There is a wide range of patient-related risk factors for the development of adult PTSD with many considerably more complex than some individual studies would suggest. Patient-related factors include adverse childhood experience, childhood abuse, low intelligence, low socioeconomic status, female gender, younger age at the time of trauma, lack of education and a family history of psychiatric illness (Brewin et al., 2000). Non-patient risk factors include a lack of social support, which likely also includes the inability to use available support due to problems with afﬁ liation. While it is not clear whether risk factors are additive, as many will cluster and some will predispose for the occurrence of others, it does appear unarguable that a child experiencing abuse of many forms from a very young age has many of these risk factors. Aetiological complexity is highlighted by previous trauma, potentially either “sensitising” or “inoculating” the individual depending upon their view of that event and their ability to cope with it (e.g., whether they felt powerless or powerful).
The two most important and interacting factors in determining how individuals respond to and cope with PTEs, and reduce their vulnerability to developing PTSD, are: ﬁrst, the ability to afﬁliate with others and accept their support, and, second, the amount of psychosocial support families and communities offer. The disrupted attachment and fear of attunement limiting afﬁliation are targeted directly with CRM, with the nested hierarchy of resources then providing a framework within which traumatic experiences may be processed. This will allow individuals to afﬁliate more readily rather than freeze and avoid, thereby making use of any psychosocial support available.
Whilst the clinical symptom of peritraumatic dissociation has been found to be a risk factor for PTSD, the authors would argue that it is also the key neurochemical factor in the chain of body responses to an adverse experience. Clinically, it appears that the survival terror accessed in treatment has been capped and compartmentalised, through a peri-traumatic dissociative adaptation of the stress-induced analgesia response; the authors regard this as the primary event in the pathogenesis of PTSD. Storage in a state-dependent “compartment” may also be a trauma-related mechanism for “splitting off” an experience. Whether one mechanism applies to extreme terror and another to a low arousal state of dissociation has not yet been empirically delineated.
The genetics of PTSD are complex and far from fully delineated, and what follows is a brief overview – the interested reader is referred to Uddin et al. (2012). There have been many published candidate gene studies examining genetic variation at loci hypothesised to be linked to the development and/or maintenance of PTSD and there are likely many more unpublished studies with negative ﬁndings. Many studies have focused on the dopaminergic system, although other systems such as serotonergic and noradrenergic, and the hypothalamic pituitary adrenal axis have also been investigated (Koenen et al., 2009). Conﬂicting results in some instances may be because of the absence of trauma exposed control groups. Of the ﬁndings reviewed by (Uddin et al., 2012), some of the most noteworthy are, ﬁrst, that independent of an individual’s genetic constitution there appears to be a level of traumatic stressor at which resilience can be extinguished in the majority of those exposed (Kolassa et al., 2010). Second, a frequently studied gene is the transporter region of SLC6A4; it has been suggested that different alleles at the same locus on SLC6A4 may confer both a risk factor and resilience to PTSD depending on contextual factors (including gender). Methodological differences may explain the variable ﬁ ndings (Uddin et al., 2012) although DNA methylation of SLC6A4 may determine whether responses to trauma are unresolved or otherwise (Zannas et al., 2015).
This chapter has set out the empirical background to, the need for and development of CRM, i.e., its rationale, its hypotheses and its methods. However, we also need to justify the inclusion of components of this chapter, speciﬁcally epigenetics – not perhaps an expected inclusion for a book introducing a psychotherapy paradigm.
Any clinician who has worked with terror connected to early attachment disruptions is likely to have found that the physiological and behavioural responses to relevant triggers are resistant to extinction, to use fear learning terms. The lessons of infancy that are not genetic can nevertheless be stamped on the psyche and on its neural substrates and are difﬁ cult to unlearn, or to be inﬂuenced by new learning in the time period required for reconsolidation. This is because the expression of genes is altered in a way which modiﬁ es the functioning of cells so that fear memories become strong and difﬁ cult to modify at the cellular level. Epigenetic mechanisms are the means whereby the memory-enhancing genes are promoted while memory-restricting genes are inhibited (Kwapis & Wood, 2014). There are many possible biochemical modiﬁ cations of the nucleosome, in which DNA is bound to histone proteins, and these include DNA methylation and hydroxymethylation, histone modiﬁ cations and noncoding RNA populations (Zannas et al., 2015). A risk factor for PTSD is the glucocorticoid-responsive FKBP5 gene that mediates speciﬁ cally the effects of childhood rather than adult trauma on stress responsivity and HPA axis functioning (Zannas et al., 2015). FKBP5 methylation and demethylation mechanisms contribute to vulnerability to PTSD or resilience and these mechanisms are described as epigenetic. Other examples include children of holocaust survivors (with PTSD) having both a higher risk of developing PTSD and lower cortisol levels, and offspring whose parents have PTSD having higher rates of PTSD as an adult (Yehuda et al., 2001). Further research on holocaust exposure involving survivors, adult offspring and comparable parent and offspring, found exposure to have an effect on FKBP5 methylation observed both in the parent and offspring (Yehuda et al., 2016). The methylation was higher than controls in the survivors but lower than controls for their offspring. This relatively small study also showed differential impact of environmental stressors (holocaust exposure and childhood adversity, respectively).
Epigenetic mechanisms not only turn short-term experiences into lessons learned for the remainder of the lifespan – they also mediate transgenerational transmission of fear learning and stress responsiveness. Preclinical studies in mice demonstrate that learned fear responses to particular odours in mice are transmitted to subsequent generations (Dias & Ressler, 2013) and are expressed into adulthood.
The CRM perspective would stress the importance of moving beyond the fear learning pathways to the:
“. . . epigenetic moldings of brain networks that result in various patterns of sensitization and desensitization in the primary-process emotional and motivational networks of the brain.” (Panksepp & Biven, 2012)
That is, epigenetic modiﬁcation of FEAR, RAGE, GRIEF/PANIC systems at brain levels below the corticolimbic learning mechanisms, such as in the brainstem (e.g., Bortolanza et al., 2010), require the resourcing and reorienting opportunities provided by CRM if change is to occur throughout the most fundamental strata of the self. When the resources are ﬁrmly in place, deepening the attention into the body sensations that have arisen with the target issue can access unexpectedly profound levels of the psyche. These effects are targeted in treatment through a combination of CRM breathing techniques and somatic attunement, with the scaffolding of CRM resources such as grids, core self and attachment/attunement work: all of which are set out in subsequent chapters.
(Excerpted from) The Comprehensive Resource Model: Effective Therapeutic Techniques for the Healing of Complex Trauma, written by Lisa Schwarz, Frank Corrigan, Alastair Hull and Rajiv Raju, published by Routledge, 2017