new life stressors.

2. Animal Model Studies

It has long been known that psychological stress in humans is often associated with the spontaneous bouts of recurrent HSV infection that occur as consequence of latent virus reactivation. Unfortunately, the lack of a reliable mouse model of spontaneous reactivation has somewhat limited the usefulness of mice in studying HSV reactivation and the associated immune response. However, the immune system of the mouse is very well characterized and is similar in many respects to that of humans. This reason, and the fact that there is a wide and continually expanding variety of reagents for studying detailed immune responses in mice, has led to mice being the species of choice for most immunological studies, including those studies which seek to better decipher the nature of stress-neuroendocrine-immune interactions.

For many years, it has been known that local trauma (e.g., hair plucking, tape stripping, chemical-induced trauma, ultraviolet light) administered to a previously infected area can result in HSV reactivation and recurrent disease. However, the ability of each of these methods to consistently induce recurrent disease is quite low (Harbour et al., 1983; Hill et al., 1978; Hill et al., 1983; Hurd and Robinson, 1977). Whether or not the above methods elicited reactivation and recurrent infection simply due to trauma on nerve endings innervating the site or whether the animal perceived the trauma as a psychological stressor is not known. However, two additional recent and reliable models of psychological stress in mice have been shown to be effective in inducing HSV reactivation and recurrent disease and, in turn, have allowed for better studies of the immunological and neuroendocrine mechanisms underlying behaviorally mediated reactivation of latent HSV and the development of recrudescent HSV infection in mice. For example, the use of a hyperthermic stress model (Sawtell, 1998; Sawtell and Thompson, 1992; Thompson and Sawtell, 1997) has been used to show that HPA axis activation plays an important role in HSV-1 reactivation in the trigeminal ganglion and that this reactivation may be associated with an increase in IL-6 expression in the ganglia itself (Noisakran et al., 1998). In addition, the use of a social stress model in mice has been shown to be effective in causing recurrent HSV infection in mice (Padgett et al., 1998b). This correlation between neuroendocrine activity, immune function, and latent HSV reactivation (Carr et al., 1998; Halford et al., 1996; Noisakran et al., 1998; Padgett et al., 1998b) is particularly interesting in light of recent findings that HSV-specific memory CD8+ T-cells are selectively activated and retained in latently infected sensory ganglia (Khanna et al., 2003). Studies are in progress to determine if stress-induced, neuroendocrine-mediated mechanisms are able to play a role in the activation of ganglia-resident CD8+ T-cells and the impact of this activation on latent HSV reactivation and recurrent infection.