Abstract
For decades, post‑traumatic stress disorder (PTSD) has been conceptualized primarily as a psychopathology requiring clinical remediation. This article argues that natural recovery from traumatic stress is the biological default, and that PTSD represents a condition of interrupted recovery within a phylogenetically ancient adaptive system. Drawing on ethology, evolutionary biology, learning theory, and clinical research, I propose that the core mechanism of both natural recovery and effective treatment is the restoration of perceived control through behavioral re‑engagement with the feared environment. Control‑Focused Behavioral Treatment (CFBT) is presented not as an exogenous clinical invention but as a systematic facilitation of this endogenous recovery process. The evidence converges from cross‑species observations, epidemiological patterns, self‑help treatment studies, and four decades of fieldwork with over 15,000 survivors of torture, war, and earthquakes. The article challenges alternative models of trauma treatment and outlines implications for public health and disaster response. Although the evidence reviewed is drawn primarily from trauma research, the principles outlined apply to anxiety and fear responses generally.
Keywords: Natural recovery, Post‑traumatic stress disorder, PTSD, Control‑Focused Behavioral Treatment, CFBT, perceived control, uncontrollability and unpredictability, avoidance, ethology, evolutionary psychology, affective neuroscience, social pain, resilience, self‑exposure, foraging–survival trade‑off, trauma treatment, earthquake survivors
Introduction: Reframing Trauma Within an Evolutionary Framework
For several decades, the dominant clinical paradigm has conceptualized post‑traumatic stress disorder (PTSD) primarily as a psychopathology—a disorder of cognition, affect, and neurobiological dysregulation requiring active clinical remediation. While this framework has generated substantial therapeutic innovation, it carries an implicit assumption that is rarely examined with sufficient rigor: that the symptomatic sequelae of catastrophic stress represent a deviation from some prior state of psychological equilibrium, rather than the expression of a fundamentally biological program whose execution has been arrested. This article proposes an alternative conceptual architecture, grounded in ethology, evolutionary biology, and behavioral medicine, which situates both trauma pathology and clinical recovery within the organism’s phylogenetically ancient adaptive repertoire.
The central thesis is that PTSD represents a condition of interrupted recovery—a state in which the organism’s adaptive survival machinery, having been activated but denied completion of its evolutionarily prescribed sequence, becomes locked in a chronic state of arousal and vigilance. From this condition, neither physiological nor behavioral resolution is achievable without renewed confrontation with the aversive stimulus environment. Correspondingly, I propose that effective trauma treatment, and in particular the model of Control‑Focused Behavioral Treatment (CFBT) that I have developed over four decades, does not represent the imposition of an exogenous clinical procedure upon a disordered system. It represents instead the systematic facilitation of a recovery process that is itself biologically mandated and phylogenetically conserved.
This reconceptualization carries significant implications not only for clinical practice but for the epistemological foundations upon which trauma science rests. If natural recovery from traumatic stress is the biological default, a position for which the epidemiological and ethological evidence reviewed herein is compelling, then the appropriate scientific question is not “What must be done to treat trauma?” It is rather “What biological, cognitive, behavioral, and emotional processes, when unimpeded, render traumatic stress self‑limiting, and what circumstances prevent their normal execution?” The answers to these questions, as I shall demonstrate, point toward a unified account of traumatic stress, its chronification, and its resolution.
This account is the product of a research program spanning four decades, involving over 15,000 survivors of torture, war, and earthquakes, and organized around two guiding hypotheses: first, that loss of perceived control during traumatic experiences is the primary determinant of traumatic stress; and second, that regaining a sense of control reverses this process and leads to resilience. These twin hypotheses, and the evidence bearing on them, form the backbone of the present article.
A unifying visual model of the learning theory framework on which CFBT is based appears as Figure 1.1 in my 2011 book (Başoğlu et al., 2011). That figure depicts the pathways from trauma exposure through loss of control, helplessness, and avoidance to traumatic stress, and the reverse pathway from enhanced control through reduced avoidance to recovery. The present article focuses on one component of this broader model: the natural recovery processes that operate when the organism’s own recovery machinery is permitted to function. The reader is referred to the 2011 book for a full review of the literature evidence supporting each pathway in the model.
This article is the third in a planned series examining the theoretical, clinical, socio‑political, and philosophical implications of a control‑focused approach to trauma. The first article (Başoğlu, 2026a) critically examined cognitive behavioral therapy and its third‑wave derivatives in light of the CFBT model. The second (Başoğlu, 2026b) compared CBT and CFBT with respect to their theoretical foundations, socio‑political contexts, and philosophical implications. The present article turns to the biological and evolutionary evidence, arguing that natural recovery is not merely a clinical observation but an ethological imperative.
Although much of the evidence reviewed in this article is drawn from trauma research—reflecting the primary focus of my own work over four decades—the principles outlined here are not specific to trauma. They apply to the full spectrum of anxiety and fear responses, including phobias, panic disorder, obsessive‑compulsive disorder, and the ordinary anxieties and fears of daily life. The core mechanism—loss of control leading to helplessness and avoidance, restoration of control leading to recovery—operates across these conditions, as our studies of panic disorder and agoraphobia demonstrate.
A note on terminology
Throughout this article, I distinguish between three related terms. Exposure refers broadly to any confrontation with feared stimuli, whether therapist‑directed, self‑initiated, or incidental. Self‑exposure denotes the deliberate, self‑initiated confrontation with feared situations aimed at restoring a sense of control. It is the active ingredient in CFBT and one important pathway to natural recovery. Re‑engagement describes the broader ethological pattern, observed across species, of resuming functional activity in a previously threatening environment. Re‑engagement can take the form of deliberate self‑exposure, or it can be driven by changing life circumstances, environmental demands, or the simple erosion of avoidance in the face of competing survival imperatives. In all cases, the mechanism of recovery is the same: contact with the feared stimulus restores the organism’s sense of control, whether or not that contact was deliberately sought.
I also use the term control throughout this article in a broad evolutionary sense. What I mean by control is not limited to behavioral action in the narrow sense. It encompasses the organism’s capacity to exercise agency over cognitions, emotions, and physiological states—all of the processes that serve to protect the organism from harm and keep it alive. When I refer to behavioral control, I am referring to this broader repertoire of adaptive responses, of which overt motor behavior is only one component.
The Evolutionary Architecture of Survival: Active Control as Biological Imperative
Any rigorous ethological account of trauma must begin with the organism’s primary defensive architecture. The fight‑or‑flight response, described in its essential neurophysiological contours by Cannon (1932) and subsequently elaborated through decades of comparative behavioral research, is not accurately characterized as a simple binary between aggression and escape. It is more precisely understood as a coordinated set of active control strategies whose shared functional objective is the restoration of perceived and actual control over an aversive or threatening stimulus environment. Both fight and flight are, at their core, instrumental behaviors: they are actions directed toward an environmental outcome, and their biological function is to terminate or distance the organism from the source of threat (Fanselow, 1994). The neurobiological substrates supporting these behaviors—activation of the hypothalamic‑pituitary‑adrenal (HPA) axis, sympathoadrenomedullary mobilization, suppression of vegetative functions incompatible with vigorous motor action—represent an extraordinarily conserved phylogenetic legacy, identifiable across vertebrate and many invertebrate taxa (Korte et al., 2005).
What is critical for the present analysis is the behavioral logic underlying this architecture. The fight‑or‑flight response is predicated on the assumption, embedded in the organism’s phylogenetic inheritance, that some form of effective action is available. The mobilization of sympathetic resources, the sharpening of attentional focus, the suppression of pain sensitivity—all of these preparatory physiological adjustments are oriented toward enabling an active response that will, with some probability, alter the organism’s relationship to the threatening stimulus. This is, in the broadest sense, a system designed for control.
I have argued throughout my work that the core experiential dimension of traumatic stress is not fear per se. It is the conjunction of fear with uncontrollability and unpredictability—the subjective and objective conditions under which the organism’s active control strategies are rendered ineffective (Başoğlu, 2011; Başoğlu & Mineka, 1992). It is precisely this conjunction that differentiates a frightening experience from a traumatizing one, and it is the failure of active control, not the intensity of aversive stimulation alone, that initiates the pathological cascade culminating in PTSD. This formulation has direct ethological grounding. In naturalistic settings, organisms exposed to controllable aversive stimulation exhibit rapid behavioral adaptation and recovery. In contrast, exposure to inescapable and unpredictable aversive events produces persistent disruptions in motivation, affect, and cognition (Maier & Seligman, 1976; Maier & Watkins, 2005).
The Foraging–Survival Trade‑off: When Avoidance Becomes Incompatible with Survival
A critical dimension of the evolutionary analysis of trauma concerns the functional limits of avoidance behavior as a survival strategy. Within the broader ethological literature, avoidance of threat is widely recognized as an adaptive behavioral response under conditions in which threat is genuine and proximate. However, the same literature provides compelling evidence that avoidance is not a biologically unconditional good. Organisms for whom avoidance becomes the dominant behavioral response to threat pay substantial fitness costs that may, under extreme conditions, render excessive avoidance incompatible with survival itself.
This tension is most elegantly formalized in the ecological concept of the foraging–predation risk trade‑off, which posits that prey organisms must perpetually balance the life‑preserving imperative of avoiding predators against the equally life‑preserving imperative of acquiring nutritional resources (Lima & Dill, 1990). Behavioral ecologists have documented this trade‑off across a wide range of taxa. Fish exposed to persistent predatory threat substantially reduce foraging activity, resulting in decreased growth, depletion of energy stores, and heightened susceptibility to other mortality risks (Siepielski et al., 2016). Ground‑dwelling foragers such as kangaroo rats alter the timing and location of their foraging under elevated predation risk, incurring significant energetic penalties (Kotler et al., 1994). Research on redshanks (Tringa totanus) demonstrated that when starvation risk forces individuals into high‑predation‑risk foraging zones, the behavioral calculus shifts: approach behavior becomes the adaptive response, and those individuals most capable of resuming normal foraging in a risky environment demonstrate superior survival outcomes (Sansom et al., 2009).
Decision‑making research on predator avoidance has formalized this logic in terms of the costs of anti‑predator behavior. Time spent hiding or in a state of hypervigilant immobility necessarily displaces time available for foraging, mate‑seeking, territorial defense, and reproductive investment (Lind & Cresswell, 2005). Organisms that persist in avoidance behavior beyond its adaptive window—that is, after the threat has genuinely resolved—suffer measurable fitness penalties relative to conspecifics that resume approach behavior earlier (Siepielski et al., 2016). The evolutionary implication is unambiguous: natural selection does not favor indefinite avoidance. It favors calibrated risk‑taking that permits the organism to re‑engage with its environment as soon as conditions allow. Avoidance that persists beyond the period of genuine threat is, in evolutionary terms, maladaptive—a biologically costly error.
This principle extends well beyond the predator–prey context. Among songbirds, individuals exposed to simulated predator attacks reduce their singing rate and shift to less conspicuous perches, but those that fail to resume normal vocalization patterns after the threat has passed suffer reduced territory defense and mate attraction (Cresswell, 2008). In social mammals, exaggerated vigilance and withdrawal from group activities in response to past predation events reduce access to cooperative hunting, allogrooming, and coalitionary support (Cheney & Seyfarth, 2007). Among rodents, rats exposed to cat odor exhibit prolonged hiding and reduced exploration, but those that resume exploratory behavior sooner show more rapid restoration of normal feeding and weight gain (Blanchard & Blanchard, 1989; Dielenberg & McGregor, 2001). Experimental work with stickleback fish has shown that individuals from high‑predation environments who fail to adjust their anti‑predator behavior when moved to low‑predation conditions suffer reduced growth and fecundity relative to more behaviorally flexible conspecifics (Bell & Sih, 2007). In field crickets, persistent hiding after predator cues have been removed delays mating and reduces reproductive success (Hedrick & Kortet, 2006). The consistency of this pattern across vertebrate and invertebrate taxa points to a fundamental evolutionary principle: anti‑predator behavior is adaptive only when it is calibrated to the actual level of threat in the environment. When it persists beyond its adaptive window, it becomes a liability.
This has direct and under‑theorized implications for the understanding of PTSD. The human individual with chronic PTSD who avoids trauma‑associated stimuli, public spaces, social engagement, occupational demands, or the full range of activities necessary for productive functioning is, in the most literal biological sense, exhibiting a pattern of avoidance that has become incompatible with adaptive functioning. The organism’s defensive system, calibrated for the acute emergency, is consuming resources and constraining behaviors that the organism’s broader survival and reproductive mandate requires. I have argued in my own work that this evolutionary tension—between the short‑term protective function of avoidance and its long‑term fitness costs—is central to understanding why natural recovery must exist and why the organism is equipped with mechanisms to overcome avoidance when it becomes excessive (Başoğlu et al., 2011, Chapter 1).
The Defensive Cascade: From Active Control to Interrupted Recovery
When neither fight nor flight succeeds—when the organism’s active control strategies are exhausted, circumvented, or rendered structurally impossible by the nature of the traumatic situation—the organism does not simply return to baseline. The biological mobilization initiated by the threat does not gracefully dissolve in the absence of behavioral discharge. Rather, a third phylogenetically ancient response pattern is activated: the immobility or freeze response, characterized by tonic behavioral suppression, attenuated motor output, and a paradoxical analgesia that may reflect the organism’s evolved preparation for the possibility of predatory capture. In non‑human animals, this freeze response is typically transient. It is followed, upon removal of the threatening stimulus, by spontaneous motor discharge—trembling, shaking, vigorous movement—that appears to serve a neurophysiological function in completing the interrupted defensive response sequence and restoring autonomic equilibrium.
In humans, however, the completion of this sequence is not guaranteed. The cognitive and linguistic capacities that distinguish the human organism—capacities for abstract self‑reflection, for the anticipatory modeling of future threat, for the narrative reconstruction of past experience—also confer the capacity to sustain, indefinitely and in the absence of any continuing environmental threat, the internal representation of the traumatic event and its associated aversive emotional state. PTSD, from this perspective, represents a condition of interrupted recovery. The threat has passed. The defensive response has not been completed. And the organism’s biology continues responding as though the emergency were ongoing. The hyperarousal, intrusive re‑experiencing, and pervasive avoidance that constitute the clinical presentation of PTSD are, on this account, not aberrant processes but the predictable functional consequences of an adaptive system that has been denied its normal resolution.
The role of conditioning in sustaining this state deserves emphasis. The traumatic event, in classical conditioning terms, constitutes an unconditioned stimulus (UCS) that produces unconditioned fear and defensive activation. Stimuli present during the traumatic event—environmental, somatic, social, and contextual—acquire the status of conditioned stimuli (CS) through their temporal and spatial contiguity with the UCS, and subsequently elicit conditioned fear responses even in the complete absence of genuine threat (Mineka & Zinbarg, 2006; Başoğlu & Mineka, 1992). This transforms the post‑traumatic environment into a pervasive threat landscape in which formerly neutral stimuli systematically elicit defensive activation. The behavioral consequence—systematic avoidance of all conditioned stimuli—is, in the short term, adaptive in that it reduces the frequency of conditioned fear responses. In the longer term, however, avoidance constitutes the central mechanism by which PTSD is maintained and the natural recovery process is impeded.
This is not merely a matter of avoiding feared situations. The disability that avoidance causes in important life areas—occupational impairment, social withdrawal, loss of meaningful activities—can itself exacerbate the helplessness response. When avoidance progressively narrows the survivor’s behavioral repertoire, the resulting loss of function in work, family, and community roles deepens the experience of uncontrollability. Helplessness, reinforced by accumulating evidence of incapacity, can give way to hopelessness, and hopelessness to depression (Alloy et al., 1990). What begins as a defensive adaptation thus becomes a self‑reinforcing cycle: avoidance produces disability, disability deepens helplessness, and helplessness strengthens the conviction that action is futile, which in turn sustains avoidance. Breaking this cycle requires not the elimination of fear but the restoration of a sense that action can produce meaningful outcomes.
My observations of both earthquake and torture survivors documented that reduced avoidance of trauma‑related cues—whether achieved deliberately or through the demands of daily life—was strongly associated with accelerated symptomatic improvement (Başoğlu et al., 2011). A subsequent controlled study provided direct evidence that reduction in behavioral avoidance was the proximate mechanism mediating exposure‑induced improvement in earthquake survivors with PTSD, underscoring the causal role of avoidance reduction in recovery (Salcıoğlu et al., 2007). All of our treatment studies, beginning with the 2003 trial of a single session with an earthquake simulator (Başoğlu et al., 2003), involved only live exposure—that is, direct confrontation with feared situations rather than imaginal or verbal processing. The consistent finding across these studies was that reduced avoidance led to recovery, providing converging evidence for the centrality of this mechanism.
The earthquake setting provided particularly compelling naturalistic evidence for the evolutionary theory. In my 2011 book (Başoğlu et al., 2011, Chapter 1), I describe how, in the aftermath of the 1999 Marmara earthquake, survivors who had initially fled their homes and relocated to tent cities or makeshift shelters often reached a point where the conditions of avoidance became unsustainable. The shelters were crowded, unsanitary, cold in winter, and incompatible with the demands of employment and family life. At a certain threshold, the costs of avoidance outweighed the perceived safety it provided. Survivors began returning to their homes—initially for brief periods, then for longer stays—not because they had been instructed to do so by a therapist, but because the survival calculus had shifted. The same behavioral pattern observed in the animal literature—the resumption of foraging when starvation risk outweighs predation risk—was playing out in human survivors. And the outcome was the same: contact with the feared environment, even when driven by circumstance rather than intention, restored a sense of control and accelerated recovery.
Uncontrollability and Unpredictability: The Core Dimensions of Traumatic Stress
The theoretical framework that I developed with Susan Mineka (Başoğlu & Mineka, 1992) identifies the dimensions of uncontrollability and unpredictability as the cardinal determinants of traumatic stress severity and chronicity. The evidence for this framework, including the original learned helplessness experiments, neurobiological studies, and our own research with torture survivors, has been extensively reviewed elsewhere (Başoğlu, 2026b). Here I will only summarize the essential points: (a) exposure to uncontrollable aversive stimulation produces lasting deficits that are not produced by equivalent but controllable stimulation; (b) unpredictability leads to generalization of fear and sustained hypervigilance; and (c) psychological preparedness for trauma (political commitment, prior knowledge, stoic training) serves as a protective factor by preserving a sense of control even under extreme duress.
I should note that I do not use the term “learned helplessness” when describing human responses to uncontrollable stressors. The term denotes a cognitive construct derived from animal models; human responses are more complex, and “learned” implies a finality that may not be warranted. I prefer the term “helplessness” to describe the state that may or may not progress to the full syndrome observed in laboratory animals. For a full review of the human evidence, the reader is referred to my earlier work (Başoğlu, 2026b; Başoğlu et al., 2011).
The evidence reviewed thus far has focused on physical threat—the dangers that predators, earthquakes, and other environmental hazards pose to survival. Yet humans, like many other social mammals, live in complex social systems in which group membership is essential for protection, resource acquisition, and reproduction. Just as evolution has shaped the organism’s physical and behavioral defenses against predators and environmental threats, it has also shaped defenses against threats to social standing, belonging, and identity. Adaptation to the social environment is not a cultural overlay on a biological substrate; it is a biological imperative in its own right. Social exclusion, humiliation, and loss of status can be as consequential for survival as physical injury, and the organism’s stress‑response systems reflect this evolutionary reality.
Although the Başoğlu and Mineka (1992) framework was developed primarily in the context of torture trauma, its core principles apply with equal force to social stressors. Evidence from affective neuroscience demonstrates that social pain—the distress caused by humiliation, ostracism, and social defeat—shares neural substrates with physical pain, particularly the dorsal anterior cingulate cortex and anterior insula (Eisenberger, 2012b; MacDonald & Leary, 2005). Threats to social standing and belonging are thus processed by the same phylogenetically ancient systems that respond to physical danger. The evolutionary depth of this response is further suggested by evidence that shame‑like appeasement displays occur in non‑human primates and other social mammals (Darwin, 1872; Keltner & Buswell, 1997) and that the nonverbal expression of shame appears to be innate, emerging even in congenitally blind individuals (Tracy & Matsumoto, 2008). The severity with which human societies have historically treated social exclusion—banishment often being the most extreme sanction short of execution—underscores the survival value of group membership (Ouwerkerk et al., 2005). Social defeat is a powerful stressor that elevates cortisol and can lead to anxiety, depression, and PTSD in both humans and other social mammals (Björkqvist, 2001; Dickerson & Kemeny, 2004). It is therefore not surprising that people often report social exclusion as more painful than physical injury (Williams, 1997)—a pattern consistent with evidence that psychological torture can be as traumatic as physical torture (Başoğlu et al., 2007) and, in some contexts, even more so (Başoğlu, 2009). (For a more detailed review of the evolutionary and neurobiological evidence on social pain, see Björkqvist, 2017.) The primacy of uncontrollability and unpredictability thus extends across physical and social domains, consistent with the evolutionary continuity of stress responses.
Collective Behavioral Responses to Uncontrollable Events: Evidence from Mass Trauma
One of the most striking observations to emerge from our work with earthquake survivors was the spontaneous, self‑organized coping behaviors exhibited by millions of people in the aftermath of catastrophic earthquakes. The 1999 Marmara earthquake, which affected a large urban population in Turkey, provided a natural laboratory for observing how human beings respond collectively to events that are, by their very nature, both unpredictable and uncontrollable. These responses are detailed elsewhere (Başoğlu, 2011, Chapter 1). To summarize, following the earthquake, vast numbers of survivors relocated to tent cities or makeshift shelters outdoors, even when their homes were structurally intact, to avoid being indoors during unpredictably occurring aftershocks. They developed elaborate strategies for monitoring seismic activity, sharing information about tremors, and organizing daily routines around the anticipated timing of aftershocks. Many individuals slept in their clothes with emergency supplies by the door. Some kept lights on throughout the night to be able to see if an earthquake occurred. Others placed objects in precarious positions on shelves so that their fall would signal the onset of a tremor and wake them. Survivors reported mentally rehearsing escape routes from every room they entered. Many avoided bathing or showering for extended periods because the bathroom was perceived as a particularly dangerous location during tremors. Parents developed protocols for reaching their children quickly in the event of an aftershock, often rehearsing these sequences with family members.
What is significant about these observations is not merely their variety but their common functional objective. Each of these behaviors, however idiosyncratic, represented an attempt to make the unpredictable predictable and thereby to restore a measure of perceived control. The survivor who slept fully clothed by the door was not actually safer from earthquake injury. But the behavior served a psychological function: it created a subjective sense of preparedness that partially restored the predictability that the earthquake had shattered. The same logic applied to the survivor who monitored seismological reports obsessively, or who developed a personal theory about the pattern of aftershocks, or who refused to enter buildings above a certain height. Each of these strategies, whether rational or not, addressed the core traumatic dimension: the loss of control over one’s physical safety.
Particularly striking was the observation that some survivors developed beliefs that were manifestly irrational, yet functionally adaptive. Some individuals became convinced that they could predict earthquakes from changes in weather, from the behavior of animals, or from physical sensations. Others developed superstitious rituals that they believed would protect them. From a clinical perspective, these beliefs might appear to be cognitive distortions. From an evolutionary perspective, they represent the organism’s fundamental drive to restore predictability and control by whatever cognitive means are available. When objective control is impossible, subjective control—even if illusory—may be the organism’s default response.
Similar patterns have been documented in survivors of torture and war trauma. In a chapter on torture trauma (Başoğlu & Mineka, 1992), we described how political activists subjected to captivity and torture spontaneously developed cognitive and behavioral strategies to maintain a sense of control over their circumstances—timing interrogations, establishing covert communication with fellow prisoners, mentally rehearsing resistance techniques, and finding small ways to exercise choice even under conditions of extreme constraint. A later publication (Başoğlu et al., 2011, Chapter 2) examining the learning theory formulation of war and torture trauma documented parallel strategies in survivors who, despite ongoing threat, found ways to resume functional activities and thereby restore a sense of control over their lives. In addition, a study of 78 former Guantánamo detainees reported strikingly similar cognitive and behavioral strategies aimed at maintaining sense of control in a helplessness‑inducing captivity environment—leading the researcher to describe the interactions between the captors and the captives as “a battle for control” (Koenig, 2017).
The convergence across such different trauma types—earthquakes, torture, and war—strengthens the argument that these coping responses are not trauma‑specific but reflect a general biological preparedness. When human beings are confronted with extreme uncontrollability and unpredictability, the organism’s default response is to attempt to restore predictability and control through whatever cognitive and behavioral means are available. This is, I have come to believe, an evolutionary mandate.
Fear of Earthquakes: An Evolutionary Perspective
The intense and persistent fear that earthquakes evoke, and the remarkable resistance of this fear to extinction, may reflect an evolutionarily determined response geared towards self‑preservation. It has long been recognized that defensive responses such as heightened vigilance, flight or fight, and avoidance of threat have played a fundamental role in the survival of species for millions of years (Marks, 1987). Several lines of evidence suggest that earthquakes have evolutionary significance for living organisms. For example, there are close parallels between human and animal responses to earthquakes. Snarr (2005) documented that animal responses to earthquakes have been observed for at least 3,000 years, including behavioral changes before, during, and after seismic events. Non‑human primates show increased restlessness, freezing, and signs of stress and fear in response to earthquakes (Shaw, 1977; Krusko et al., 1986; Antilla, 2001). In a study of wild mantled howlers in Honduras, the monkeys’ response to seismic activity was very similar to their response to a ground threat such as an approaching predator (Snarr, 2005). Moreover, Kirschvink (2000) suggested that evolutionary processes might have led to tilt, hygroreception, electric, and magnetic sensory systems in animals that enable them to detect certain earthquake precursors, such as P waves. Given that tectonic plate activities have existed for at least two billion years, there has been sufficient time for natural selection to favor organisms capable of detecting and responding to seismic cues. Kirschvink argued that even a small selection pressure acting over vast geological time can be as effective as stronger selection over shorter intervals, and that evasive action taken prior to an earthquake can reduce mortality and preserve fitness.
Preparedness theory in fear acquisition
Further evidence comes from the preparedness theory of fear acquisition. Öhman and Mineka (2001) and Seligman (1971) proposed that primates may have a preparedness to acquire fear of certain kinds of objects or situations that have evolutionary significance. Mineka and Zinbarg (2006) noted that people are much more likely to develop phobias of snakes, heights, or enclosed spaces than of bicycles or cars, even though modern objects may be equally associated with trauma. This is because there may have been a selective advantage in the course of evolution for primates who rapidly acquired fear of stimuli that posed threats to their early ancestors. Prepared fears are not seen as innate but as very easily acquired and especially resistant to extinction.
Experimental work supports this view. Using mild shock as an unconditioned stimulus, Öhman and his colleagues found superior conditioning effects with fear‑relevant conditioned stimuli such as snakes and spiders than with fear‑irrelevant stimuli (e.g., flowers, mushrooms; Öhman & Mineka, 2001). In addition, using videotaped model monkeys, Cook and Mineka (1989; 1990) showed that naïve monkeys rapidly learned fear to fear‑relevant stimuli (a toy snake or crocodile) but not to fear‑irrelevant stimuli (flowers or a toy rabbit). Mineka and Zinbarg (2006) concluded that in both monkeys and humans, evolutionary fear‑relevant stimuli more readily enter into selective associations with aversive events, and the special characteristics of fear learning seen with such stimuli – its automaticity and resistance to higher cognitive control – suggest that phobia acquisition involves a primitive, basic emotional level of learning shared with many other mammalian species.
Earthquakes present a particularly interesting case. The sudden, unpredictable shaking of the ground beneath one’s feet is, in evolutionary terms, a superordinate threat that has been present throughout mammalian history. Our own field surveys have consistently demonstrated that, among all traumatic stressors that occur during an earthquake and subsequently in the early phases of the disaster, fear evoked by the earthquake tremors themselves is the single most important predictor of PTSD in the long term (Başoğlu et al., 2002; Başoğlu et al., 2004; Livanou et al., 2005). This finding suggests that the fear of earthquakes is not merely a rational response to a dangerous event. It is a response that may be prepared in the same sense that fear of predators or heights is prepared – selected over evolutionary time because the ground shaking signals a threat to survival for which rapid defensive mobilization is adaptive.
Thus, preparedness theory may explain why people respond to earthquakes with such intense fear, rapidly acquire conditioned fears and avoidance to a wide range of situations, and why such fear is resistant to extinction in the long term. The theory would predict a higher rate of fear and avoidance associated with earthquakes than with other life‑threatening events that lack such evolutionary significance – a hypothesis well worth testing in future research.
Observational learning of fear
The widespread conditioned fears and avoidance among earthquake‑exposed people are consistent with the effects of inescapable shocks in animal experiments (Desiderato & Newman, 1971; Mineka et al., 1984; Warren et al., 1989). However, another contributing factor may be the acquisition of fear through observational learning. Experiments with animal and human subjects have shown that observing others experiencing a traumatic event or acting fearfully can lead to the development of phobias (Mineka & Öhman, 2002; Mineka & Zinbarg, 2006; Öhman & Mineka, 2001). Mineka and Zinbarg (2006) also noted that humans are susceptible to acquiring fear vicariously through watching movies and television.
Major earthquakes provide ample opportunities for observational learning of fear. In the early aftermath of a disaster, survivors witness people in distress, panic, screaming, and suffering. Those who participate in rescue efforts have even more intense exposure. During the period of aftershocks, people observe others acting fearfully, panicking during tremors, and avoiding a wide range of daily situations. The media also play a role. Following the 1999 Marmara earthquake, Turkish television channels endlessly broadcast graphic images of severely injured, distressed, or bereaved survivors, people trapped under rubble, and rescue efforts. In the Şalcıoğlu (2004) study, among survivors who had no direct personal experience of such events, 51% reported that watching television in the early days of the disaster markedly increased their anticipatory fear of earthquakes; a further 17% reported a slight increase. Women and those who experienced greater fear and loss of control during the earthquake were more vulnerable to such media effects. This increase in fear was associated with more severe and extensive avoidance behaviors. Such findings are consistent with reports of an association between exposure to television images of the 9/11 attacks and subsequent PTSD (Blanchard et al., 2004; Schlenger et al., 2002).
Thus, observational learning, including through mass media, can transmit fear and avoidance on a societal scale. Yet the same mechanisms can also transmit adaptive coping: survivors who observe others successfully re‑entering damaged buildings, resuming work, or maintaining calm during aftershocks receive vicarious evidence that behavioral re‑engagement is possible and that control can be restored.
Natural recovery processes
Epidemiological evidence consistently demonstrates that the modal outcome following traumatic exposure is recovery without formal clinical intervention (Kessler et al., 1995; Breslau et al., 1998; Morina et al., 2014; Burden et al., 2022). Natural recovery, as I define it, is sufficient remission in traumatic stress reactions to allow near‑baseline functioning in important life areas. Reduction in anxiety or fear is not necessary for sufficient improvement in functioning, although increased sense of control often leads to substantial reduction in these emotions in most cases.
What distinguishes those who recover naturally from those who develop chronic PTSD? The ethological literature provides a critical clue. In a review of evolutionarily determined defensive responses, Cantor (2005) noted that vigilant avoidance was the most commonly used strategy early in our evolutionary history, because of reptilian energy limitations. However, the use of this strategy depends on an appraisal of the relative costs and benefits of avoidance behavior – what Kavaliers and Choleris (2001) termed the ‘cost‑benefit ratio’. Avoidance has survival value only as long as it does not interfere with feeding, mating, and other fitness‑related activities. Animals are prepared to take greater risks of predation when they are hungry (Lima, 1998). If this evolutionary logic applies to humans, the persistence of avoidance following trauma should be conditional on the costs of avoidance outweighing its perceived benefits. When the costs – such as living in crowded, unsanitary, cold shelters; inability to work; loss of social contact; disruption of family life – exceed the perceived safety benefits, the organism should resume approach behavior, even in the presence of continuing fear.
Our own observations of earthquake survivors provided direct, naturalistic evidence for this prediction. Following the 1999 Marmara earthquake, a large proportion of survivors whose homes were structurally undamaged relocated to tent cities or makeshift shelters to avoid being indoors during unpredictable aftershocks. However, as the winter of 1999 set in, the conditions in the shelters became increasingly difficult. In a study of 156 survivors who had relocated to shelters, the mean time to resettlement – returning to their homes or to other concrete buildings – was 126 days (Şalcıoğlu, 2004; Başoğlu et al., 2011, Chapter 1). The most commonly stated reason for resettlement was the inconvenience and hardships of living in shelters (67% of survivors). Only 4% reported that they had lost their fear before resettlement. Thus, the decision to re‑engage with the feared environment was driven by a cost‑benefit calculation, not by fear reduction. This pattern mirrors exactly the foraging–predation trade‑off observed in the animal literature: when the costs of avoidance become too high, the organism takes risks and re‑engages, even while threat continues.
Crucially, such risk‑taking behavior is the most important factor that reverses the traumatization process and protects against the chronic effects of trauma (Başoğlu et al., 2011, Chapter 1). Once survivors began returning to their homes – initially for brief periods, then for longer stays – they inadvertently exposed themselves to the very stimuli that evoked fear. This contact with the feared environment, even when driven by necessity rather than intention, restored a sense of control and accelerated recovery. Remarkably, some survivors discovered the beneficial effects of exposure after an unintended encounter with a feared situation and then intentionally applied the same strategy to overcome other fears. A woman who had successfully used self‑exposure to overcome her earthquake‑related fears later told us that she had treated her snake phobia by searching for snakes in the region, eventually finding some and returning home free of her phobia (Başoğlu et al., 2011, Chapter 1).
Perhaps the most vivid illustration of natural recovery is the spontaneous use of graduated self‑exposure by survivors who had no formal treatment. One such survivor, a woman we called Semra, had lived with her family in a ground‑floor flat that survived the earthquake with minimal damage. For a month after the earthquake, she lived in a tent city, unable to return home because of pervasive fear. Faced with the hardship of shelter life, she decided to overcome her fear. When we met her in a café, she was about to enter her flat for the first time. Despite intense anxiety, she summoned the courage to go inside. Half an hour later, she emerged in a state of joy, repeatedly saying, “I’ve done it! I have beaten my fear!” She then went around the flat, deliberately focusing on cracks in the wall and broken objects – fear‑evoking cues – in an effort to challenge her fear, exactly as a therapist might prescribe during an exposure session. She returned to her flat repeatedly, stayed longer each time, and within a month was living there with her family, almost completely free of fear (Başoğlu et al, 2011, Chapter 1). This case exemplifies the central claim of this article: that the organism is equipped with an innate capacity for recovery, and that all that is required is for the behavioral obstacle of avoidance to be overcome – whether by the demands of daily life, by a conscious decision to take risks, or by a structured therapeutic intervention.
Further evidence for the endogenous nature of recovery comes from the phenomenon of stress immunization. In the animal literature, prior experience with controllable stress confers resistance to the effects of subsequent uncontrollable stress (Seligman & Maier, 1967; Williams & Maier, 1977). This effect can occur even when different types of aversive stimuli are used in the immunization and helplessness induction phases – for example, experience escaping from cold water immunized rats against the effects of uncontrollable foot shocks (Williams & Maier, 1977). Our earthquake survivor studies provided a human analogue. Survivors who had prior experience with earthquake‑like shaking sensations – for instance, sailors accustomed to the motion of ships, or people living near busy roads used by heavy trucks or near railway bridges – reported less fear of earthquakes and a greater sense of control over aftershocks (Başoğlu et al, 2011, Chapter 1). This finding suggested that even incidental, non‑traumatic exposures to controllable shaking could have protective effects, and it inspired the development of the earthquake simulator treatment (Başoğlu et al., 2003; Şalcıoğlu & Başoğlu, 2010). The Şalcıoğlu (2004) study provided direct quantitative evidence on how fear changes over time in the general population of earthquake survivors. When participants were asked, on average 21 months after the earthquake, whether they had experienced any change in their fear of earthquakes, 60% reported some decrease (from slight to very much), 25% reported no change, and 15% reported a slight to very much increase. Thus, fear reduction occurred in the majority of survivors, despite ongoing aftershocks and the persistent threat of future major earthquakes. Importantly, a regression analysis showed that increased sense of control over aftershocks and fear reduction were associated with prior experiences of earthquake‑like shaking sensations. This indicates that learning of control – including through repeated exposures to the aftershocks themselves – can reduce fear and helplessness. In other words, the aftershocks, which are initially a source of uncontrollable threat, can become an immunizing experience when the survivor learns that they can tolerate them and remain in control. Fear reduction is therefore not merely a function of time or passive extinction; it is actively driven by experiences that enhance perceived control.
To summarize: natural recovery from traumatic stress is not a passive process of waiting for fear to extinguish. It is an active, biologically driven process of risk‑taking and behavioral re‑engagement. The organism is equipped with a phylogenetically conserved mechanism that, when unimpeded, restores a sense of control through contact with the feared environment. The obstacles to this process are not primarily cognitive or emotional – they are behavioral. Remove the obstacle of avoidance, and recovery follows – not because the clinician has healed the patient, but because the patient’s own biology has been permitted to complete the work that trauma interrupted.
The Likely Mechanism of Change in Natural Recovery: Restoring Perceived Control
What drives fear reduction during successful treatment or natural recovery? The clinical literature often contrasts two models: habituation‑extinction (progressive attenuation of conditioned fear through repeated non‑reinforced exposure) and control enhancement (restoration of the organism’s sense of agency over the aversive stimulus environment). A detailed review of the evidence favoring the control‑enhancement model – including our panic disorder attribution studies, the dissociation between functional recovery and fear reduction in earthquake survivors, and the self‑efficacy literature – is available elsewhere (Başoğlu, 2026b; Başoğlu et al., 2011, Chapter 6). Here I focus on the evolutionary rationale, which has been less developed in the clinical literature, and on the conceptual question of whether control is merely one mechanism among many or the fundamental pathway through which recovery occurs.
The evolutionary limitations of habituation
From an evolutionary perspective, the habituation‑extinction mechanism has a serious limitation. Fear reduction acquired through extinction is often context‑dependent. An organism that learns that a feared stimulus is safe in one context may continue to fear it in a different context, because extinction learning does not erase the original fear memory but rather creates a new, context‑bound memory that competes with it. This phenomenon, known as renewal, has been extensively documented in animal research. In natural environments, threats rarely occur in identical contexts repeatedly. A prey animal that learns that a particular predator is not present in one specific location may still need to fear that predator in other locations. A mechanism that required separate extinction experiences for every possible context would be metabolically expensive and ecologically maladaptive.
The control‑enhancement mechanism does not suffer from this limitation. When the organism learns that it can tolerate fear and remain in control – not that a particular stimulus is safe in a particular context – the learning generalizes across situations. What changes is not the organism’s representation of the external threat but its representation of its own capacity to cope. This is a more fundamental and durable form of learning. Once the organism has discovered that it can act effectively in the presence of fear, it does not need to re‑learn this lesson for each new context. Natural selection would therefore favor the control‑enhancement mechanism over the habituation‑extinction mechanism.
Control as the common pathway
If this evolutionary logic is correct, then restoring a sense of control is not merely one therapeutic mechanism among many; it is the common pathway through which any effective recovery – whether natural or clinically assisted – must ultimately operate. Consider the alternatives. Habituation, as classically conceived, reduces fear by repeated exposure without reinforcement. But why does repeated exposure reduce fear? The parsimonious answer is that, with each non‑reinforced encounter, the organism learns that the feared stimulus is manageable – that it can be tolerated, that it does not lead to catastrophe, and that the organism can remain in control. The learning is not about the absence of reinforcement; it is about the presence of control. Similarly, cognitive restructuring, when it works, does not directly alter the external threat; it alters the individual’s appraisal of their capacity to cope. The belief that “I can handle this” is, at its core, a belief about control.
Thus, while different therapies use different methods – exposure, cognitive reappraisal, medication, self‑help, or simply the demands of daily life – their common therapeutic currency may be the restoration of perceived control. The same logic applies to natural recovery. The earthquake survivor who returns home because the shelter has become uninhabitable is not engaging in cognitive restructuring. But through the act of returning, they discover that they can tolerate fear and remain in control. The change is not in their beliefs about the earthquake but in their sense of agency.
Why exposure to unconditioned stimuli is particularly effective
Not all exposure is equal. In the trauma literature, a distinction is made between exposure to conditioned stimuli (CS) – the environmental cues that have come to signal danger – and exposure to the unconditioned stimulus (UCS) itself – the primary aversive event, such as an earthquake tremor, an explosion, or the sensation of being under attack. Most traditional exposure treatments target CS. However, exposure to UCS has stronger and more durable effects, for reasons that are directly relevant to natural recovery.
In natural environments, UCS events are not rare exceptions; they are common and often recurrent. Predators return, aftershocks follow major earthquakes, and combat zones involve repeated attacks. An organism whose defensive system can only learn from CS would be at a disadvantage, because CS are mere predictors; their reliability can change, and their absence does not guarantee safety. Exposure to the UCS itself, by contrast, engages the core defensive system directly. When an organism confronts the UCS and discovers that it can tolerate it and remain in control, the learning is not about a specific predictive cue but about the organism’s own capacity to cope. This learning generalizes broadly, because what has changed is the individual’s sense of agency. Once a survivor has endured a powerful UCS and remained in control, they do not need to re‑learn this lesson for every associated CS. This is precisely the pattern observed in natural recovery: survivors who faced the tremors themselves – whether through necessity or choice – showed rapid and durable improvement, even while aftershocks continued (Başoğlu et al., 2003; Şalcıoğlu & Başoğlu, 2010). The same principle explains the high recovery rates in war and torture survivors who confronted simulated UCS (Başoğlu, 2022).
Thus, exposure to UCS is evolutionarily superior to exposure to CS because it (a) directly engages the organism’s core defensive system, (b) produces learning that is context‑independent and generalizable, and (c) can operate effectively even under ongoing threat. This is why natural recovery can occur in ongoing trauma situations – and why CFBT, which facilitates confrontation with UCS, is particularly effective.
Are there alternative mechanisms?
One might argue that claiming control as the mechanism of recovery is an overstatement – that other processes, such as social support, passage of time, or incidental extinction, might also contribute. This objection, however, confuses the pathway with the endpoint. Social support, for example, may enhance recovery by providing encouragement, reducing isolation, or facilitating behavioral re‑engagement. But if it works, it works because it helps the individual regain a sense that they are not helpless – that they have resources, that others believe in them, that they can act. The supportive relationship is a means; the restoration of perceived control is the end. Similarly, the passage of time alone rarely heals trauma; what heals is what happens during that time – the accumulation of experiences that, one way or another, demonstrate controllability. The evolutionary argument is not that control is the only variable of interest. It is that, at the most fundamental level, the organism’s survival depends on its ability to distinguish controllable from uncontrollable threats and to act when action is effective. No other psychological construct can substitute for this function. Fear reduction without control may be transient; symptom suppression without agency may leave the organism vulnerable to relapse.
In summary, the control‑enhancement model is not merely one of several equally plausible accounts of recovery. It is the account that best fits the evolutionary logic of survival, the clinical evidence on durability and generalization, and the observed phenomenology of natural recovery. Different pathways – exposure, cognitive change, social support, self‑help – all converge on the same endpoint: the restoration of perceived control. Therefore, I propose that the likely mechanism of change in natural recovery is the restoration of perceived control, and that this is not an overstatement but a defensible theoretical position grounded in both evolutionary biology and clinical science.
Self‑Exposure as Phylogenetically Conserved Survival Mechanism
The central ethological claim of this article is that the mechanism of recovery from traumatic stress – re‑engagement with the aversive stimulus environment – is not a culturally specific or cognitively mediated human behavior. It is a phylogenetically ancient and broadly conserved biological strategy. The empirical basis for this claim is found across multiple levels of biological organization and across widely disparate taxonomic groups.
At the most fundamental level, the capacity to update threat representations through non‑reinforced exposure to feared stimuli has been demonstrated in virtually every species in which it has been systematically investigated, including insects, mollusks, fish, amphibians, birds, and mammals (Bouton, 2004; Rescorla, 2001). This process is not passive forgetting. It is an active, neurobiologically mediated learning process that requires behavioral contact with the feared stimulus. In naturalistic settings, this contact is accomplished through the organism’s spontaneous behavioral tendencies toward environmental exploration – tendencies that are themselves under strong evolutionary selection pressure. Organisms that fail to update their threat representations in response to changing environmental conditions are at a significant adaptive disadvantage (Fanselow & Lester, 1988).
Ethological observation of animals following exposure to predatory threat provides particularly compelling illustration. Prey species that have undergone a genuine predatory encounter do not, following escape, universally withdraw from the environment in which the encounter occurred. Rather, many species exhibit what has been described as post‑encounter risk assessment – a pattern of cautious but active re‑engagement with the threatening environment that serves the functional purpose of updating threat representations and re‑establishing behavioral competence in the formerly dangerous location (Blanchard & Blanchard, 1989; Eilam, 2005). This spontaneous risk‑taking in the immediate aftermath of threat exposure is precisely analogous, at the phylogenetic level, to what I have identified as the behavioral mechanism underlying natural recovery in human trauma survivors: those who recover naturally do so because they re‑engage with the circumstances and environments associated with the traumatic event. The convergence of evidence across species – from insects to primates – strongly suggests that self‑exposure is not a learned cultural practice but an evolutionarily conserved survival strategy. For a detailed review of the human clinical evidence supporting this mechanism, the reader is referred to my earlier work (Başoğlu et al., 2011, Chapter 1; Başoğlu, 2026b).
The Neurochemical Foundations of Natural Recovery: Endogenous Opioids and Oxytocin
If the behavioral capacity for recovery from threat is phylogenetically conserved—as the ethological evidence reviewed above suggests—then there should also be evidence for an endogenous neurochemical system that supports this recovery. Such a system would need to meet two criteria: first, it must be activated by the same stimuli that trigger defensive responses; second, it must promote the restoration of physiological and behavioral equilibrium once the threat has passed. A substantial body of research in affective neuroscience indicates that the endogenous opioid and oxytocin systems serve precisely these functions, and that they operate across physical and social domains of pain alike.
The discovery that social pain shares neural substrates with physical pain—particularly the dorsal anterior cingulate cortex, the anterior insula, and the periaqueductal gray—has been reviewed in detail elsewhere (Eisenberger, 2012b; MacDonald & Leary, 2005). What is less often emphasized in the trauma literature is that these shared substrates also entail shared mechanisms of alleviation. Panksepp (1998) was the first to propose that the social attachment system “piggybacked” onto the opioid substrates of the physical pain system during mammalian evolution. Endogenous opioids, long known for their role in physical pain relief, also reduce separation distress in infant animals and social distress in adults (Herman & Panksepp, 1978; Panksepp et al., 1978). Conversely, opioid receptor antagonists increase distress vocalizations, demonstrating that the endogenous opioid system tonically regulates social comfort and distress. In other words, the organism possesses a built‑in chemistry for social soothing.
Oxytocin plays a complementary role. Best known for its functions in lactation and mother–infant bonding, oxytocin also reduces pain sensitivity and separation distress across mammalian species (Insel & Winslow, 1991; Ågren et al., 1995). Gentle physical touch elevates oxytocin levels and reduces both physical pain and the neural response to social exclusion (Eisenberger et al., 2011). Thus, the same neurochemical that bonds mother to infant, and that is released by physical contact, also dampens the pain of threat and isolation.
The evolutionary implication is clear. The organism is not merely a passive recipient of painful stimuli; it is equipped with an endogenous pharmacology that actively counteracts the distress caused by threat, whether physical or social. This neurochemical recovery system is not a human novelty; it is present in rodents, in non‑human primates, and across social mammals. It is phylogenetically ancient and biologically conserved—exactly what the evolutionary framework advanced in this article would predict.
This neurochemical perspective also sheds light on the mechanism through which behavioral re‑engagement restores a sense of control. When a survivor deliberately confronts a feared situation, the act of enduring the experience and discovering that it can be tolerated is not merely a cognitive or behavioral event. It is also a neurochemical one. Successful coping with threat activates the same endogenous opioid and oxytocin systems that mediate comfort upon reunion and relief after pain. The subjective sense of control that follows successful self‑exposure may thus be the phenomenological correlate of a neurochemical process that has been conserved over millions of years to restore equilibrium after stress.
From this standpoint, natural recovery is not simply a behavioral process supported by evolutionary logic; it is a physiological process built into the organism’s neurochemistry. CFBT and other effective behavioral interventions can therefore be understood as external catalysts that activate an internal, pharmacologically mediated recovery system. The therapist does not provide the chemistry of healing; the organism already possesses it. The task of treatment is to create the conditions—through behavioral re‑engagement—that trigger its release.
Control‑Focused Behavioral Treatment: Facilitating the Reactivation of Natural Recovery
The foregoing analysis provides the conceptual foundation for understanding Control‑Focused Behavioral Treatment not as an externally imposed clinical invention, but as a structured means of removing the behavioral obstacles that prevent the organism’s own recovery machinery from operating. If natural recovery is driven by the organism’s spontaneous tendency toward re‑engagement, and if PTSD represents the condition in which this tendency has been overridden by conditioned avoidance, then the logical therapeutic objective is to unblock a process that the organism is already equipped to execute.
CFBT operates by enabling the survivor to demonstrate, through direct behavioral evidence, that the feared stimulus environment is manageable—that control can be restored. The therapist does not provide reassurance, process emotions, or restructure cognitions; evidence indicates that cognitive change occurs without direct intervention following recovery (Başoğlu et al., 2011, Chapter 6; Foa et al., 1999; Foa & Rauch, 2004; Livanou et al., 2002). Instead, the therapist encourages the patient to test their own capacity for control through systematic self‑exposure.
A frequently observed clinical phenomenon is the rapidity with which symptomatic recovery occurs once avoidance behavior is consistently overcome. In our treatment studies, a single session of CFBT achieved improvement rates of 76% to 92% in earthquake survivors (Başoğlu et al., 2003a, 2003b, 2005, 2007). These response rates are difficult to reconcile with models requiring extensive habituation, cognitive restructuring, or emotional processing. They are, however, consistent with the hypothesis that the intervention is reactivating a pre‑existing, phylogenetically prepared recovery program that requires only a sufficient behavioral catalyst to proceed. A full description of the CFBT model, its evidence base, and a meta‑analytic comparison with other trauma‑focused treatments is available elsewhere (Başoğlu, 2026b).
Self‑administered recovery and the role of therapist‑free interventions
If the mechanism of recovery is the restoration of perceived control through re‑engagement with the feared environment, a testable prediction follows: the critical ingredient of recovery is the act of re‑engagement itself, not the professional credentials, relational qualities, or clinical expertise of the person who supervises it. If natural recovery is driven by the organism’s own behavioral repertoire, then facilitated recovery should be achievable through any medium that successfully delivers the behavioral imperative of approach to the feared environment.
Our own treatment research provides direct evidence in the trauma domain. In a series of single‑case experimental studies and controlled trials with earthquake survivors, CFBT delivered as a self‑help manual – following initial brief contact to establish the therapeutic rationale – produced outcomes comparable to those of therapist‑delivered CFBT, with approximately 60% reduction in posttraumatic stress symptoms and global improvement in 80% of treated survivors (Başoğlu et al., 2011; Başoğlu et al., 2009). The manual’s capacity to produce effects comparable to therapist‑administered treatment is consistent with the hypothesis that the critical factor is the effective delivery of the behavioral ingredient – the induction of self‑exposure and the consequent enhancement of perceived control – rather than the therapeutic relationship per se.
This conclusion is supported by a substantial independent literature on self‑administered behavioral treatment in anxiety disorders. In obsessive‑compulsive disorder, fully interactive computer‑assisted self‑help based on exposure and response prevention has been shown to be efficacious with minimal scheduled clinician support (Marks et al., 2006; Norbye et al., 2022). In the phobia and panic domain, internet‑delivered self‑exposure programs have demonstrated outcomes comparable to therapist‑administered treatment (Marks et al., 2004; Carlbring et al., 2001; Klein et al., 2006). Comparable findings have been reported for social anxiety (Andersson et al., 2006) and for virtual reality‑based self‑administered exposure (Stefaniak et al., 2022).
The convergent implication for the evolutionary model is substantial. A treatment that is deliverable through a printed manual, a computer program, or a self‑help protocol – without requiring the ongoing presence of a trained clinician – is, almost by definition, not introducing a novel therapeutic mechanism. It is facilitating a process that the organism’s own biology is configured to execute. The evolutionary framework predicts precisely this: that any reliable means of delivering the behavioral message “approach the feared environment and experience the consequences” will activate the phylogenetically conserved machinery of control restoration that constitutes the organism’s natural recovery program.
Converging lines of evidence
The evidence for this unified account converges from multiple sources. Epidemiological data consistently show that the majority of trauma‑exposed individuals recover without formal treatment. Ethological observations document spontaneous post‑threat exploratory behavior across a wide range of species – behavior whose functional purpose is the restoration of behavioral competence in previously dangerous environments. Learning theory research demonstrates that controllability, not mere exposure, is the critical variable determining whether aversive experience leads to pathology or to resilience. Affective neuroscience adds a further layer, showing that social and physical pain share common neural substrates, underscoring the evolutionary continuity of stress responses across domains (Eisenberger, 2012b; MacDonald & Leary, 2005). Clinical trial data show that brief, control‑focused interventions produce rapid and durable improvement, even during ongoing threat. Self‑help outcome studies demonstrate that recovery can occur without a therapist, consistent with the claim that the recovery mechanism is endogenous rather than externally imposed. And four decades of fieldwork with over 15,000 mass trauma survivors – spanning torture, war, and earthquake contexts – have provided extensive observational confirmation of the parallels between natural recovery processes and CFBT.
The twin hypotheses that have guided this work – that loss of control during trauma leads to traumatic stress, and that regaining control reverses this process – have been consistently supported across four decades of research. The framework is general. It applies not only to extreme trauma but to the ordinary stressors of daily life, where the same principles of controllability and unpredictability govern the relationship between aversive experience and psychological outcome.
A challenge to alternative models
The evidence reviewed in this article poses a direct challenge to alternative theoretical frameworks in trauma treatment. A single session of behavioral treatment that does nothing more than encourage self‑exposure to feared situations, with no systematic cognitive restructuring, no emotional processing, and no extended therapeutic relationship, produces clinically significant and durable improvement in the vast majority of treated survivors. How is this possible?
In our first treatment study of earthquake survivors (Başoğlu et al., 2003a), 231 survivors with chronic PTSD received a single session of CFBT. Among those who completed treatment, the cumulative improvement rates were 76% after the first session, 88% after the second, 97% after the third, and 100% after the fourth session. We examined a comprehensive range of potential predictors of improvement, including age, sex, education, marital status, personal or family psychiatric history, history of past trauma, presence of prolonged grief, presence of comorbid illnesses, having been trapped under rubble, loss of family members, loss of property, participation in rescue work, additional drug treatment, intensity of fear during the earthquake, time since trauma, number of days between baseline and last available assessment, treatment modality, and baseline PTSD and depression scores. None of these variables predicted clinical response. The treatment effect explained most of the variance in outcome data, leaving little variance for other factors to explain. The single most important predictor of outcome was compliance with treatment. If patients stayed in treatment to the very end and complied with treatment instructions, they all improved.
This finding presents a challenge that any comprehensive theory of trauma recovery must address. If cognitive restructuring is the essential mechanism of recovery, how does improvement occur so rapidly and with no cognitive intervention? If emotional processing of traumatic memories is necessary, how does a treatment that focuses exclusively on avoidance behavior in the present produce such profound change? If the therapeutic relationship is a core ingredient, how do self‑help manuals achieve comparable results? If recovery requires the passage of time and the gradual extinction of conditioned fear, how does it occur during ongoing threat when the unconditioned stimulus continues to recur?
The answer I have offered is that these treatments work because they facilitate a recovery process that the organism is already prepared to execute. The mechanism is not extinction, habituation, or cognitive restructuring. It is the restoration of perceived control through behavioral re‑engagement. This mechanism is phylogenetically ancient, biologically conserved, and activated whenever the organism’s avoidance behavior is overcome – whether by deliberate self‑exposure, by the demands of daily life, or by the structured encouragement of a brief clinical intervention. The challenge to proponents of alternative models is to explain the same body of evidence – and particularly the rapid, durable, single‑session improvement – in terms that are at least as parsimonious and empirically grounded as the account presented here.
Implications for Public Health and Disaster Response
Mass trauma contexts—earthquakes, conflicts, refugee crises—demand interventions that are scalable, brief, and disseminable through means other than highly trained specialists. The recognition that natural recovery is the biological default shifts the intervention paradigm: the most powerful public health strategy is the systematic reduction of barriers to natural recovery.
The earthquake setting provides a concrete illustration. Following major earthquakes, many survivors whose homes are structurally undamaged nevertheless relocate to shelters or tent cities out of fear. While shelters serve an essential humanitarian function in the immediate aftermath, their prolonged use can inadvertently promote a “culture of avoidance.” Survivors in shelters are continuously exposed to the fear responses of others—their vigilance, panic during aftershocks, and collective anxiety—which can reinforce and even augment their own avoidance behaviors. The longer survivors remain in such environments, the more entrenched their avoidance becomes. Government policies that prolong the duration of stay in shelters, however well‑intentioned, may therefore delay recovery. Our research has shown that survivors experience significant reduction in traumatic stress reactions after they resettle in permanent housing (Şalcıoğlu et al., 2007; Şalcıoğlu et al., 2008). Policies that expedite resettlement—by providing timely housing solutions, financial assistance, and logistical support—can directly accelerate recovery by removing the environmental conditions that sustain avoidance.
Beyond shelter policies, public health measures such as early provision of accurate information, community‑based programs that encourage social connectedness, and media campaigns that model adaptive coping can collectively create conditions that permit the organism’s own recovery machinery to function unimpeded. Each of these measures, individually modest, amplifies natural processes rather than substituting for them.
This approach does not replace the need for clinical care. It redefines the priorities of care. If therapists are not essential for recovery—as the self‑help evidence reviewed earlier suggests—then self‑help materials, community‑based facilitation, and media‑delivered behavioral guidance become evidence‑based alternatives rather than compromises. For a broader discussion of the socio‑political implications of this paradigm shift, including the decolonization of mental health care in developing countries, the reader is referred to my earlier work (Başoğlu, 2026b; see also Başoğlu et al., 2011, Chapter 7).
What Blocks Natural Recovery? Limitations and Unresolved Questions
If natural recovery is the biological default, and if the mechanism of recovery is the restoration of perceived control through re‑engagement with feared stimuli, then the critical question is not whether natural recovery exists but why it fails to occur in the minority of trauma‑exposed individuals who develop chronic PTSD. What blocks the natural recovery process?
We do not yet have a definitive answer. It is possible that in some cases, the helplessness response is so severe, and the hopelessness that follows so profound, that the survivor’s motivational capacity to initiate re‑engagement is compromised beyond what spontaneous recovery mechanisms can overcome. When anxiety and depression reach levels that are themselves disabling, the organism may be unable to generate the behavioral activation necessary to test its own capacity for control. In such cases, some degree of therapist intervention—even if brief—may be required to initiate the recovery process.
Our treatment data are instructive in this regard. The finding that 100% of treatment completers in our first earthquake survivor study improved, and that no baseline variable predicted outcome, suggests that recovery is universally achievable once the behavioral obstacle of avoidance is overcome. The challenge is not that some individuals are incapable of recovery. It is that some individuals, for reasons we do not fully understand, are unable to overcome avoidance without external support. Understanding the factors that differentiate those who spontaneously re‑engage from those who require facilitation is an important direction for future research.
A legitimate observation about the theory of natural recovery is the indirect nature of the evidence that supports it, as reviewed in this article. The ideal study would take a representative sample of the general population who developed PTSD or a phobia, examine prospectively how symptoms progress over time, and measure the extent to which exposure to feared cues—whether deliberate or incidental—plays a role in recovery. Such a study does not exist, and it would be exceptionally difficult to conduct over the extended timeframe required. A more feasible alternative would be a retrospective study of individuals who developed a phobia or PTSD at some point in their lives and subsequently recovered, asking them whether their recovery followed any form of exposure, intentional or otherwise. Such a study would have the limitations inherent in retrospective designs but would nevertheless have value.
How significant is this limitation? One might argue that it is only as significant as the limitations of Darwin’s theory of evolution. To the best of my knowledge, Darwin’s theory was also built on observations of living organisms—observations of patterns in nature, of variation within species, of the distribution of forms across geographical space and geological time. He did not have experimental proof of natural selection in the modern sense. What he had was a convergence of observational evidence from multiple independent sources—comparative anatomy, biogeography, paleontology, animal and plant breeding—that together pointed toward a unified account. The evidence for natural recovery from trauma, as reviewed in this article, is of a similar character. Epidemiological patterns, ethological observations, learning theory experiments, clinical trial data, self‑help outcomes, and four decades of field observations with mass trauma survivors converge on the same conclusion: that the organism is equipped with a phylogenetically conserved recovery program whose core mechanism is the restoration of perceived control through re‑engagement with the feared environment.
Some might argue that social and environmental factors—poverty, displacement, ongoing threat, lack of social support—undermine the natural recovery process by preventing re‑engagement. This may be true in some cases. A survivor who wishes to return to work but has no job to return to, or who lives in conditions where safety is genuinely uncertain, faces obstacles that are structural rather than psychological. However, it is also true that deprivation and hardship do not necessarily undermine a sense of control. Indeed, many cultural and religious traditions—Buddhist monastic training, the Mevlevi order in Islam, military training across cultures—have long recognized that voluntary exposure to deprivation and hardship can enhance resilience by strengthening the individual’s sense of mastery over their own responses to adversity. The relationship between external circumstances and internal sense of control is not a simple one. The same conditions that might appear to block re‑engagement can, under different psychological framing, provide the very experiences of mastery that drive recovery.
The question of cultural variability also deserves brief comment. The core mechanism I have described—loss of control leading to traumatic stress, restoration of control leading to recovery—has been observed across the diverse cultural contexts in which we have worked. The specific forms that avoidance and re‑engagement take are undoubtedly shaped by cultural norms, beliefs, and practices. But the underlying process is universal. Whether an earthquake survivor in Turkey copes by returning to a damaged home, or a torture survivor in a different cultural context copes by re‑engaging with political activity, the mechanism is the same: behavioral contact with the feared stimulus restores the sense of control, and recovery follows. Cultural variation in the form of the behavior does not challenge the universality of the process.
Future research might usefully pursue several directions. Direct empirical tests of the control‑enhancement mechanism versus the extinction mechanism, ideally through experimental designs that manipulate the degree to which exposure participants experience themselves as active agents versus passive recipients of safety signals, would help to clarify the theoretical questions at stake. Neurobiological investigation of the specific processes underlying enhanced control—as distinct from fear reduction—remains an important direction for future work. And systematic examination of the factors that facilitate or impede spontaneous re‑engagement following trauma, whether through prospective or retrospective designs, would deepen our understanding of why natural recovery succeeds in the majority of cases and fails in a minority.
Conclusion: The Evolutionary Mandate of Recovery
I have argued that PTSD represents a condition of interrupted recovery within a biological system that is fundamentally oriented toward healing. Natural recovery from traumatic stress is the biological default, driven by the restoration of perceived control through re‑engagement with the feared environment. Control‑Focused Behavioral Treatment is the systematic facilitation of this endogenous process—the removal of the obstacle of avoidance so that the organism’s own recovery machinery can operate. The evidence for this account converges from ethology, epidemiology, learning theory, clinical trials, self‑help research, affective neuroscience, and four decades of fieldwork with mass trauma survivors. The organism’s phylogenetic heritage has equipped it with the machinery for recovery. The obligation of trauma science is to understand this machinery with sufficient precision to facilitate its operation. This represents a paradigm shift in how we think about psychological trauma. The appropriate question is not “What must be done to treat trauma?” It is “What prevents the organism from doing what it is already prepared to do?” The answer, I have argued, is avoidance—a behavior that is adaptive in the short term but that, when it persists beyond its adaptive window, becomes the central obstacle to the natural recovery that evolution has prepared for us. Remove that obstacle, and recovery follows—not because the clinician has healed the patient, but because the patient’s own biology has been permitted to complete the work that trauma interrupted.
This article has brought together several lines of evidence that have previously remained largely separate. Ethologists have described the defensive cascade and the foraging–survival trade-off. Learning theorists have established the centrality of controllability. Affective neuroscientists have mapped the shared neural and neurochemical substrates of physical and social pain, and clinicians have documented the phenomenon of natural recovery. What has been missing—and what this article has sought to provide—is a unified framework that places these observations within a single evolutionary logic. The core proposition, that recovery from traumatic stress is the biological default, driven not by the extinction of fear but by the restoration of perceived control, and that an effective treatment such as Control‑Focused Behavioral Treatment functions by removing the behavioral obstacle that prevents this endogenous recovery program from operating, has not, to my knowledge, been advanced in this specific form in the published literature. If similar ideas have been proposed elsewhere, the present argument should be understood as an independent convergence on the same principles, and I welcome the opportunity for further dialogue and refinement.
Disclosure and acknowledgment
The author is the developer of Control‑Focused Behavioral Treatment, which is discussed in this article. The evidence presented is drawn from published, peer‑reviewed studies, and the author has attempted to present it fairly. During the writing process, he selected the main points for discussion, formulated the arguments, and discussed them with an AI language model (Deepseek). The AIs also helped with literature search and offered suggestions for the content, structure, and wording of the manuscript, all of which were carefully reviewed by the author and revised as necessary. All conclusions are the author’s own, based on the evidence.
References
Ågren, G., Lundeberg, T., Uvnäs-Moberg, K., & Sato, A. (1995). The oxytocin antagonist 1-deamino-2-D-Tyr-(Oet)-4-Thr-8-Orn-oxytocin reverses the increase in the withdrawal response latency to thermal, not mechanical nociceptive stimuli following oxytocin administration or massage-like stroking in rats. Neuroscience Letters, 187, 49−52.
Alloy, L. B., Kelly, K. A., Mineka, S., & Clements, C. M. (1990). Comorbidity of anxiety and depressive disorders: A helplessness-hopelessness perspective. In J. D. Maser & C. R. Cloninger (Eds.), Comorbidity of mood and anxiety disorders (pp. 499–543). American Psychiatric Press.
Andersson, G., Carlbring, P., Holmstrom, A., Sparthan, E., Furmark, T., Nilsson-Ihrfelt, E., Buhrman, M., & Ekselius, L. (2006). Internet-based self-help with therapist feedback and in vivo group exposure for social phobia: A randomized controlled trial. Journal of Consulting and Clinical Psychology, 74(4), 677–686.
Antilla, A. (2001). Orangutans react to earthquake in Seattle. Long Call, 6, 4.
Başoğlu, M. (2009). A multivariate contextual analysis of torture and cruel, inhuman, and degrading treatments: Implications for an evidence-based definition of torture. American Journal of Orthopsychiatry, 79(2), 135–145.
Başoğlu, M. (2011). A mental healthcare model for mass trauma survivors: Control-focused behavioral treatment of earthquake, war, and torture trauma. Cambridge University Press.
Başoğlu, M. (2017). Introduction. In M. Başoğlu (Ed.), Torture and its definition in international law: An interdisciplinary approach (pp. 3–30). Oxford University Press.
Başoğlu, M. (2022). Control-Focused Behavioral Treatment: A brief intervention for survivors of war and torture. Torture, 32(1-2), 251–263.
Başoğlu, M. (2026a). A critical look at cognitive behavioral therapy and its “third wave” derivatives. DABATEM. https://dabatem.org/a-critical-look-at-cognitive-behavioral-therapy-and-its-third-wave-derivatives/
Başoğlu, M. (2026b). Cognitive behavior therapy and Control-Focused Behavioral Treatment: A critical comparison of their theoretical, socio-political, and philosophical implications. DABATEM. https://dabatem.org/cognitive-behavior-therapy-and-control-focused-behavioral-treatment-a-critical-comparison-of-their-theoretical-socio-political-and-philosophical-implications/
Başoğlu, M., & Mineka, S. (1992). The role of uncontrollable and unpredictable stress in post-traumatic stress responses in torture survivors. In M. Başoğlu (Ed.), Torture and its consequences: Current treatment approaches (pp. 182–225). Cambridge University Press.
Başoğlu, M., & Paker, M. (1995). Severity of trauma as predictor of long-term psychological status in survivors of torture. Journal of Anxiety Disorders, 9(4), 339–350.
Başoğlu, M., & Şalcıoğlu, E. (2011). A mental healthcare model for mass trauma survivors: Control-focused behavioral treatment of earthquake, war, and torture trauma. Cambridge University Press.
Başoğlu, M., Kılıç, C., Şalcıoğlu, E., & Livanou, M. (2004). Prevalence of posttraumatic stress disorder and comorbid depression in earthquake survivors in Turkey: An epidemiological study. Journal of Traumatic Stress, 17, 133–141.
Başoğlu, M., Livanou, M., & Crnobarić, C. (2007). Torture vs other cruel, inhuman, and degrading treatment: Is the distinction real or apparent? Archives of General Psychiatry, 64(3), 277–285.
Başoğlu, M., Livanou, M., & Şalcıoğlu, E. (2003a). A brief behavioural treatment of chronic post-traumatic stress disorder in earthquake survivors: Results from an open clinical trial. Psychological Medicine, 33(4), 647–654.
Başoğlu, M., Livanou, M., & Şalcıoğlu, E. (2003b). A single session with an earthquake simulator for traumatic stress in earthquake survivors. American Journal of Psychiatry, 160(4), 788–790.
Başoğlu, M., Livanou, M., Crnobarić, C., Frančišković, T., Suljić, E., Đurić, D., & Vranešić, M. (2005). Psychiatric and cognitive effects of war in former Yugoslavia – Association of lack of redress for trauma and posttraumatic stress reactions. Journal of the American Medical Association, 294(5), 580–590.
Başoğlu, M., Livanou, M., Şalcıoğlu, E., & Kalender, D. (2003a). A brief behavioural treatment of chronic post‑traumatic stress disorder in earthquake survivors: Results from an open clinical trial. Psychological Medicine, 33(4), 647-654.
Başoğlu, M., Marks, I. M., Kılıç, C., Brewin, C. R., & Swinson, R. P. (1994b). Alprazolam and exposure for panic disorder with agoraphobia: Attribution of improvement to medication predicts subsequent relapse. British Journal of Psychiatry, 164(5), 652–659.
Başoğlu, M., Marks, I. M., Kılıç, C., Noshirvani, H., & O’Sullivan, G. (1994a). The relationship between panic, anticipatory anxiety, agoraphobia, and global improvement in panic disorder with agoraphobia treated with alprazolam and exposure. British Journal of Psychiatry, 164(5), 647–652.
Başoğlu, M., Mineka, S., Paker, M., Aker, T., Livanou, M., & Gök, Ş. (1997). Psychological preparedness for trauma as a protective factor in survivors of torture. Psychological Medicine, 27(6), 1421–1433.
Başoğlu, M., Paker, M., Özmen, E., Taşdemir, O., & Şahin, D. (1994b). Factors related to long‑term traumatic stress responses in survivors of torture in Turkey. Journal of the American Medical Association, 272(5), 357-363.
Başoğlu, M., Paker, M., Özmen, E., Taşdemir, O., Şahin, D., Ceyhanlı, A., & İncesu, C. (1996). Appraisal of self, social environment, and state authority as a possible mediator of posttraumatic stress disorder in tortured political activists. Journal of Abnormal Psychology, 105(2), 232-236.
Başoğlu, M., Paker, M., Paker, Ö., Özmen, E., Marks, I., Incesu, C., Şahin, D., & Sarimurat, N. (1994a). Psychological effects of torture: A comparison of tortured with nontortured political activists in Turkey. American Journal of Psychiatry, 151(1), 76–81.
Başoğlu, M., Şalcıoğlu, E., & Livanou, M. (2002). Traumatic stress responses in earthquake survivors in Turkey. Journal of Traumatic Stress, 15, 269–276.
Başoğlu, M., Şalcıoğlu, E., & Livanou, M. (2007). A randomized controlled study of single‑session behavioural treatment of earthquake‑related post‑traumatic stress disorder using an earthquake simulator. Psychological Medicine, 37(2), 203-213.
Başoğlu, M., Şalcıoğlu, E., & Livanou, M. (2011). A mental healthcare model for mass trauma survivors: Control‑Focused Behavioral Treatment of earthquake, war, and torture trauma. Cambridge University Press.
Başoğlu, M., Şalcıoğlu, E., Livanou, M., & Kalender, D. (2009). Single-case experimental studies of a self-help manual for traumatic stress in earthquake survivors. Journal of Behavior Therapy and Experimental Psychiatry, 40(1), 50–58.
Başoğlu, M., Şalcıoğlu, E., Livanou, M., Kalender, D., & Acar, G. (2005). Single‑session behavioral treatment of earthquake‑related posttraumatic stress disorder: A randomized waiting list controlled trial. Journal of Traumatic Stress, 18(1), 1-11.
Başoğlu, M., Şalcıoğlu, E., Livanou, M., Özeren, M., Aker, T., Kılıç, C., & Mestçioğlu, Ö. (2003). A single session with an earthquake simulator for traumatic stress in earthquake survivors. American Journal of Psychiatry, 160, 788–790.
Bell, A. M., & Sih, A. (2007). Exposure to predation generates personality in threespined sticklebacks (Gasterosteus aculeatus). Ecology Letters, 10(9), 828–834.
Björkqvist, K. (2001). Social defeat as a stressor in humans. Physiology & Behavior, 73, 435–442.
Björkqvist, K. (2017). An evolutionary approach to humiliation and shame induced by inhuman and degrading treatment. In M. Başoğlu (Ed.), Torture and its definition in international law: An interdisciplinary approach (pp. 101–130). Oxford University Press.
Blanchard, E. B., Kuhn, E., Rowell, D. L., Hickling, E. J., Wittrock, D., Rogers, R. L., Johnson, M. R., & Steckler, D. C. (2004). Studies of the vicarious traumatization of college students by the September 11th attacks: effects of proximity, exposure and connectedness. Behaviour Research and Therapy, 42, 191–205.
Blanchard, R. J., & Blanchard, D. C. (1989). Antipredator defensive behaviors in a visible burrow system. Journal of Comparative Psychology, 103(1), 70–82.
Bouton, M. E. (2004). Context and behavioral processes in extinction. Learning & Memory, 11(5), 485–494.
Breslau, N., Kessler, R. C., Chilcoat, H. D., Schultz, L. R., Davis, G. C., & Andreski, P. (1998). Trauma and posttraumatic stress disorder in the community. Archives of General Psychiatry, 55, 626–632.
Burden, G., Wiseman, H., & Meiser-Stedman, R. (2022). Change in prevalence of post‑traumatic stress disorder in the two years following trauma: A meta‑analytic study. European Journal of Psychotraumatology, 13, Article 2066456.
Cannon, W. B. (1932). The wisdom of the body. W. W. Norton.
Cantor, C. (2005). Evolution and posttraumatic stress: Disorders of vigilance and defence. Routledge.
Carlbring, P., Ekselius, L., & Andersson, G. (2001). Treatment of panic disorder via the internet: A randomized trial of CBT vs. applied relaxation. Journal of Behavior Therapy and Experimental Psychiatry, 34(2), 129–140.
Cheney, D. L., & Seyfarth, R. M. (2007). Baboon metaphysics: The evolution of a social mind. University of Chicago Press.
Cook, M., & Mineka, S. (1989). Observational conditioning of fear to fear‑relevant versus fear‑irrelevant stimuli in rhesus monkeys. Journal of Abnormal Psychology, 98, 448–459.
Cook, M., & Mineka, S. (1990). Selective associations in the observational conditioning of fear in rhesus monkeys. Journal of Experimental Psychology: Animal Behavior Processes, 16, 372–389.
Cresswell, W. (2008). Non-lethal effects of predation in birds. Ibis, 150(1), 3–17.
Darwin, C. (1872). The expression of the emotions in man and animals. John Murray.
Desiderato, O., & Newman, A. (1971). Conditioned suppression produced in rats by tones paired with escapable or inescapable shock. Journal of Comparative and Physiological Psychology, 96, 427–431.
Dickerson, S. S., & Kemeny, M. E. (2004). Acute stressors and cortisol responses: A theoretical integration and synthesis of laboratory research. Psychological Bulletin, 130, 355–391.
Dielenberg, R. A., & McGregor, I. S. (2001). Defensive behavior in rats towards predatory odors: A review. Neuroscience & Biobehavioral Reviews, 25(7-8), 597–609.
Eilam, D. (2005). Die hard: A blend of freezing and fleeing as a dynamic defense—implications for the control of defensive behavior. Neuroscience & Biobehavioral Reviews, 29(8), 1181–1191.
Eisenberger, N. I. (2012b). The pain of social disconnection: Examining the shared neural underpinnings of physical and social pain. Nature Reviews Neuroscience, 13, 421–434.
Eisenberger, N. I., Lieberman, M. D., & Williams, K. D. (2003). Does rejection hurt? An fMRI study of social exclusion. Science, 302, 290–292.
Eisenberger, N. I., Master, S. L., Inagaki, T. K., Taylor, S. E., Shirinyan, D., Lieberman, M. D., & Naliboff, B. (2011). Attachment figures activate a safety signal-related neural reward system. Proceedings of the National Academy of Sciences, 6, 11721–11726.
Fanselow, M. S. (1994). Neural organization of the defensive behavior system responsible for fear. Psychonomic Bulletin & Review, 1, 429–438.
Fanselow, M. S., & Lester, L. S. (1988). A functional behavioristic approach to aversively motivated behavior: Predatory imminence as a determinant of the topography of defensive behavior. In R. C. Bolles & M. D. Beecher (Eds.), Evolution and learning (pp. 185–212). Erlbaum.
Foa, E. B., & Rauch, S. A. M. (2004). Cognitive changes during prolonged exposure versus prolonged exposure plus cognitive restructuring in female assault survivors with posttraumatic stress disorder. Journal of Consulting and Clinical Psychology, 72(5), 879-884.
Foa, E. B., Dancu, C. V., Hembree, E. A., Jaycox, L. H., Meadows, E. A., & Street, G. P. (1999). A comparison of exposure therapy, stress inoculation training, and their combination for reducing posttraumatic stress disorder in female assault victims. Journal of Consulting and Clinical Psychology, 67, 194-200.
Hedrick, A. V., & Kortet, R. (2006). Hiding behaviour in male field crickets, Gryllus integer, after exposure to a predator cue. Animal Behaviour, 72(5), 1101–1108.
Herman, B. H., & Panksepp, J. (1978). Effects of morphine and naloxone on separation distress and approach attachment: Evidence for opiate mediation of social affect. Pharmacology, Biochemistry and Behavior, 9, 213–220.
Insel, T. R., & Winslow, J. T. (1991). Central administration of oxytocin modulates the infant rats response to social isolation. European Journal of Pharmacology, 203, 149–152.
Kavaliers, M., & Choleris, E. (2001). Antipredator responses and defensive behavior: ecological and ethological approaches for the neurosciences. Neuroscience and Biobehavioral Reviews, 25, 577-586.
Keltner, D., & Buswell, B. N. (1997). Embarrassment: Its distinct form and appeasement functions. Psychological Bulletin, 122, 250–270.
Kessler, R. C., Sonnega, A., Bromet, E., Hughes, M., & Nelson, C. B. (1995). Posttraumatic stress disorder in the National Comorbidity Survey. Archives of General Psychiatry, 52, 1048–1060.
Kirschvink, J. L. (2000). Earthquake prediction by animals: evolution and sensory perception. Bulletin of the Seismological Society of America, 90, 312–323.
Klein, B., Richards, J. C., & Austin, D. W. (2006). Efficacy of internet therapy for panic disorder. Journal of Behavior Therapy and Experimental Psychiatry, 37(3), 213–238.
Koenig, K. A. (2017). Control in captivity: The role of perceived control in the development and resolution of posttraumatic stress symptoms among former Guantanamo detainees. In M. Başoğlu (Ed.), Torture and its definition in international law: An interdisciplinary approach (pp. 101–132). Oxford University Press.
Korte, S. M., Koolhaas, J. M., Wingfield, J. C., & McEwen, B. S. (2005). The Darwinian concept of stress: benefits of allostasis and costs of allostatic load and the trade‑offs in health and disease. Neuroscience & Biobehavioral Reviews, 29, 3–38.
Kotler, B. P., Brown, J. S., & Mitchell, W. A. (1994). The role of predation in shaping the behavior, morphology and community organization of desert rodents. Australian Journal of Zoology, 42(4), 449–466.
Krusko, N., Dolhinov, P., Anderson, C., Bortz, W., Kastlen, J., Flesher, K., Flood, M., … & Read, E. (1986). Earthquake: Langur monkey’s response. Laboratory Primate Newsletter, 25, 6–7.
Lima, S. L. (1998). Stress and decision‑making under the risk of predation: recent developments from behavioral, reproductive and ecological perspectives. Advances in the Study of Behavior, 27, 215-290.
Lima, S. L., & Dill, L. M. (1990). Behavioral decisions made under the risk of predation: A review and prospectus. Canadian Journal of Zoology, 68(4), 619–640.
Lind, J., & Cresswell, W. (2005). Determining the fitness consequences of anti-predation behavior. Behavioral Ecology, 16(5), 945–956.
Livanou, M., Başoğlu, M., Marks, I. M., De Silva, P., Noshirvani, H., Lovell, K., & Thrasher, S. (2002). Beliefs, sense of control and treatment outcome in post‑traumatic stress disorder. Psychological Medicine, 32(1), 157-165.
Livanou, M., Kasvikis, Y., Başoğlu, M., Mytskidou, P., Sotiropoulou, V., Spanea, E., Mitsopoulou, T., & Voutsa, N. (2005). Earthquake‑related psychological distress and associated factors 4 years after the Parnitha earthquake in Greece. European Psychiatry, 20, 137–144.
MacDonald, G., & Leary, M. R. (2005). Why does social exclusion hurt? The relationship between social and physical pain. Psychological Bulletin, 131, 202–223.
Maier, S. F., & Seligman, M. E. P. (1976). Learned helplessness: Theory and evidence. Journal of Experimental Psychology: General, 105, 3–46.
Maier, S. F., & Watkins, L. R. (2005). Stressor controllability and learned helplessness: The roles of the dorsal raphe nucleus, serotonin, and corticotropin‑releasing factor. Neuroscience & Biobehavioral Reviews, 29, 829–841.
Marks, I. M. (1987). Fears, phobias, and rituals. Oxford University Press.
Marks, I. M., Kenwright, M., McDonough, M., Whittaker, M., & Mataix-Cols, D. (2004). Saving clinicians’ time by delegating routine aspects of therapy to a computer: A randomized controlled trial in phobia/panic disorder. Psychological Medicine, 34(1), 9–17.
Marks, I. M., Mataix-Cols, D., Kenwright, M., Cameron, R., Hirsch, S., & Gega, L. (2006). Self-help with minimal therapist contact for obsessive-compulsive disorder: A review. European Psychiatry, 21(2), 75–80.
Mineka, S., & Cook, M. (1993). Mechanisms involved in the observational conditioning of fear. Journal of Experimental Psychology: General, 122(1), 23–38.
Mineka, S., & Öhman, A. (2002). Phobias and preparedness: The selective, automatic, and encapsulated nature of fear. Biological Psychiatry, 52, 927–937.
Mineka, S., & Zinbarg, R. (2006). A contemporary learning theory perspective on the etiology of anxiety disorders – It’s not what you thought it was. American Psychologist, 61, 10–26.
Mineka, S., Cook, M., & Miller, S. (1984). Fear conditioned with escapable and inescapable shock: effects of a feedback stimulus. Journal of Experimental Psychology: Animal Behavior Processes, 10, 307–323.
Morina, N., Wicherts, J. M., Lobbrecht, J., & Priebe, S. (2014). Remission from post‑traumatic stress disorder in adults: A systematic review and meta‑analysis of long‑term outcome studies. Clinical Psychology Review, 34, 249–255.
Norbye, A. D., Hagen, R., & Thilesen, A. (2022). Unguided computer-assisted self-help interventions without human contact in patients with obsessive-compulsive disorder: Systematic review and meta-analysis. JMIR Mental Health, 9(5), e35737.
Öhman, A., & Mineka, S. (2001). Fears, phobias, and preparedness: Toward an evolved module of fear and fear learning. Psychological Review, 108, 483–522.
Ouwerkerk, J. W., Kerr, N. L., Galluci, M., & Van Lange, P. A. M. (2005). Avoiding the social death penalty: Ostracism and cooperation in social dilemmas. In K. D. Williams, J. P. Forgas, & W. von Hippel (Eds.), The social outcast: Ostracism, social exclusion, rejection, and bullying (pp. 321–332). Psychology Press.
Panksepp, J. (1998). Affective neuroscience: The foundation of human and animal emotions. Oxford University Press.
Panksepp, J., Herman, B. H., Conner, R., Bishop, P., & Scott, J. P. (1978). The biology of social attachments: Opiates alleviate separation distress. Biological Psychiatry, 13, 607–618.
Rescorla, R. A. (2001). Experimental extinction. In R. R. Mowrer & S. B. Klein (Eds.), Handbook of contemporary learning theories (pp. 119–154). Lawrence Erlbaum.
Şalcıoğlu, E. (2004). The effect of beliefs, attribution of responsibility, redress and compensation on posttraumatic stress disorder in earthquake survivors in Turkey. PhD dissertation, Institute of Psychiatry, King’s College London.
Salcıoğlu, E., & Başoğlu, M. (2010). Control-focused behavioral treatment of earthquake survivors using live exposure to conditioned and simulated unconditioned stimuli. Cyberpsychology, Behavior, and Social Networking, 13(1), 13–19.
Salcıoğlu, E., Başoğlu, M., & Livanou, M. (2007). Effects of live exposure on symptoms of posttraumatic stress disorder: The role of reduced behavioral avoidance in improvement. Behaviour Research and Therapy, 45(10), 2268–2279.
Sansom, A., Lind, J., & Cresswell, W. (2009). Individual behavior and survival: The roles of predator avoidance, foraging success, and vigilance. Behavioral Ecology, 20(6), 1168–1174.
Schlenger, W. E., Caddell, J. M., Ebert, L., Jordan, B. K., Rourke, K. M., Wilson, D., Thalji, L., Dennis, J. M., Fairbank, J. A., & Kulka, R. A. (2002). Psychological reactions to terrorist attacks – Findings from the national study of Americans’ reactions to September 11. Journal of the American Medical Association, 288, 581–588.
Seligman, M. E. P. (1971). Phobias and preparedness. Behavior Therapy, 2, 307–320.
Seligman, M. E. P. (1975). Helplessness: On depression, development, and death. W. H. Freeman.
Seligman, M. E. P., & Maier, S. F. (1967). Failure to escape traumatic shock. Journal of Experimental Psychology: Animal Behavior Processes, 74, 1–9.
Shaw, E. (1977). Can animals anticipate earthquakes? Natural History, 86, 14–20.
Siepielski, A. M., Fallon, E., & Boersma, K. (2016). Predator olfactory cues generate a foraging–predation trade-off through prey apprehension. Royal Society Open Science, 3(2), Article 150537.
Snarr, K. A. (2005). Seismic activity response as observed in mantled howlers (Alouatta palliata), Cuero y Salado Wildlife Refuge, Honduras. Primates, 46.
Stefaniak, I., Hanusz, K., Mierzejewski, P., Bienkowski, P., Parnowski, T., & Murawiec, S. (2022). Preliminary study of efficacy and safety of self-administered virtual exposure therapy for social anxiety disorder vs. cognitive-behavioral therapy. Brain Sciences, 12(9), Article 1236.
Tracy, J. L., & Matsumoto, D. (2008). The spontaneous expression of pride and shame: Evidence for biologically innate nonverbal displays. Proceedings of the National Academy of Sciences, 105, 11655–11660.
Warren, D., Rosellini, R., & Maier, S. (1989). Fear, stimulus feedback and stressor controllability. In G. Bower (Ed.), The psychology of learning and motivation (Vol. 24, pp. 167–206). Academic Press.
Williams, J., & Maier, S. (1977). Transsituational immunisation and therapy of learned helplessness in the rat. Journal of Experimental Psychology: Animal Behavior Processes, 3, 240–252.
Williams, K. D. (1997). Social ostracism. In R. Kowalski (Ed.), Aversive interpersonal behaviors (pp. 133–170). Plenum Press.
Leave a Reply