Acute stressors and cortisol resp...
Acute Stressors and Cortisol Responses: A Theoretical Integration and Synthesis of Laboratory Research Sally S. Dickerson and Margaret E. Kemeny University of California, Los Angeles This meta-analysis reviews 208 laboratory studies of acute psychological stressors and tests a theoretical model delineating conditions capable of eliciting cortisol responses. Psychological stressors increased cortisol levels however, effects varied widely across tasks. Consistent with the theoretical model, motivated performance tasks elicited cortisol responses if they were uncontrollable or characterized by social-evaluative threat (task performance could be negatively judged by others), when methodological factors and other stressor characteristics were controlled for. Tasks containing both uncontrollable and social-evaluative elements were associated with the largest cortisol and adrenocorticotropin hormone changes and the longest times to recovery. These findings are consistent with the animal literature on the physiological effects of uncontrollable social threat and contradict the belief that cortisol is responsive to all types of stressors. An extensive animal and human literature documents that psy- chological factors can influence the hypothalamic���pituitary��� adrenocortical (HPA) axis, which regulates the release of cortisol, an important hormone associated with psychological, physiologi- cal, and physical health functioning. Over the past half century, hundreds of studies have specifically focused on the effects of psychological stressors on cortisol activation. Despite the magni- tude of this research enterprise, only two broad conclusions can be drawn from this literature as a whole. First, like physical stressors (e.g., electric shock, prolonged exercise), psychological stressors are indeed capable of activating the HPA axis a number of studies have reported that laboratory tasks such as public speaking or mental arithmetic can increase cortisol levels (e.g., Kirschbaum, Pirke, & Hellhammer, 1993). Second, the effects of psychological stressors on this physiological system are highly variable. Many studies have failed to find cortisol changes (e.g., Manuck, Cohen, Rabin, & Muldoon, 1991), and recent narrative reviews have highlighted the inconsistent effects of psychological stressors on cortisol activity (e.g., Biondi & Picardi, 1999). The tremendous heterogeneity in the literature suggests that all types of negative situations may not uniformly trigger cortisol changes (Mason, 1968). Essential elements, present only in contexts that elicit cortisol responses, have yet to be clearly delineated. What is it, then, about certain conditions that would make them capable of inducing a cortisol response? For decades, this funda- mental question has generated a spectrum of hypotheses. Hans Selye (1956) argued that the stress response, which includes HPA activation, was nonspecific: All stressors, whether physical or psychological, would elicit the same physiological reaction. Others have concluded from the early work investigating the effects of severe traumatic experiences on cortisol activity (e.g., electric shock, injury) that only extreme or prolonged stressful conditions trigger cortisol elevations. Some have focused on the specific characteristics of the stressor, hypothesizing that contexts that are novel (Rose, 1980), unpredictable (Mason, 1968), uncontrollable (Henry & Grim, 1990 Sapolsky, 1993), or threatening, with the potential for harm or loss (Blascovich & Tomaka, 1996 Dienst- bier, 1989), would be most likely to activate this system. Although a number of hypotheses have been offered, many have never been empirically tested, and in other cases, the evidence is not as conclusive as popular wisdom may suggest. For example, although uncontrollable contexts are commonly thought to elicit cortisol responses, the support for this association stems primarily from nonhuman animal studies primates or other animals that had control over electric shocks or blasts of noise showed attenuated cortisol responses compared with ���yoked��� animals that received identical stimuli without control (Davis et al., 1977 Dess, Lin- wick, Patterson, Overmier, & Levine, 1983 Hanson, Larson, & Snowdon, 1976 Swenson & Vogel, 1983 Weiss, 1971). However, there is surprisingly little empirical evidence for a relationship Sally S. Dickerson, Department of Psychology, University of California, Los Angeles Margaret E. Kemeny, Department of Psychology and De- partment of Psychiatry and Biobehavioral Sciences, University of Califor- nia, Los Angeles. Margaret E. Kemeny is now at the Department of Psychiatry, University of California, San Francisco. Preparation of this article was supported in part by a National Science Foundation Graduate Fellowship to Sally S. Dickerson, a National Institute of Mental Health Psychology Training Grant Predoctoral Fellowship to Sally S. Dickerson, and Research Scientist Development Award MH00820 to Margaret E. Kemeny. We thank Yoon-Soo Cynthia Bae and Shivani Chopra for their diligent coding Shelly Gable and Kevin Kim for their statistical consulting Juli- enne Bower, Naomi Eisenberger, Roberta Mancuso, Traci Mann, Wendy Berry Mendes, Gregory Miller, and Shelley Taylor and her Psychology 421 group for their thoughtful comments on a previous version of this article and Tara Gruenewald for her invaluable suggestions and support through- out this project. Their contributions are gratefully acknowledged. We also thank the authors of the primary studies, whose empirical contributions made this meta-analysis possible. Correspondence concerning this article should be addressed to Sally S. Dickerson, Department of Psychology, Franz Hall, Box 951563, University of California, Los Angeles, CA 90095-1563. E-mail: email@example.com Psychological Bulletin Copyright 2004 by the American Psychological Association 2004, Vol. 130, No. 3, 355���391 0033-2909/04/$12.00 DOI: 10.1037/0033-2909.130.3.355 355
between acute, uncontrollable conditions and cortisol activation in humans (for review, see Peters et al., 1998). Although it remains unclear whether psychological stressors with specific characteristics preferentially elicit cortisol changes in humans, research in animals supports the premise that there could be stressor-specific pathways to cortisol activation. For example, exposing animals to distinct types of physical, or systemic, stres- sors (e.g., heat, shock) can lead to different effects on the HPA system (Weiner, 1992). Systemic stressors have been differenti- ated from psychological (neurogenic) stressors in terms of their neural correlates and downstream physiological effects, including activation of components of the HPA system (e.g., Sawchenko & Ericsson, 2000). In addition, distinctive physiological correlates have been found for different stress-relevant behavioral patterns in animals (e.g., fighting, fleeing, submitting Weiner, 1992). How- ever, little is known about the differential impact of types of psychological stressors on the cortisol system in humans. Elucidating the conditions in which psychological stressors ac- tivate the cortisol system has several important implications, not only for the field of psychobiology, but for broader psychological theory and research as well. First, psychological stressors affect physiology by activating specific cognitive and affective processes and their central nervous system underpinnings. The thalamus and frontal lobes (e.g., prefrontal cortex) first integrate sensory infor- mation and evaluate or appraise the significance or meaning of environmental stimuli. These cognitive appraisals can lead to the generation of emotional responses via extensive connections from the prefrontal cortex to the limbic system (e.g., the amygdala and hippocampus). The limbic structures, which connect to the hypo- thalamus, serve as a primary pathway for activating the HPA axis (see Feldman, Conforti, & Weidenfeld, 1995, or Lovallo, 1997, for reviews on central nervous system inputs to the HPA system). Activation of the HPA axis is initiated by the hypothalamic release of corticotropin releasing hormone (CRH), which stimu- lates the anterior pituitary to secrete adrenocorticotropin hormone (ACTH), which in turn triggers the adrenal cortex to release cortisol into the bloodstream (for review, see Lovallo & Thomas, 2000 Sapolsky, Romero, & Munck, 2000). In particular, the paraventricular nucleus of the hypothalamus, a cell group that expresses CRH, is believed to play a key role in translating the differentiated neural activation patterns generated under specific environmental conditions into specific patterns of physiological and behavioral responses, including activation of the HPA axis (Sawchenko & Ericsson, 2000). Research documenting an associ- ation between specific stressors and cortisol responses might in- form an understanding of the links between the cognitive and affective responses associated with specific stressful circum- stances, the neural substrates of these responses, and activation of the HPA system. Second, the HPA axis is vital for supporting normal physiolog- ical functions and regulating other systems. Cortisol plays a critical role in metabolism by mobilizing energy resources to provide ���fuel��� for the body. This is primarily accomplished by elevating blood glucose levels (by stimulating the conversion of amino acids and other substrates to glucose in the liver, and promoting the breakdown of protein and fat stores in the tissue) the net result is the release of energy reserves that allow adequate metabolic func- tioning. Cortisol is an important regulator of other physiological systems. For example, cortisol can inhibit many aspects of immune system functioning. It can be considered the body���s own natural anti-inflammatory because it can preferentially inhibit proteins that play a central role in regulating inflammation. Cortisol also has permissive effects, which allow other physiological systems to function effectively. For example, certain levels of this hormone are necessary for the catecholamines and other sympathetic prod- ucts to exert effects on the cardiovascular system (e.g., induce vasoconstriction, increase heart rate). Therefore, the specific con- ditions that elevate cortisol levels also have the potential to influ- ence the variety of critical physiological processes that can be affected by HPA activity. Third, when the HPA system is activated, it is associated with important cognitive and affective processes and is thought to have implications for health and disease. Heightened HPA activity has been associated with depressive symptomology (E. S. Brown & Suppes, 1998 Heim & Nemeroff, 1999) and can have effects on memory (e.g., Buchanan & Lovallo, 2001 Kirschbaum, Wolf, May, Wippich, & Hellhammer, 1996 Lupien et al., 1997). Pro- longed cortisol activation (produced by frequent exposure to stres- sors or by failing to shut down this response after stressor termi- nation) is associated with a number of negative biological and health effects, including suppression of aspects of the immune system (e.g., decreased lymphocyte proliferation and cytokine production) damage to hippocampal neurons and the develop- ment and/or progression of certain chronic diseases, such as dia- betes and hypertension (Boomershine, Wang, & Zwilling, 2001 McEwen, 1998). Therefore, determining whether specific stressors activate the cortisol system could delineate the conditions capable of contributing to the onset or exacerbation of certain health outcomes. A meta-analytic review of the studies examining acute stressors and cortisol responses provides an opportunity to address the theoretical debate on the elicitors of this system as well as helps to explain the tremendous variability in this literature. Although several narrative reviews have provided overviews of topics rele- vant to acute stressors and cortisol responses (e.g., Biondi & Picardi, 1999 Kirschbaum & Hellhammer, 1994 Lovallo & Thomas, 2000 Stansbury & Gunnar, 1994), in most cases, their primary purpose was not to address the specific conditions that elicit cortisol activation there has not been a quantitative review that evaluates this literature as a whole. This type of research synthesis could systematically assess the characteristics that pre- dict cortisol responses across a comprehensive set of acute psy- chological stressor studies. The purpose of this meta-analysis is twofold: (a) to present a quantitative review of 208 acute psychological laboratory stressor studies that assess cortisol as an outcome, and (b) to test a theo- retical framework that delineates the conditions most likely to elicit cortisol responses. Drawing on theory and empirical research in animals and humans, we propose that uncontrollable threats to the goal of maintaining the ���social self��� would trigger reliable and substantial cortisol changes. In the subsequent sections, we outline the theoretical rationale and empirical support for specifically linking uncontrollability and threats to the social self (e.g., social- evaluative conditions) to cortisol activation. Then, through meta- analysis, we test whether these specific threats influence both the overall magnitude of the cortisol response and patterns of recovery (i.e., the degree to which elevations persist after the stressor ends). 356 DICKERSON AND KEMENY
In addition, using a subset of the studies, we determine the effects of these specific stressors on ACTH secretion. Recovery may be a critical issue because failing to shut down the cortisol system after provocation could lead to greater overall exposure to this hormone, which could have deleterious effects on health (e.g., Linden, Earle, Gerin, & Christenfeld, 1997 McEwen, 1998 Sapolsky et al., 2000). Despite the potential implications, very few studies have examined factors that contribute to delayed recovery (cf. Earle, Linden, & Weinberg, 1999 Matthews, Gump, & Owens, 2001 Roy, Kirschbaum, & Steptoe, 2001) the research synthesis provides an opportunity to examine whether uncontrol- lable contexts that threaten the social self influence recovery processes. In addition, whereas some studies have reported strong correla- tions between ACTH and cortisol responses to stressors (e.g., Kirschbaum, Kudielka, Gaab, Schommer, & Hellhammer, 1999), others have found dissociations between these two indicators of HPA activity (e.g., Cacioppo et al., 1995 van der Pompe, Antoni, & Heijnen, 1996). By examining the subsample of studies that also assessed ACTH secretion, we can determine, through meta- analysis, whether patterns of stress-induced ACTH and cortisol changes occur in concert, and whether social-evaluative, uncon- trollable conditions are associated with heightened activity across multiple levels of the HPA system. Theoretical Model Activation of the HPA System Although the HPA axis is often considered a general system that can be activated in response to a variety of negative situations (or in response to all types of ���stress��� e.g., Selye, 1956), an alterna- tive perspective argues that cortisol is released in response to a more circumscribed set of eliciting conditions. According to Weiner (1992), The behavioral and physiological responses of the organism to a particular stressful experience, unless overwhelming, are very specific (not general). . . . [Hormone] secretion subserves the metabolic and behavioral requirements of the organism in its efforts to survive and overcome danger and challenge. (p. 243) It has been argued that the cortisol system is activated under conditions in which central goals are threatened or impediments to attaining desired goals are encountered (Blascovich & Tomaka, 1996 Carver & Scheier, 1999 Dienstbier, 1989 Lazarus & Folk- man, 1984). This motivational perspective assumes that ���without goal commitment, there would be nothing of adaptational impor- tance at stake in an encounter to arouse a stress reaction��� (Lazarus, 1999, p. 76). Although a variety of circumstances can elicit neg- ative feeling states, only those that threaten a central goal are considered capable of triggering this particular physiological response. For example, threats to the goal of physical self-preservation (i.e., survival, safety) can elicit cortisol changes. Responses to these survival threats include activation of the HPA system, pre- sumably because cortisol mobilizes energy resources and modu- lates other physiological systems to effectively respond to the short-term metabolic demands of the threat (Lovallo & Thomas, 2000 Sapolsky et al., 2000). The mobilization of energy-relevant systems and the reduction in restorative systems are adaptive when behavioral output is needed to reduce the threat. Although threats to the central goal of physical self-preservation are regarded as the prototypical conditions that trigger HPA activation (Sapolsky et al., 2000), a growing animal and human literature indicates that threats to other central goals could activate this system as well. Social Self-Preservation Theory Similar to the motive of preserving the physical self, we propose that the motive to maintain and preserve the social self is supported by specific biological processes that include HPA activation (Dickerson, Gruenewald, & Kemeny, in press Kemeny, Gru- enewald, & Dickerson, 2004). This system, which we term the social self-preservation system, monitors the environment for threats to one���s social esteem or social status and coordinates psychological, physiological, and behavioral responses to cope with such threats. Responses to these threats include increases in negative self-evaluations (i.e., negative self-related cognitions and emotions), increases in cortisol, and changes in other physiological parameters. The magnitude of these responses depends on the intensity of the threat, its context, and the presence of vulnerability and protective factors in the individual and social environment. The social self reflects one���s social value, esteem, and status and is largely based on others��� perceptions of one���s worth (de Waal, 1989 Gilbert, 1997). Individuals who possess qualities that are valued by the group are positively regarded, respected, and es- teemed by others and have high social standing. Conversely, those that lack these valued attributes or have undesired characteristics receive signals of rejection or disinterest from group members and are lower on the social hierarchy. The quality and valence of the social self is formed through these social assessments. Humans are driven to preserve the social self and are vigilant to threats that may jeopardize their social esteem or status. A number of theories propose the existence of motives and goals similar to social self-preservation, including the need for positive self- presentation, social status, and positive self-regard (Allport, 1937 Baumeister & Leary, 1995 Bowlby, 1969 James, 1890/1950 Leary & Kowalski, 1990 Maslow, 1987 McClelland, 1984 Tay- lor & Brown, 1988). This motivational domain can also be seen across a wide variety of species nonhuman primates and other animals have developed adaptive psychobiological responses to threats to social status in hierarchies (Sapolsky, 1993). Although the social self-preservation system takes a more complex form in humans, we believe that the phylogenetic roots for this system can be observed in other social animals. Primates have complex social systems in which hierarchies emerge, providing a salient marker of rank or social status relative to the others in the troop. The hierarchy is maintained through aggressive displays by dominants that are reciprocated by submis- sive behavior by subordinates, which continually reinforces the latter���s lower status. Subordinate, low-ranking primates consis- tently have higher levels of HPA activation when compared with those of higher rank (e.g., Sapolsky, 1993), and the frequency of submissive display behavior correlates with cortisol activity (Shively, Laber-Laird, & Anton, 1997). Uncontrollable contexts can augment this effect cortisol levels of subordinate primates are particularly elevated when conditions are uncontrollable or unsta- ble (Sapolsky, 1993). Studies that have manipulated social position 357 ACUTE STRESSORS AND CORTISOL RESPONSES
in the hierarchy demonstrate the acute effects of lowered social status. Shifting from dominant to subordinate rank is associated with concomitant increases in cortisol levels (Shively et al., 1997). After an antagonistic encounter, an animal that is defeated and drops in social rank shows greater cortisol activity compared with the victor (e.g., Kollack-Walker, Watson, & Akil, 1997 Pich et al., 1993). Taken together, these studies indicate that acute or chronic threats to social status can lead to increases in cortisol activity in primates and other animals, particularly when conditions are un- controllable comparable forms of social threat could trigger cor- tisol changes in humans as well. Many theorists have argued that social hierarchies exist within human groups across cultures like nonhuman primates, humans organize their social groups so that some individuals are more highly regarded and have higher status relative to others (e.g., Fiske, 1992). Status can be conferred in humans, as in lower animals, through power, dominance, and ability to influence by means of a threat-based, agonic system that relates to access to resources. However, status is more commonly obtained in humans through hedonic processes that relate to re- spect, social esteem, acceptance, and positive social attention (de Waal, 1989 Gilbert, 1997 Gilbert & Trower, 1990). Although threats to social esteem and dominance may often overlap (e.g., situations that threaten one���s social esteem, respect, and/or accep- tance could also threaten how much influence or dominance one has), they do not always co-occur (for discussion, see Leary & Baumeister, 2000 Leary, Cottrell, & Phillips, 2001). We argue that threats to social esteem, respect, and acceptance, either in or outside the context of dominance, can activate the HPA system, causing the release of cortisol. These threats may provide the human analogue to social status threats in animals and cause activation of this system (Gilbert, 1997). Threats to the goal of preserving the social self in humans would include situations that require displays of valued attributes or skills in the presence of others, as demonstrating a lack of these qualities (through poor performance or failure) could lead to a loss of social esteem and/or social status. These social-evaluative conditions are characterized by potential or explicit social rejection and therefore could have implications for other social goals. For example, the need to preserve the social self can overlap with the need for interpersonal belonging, as failing to maintain social esteem may decrease the likelihood of forming close personal ties with others (i.e., friendship). Conditions that threaten the social self can elicit negative self- evaluations, as assessments of how we are viewed by others fundamentally affects how we see ourselves (e.g., Baumeister, 1998 Cooley, 1902/1983 Hardin & Higgins, 1996 Mead, 1934). Several lines of research indicate that social evaluation can lead to changes in self-esteem and self-related emotion (e.g., shame, em- barrassment). Leary and colleagues (Leary & Baumeister, 2000 Leary, Tambor, Terdal, & Downs, 1995) have proposed that self- esteem and self-related emotion are driven by the degree to which others are accepting or rejecting of the self perceived threats to social esteem or acceptance lead to increases in negative self- evaluative states (Gilbert, 1997 Leary et al., 1995, 2001). The presence and/or evaluation of others can lead to social compari- sons (e.g., Swallow & Kuiper, 1988 Taylor, Neter, & Wayment, 1995) or self-awareness (Carver & Scheier, 1981 Pyszczynski & Greenberg, 1987), which can also initiate negative self-evaluative processes. The resulting negative self-related states may mediate the effects of threats to the social self on physiological systems (Dickerson, Gruenewald, & Kemeny, in press). Social-Evaluative Threat We hypothesize that contexts characterized by social evaluation would elicit a significant cortisol response, as a result of the salient threat that it would pose to the goal of maintaining the social self. Social-evaluative threat occurs when an important aspect of the self-identity is or could be negatively judged by others. We pro- pose that social-evaluative threat is most likely to occur when failure or poor performance could reveal lack of a valued trait or ability. Whereas certain characteristics may be important under circumscribed conditions or among certain groups (e.g., athletic ability), others, such as intelligence or competence, are considered core attributes that are widely valued across diverse domains (e.g., Crocker & Wolfe, 2001 Kirkpatrick & Ellis, 2001 Leary & Baumeister, 2000). In the laboratory, motivated performance sit- uations provide conditions in which these core attributes are vul- nerable, because they are active performance tasks that require or demand overt or cognitive responses and have the potential for evaluation (e.g., mental arithmetic, speech task Blascovich & Mendes, 2000 Blascovich & Tomaka, 1996). Because social- evaluative threat creates the potential for loss of social esteem, it could heighten the stakes for failure in a performance-relevant situation (Seta & Seta, 1995). There is emerging empirical evidence for this relationship be- tween social-evaluative threat and cortisol responses. One exper- imental study has demonstrated that social exclusion increases cortisol levels (Stroud et al., 2000). Individuals with characteristics that would make them particularly sensitive to social evaluation show exaggerated cortisol responses to acute stressors. For exam- ple, children low in social competence show greater cortisol changes to a social-evaluative stressor (peer self-presentation task Schmidt et al., 1999), and several studies have demonstrated that individuals with low-self esteem show elevated cortisol responses to laboratory stress tasks (Kirschbaum, Pruessner, et al., 1995 Pruessner, Hellhammer, & Kirschbaum, 1999 Seeman, Berkman, et al., 1995). Although these studies demonstrate that those who might be vulnerable to social evaluation show heightened cortisol activity, a more direct test of our hypothesis would compare contexts that vary in social-evaluative threat to elucidate the spe- cific conditions that trigger the cortisol response. Uncontrollability The animal literature suggests that cortisol responses to social status threats can be heightened when conditions are uncontrolla- ble. Uncontrollability could impede the process of attaining social esteem and/or social status in humans, which could increase acti- vation of the cortisol system when the social self is threatened. In uncontrollable conditions, a behavioral response cannot affect an outcome (Averill, 1973 Levine & Ursin, 1991 Thompson, 1981 Weiner, 1992). This creates a context of forced failure, in which participants are unable to avoid negative consequences or cannot succeed despite their best efforts. Because there is nothing that can be done to change the situation, uncontrollability could greatly amplify the goal threat, which therefore could lead to exaggerated 358 DICKERSON AND KEMENY
cortisol responses. Many have posited that uncontrollability is the specific stressor dimension that triggers cortisol activation (e.g., Henry & Grim, 1990 Sapolsky, 1993), and a number of nonhuman animal studies support this contention. There has been surprisingly little empirical work in humans that has examined the relationship between acute, uncontrollable psy- chological situations and cortisol responses. Several studies offer indirect support for an association between cortisol and uncontrol- lability. Lovallo, Pincomb, Brackett, and Wilson (1990) found that among high heart rate reactors, cortisol levels increased after an aversive task (reaction time task with punishment), whereas no changes were found after a more controllable appetitive task (reaction time task with monetary incentive). Lundberg and Fran- kenhaeuser (1980) factor analyzed urinary cortisol output levels and subjective responses to five experimental tasks completed on separate days, and found that cortisol excretion loaded on a distress factor. Because uncontrollable tasks are thought to induce effort with distress (Frankenhaeuser, 1991), this factor analysis has been interpreted as support for the association between uncontrollable conditions and cortisol responses. When uncontrollability has been experimentally manipulated, results have been mixed some stud- ies have found support for the cortisol���uncontrollability link (Breier, 1989 Croes, Merz, & Netter, 1993 Peters et al., 1998), whereas others have not (Bohlin, Eliasson, Hjemdahl, Klein, & Frankenhaeuser, 1986 Bohlin, Eliasson, Hjemdahl, Klein, Fredrikson, & Frankenhaeuser, 1986 Steptoe, Fieldman, Evans, & Perry, 1993). Despite strong support from the animal literature, the evidence for whether cortisol is released specifically in response to uncontrollable situations in humans is inconclusive therefore, this remains a key theoretical question. Uncontrollable conditions may have greater effects on cortisol responses when the outcome of the situation affects an important domain or impedes progress toward a salient goal. In other words, the combination of threat to a central goal and an inability to overcome that threat may lead to substantial HPA activation. For example, in many of the animal studies, procedures (e.g., electric shock) directly threatened the physical integrity of the animal, suggesting that the uncontrollability occurred in a goal-relevant context. In humans, motivated performance situations with social- evaluative threat could provide one set of conditions in which an important goal is threatened. The Research Synthesis A research synthesis provides the opportunity to look across all of the acute laboratory stressor studies to examine the specific experimental conditions that elicit cortisol responses. This ap- proach allows us to test one component of our theoretical model: that uncontrollable threats to the goal of maintaining the social self trigger cortisol activation. Specifically, we hypothesized that un- controllable motivated performance situations with social- evaluative threat (goal-relevant conditions in which others could observe the performance and failure is the likely outcome) would lead to larger cortisol elevations than stressors without these characteristics. A meta-analytic framework could be particularly germane for clarifying the relationship between acute psychological stressors and cortisol responses because methodological and procedural factors could contribute to the inconsistent results in the literature. For example, cortisol levels show a circadian rhythm, in which levels increase dramatically on awakening and gradually decrease throughout the day, reaching the lowest levels late in the evening therefore, the time of day that the study was conducted could be a confounding variable. The timing of cortisol assessment from stressor onset could lead some studies to miss changes in cortisol, as there is a time lapse between the onset of an acute stressor and the peak cortisol response. The time of day, timing of assessment, and other methodological variables could preclude eliciting and/or capturing cortisol responses to acute laboratory stressors (e.g., Kirschbaum & Hellhammer, 1994 Lovallo & Thomas, 2000 Mason, 1968). These factors could not only obscure possible relationships between psychological stressors and cortisol activa- tion, but also greatly hinder the ability to compare results across studies. Meta-analysis provides the opportunity to first identify the methodological factors associated with cortisol responses and then statistically control for them, potentially elucidating previously masked relationships between specific eliciting conditions and cortisol activation. We limited the research synthesis to studies that assessed cor- tisol responses in healthy adults because the pathophysiology that accompanies many psychological or physical disorders could re- duce the interpretability of meta-analytic results. Furthermore, we examined acute stressors in a laboratory setting because it permits greater standardization of the stressor task and control over con- founding variables, and allows for direct causal inferences between stressful conditions and cortisol changes. Therefore, this meta- analysis does not address stressful circumstances of long duration and those that cannot be modeled in a laboratory. Although it is clear that individual difference factors and appraisal processes are important for understanding intraindividual variation in response to stressors, a solid conceptual understanding of the contexts that reliably trigger cortisol responses across individuals paves the way for the second generation of research questions, leading to more focused research on those factors that may be particularly relevant for understanding individual variability in cortisol responsivity. A sophisticated quantitative assessment of the conditions asso- ciated with cortisol changes can address several fundamental ques- tions regarding the elicitors of this system. First, studies conducted in this area have used a number of different stressor tasks that can vary immensely along dimensions such as duration, controllability, and relevance for important goals. We capitalize on this heteroge- neity and include in the meta-analysis the broad range of tasks commonly used in the stress reactivity literature. Thus, the meta- analysis provides an estimate of the magnitude of the cortisol response to acute psychological stressors across all of the tasks used in this area, and determines whether this activation is non- specific with regard to the nature of the stressor. Second, by coding the stressor category and characteristics of the tasks, we system- atically evaluate the conditions associated with cortisol responses, and specifically test our theoretical model that uncontrollable threats to maintaining the social self are capable of triggering relatively large changes in this system. Third, because the process of recovery may have different predictors than the overall magni- tude of the cortisol response (e.g., Linden et al., 1997), we also determine whether these conditions affect the degree to which cortisol elevations may persist after stressor termination. Finally, we can examine whether social-evaluative, uncontrollable condi- 359 ACUTE STRESSORS AND CORTISOL RESPONSES