Epigenetics and Primal Therapy: The Cure for Neurosis (Part 1/20)

This is the first part of a series I wrote on Epigenetics and Primal Therapy. The whole article will publish soon in the "Activitas Nervosa Superior" Journal of the World Psychiatry Association (http://www.activitas.org/)



Sometimes I realize I am getting science-heavy but what is happening today is so exciting, especially since it supports what I have been writing about for almost 50 years. Almost every week, it seems, scientists announce new research confirming much of the primal position. This is especially true in the burgeoning field of epigenetics, the study of how experience changes an individual’s genetic code, previously considered inalterable. An article recapping the groundbreaking work by pioneering researchers from McGill University in Montreal proclaimed that “the emerging field of epigenetics is revolutionizing the study of mental health – and challenging the belief that DNA is destiny”(1). 

 Moreover, in terms of the history of science, the new developments augur the convergence of previously distinct fields, psychology and biology. In one report regarding research that shows a link between early-life adversity and changes in a person’s genetic make-up, the Canadian researchers come to this sweeping conclusion: “Epigenetics could serve as a bridge between the social sciences and the biological sciences, allowing a truly integrated understanding of human health and behavior.” (McGowan & Szyf, 2010, p. 71) In short, there is a growing understanding that mental illness has a crucial physical component, which has been a basic tenet of Primal Theory from the start. We have always maintained that neurosis is a disturbance of mind and body. And in our treatment, both mind and body must be involved for a cure. Now, science is showing us how that is possible at a cellular level. Unlike genetic mutations, the researchers state, “epigenetic alterations are potentially reversible” (McGowan & Szyf, 2010, p. 66). And that is the most promising finding of all. 

 I have discussed epigenetics in my blog and my books, about how adversity early on changes the switches for key genes that then serves to compound repression or inhibition. These switches turn the gene on or off, and thus help set in what seem like genetic changes. In Primal terms, it is the mechanism of closing the gates of feeling or opening them. And there are different chemicals that accompany the epigenetic events, methyl and acetyl groups, for example. The critical work in this field shows how imprints can be passed down through generations – from parent to child and grandchild – primarily through the biochemical processes known as methylation and acetylation. We need to differentiate, however, between healthy and unhealthy methylation. Under normal conditions, methylation is a necessary and naturally occurring process that helps regulate the expression of an individual’s genetic make-up. But excess methylation becomes pathological and leads to disease. The process goes awry when the individual suffers physical or psychological trauma, especially in the womb and in infancy. It seems that for each and every pain we endure during gestation and at birth there is a change in the chemicals that enhance the repression of pain. When the pain or adversity is prolonged, the system is overtaxed and we now have the mechanism of leaky gates; that is, repression begins to falter due to an overload of chronic pain. 

 It is the consistency of the pain that causes the overload. There is a limit that the brain can handle. Beyond that, the gates become vulnerable and do not do well. It takes very little trauma after that to produce a symptom such as ADD, Attention Deficit Disorder. The chemical methyl group is recruited when there is a traumatic event, and helps embed that memory. It seems that when there is a surge of methylation part of it attaches to cytosine, one of the four nucleobases of DNA. The imprint of the pain is now part of the DNA and blocks the expression of various genes. Concurrently, methyl and acetyl groups attached to the histones (protein structures which allow the DNA to coil up) may interfere with the timely coiling or uncoiling of the DNA. This disrupts the proper expression of certain hormones and other neurochemical processes. That is part of the reason it is so easy to confuse genetics with epigenetics: our moods and personalities are shaped early on, so we believe psychological disorders are passed down through the bloodlines. After all, if both the parents have blue eyes, it is not a mystery that their child also has blue eyes. 

 But when it comes to behavior and feelings, it is another matter. Controlled by the epigenome, genetic expression can be restricted through experiences the fetus undergoes while in the womb. And it is here that some of the mystery of cancer may be uncovered; for it may be that cancerous cells would evolve as normal cells if not for the physiologic force of repression provoked by maternal stress. This creates lifelong chronic stress in the offspring. It may be that as benign cells surge forward along preordained pathways, they are blocked from their destinations. They are then “crushed” or deviated and can no longer be themselves; they lose their identity and become lethal. As they are changed, we are changed. (More on cancer in a moment.) What all this means is that by examining our womb-life in detail we can often predict our future: our sexual problems, the possibility of later cancer, psychosis, heart problems, Alzheimer’s disease, and a whole host of afflictions (Johnstone & Baylin, 2010). 

 One study suggests that the biological underpinnings of bipolar affective disorder are not primarily genetic, but are epigenetic (Rutten & Mill, 2009). Even an individual’s tendency toward violence, once thought to be a brain disorder, is being shown to have epigenetic roots. In research with rats, investigators at Switzerland’s Ecole Polytechnique Fédérale de Lausanne found that animals subjected to trauma in childhood showed changes in two parts of the brain – the orbitofrontal cortex and the amygdala (Márquez et al., 2013). Those changes taken together combined to lower the threshold of aggressive impulses and weaken the ability to control them. (A report summarizing the findings was also released by the Swiss research university under the title, “Childhood Trauma Leaves its Mark on the Brain.”(2) The results were surprisingly similar to changes found in the human brains of traumatized children who grew up to be violent adults. In addition, the scientists also measured changes in genes known to be associated with aggressive behavior. Here, they found that the psychological stress experienced by the rats caused an alteration in the way these genes were expressed, specifically an increase in the level of MAOA gene expression in the prefrontal cortex, according to Prof. Carmen Sandi, head of the Swiss school’s Laboratory of Behavioral Genetics and director of the Brain-Mind Institute. Researchers were able to reduce the levels of aggression with antidepressants, specifically an MAOA gene inhibitor. In short, childhood stress produced epigenetic changes that heightened violent tendencies. Drug treatment later tamped down the violence, reversing the long-term impact of early trauma. In our own work, we have found that the deeper patients descend down the levels of consciousness the more likely there can be rage and violence. 

 Until recently, the role of epigenetic mechanisms in transmitting trauma across generations has been demonstrated in animals but not in humans. A new study, involving Holocaust survivors and their children, shows for the first time how the epigenetic impact of stress, the cellular changes, can also be passed down among humans, from one generation to the next (Yehuda et al., 2015). Researchers found that children of Holocaust survivors frequently gave birth to anxious children. At first, they thought it was because the parents told horrible stories to the children, but later they discovered that the anxiety came down through the genetic chain, as we shall see in more detail shortly. The point is that the genetic effect of wartime stress had descended from the mother’s physiology through epigenetics. (More on this study in a moment.) 

 I will discuss the clinical implications of the research in the second half of this article. Suffice to say for now that pharmacological treatment may not be the only way to reverse epigenetic changes. We propose that the effects of methylation – as an agent of repression – can be reversed during Primal Therapy, which revisits and resolves the traumatic events that triggered the repressive chemical process to begin with. The real revolution lies in the possibility that people no longer have to live with their genetic inheritance but can actually take charge and change it through Primal Therapy. We believe we may have the method for reversing the long-term deleterious effects of epigenetics, and we are undertaking new research to study that point. If it is life experience that caused changes in the biochemistry and neuronal circuitry, then it is not a fixed entity. It can be altered; the way this is done is by retrieving and reliving key imprints, as I will explain. Heredity is irreversible, but epigenetics is not. It is reversible, which is something I propose we have been doing for almost 50 years. 

 (1) McDevitt, N. (2006, Fall). The nurture of things. Headway. Retrieved from http://www.mcgill.ca/research/files/research/headway-fall-06.pdf 
 (2) Childhood trauma leaves its mark on the brain. (2013, January 15). Ecole Polytechnique Fédérale de Lausanne. Retrieved from http://www.sciencedaily.com/releases/2013/01/130115090215.htm