Our increasing knowledge of the neural and molecular processes involved in learning and memory—as well as in thoughts, feelings and behaviors—freshly provokes ancient questions about the relationship between mind and matter. Our intent here is simply to touch briefly on certain aspects of this fascinating topic and offer a prediction.
Neuroscience researchers consistently refer to the identified neurobiological and biomolecular processes as “subserving”
subjective psychological processes or as being “substrates” or
“correlates” of such processes. They describe subjective or behavioral responses as “recruiting” neurobiological processes.
These terms suggest an intricate, mutually dependent interplay of the
“top” and “bottom” domains without implying that one is fundamentally the cause or source of the other. There are, of course, specific instances where one domain clearly drives effects in the other—such as a stroke destroying specific areas of subjective functioning, or (illustrating what neuroscientists term “experience-driven” neural effects) chronic despair and depression over major personal losses causing measurable changes in brain chemistry, synapse firings, and epigenetic alteration of gene expression. Use of the clinical methods described in this book lays bare what appears to be a top-down, meaning-driven causation of therapy clients’
symptoms. Moreover, the clinical ability to retrieve the contents of emotional implicit memory, revealing its coherence, combined with our research-based understanding of the longevity of such a memory enable us to recognize that even in generating responses regarded as
symptoms, a person’s brain has functioned as it was set up to do by evolution and is not malfunctioning—suggesting again that the causation of symptoms based in memory is not bottom-up.
These issues may become particularly relevant in the context of epigenetics, an emerging field of great importance to the scientific understanding of learning, memory, and symptom production. The term refers to a complex system of molecular machinery that carries out experience-driven (that is, learning-driven) modifications of gene expression without mutating the genes themselves. In the complex interplay of nature and nurture, epigenetic mechanisms deliver the influences of nurture to our genes—in the form of molecular units or tags that are attached to or removed from genes or nearby structures, influencing the level of gene activity in response to environmental experiences. Researchers have made significant progress in delineating the detailed epigenetic markers and corresponding changes in gene expression in the brain that result from, for example, experiences that induce depression or attachment insecurity and distress (e.g., Franklin et al., 2010; Tsankova, Renthal, Kumar, &
Nestler, 2007).
All meaning-driven behaviors, emotions and thoughts—including those regarded as clinical symptoms—undoubtedly do have a neural and molecular substrate, but what is a meaningful definition of causation? We suggest that depression- or insecurity-generating experiences, for instance, may drive epigenetic molecular tagging not directly but through the long-lasting negative meanings and constructs that these experiences set up in implicit memory (even in animals). It is these chronically operating, implicit, subjective meanings, we propose, that drive emotional and behavioral responses which, in turn, drive the epigenetic tagging process in a top-down manner. In this view, epigenetics research is showing us more of what’s “under the hood.” Knowing the molecular details of what’s under the hood, though, does not logically imply a change in our recognition of top-down causation. In the car analogy, the cause of the car turning left continues to be the subjective desire and will of the person at the wheel, not the movements of the mechanical parts under the hood,
because those movements are recruited by and subserve the driver’s subjective world of meaning—and no less so if we know in detail what those movements are.
The view that the fundamental cause of many clinical symptoms lies in implicit emotional meanings, and that those same meanings drive changes at the molecular level, generates the prediction that if epigenetic tags created by depression-inducing events are removed by chemical agents, the tags and associated symptoms of mood and behavior would recur when the chemical agent ceases to be applied, because the causal meanings in implicit memory are not removed by the chemical agent and would therefore once again drive production of tags and symptoms in the absence of the chemical intervention.
This prediction is supported by observations that the antidepressant imipramine removes or blocks some of the depression-related epigenetic tags and dispels symptoms of mood and behavior (e.g., Tsankova et al., 2007), and that symptoms return when imipramine is discontinued. The same prediction implies that the induced molecular tags would disappear lastingly as a result of erasure, through memory reconsolidation, of the learned meanings that generated them. To test this key prediction, methods already demonstrated by neuroscientists to erase a learned fear (Monfils et al., 2009; Schiller et al., 2010) could be complemented by epigenetic monitoring.
Conclusion
In this chapter we have seen how memory reconsolidation works and, as demonstrated in a large body of quite recent research by neuroscientists, how it unlocks the neural circuits of a targeted emotional learning, allowing that learning to be unlearned and erased by other learning. Emotional learnings are extremely tenacious and otherwise normally last for a lifetime. Based on these findings, we defined the therapeutic reconsolidation process as a general template for utilizing reconsolidation in psychotherapy for
elimination of learned responses down to their emotional and neural roots.
Since the 1950s, the beliefs of psychotherapists regarding symptom causation have drifted ever farther away from psychological causation, and have increasingly embraced biochemical, neurological, and/or genetic causation of symptoms, often despite weak or faulty evidence for the latter views. (For example, see Toomey and Ecker, 2009 for a review of the invalid empirical evidence surrounding the rise of antidepressant SSRIs and the view that depression is caused by imbalances of neurotransmitters.) However, as reconsolidation and memory erasure enter more and more into clinicians’ thinking and practices, and therapists repeatedly witness a symptom such as long-term depression or anxiety attacks ceasing permanently as a result of a process known to bring about erasure of emotional learnings, psychological causation will speak for itself compellingly, particularly when this is observed for many different kinds of symptoms (see Table 3.1 and supplemental online list of published case studies indexed by symptom).
Of course, we must not overshoot in this direction either; as we noted earlier in this chapter, there are important categories of symptom that we reliably can believe have genetic and/or neurobiological, but not psychological, causes. And it may be found in the future that, for example, most cases of depression are due to psychological causes—that is, emotional learnings in implicit memory—while some smaller fraction of depression cases may have physical, non-psychological causes that have not been identified as yet. Overall, as a result of reconsolidation research having put emotional memory erasure into the clinical picture, the psychological causation of symptoms can become clearly apparent to therapists as never before.
The rest of this book moves on to show a wide range of clinical methods, skills, and processes that are well suited for facilitating deep, transformational change based on these principles. Therapists who understand that the brain requires a definite process for erasing an emotional learning are in a position to use their preferred methods
to fulfill that process, regularly deliver therapy of exceptional, liberating potency, and enjoy a level of effectiveness in day-to-day practice well beyond what previously seemed possible in the clinical field, as shown in the many case examples throughout this book.
This is a wonderful moment in the ongoing advancement of psychotherapy— the moment when, for the first time in the course of evolution, we understand how to free ourselves from limiting emotional learnings formed earlier in life. This book is dedicated to spreading that knowledge throughout the field of psychotherapy.