Cultic Studies Review, Vol. 1, No. 1, 2002, 351-373
The Psychobiology of Trauma and Child Maltreatment
Doni Whitsett, Ph.D., L.C.S.W.
University of Southern California
The exploding field of Neurobiology has provided a new dimension to our understanding of child neglect and abuse. The effects of early stress on the developing brain and nervous system is now well-documented in the literature. Many of the symptoms experienced by former cult members and observed by clinicians can now be conceptualized as a sub-optimal stress response resulting in affect dysregulation in its various forms. Due to the inadequate and often abusive parenting practices to which members were often exposed it is not surprising that symptoms such as anxiety, depression, rage, dissociation, emotional constriction, and substance abuse/dependence might occur. This article seeks to explain how these symptoms develop and what might be done to repair the harm.
Once upon a time, not so long ago, there lived a group of neurobiologists and mental health practitioners (psychiatrists, psychologists, psychotherapists) who did not talk to one another. While not everyone could remember how the rift began, many believed it had something to do with a neurologist named Sigmund Freud who abandoned his pursuit of medicine in favor of some strange ideas about the mind. Thus, a Great Divide developed that none dared cross. However, Freud anticipated that at some future date the physical and behavioral sciences would have to reunite. “We shall have to find a contact point with biology,” Freud stated in 1895 (as quoted in Schore, 1997, 807).
As predicted, in the modern age it became apparent that both the neurobiology and mental health camps were equally limited in their individual attempts to explain human behavior because each was knowledgeable about only a part of the “elephant.” Gradually, perhaps reluctantly at first, these two eminent groups began a dialogue. And, lo and behold, they discovered, and continue to discover, that they aren’t so far apart after all, and that each knowledge base appears to add explanatory power to the other. Thus began the rapprochement (Schore, 1997) between the neurobiology and mental health communities as each opened their hearts and their minds to the other.
The trauma field has been one of the platforms upon which this dialogue has taken place. Although clinicians had long suspected that the affective and behavioral differences observed between traumatized people and “normals,” and between people with one type of early childhood history versus another had underlying physiological substrates, these suspicions could not be empirically validated. However, with the advent of new technologies, particularly the fMRI, which has enabled scientists to view the living brain as it thinks and feels, areas of inquiry previously closed to exploration have opened up.
Child maltreatment includes all intentional and unintentional harm to, or avoidable endangerment of, anyone under age 18 (Berger, 2005). This definition includes emotional neglect and physical, sexual, and emotional/verbal abuse. Neglect as a form of child maltreatment occurs when caregivers fail to meet a child’s basic needs, including stimulation and education. Abuse includes all actions that are harmful to a child’s well-being, whether deliberately inflicted or not. The victim does not have to be directly affected; witnessing abuse is just as life changing, if not more so (Perry, 2002).
In the past decade, much has been written on this topic of the psychobiology of trauma; a review of that literature is beyond the scope of this article (for some excellent comprehensive review articles, see van der Kolk, 2003; Bremner, 2003; and Perry, 2002). Thus, I have chosen to focus on specific aspects of the psychobiology of trauma—i.e., affect regulation, the stress responses, and information processing as important consequences of child maltreatment.
Some of the most robust findings in the psychopathology literature are the negative effects of maltreatment on the child’s (and later the adult’s) ability to regulate his/her emotions. Without affect regulation, dealing with life’s ups and downs becomes a daily roller coaster ride that has an impact upon all aspects of a person’s life. Affect regulation refers to the ability to soothe and comfort oneself when one is agitated or anxious, as well as the ability to enliven oneself when one is depressed, bored, or dissociated (i.e., to regulate up or down, respectively). From a neurobiological standpoint, affect regulation can be seen as at the core of healthy development and affect dysregulation as at the core of psychopathology. Symptoms such as anxiety, panic attacks, or depression can be conceptualized as failures of regulation. Coping and defense mechanisms can be viewed as strategies to regulate affect and return the organism to a state of homeostasis (Applegate & Shapiro, 2005).
Thus, we have an affect-regulation spectrum. On the adaptive end are coping mechanisms, such as exercising, listening to music, or doodling during a long lecture. At the dysfunctional end of the spectrum are addictions (alcoholism, drug abuse) and other maladaptive behaviors such as fighting.
There are times, however, when even the healthiest person cannot manage to shift her/himself out of a dysregulated state, and in that case s/he needs to be able to reach out to others for this kind of assistance. People who are unable to do so would live a very schizoid existence. Likewise, people who always use others to help shift them out of dysregulated states—i.e., who are incapable of self-regulation—wear out their friends and family, and might be viewed as having a dependent or borderline personality disorder. In summary then, the ability to both self- and other-regulate are hallmarks of good mental health.
These hallmarks of good mental health should not be construed absolutely, for cultural contexts will influence what is considered to be healthy or dysfunctional. In some Asian cultures, for instance, there may be greater pressure to self-regulate; other-regulation might be seen as shameful or pathological.
The Stress Response
Childhood abuse and neglect damage the ability for affect regulation. To better understand this, we need to understand the physiology of the normal stress response. We’ve inherited this response from our reptilian ancestors, and our fight/flight/freeze reactions are rooted in a primitive part of our brain, primarily the amygdala. (The less-known freeze response is exemplified by the “deer in the headlights” phenomenon, another survival mechanism we acquired from our animal ancestors. A predator was less likely to attack a “dead” animal, so a trapped animal would become immobile to simulate that state. Additionally, a freeze state is a dissociated one.)
A simple explanation for the normal stress response is as follows: Faced with immediate danger, the body pumps out the adrenaline hormones known as cortisol and epinephrine. Epinephrine is fast acting, efficient, and short lasting; in contrast, cortisol is slower to rise but stays in the blood stream longer. These hormones go to our heart, which begins beating faster, and to our muscles, to prepare our bodies either to fight or to run away when we don’t think we have a chance of winning the fight. In addition, epinephrine and its derivative, norepinephrine, are responsible for narrowing attention so that we don’t get distracted but are able to bring all our mental faculties to bear on the present danger (Cozolino, 2002). Obviously, this response has survival value and, thus, has survived evolutionary modifications over time.
The Hypothalmic-Pituitary-Adrenal Axis
There is a wonderful feedback loop in the brain, known as the HPA (Hypothalmic-Pituitary-Adrenal) axis, which lets the body know when the danger is over and to return to baseline. This response occurs when cortisol reaches a certain critical level. When that happens, the body gets the message that the emergency chemicals are no longer needed, so the body can relax (Harvard Mental Health Letter, 2002). For example, when we slam on the car brakes because we almost went through a red light, cortisol levels are elevated in our bloodstream. Soon afterward, when we catch our breath and realize we are safe and there are no cops around, the brain sends signals that tell the pituitary and adrenal glands responsible for cortisol levels that everything is okay, and the body returns to its former homeostatic state. In this way, we have warp speed when we need it to cope with the crisis, but we don’t live there. This feedback loop is important because although cortisol is necessary in the short-run, it is toxic in the long run. And while epinephrine gets in and out of the body quickly, as previously mentioned, cortisol is slower to return to baseline and, therefore, can be harmful to the organism. If left in the bloodstream too long, cortisol actually burns out synaptic connections in the brain and wears out bodily organs, which can lead to various illnesses—ulcers, heart disease, and so on. In other words, under chronic stress, these hormone levels, especially that of cortisol, are turned ON but unable to turn OFF.
For children who have been maltreated, the problem is that they do, in fact, live in this chronic state of emergency, and their bodies continue to be “at the ready” to fight or flee. Initially, adrenaline levels rise more quickly, but cortisol levels fail to reach the critical level for shutdown. One theory for this phenomenon is that the brains of traumatized people have fewer cortisol receptors, paradoxically making them less sensitive to knowing when the emergency is over, and thus leaving them in a highly anxious state (Applegate & Shapiro, 2005). This chronic state of readiness puts a tremendous strain on their bodies. Research has shown, for example, that traumatized children are from 10 percent to 15 percent more likely to suffer from cancer, heart disease, and diabetes as adults (see, for example, Fellitti, et. al, 1998).
To explain further, the amygdala, a primitive brain structure situated at the top of the brain stem, “acts as a sensory gateway to the limbic system” (Schore, 2003, p. 236), or emotional brain. The amygdala can become sensitized to fear and danger. Repeated stress causes the amygdala to become irritable and reactive, which results in a situation known as kindling. This is an appropriate term because, just as a small spark can set a whole neighborhood up in flames, the neurons neighboring an irritable amygdala can be set off easily. Support for this idea comes from studies of other limbic regions. Teicher, Glod, Surrey, & Swett (1993) reported increased limbic system activity, suggestive of temporal lobe epilepsy, in 253 patients who had been physically (38 percent increase) or sexually (49 percent increase) abused as children. Those who had survived both types of maltreatment had a 113 percent increase in limbic excitation. A very recent study by Teicher, Samson, Polcari, and McGreenery (2006), which examined the effects of parent verbal aggression, a less-studied form of child maltreatment, found significant robust effects on measures of limbic irritability and dissociation among other variables.
Heightened levels of sustained cortisol also inhibit the normal functioning of another brain structure, the hippocampus. The hippocampus functions much like a filer, putting information into its proper time and space folders. The hippocampus is also implicated in long-term memory consolidation. Thus, if your hippocampus is functioning normally, it will tell you that you are reading this article in this journal in this particular year (where and when). The hippocampus, however, is especially sensitive to stress. During trauma it gets flooded with cortisol, the stress hormone, and when that happens, it goes offline. Therefore, the traumatic memory does not get placed into its rightful chronological and spatial folders. Subsequently, when a stimulus reminiscent of the original trauma triggers the memory, the person responds as if the event were happening here and now instead of there and then. The ubiquitous phenomena of flashbacks and intrusive thoughts characteristic of PTSD are the result. To further elucidate this process I turn now to a discussion of how memories are encoded in the brain.
Implicit and Explicit Memory
Discussion of the psychobiology of trauma would be incomplete without a discussion of different types of memories and how traumatic memories get reactivated. Implicit memory, also known as nondeclarative and procedural memory, characterizes the right brain (where the limbic system primarily resides). Since the right brain is dominant for the first three years of life, memories of our earliest experiences are laid down in the right brain, in implicit or procedural memory. These early bedrock imprints exert a powerful influence over us in subsequent years.
Around four years of age, our left brain becomes dominant and, along with it, explicit memory, which begins to develop approximately two years earlier. Explicit memory, also called declarative memory, becomes possible because language is more developed by this time and memories are laid down in the symbols of the culture—i.e., language. Explicit memory is also conscious memory.
As noted, the hippocampus is a major structure that functions to consolidate long-term explicit memories. Therefore, when the hippocampus is inhibited from functioning, as in traumatic situations, explicit memory cannot occur. Although the amygdala registers the trauma, the hippocampal “secretary” has not filed it properly. The trauma is “remembered” in implicit memory in perceptual, behavioral, and emotional ways only (Applegate & Shapiro, 2005). Later on, other perceptual, behavioral, and emotional stimuli reminiscent of the traumatic event will “trigger” these unprocessed implicit memories, and the amygdalic urge to fight or flee will often be the result.
For example, a woman molested as a child reacts with disgust and withdraws when her husband initiates sex. Her response is automatic, driven by her amygdala. Both she and her husband are confused by this reaction because she truly loves him and wants to be close. However, the roots of her reaction have been dissociated from consciousness and her conditioned reaction to the molestation is encoded in her implicit memory’s neural circuits. The hippocampus has not registered important information (time and context) of the earlier event, so the woman’s amygdala is in charge of the present interaction.
Another piece of this puzzle has to do with other aspects of information processing, which warrant brief discussion. LeDoux (1996) has pointed out that there are two information processing pathways—the primitive “low road” pathway that we inherited from our reptilian ancestors and a more evolved “high road” pathway via the cortex. When information comes in to the thalamus from the somatosensory cortex where sound, sight, touch, and taste are received (smell goes directly into the limbic system), that information is relayed to both the amygdala and the prefrontal cortex (PFC). The PFC is part of the neo-cortex, which evolved later in time; the PFC functions to organize, plan, reason, and judge information coming in.
The information and its significance then goes on to the amygdala. In contrast to the more direct thalamus-amygdala route “this pathway permits a more detailed and accurate representation of the stimulus.” (Applegate & Shapiro, p. 186.) However, because of its evolutionary heritage, the more primitive pathway is much quicker. (According to van der Kolk, there is only one synapse between the thalamus and amygdala “low road,” while there are seven synapses from the thalamus to the PFC, the “high road” ). The amygdala scans the data to see whether it resembles other fearful events and, if so, sends signals to the adrenal glands to get those fight-or-flight hormones pumping. The body goes into a hyperaroused state characteristic of PTSD before the PFC has a chance to determine the actual significance of the cue—i.e., is this really a dangerous situation? Thus, the woman discussed above reacts unconsciously and automatically first, before the PFC can kick in and reality-test the situation—i.e., is this her husband whom she loves, or is this the early perpetrator making sexual advances that disgust her?
Research on PTSD confirms that hippocampal volume is lower in people who develop PTSD following a trauma compared to those similarly exposed who do not develop the disorder (van der Kolk, 2003). Therefore, the files of those who develop PTSD are less likely to be in chronological order because of the lower number of hippocampal neurons. However, the causal direction has not been definitively established to date; in other words, does chronic stress burn out hippocampal neurons, in turn resulting in PTSD (see, for example, Bremner & Narayan, 1998), or do people who develop PTSD have smaller hippocampal volume to begin with? Tempting though it may be to presume the former, recent research seems to point in the other direction—i.e., that people with smaller hippocampi prior to the trauma are more likely than others to develop PTSD when traumatically exposed (Lyons, 2006). However, this finding, that people with reduced hippocampal volume are more at risk for PTSD, does not resolve the nature/nurture controversy because it does not necessarily mean they are born with a smaller hippocampus. Prior trauma, such as a childhood history of abuse, might explain the hippocampal reduction. In fact, Bremner and colleagues (1998) tested this hypothesis and found that the left hippocampus in survivors of childhood physical and sexual abuse was 12 percent smaller than that in controls. On the other hand, other studies (e.g., DeBellis et al., 1999 and Carrion et. al, 2001) failed to confirm these findings. Research on humans is appropriately hampered in resolving these issues since we can’t induce trauma intentionally and then see what happens.
The False Memory Controversy
Impairment of the hippocampus during trauma also lends support to the controversial phenomenon of delayed recall (a.k.a. “recovered” or “false” memory). In psychotherapy, as patients begin to talk about their earlier trauma, hippocampal activation occurs and memory fragments are consolidated into an integrative whole. Implicit memory circuits link up with explicit memory circuits to form a coherent neural network. In this way, a previously “forgotten” memory, or one that had lain in shadow, may come to consciousness or be further clarified.
Conversely, we also know that children can be suggestible and many variables influence accurate recall (age, interval between occurrence and recall, stress arousal levels, etc.—Doris, 1991). For example, Goldberg (1997) has shown how “false memories” can be implanted by therapists with an agenda, and how unconscious processes can influence autobiographical (explicit) memory. Additionally, Herman (1992) has pointed out how people with certain diagnostic traits (e.g., Borderline Personality Disorder) may lay claim to recovered memories as they attempt to organize and make sense of their symptoms. Nevertheless, because dissociated memories are sometimes implicit memories, a traumatized person in therapy may resurrect these implicit memories and place them in a context of explicit memories directly or indirectly associated with the implicit memory of the trauma in order to construct a cathartic explanation for the implicit traumatic memories. This constructed explanation may then function as an explicit memory of the trauma, which gives the person a capacity to process the trauma in ways that free him/her from its negative effects. This constructed memory/explanation may reflect the objective situation with varying degrees of accuracy, which, because therapists can rarely test the objective truth of the constructed memory, accounts in part for the controversy surrounding “recovered memories.” However, even if some details of the “memory” are inaccurate, the essence of the experience, i.e., the implicit emotional memories, may nonetheless be captured in the therapeutic construct, which, regardless of its accuracy of detail, can help liberate clients from the intrusive automaticity of improperly processed, nonverbal, implicit memories of trauma.
Other Brain Impairments
Maltreatment also results in diminished left hemispheric development. Each brain hemisphere has its own memory/learning system as noted above and is specialized for certain functions. The right hemisphere is more specialized for affect since the limbic system, the emotional brain, if you will, is more plugged into that half. The left hemisphere, the linguistic brain, is specialized for language, giving voice to right hemispheric experiences. The two hemispheres communicate with one another through the modem of the corpus collosum, nerve fibers that connect the right and left hemispheres (Applegate & Shapiro, 2005). In people with abuse histories as well as in people with PTSD, the corpus collosum has been found to be thinner so that the left hemisphere is handicapped in putting words onto emotional experiences (Teicher, Andersen, Polcan, Anderson, Navalta, & Kim, 2003). Additionally, during trauma the area in the brain responsible for speech, known as Broca’s area, shuts down, resulting in the well-known phenomenon of “speechless terror” (Cozolino, 2002).
The ability to put feelings into words is an important component for affect regulation in adults. Clinicians have intuitively known this, so that psychotherapy involves helping the client “talk about” his/her experiences—i.e., put left-brain symbols on right-brain emotions/experiences. The inability to do so keeps the traumatic experiences “stored” in the right brain/limbic areas and unavailable for exploration. This then puts people at risk for all forms of psychopathology. Teicher et al. (2003) propose that the emotional lability noted in people with Borderline Personality Disorder, who often vacillate between states of idealization and devaluation, might be a function of this lack of corpus collosum integration. More recent literature on the backgrounds of this clinical population often reveals extensive traumatic childhood histories (see, for example, Herman, 1992; Sable, 2000; Gunderson & Berkowitz, 2003). Thus, these two bodies of research are consistent with one another and support the premise of this paper that child maltreatment has serious consequences for affect dysregulation and psychiatric disturbance.
Norepinephrine and Dissociation
The other stress hormone mentioned earlier, norepinephrine (NE), may have other consequences. As previously noted, NE focuses attention, and, like cortisol, is helpful as a short-term response but detrimental long term. When attention is narrowed to certain stimuli, other stimuli are shut out. NE is one of the chemicals behind the flashbulb memories mentioned earlier. From an evolutionary perspective, this focusing response is desirable. If a hunter is being attacked by a wild boar, he is more likely to survive if he can focus all his attention on the boar’s distance and speed, and not get distracted by the beautiful waterfall behind the boar or thoughts about his beloved waiting at home. Thus, while NE allows some data to be remembered in bold relief and placed into long-term, hippocampal memory, other data may be tuned out. In the case of child sexual abuse, for example, NE may cause the child to focus on only a part of the event, entering it into long-term memory, but losing other information that might be important. Consequently, the smell of semen might be easily recalled along with an associated feeling of disgust, but the abuser himself may have been excluded from conscious awareness. As an adult, then, the victim/survivor might feel nauseous during a sexual encounter with an appropriate partner (as in our previous example) and lose all enjoyment that sexual activity might otherwise bring. In other words, knowledge of the abuser may be dissociated from the rest of the event, a common characteristic of PTSD. A former client of mine told me how she had focused on a doll in her room while her father was sexually violating her. She is now phobically avoidant of dolls but has little (explicit) memory of the abuse. The problem with dissociated material is that it doesn’t remain unconscious; it leaks out in many of the symptoms characteristic of PTSD: nightmares, flashbacks, autonomic hyperarousal, intrusive memories, and somatic complaints.
Additionally, people who have been sexually abused are prone to the oft-noted clinical phenomenon of revictimization; that is, people who have been abused as children too often become subsequent victims of rape or domestic violence. Prone to using dissociation as a way of coping with stress, they may tune out cues that alert other people to potential danger. Another theory proposed to explain this phenomenon is that, because the stress response is less sensitive in many cases, the person does not pick up the danger signals that would alert others to leave. Potentially dangerous situations might feel familiar and not raise concern for the formerly abused person.
Another aspect of brain development that is important to understand in looking at the psychobiology of trauma has to do with the connections between the lower, more primitive brain regions (limbic and reptilian areas) and the higher cortical regions (neo-cortex, frontal lobes) that enable us to think, reason, organize, judge, and so on. A well-functioning brain has strong connections up and down so that people can integrate thinking and feeling. Otherwise, they either “live in their heads,” as we say, where they are cut off from their feelings, or, on the flip side, they are flooded with affect and cannot reason. Neither situation is desirable.
A key factor in how these synaptic connections form and how strong they are appears to be the relationship between the primary caregiver, usually the mother, and the infant (Schore, 1994). When the mother is attuned to the infant’s cues and able to respond sensitively, contingently, and in a timely fashion to her child, a proliferation of dendritic growth in the child’s right brain connects these lower and higher cortical regions. Additionally, the “good-enough mother” (Winnicott, 1965) acts as a psychobiological regulator, calming and soothing the child when s/he is distressed and enlivening her/him when s/he is bored or dissociated (Schore, 1994). The child then develops a secure attachment to the mother. Eventually, the baby will be able to internalize these functions and become able to regulate his/her own affect. But if these functions are lacking in the primary caregiver, they will have serious consequences for the child. Michael Meaney (2001) at McGill University demonstrated that when baby rats were licked and groomed a lot they were less anxious and fearful as adults; that is, they were able to be calm in the face of stress. Attentive maternal behaviors such as licking predicted calm nervous systems, as well as how nurturing the pups would be to their own offspring. Thus, we see biological underpinnings of the intergenerational transmission of maternal behavior and affect regulation.
Although it is never clear how generalizable animal research is to human behavior, studies from the field of attachment appear to confirm these findings. For instance, EEGs have shown that the human infants of depressed mothers exhibited excessive right frontal lobe activity, which is biased for negative emotions, emotional reactivity, and psychopathology (Teicher, 2002). Researchers at Baylor Medical Center also found that babies of depressed mothers, who were unable to play with their children, had smaller and less complex brains than babies of nondepressed mothers, (Perry, 2002). And brain scans of two-year-old Romanian orphans who had not been held and played with showed little or no activity in the parts of their brains dedicated to emotions. Thus, they were unable to attach because they could not feel. Perry (2002), reporting on some of the findings of the Romanian adoptee research team, stated that “chaotic, inattentive, and ignorant caregiving can produce pervasive developmental delays” and meet criteria for a DSM diagnosis (p. 89). Thus, not just the obvious forms of child maltreatment (abuse) but also neglect appear to have major consequences for healthy development.
An insecure attachment has been shown to put people at risk for psychopathology. Specifically, the attachment category known as disorganized/disoriented appears to create a vulnerability to developing PTSD after experiencing a traumatic event as an adult. This may be due to the fact that children with this “D” attachment style learned to use dissociation to cope with early childhood stress. Unable to fight or flee as children, they froze or dissociated (they “got away” psychologically) as a way of coping, and this behavior became their preferred mode of dealing with stress. From the trauma literature we know that people who dissociate during a traumatic event are more likely than others exposed to the same event to develop PTSD. A logical interpretation of this finding would suggest that people who grow up in chaotic, neglectful, and/or abusive homes that foster disorganized attachment are more at risk for PTSD. This is borne out in research on foster children, where the most prevalent attachment category observed was “D" (about 80 percent of the children in foster homes—Cicchetti, 1996). It would not be such a great leap then to assume that people who grow up in cults, where parents are distracted, frustrated, confused, shamed, deprived, and angry would develop disordered attachment and thus be at risk for PTSD.
Neurobiology, Trauma, and Cults
This article has focused on the effects of the biological component of trauma on the normal stress response, affect regulation, and information processing. Understanding this component helps create a more comprehensive clinical picture that informs treatment of survivors. Traumatic experiences and child maltreatment have been extensively documented in the cult literature (e.g., Markowitz & Halperin, 1984; Langone & Eisenberg, 1993; Ayella, 1998; Whitsett & Kent, 2003) but to date the biological component has not been addressed in relation to those experiences. A neurobiological perspective may illuminate some of the trauma-related symptoms observed in cult survivors.
Post-traumatic Stress Disorder (PTSD) is a three pronged phenomena characterized by the following:
Re-experiencing (in the form of nightmares, intrusive thoughts, and “flashbacks”)
Avoidance (of the reminders, which act as “triggers”)
Heightened arousal (a dysregulated physiological state resulting in insomnia, irritability, and a startle response).
Re-experiencing and Avoidance
Biological explanations can shed much light on the symptoms of re-experiencing and avoidance. Trauma survivors are prone to re-experiencing because the information they initially received was not processed completely due to the overwhelming emotional affect accompanying it. Parts of the experience were dissociated and not entered into explicit memory. Thus, these portions remain unintegrated in implicit memory circuits, in perceptual, emotional, and behavioral networks. The dissociated material (sights, sounds, smells, etc.) acts as “triggers” later on, flooding the survivor with emotions similar to those accompanying the original event. Conversely, triggers can induce dissociated states, sometimes called “floating,” (Lalich and Tobias, 2006), which may appear in the form of “flashbacks,” intrusive thoughts, and nightmares.
To clarify further, “flashbacks” are implicit memories made up of sensations, perceptions, emotions, and behavioral tendencies. They can be conceptualized as experiences that were not processed explicitly because Broca’s area (the speech center) shuts down during high emotional states and the hippocampus goes offline. Clinicians should take advantage of occurrences such as flashbacks, since it is at these times that implicit memories are most available for processing. Helping the client put words (left brain symbols) on the limbic experiences (right brain) will bring down the autonomic arousal. Applegate and Shapiro state: “One goal of intervention is to use the conscious linguistic structures of the high road to inhibit and render more manageable the reactive, unconscious, and preverbal appraisals of the low-road pathways” (P. 186).
Without such intervention, the dissociated experiences remain trapped in the limbic system, forever vulnerable to “triggering” attacks. Within the safety of the empathic therapeutic relationship the survivor can begin to “speak of the unspeakable” and gain some control over his/her internalized cult world.
A compelling case in point, for which the therapist obtained some corroboration (Paul Martin, Personal Communication), concerns a woman who spent her earliest childhood in a group that practiced sadistic ritual abuse (Woznick, 2006). Woznick’s account describes methods used to instill dissociation. She was, for example, shocked with a cattle prod in her childhood to stop her crying and threatened with additional shocks if she should ever show emotion again. She states, “So began our conditioning to hold our feelings inside no matter what horrific atrocities we would witness” (such as being forced to observe a woman literally being torn apart by wild dogs). The cattle prod was only one means of intimidation in a long history of threats and terrorizing experiences. Her inability to leave the cult resulted in severe Dissociative Identity Disorder when her mind could no longer keep the walled off material out of consciousness. Although the actual memories were not repressed, the affect associated with them had been compartmentalized and relegated to her unconscious. By her early 30’s Woznick was experiencing fugue states where she lost time and found herself in strange places without knowing how she got there or why people were calling her by other names.
The third prong of PTSD, heightened arousal, is also further clarified through greater neurobiological understanding. Affect dysregulation is at the core of heightened arousal—an inability to regulate emotional states. These include such post-trauma characteristics as the startle response and emotional volatility. The startle response is an amygdala reaction, the early warning system we inherited from our reptilian ancestors. Once the amygdala registers a particular stimulus as dangerous, that stimulus gets generalized to others and the survivor loses the ability to discriminate among threats. As van der Kolk, McFarlane, and van der Hart (1996) put it, “Autonomic arousal, which serves the essential function of alerting the organism to potential danger, loses that function in people with PTSD. The easy triggering of somatic stress reactions … causes them to react to all reminders of the trauma as an emergency” (P.421). Constantly hypervigilant, sleep becomes problematic and results in insomnia and other sleep difficulties often noted in trauma survivors, who not only fear losing control but are afraid of their dreams.
Likewise, emotional volatility and irritability are characteristic of heightened arousal. As noted in an earlier section the pre-frontal cortex is inhibited during high amygdala activation. Heightened arousal results because there are no breaks put on the fight or flight reaction. The person goes from 0 to 100 in a split second; aggression and rage may result. Overwhelmed and ashamed by their own behavior, traumatized people attempt to control these eruptions through suppression and avoidance. However, these attempts at containment inevitably fail because they cannot hold back the flood of affect pushing for release. A vacillation between emotional constriction and emotional volatility results. Trauma expert Judith Herman (1992) calls this vacillation the dialectic of trauma.
Because survivors are prone to states of indiscriminate heightened arousal they often avoid activities that stimulate the sympathetic branch of the autonomic nervous system (ANS). Additionally, any body arousal can act as a trigger. Thus, survivors learn to distrust their bodies and become unable to use emotional signals to inform their decisions. Clinicians should assist clients in regaining a sense of safety in, and control over, their bodies through such techniques as hierarchical desensitization, muscle relaxation, a titrated exercise program, EMDR, and sensory integration techniques (Fosha, 2000). However, two cautions must be noted here. First, the clinician should be knowledgeable about the kinds of techniques utilized by a particular cult to induce dissociated states; otherwise s/he might trigger “relaxation-induced anxiety” inadvertently. For instance, in Eastern-based cults where meditation and listening to “heavenly music” is part of the daily routine, clients coming out of these groups may have conditioned dissociated responses if advised to meditate. Likewise, survivors often used self-hypnosis to “get away” in their mind during their time in the cult. Thus, hypnosis for these clients would be questionable.
From the perspective of neurobiology, behaviors such as aggression, substance abuse, and domestic violence can be seen as attempts to regulate affect. Depression and anxiety can be viewed as failures to do so. Obviously, this applies to all kinds of trauma survivors, not just those exiting cults. Cult survivors, however, may be unique among trauma victims in that the cult actually predicts that these behaviors will occur. As a means of control members are given “dread” messages about what will happen if they leave the group. This prophesy often comes true because the cult member lacks healthy emotion regulation and the life skills necessary to function in the world. She often has to leave family and friends behind and, thereby, give up a support network that, however imperfect, was all that she had. Without the ability to regulate affect, interpersonal relationships become a challenge, leaving the former member isolated and believing that “the world really is a cold, uncaring place,” just as the cult leader said it was. The ex-member then turns to whatever sources of relief may be available—drugs, alcohol, promiscuous sexuality, and other addictions— to regulate his or her heightened affect.
As mentioned previously, early attachment experiences are the key ingredient to optimal brain development, particularly the right (emotional) brain, which is dominant for the first three years of life (Schore, 2001). Since the limbic system is primarily in the right brain, emotional experiences will be “stored” there. Schore (2001) and Siegel (2003), among other infant mental health researchers, emphasize the unconscious interaction between mothers and infants and how the baby essentially “downloads” the mother’s emotional right brain. This implies that the mother’s right brain needs to be in good shape; otherwise she is giving faulty information to the child about the world and him/herself. Likewise, the mother’s autonomic nervous system (ANS) must regulate the less mature infant’s ANS. Since the parasympathetic branch of the ANS does not even begin developing until around 18 months, the child is unable to regulate his own affect. Thus, the infant is dependent upon the mother’s more mature brain and ANS either to enliven him when he is depressed or to soothe him when he is agitated. A mother who is frustrated, angry, and consumed with anxiety herself, as is often the case with mothers in cults, is unable to regulate her own affect let alone that of her child. Thus, the child may be left in prolonged negative affect states that stress his or her immature nervous system.
Likewise, in an environment such as certain polygamist Mormon groups (e.g., the Fundamentalist Latter-Day Saints, or FLDS), where mothers are required to have a child per year, resulting in litters of children, mothers may not be able to provide the one-on-one dyadic relationship necessary for optimal brain development. When parents’ roles are hijacked by the leader who regulates his/her own affect by manipulating, controlling, and often abusing his/her followers, parents are likely to displace their frustration/anger onto the more vulnerable members of the community, the children. This may have been the case with Lisa Woznick’s mother who is described as irrationally abusive:
“She’d lash out at me, screaming, and attack me with our shag carpet rake—often with no provocation. She’d beat me with it, or whatever else she could get her hands on, for my purported transgressions, or any other reason she used to justify her abusive behaviors. She slammed me into the walls at times for getting in her way, even though I was just playing silently in our den or living room.” (Woznick, 2006, p. 2)
Whitsett and Kent (2003), Ayella (1998), Stein (1997) and others have described the systematic destruction of the mother-child bond. In God’s Brothel Andrea Moore-Emmett (2004) describes sister-wives who often take their frustrations out on the numerous children in their care. Dysregulated themselves, the parents are unable to provide the calm, consistent, nurturing environment a developing brain requires. Additionally, in an environment lacking in stimulation, where education is prohibited and extracurricular activities denied, the brain cannot develop robust synaptic connections. The primitive amygdala impulses do not get mediated by the more evolved prefrontal cortex. The result is that raw emotions are not metabolized or clarified by thinking, and thoughts are not given emotional significance. Thus do the various forms of child maltreatment pass on intergenerationally. The memory traces of interactions with dysregulated others are laid down in implicit memory banks and get reactivated in subsequent attachment situations, that is, with their own children. And so it is that the consequences of child maltreatment also get passed from generation to generation.
As M. Teicher (2002) puts it:
Society reaps what it sows in the way it nurtures its children. Stress sculpts the brain to exhibit various antisocial, though adaptive, behaviors. Whether it comes in the form of physical, emotional, or sexual trauma or through exposure to warfare, famine, or pestilence, stress can … permanently wire a child’s brain to cope with a malevolent world. Through this chain of events, violence and abuse pass from generation to generation as well as from one society to the next. (75)
The good news is that the brain remains plastic throughout life, and new neural networks can be formed in the context of a nurturing, empathically attuned environment. Psychotherapy and/or a secure relationship can override the earlier traumatic experiences, healing and reshaping the brain.
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Cultic Studies Review, Vol. 1, No. 1, 2002,Page
 Very strong implicit memories were first called flashbulb memories by Brown and Kulik in 1977, and the term has stuck (as cited in van der Kolk, et al, 1996). The classic example usually given is that almost everyone in this country has a flashbulb memory for where they were when they heard that President Kennedy had been shot. It is like a snapshot had been taken for that moment in time and remains etched into memory (although the memory is not always completely accurate).
 The concept of “contingency” is similar to that of “mirroring.” Contingency refers to the emotional resonance and accurate understanding of the needs of the infant by the caregiver. For a more extensive discussion, see Siegel and Hartzell (2003).
About the Author
Doni Whitsett, Ph.D, L.C.S.W.. is on the faculty of the School of Social Work at the University of Southern California. Dr. Whitsett taught various courses in Practice, Behavior, and Mental Health. Dr. Whitsett has been working with cult-involved clients and their families for over ten years, and gives lectures to students and professionals in this area. Her publications include “A Self psychological Approach to the Cult Phenomenon” (Journal of Social Work, 1992) and “Cults and Families” (Families in Society, Vol. 84, No. 4, 2003), which she co-authored with Dr. Stephen Kent.