Proposed theories of the etiology and function of SIV typically involve biological and psychological explanations. The literature suggests a number of conditions that might predispose an individual to SIV including loss of a parent, childhood illness or surgery, childhood sexual or physical abuse, alcoholism in the family, witnessing family violence, peer conflict, intimacy problems, body alienation, and impulse-control disorders (Walsh & Rosen, 1988).
Of these potential etiologic factors, recent research has focused on childhood sexual and physical abuse and the subsequent posttraumatic sequelae as being associated most powerfully with the development of SIV behavior. Biological theories of the etiology of SIV include the ideas that people have biological vulnerabilities or chemical imbalances effecting brain structure and function predisposing them to SIV behaviors (Bremner, 2005; Canli, Zhao, Brewer, Gabrieli, & Cahill, 2000; Carrion, Weems, & Reiss, 2007; Herman, 1992; LeDoux, 1996; Pies & Popli, 1995; Sachsse, von der Heyde, & Huether, 2002; van der Kolk, Perry, & Herman, 1991).
Animal models of traumatic stress have guided our understandings of the psychophysiological effects of prolonged exposure to trauma, and more recently functional brain imaging focused on individuals, especially children, who have been exposed to chronic traumatic experiences has wielded important information as well (Bremner, 2005, Carrion, 2007). The majority of empirical research on the risk factors for SIV has focused on the childhood experiences associated with risk for SIV in adulthood. In particular, most research has centered on the role of childhood sexual abuse.
The preponderance of evidence suggests that there is a strong relationship between childhood maltreatment and SIV in adulthood (Boudewyn & Liem, 1995; Briere & Gil, 1998; van der Kolk et al. , 1991). In van der Kolk et al. ’s longitudinal study with 39 women and 35 men (N=74), childhood trauma and disrupted attachment appeared to be associated with SIV behavior. The participants were administered the Traumatic Antecedents Questionnaire, which inquires about primary caretakers and other important relationships.
The researchers found that childhood sexual abuse, and emotional neglect and abuse were powerful predictors of subsequent adult SIV, the functions and meanings of which are discussed in a later section. Neurobiological Theories Researchers have only just begun to describe the underlying neurobiology of the long-term effects of traumatic stress. Theories suggest childhood maltreatment can engender trauma-related stress and the subsequent emotional regulation and tension-reduction function of SIV, but the link is still unclear.
A growing body of research evidence (Bremner, 2005; Carrion, 2007; van der Kolk, 1994) on children demonstrates persistent biologic changes associated with childhood maltreatment involving the hippocampal and amygdalar brain structures and functions, the HPA axis, and the regulation of cortisol, catecholamines, opiods, and serotonin levels as possible biological explanations for continued stress reactions even after the initial trauma has subsided.
The hippocampus, amygdala, and hypothalamus comprise most of the limbic system, and it is these brain structures that regulate cortisol, catecholomines, opiates, and serotonin, the body’s stress hormones. Neuronal activity in the limbic area is responsible for memory, attachment, affect regulation, and aspects of emotion (Bremner, 2005). These biological systems’ reactions to chronic emotional stress are persistently but not permanently changed, resulting in emotional dysregulation and the possible manifestation of SIV behavior later in life when past trauma memories or unconscious triggers emerge (Bremner; van der Kolk, 1994).
Repeated abuse during childhood may leave the limbic system with highly excitable nerve cells (neurons)—a process called kindling—where the body maintains stress hormones at continuously high levels and is constantly primed to react to stress; even minor life stressors can cause an individual to react as though she or he were faced with a threatening or dangerous situation (Bremner; van der Kolk). The activity of the brain structure known as the amygdala is central to understanding the biological effects of trauma exposure and its multifarious manifestations (Canli et al.
, 2000; LeDoux, 1996; McEwen, 1998). The distinction between conscious and unconscious memory suggests that memory involves two brain systems: the hippocampus and the amygdala. While conscious memory is mediated by the hippocampus, the amygdala is implicated in unconscious emotional memory. The amygdala, a primitive brain area that hangs off the forward-most part of the hippocampus, is a small, walnut-shaped collection of nuclei in the core of the brain that controls the fear response; it receives and integrates all sensory input to determine the level of threat in the environment.
If the input (threat) is sufficiently intense to initiate an action potential, the amygdala triggers other areas of the brain, which then induces the physiological response that is interpreted as fear (fight, flight, or freeze). Danger has been recognized. Retrieval of prior memories of traumatic events has survival value in a legitimately threatening situation; however, if retrieval occurs repeatedly in non-threatening situations it can become maladaptive and may result in behaviors such as SIV (Bremner, 2005).
Bremner, Herman (1992), and van der Kolk (1996) have all hypothesized that the differences between explicit (conscious) and implicit (unconscious) memory access systems play a role in dissociation. In addition, van der Kolk proposed that a narrowing of awareness is partially responsible for the difficulty of retrieving memories of trauma. Moreover, traumatic memories are encoded without words and as a result become difficult to access consciously (Bremner; van der Kolk, 1994, 1996).
The amygdala is involved in the fear response as well as the memory of fear. When Canli et al. (2000) used functional magnetic resonance imaging (fMRI) scans to measure amygdala activity while showing study participants a number of frightening images and neutral images; they measured the degree of amygdalar activity and found it a good predictor of both fear level and of the ability several weeks later to recall having seen the images.
This evidence, along with other studies with similar findings, has made the amygdala a primary target of neurobiological research on posttraumatic stress (Canli et al. ; Carrion et al. , 2007), but it continues to raise the question of mechanism. Bremner (2005) posited that the answer might lie in classic fear-conditioning. In conditioning experiments conducted by LeDoux (1996), rats were administered a mild electric shock in conjunction with an auditory tone.
Predictably, the rats soon responded to the tone alone with a fearful response including increased blood pressure, faster breathing, and motionlessness. This may explain the recurrence of emotional responses in PTSD. Just as a non-threatening stimulus (the tone) associated with a threatening one (the shock) could trigger the same emotional response in the conditioned rats, so can an innocuous sound, sight, smell, or person associated with a trauma trigger an intense re-experiencing of emotions in a traumatized individual.
As a result, traumatic memories are encoded without words and are difficult to access (Bremner, 2005; van der Kolk, 1994, 1996), leading to an emotional rather than verbal programming of memories For this reason, individuals who suffer severe trauma often literally cannot verbalize their experiences or even consciously perceive them (Chu, 1992; Levenkron, 1998). The human body employs powerful mechanisms in order to cope with stress. Among these mechanisms is the stress hormone cortisol—without it, we cannot respond appropriately to different types of stress.
Because cortisol affects a wide range of physiological processes, its secretion is regulated by interactions among three bodily structures: the hypothalamus, the pituitary gland, and the adrenal gland, collectively known as the hypothalamic-pituitary-adrenal (HPA) axis. In response to stimulation from the brain, the hypothalamus produces corticotropin-releasing hormone (CRH), which is then channeled to the pituitary gland, situated just beneath hypothalamus. CRH acts to stimulate the release of adrenocorticotropic hormone (ACTH) from the pituitary gland.
When this ACTH arrives at the adrenal cortex via the bloodstream, it stimulates the secretion of cortisol, which travels through the bloodstream exerting its effects on those organs involved in sympathetic nervous system arousal and response to threatening situations (Bremner, 2005). Endogenous opiods provide continuous inhibition of cortisol, which may explain the physiological relief felt by individuals immediately after engaging in acts of SIV and the addictive quality of SIV. Carrion et al.
(2007) studied 15 children, ranging in age from age 7 to 13, who suffered posttraumatic stress. After measuring the volume of each child’s hippocampus at the beginning and the end of their 12- to 18-month study period, the researchers found that children who experienced more severe posttraumatic symptoms and higher bedtime cortisol levels at the start of the study were more likely to have measurable reductions in their hippocampal volumes at the end of the study than their less-affected peers.
That the change in the hippocampal volume corresponds to both posttraumatic symptom severity and increased cortisol levels is significant: Cortisol has been shown to kill hippocampal neuronal cells in animals. In a vicious cycle, a reduction in hippocampal size can make it more difficult for an individual to process and deal with traumatic events, which in turn may raise both stress and cortisol levels and compound damage to the hippocampus (Carrion et al. ; McEwan, 1998).
Long-term posttraumatic exposure theory posits that everyone carries an ongoing stress burden that accumulates throughout life. Once a certain threshold is reached through chronic high levels of stress, adults and children may begin to exhibit posttraumatic symptoms such as re-experiencing trauma (i. e. flashbacks, intrusive thoughts, or nightmares), avoidance and emotional numbing, and physiological hyperarousal (e. g. elevated resting heart rate and increased blood pressure). These symptoms are hallmark criteria for the diagnosis of PTSD as outlined by the DSM-IV-TR (APA, 2000).
The most significant and distinguishing feature of the brain’s neuronal tissue is that it changes in response to external signals and stimulus, a capacity that allows us to be immediately responsive to our environment (Bremner, 2005; Herman, 1992; van der Kolk, 1994). Individuals predisposed to posttraumatic stress by environmental circumstances may be more likely to develop PTSD in response to emotional trauma, perhaps because their responses to other life experiences have left them closer to that threshold of accumulated stress (Bremner, 2005; Herman, 1992; van der Kolk, 1994).
Further studies may help researchers clarify certain physical traits that could help identify individuals at risk for developing posttraumatic stress, as well as later adult psychopathology that might manifest as SIV behavior. However, biological factors need to be placed in context with environmental factors, concerns such as social constructs, family situations, and childhood maltreatment, as well as with the qualitative differences in felt emotions among individuals, which in turn may meditate the development of later trauma symptoms such as SIV (Herman, 1992; Linehan, 1987).