Epigenetics and Primal Therapy: The Cure for Neurosis (Part 7/20)

A key point in all of this is that physiologic reactions are the basis upon which feelings are constructed. Thus, what distorts physiologic responses will distort psychological reactions, as well. If the system is highly activated due to early trauma, chances are we will find, later on, a hyperactive individual who will search out projects to keep himself active and busy. If dopamine and other alerting chemicals are in short supply, we may have someone, instead, who is passive and phlegmatic, who concocts reasons for not doing anything, for not following through. It is not a one-to-one relationship, but physiology does direct our psychology, only after psychology has its say.

Neuroscientists in Italy did a complete literature search of many databases for panic disorders (Perna, Guerriero, Brambilla & Caldirola, 2014). Yes, the brainstem was involved. The brainstem, which registers very early trauma and sets the tone for how we respond to it later in life. So mother’s drug- taking and later birth anesthesia sets up a panic reaction to lack of oxygen. Later in life, closed doors or windows become a threat and can set up a panic attack. Their summary was as follows: “Panic patients tend to have abnormal brainstem activation to emotional stimuli when compared with healthy controls.” Let’s be wary of concentrating on the brainstem without acknowledging the milieu it lives in. The brainstem is the mechanism for the process of translating terror, but where does the terror come from? We will never find that out by a detailed examination of the brain cells. We will find out through knowing the terror that the mother has undergone while pregnant. I saw a patient recently whose mother underwent a severe auto crash with baby in the car. This child had a lifelong anxiety state. Her brainstem was constantly reacting to the imprint.

Here are my questions for researchers: where does that state come from? What causes that brainstem reaction? Or does the brainstem just go off and do its own special thing? What is the exact relationship between certain experiences and brainstem activation? Those are the answers that will lead to proper therapies, but they cannot be answered by research alone. Above all, why is the brainstem so involved? Maybe the damage is registered there because it dominates during the first weeks or days of life in the womb. And the brainstem becomes methylated early on. And as I say, it is the earliest imprints that are the most damaging. There is where therapy needs to begin. It is clear that if we want cure, we need to descend to the lower depths, the zone of the interior to read the notes from the underground. Those notes have a most painful message, one which can only be read a bit at a time. If you do not believe in imprints then all is lost and you will never arrive at the generating sources of an affliction or symptom.

When can a fetus begin to feel pain? A better question might be this: when can the fetus signify pain? Research from K. J. S. Anand, a professor of pediatrics and neurobiology at the University of Tennessee, suggests this happens once the neural circuits are in place (Anand & Hickey, 1987). When Anand placed a needle into a fetus (in a process known as amniocentesis), the fetus grimaced in pain and its stress hormone levels rose dramatically. Not only did the baby suffer but, from our point of view, that suffering can be coded and registered in the memory system, thereafter awaiting connection. This is what we in feeling therapy are about — connection— restoring the missing links in the circuitry. Some serious diseases have been considered only in the domain of inheritance, muscular dystrophy being one of many. The cures for these afflictions have been slow in coming, in my view, because our emphasis has been on inherited factors rather than in-utero experience. If we don’t regard gestation as critical, our diagnoses and treatments are bound to be flawed.
Beyond gestation and birth, early childhood is important, as well, when attempting to identify the origins of later life problems, as evidence of imprinting can be seen in the experiences of very young children. There is a study by a Canadian group from the Douglas Mental Health University in Montreal that found when child abuse exists there is a change in the gene NR3C1 (glucocorticoid receptor gene) that affects how the child will deal with the abuse (McGowan et al., 2009). Measures of the gene’s function were much lower in abuse victims who eventually took their own lives. It appears that childhood abuse had changed the gene’s structure, making the gene less active. And these modifications endured throughout the children’s lives. Epigenetics had affected the function of the stress apparatus, what is called the hypothalamic- pituitary-adrenal axis (HPA), a complex part of the neuroendocrine system that controls reactions to stress and regulates many body processes, including digestion, the immune system, mood and emotions, sexuality and energy storage and expenditure.

Patrick McGowan, one of the study’s principal researchers, implies that the changes are more or less permanent; they alter the gene’s activity, leading to later illness and suicidal tendencies. When the NR3C1 gene is ineffective, it cannot produce the kind of alerting, galvanizing chemicals that help one fight through things. (Clearly, such trauma also diminishes an individual’s adaptive capacity, as I discuss below.) As a result, the body behaves as though it were constantly under stress. Moreover, what this research group believes is that mothers can affect the fate of their children even before they are born. Epigenetic changes passed on during gestation may contribute to depression and suicidal thoughts later on. So what looks like genetics, in reality, is a much more complex interaction between biological and environmental factors, an intricate “if-then” sequence which spans generations. What this may mean is that my notion of the imprint has to be wound way back. A more accurate framework holds that the experience of the parent leaves an imprint on the sperm and egg. One experiment by researchers at the University of New South Wales was done with male rats that were fed a high-fat diet (Ng et al., 2010). Their sperm seemed to change — that is, many of their babies had adult-onset disease, even though the mothers were normal. The children had a greater frequency for deviated insulin and glucose resistance, hence a propensity for diabetes, even though the fathers had no previous history of the disease. So what looks like pure heredity is actually a molecular memory of the experiential effects on that heredity. These research animals had defects with their on/off switches. This imprint endures and affects our physiology for perhaps a lifetime, sowing the seeds for later adverse effects on the kidney, liver, or heart. For humans, this may mean the tendency to be fat derives, in part, from what a father ate before conception. If that father over-ate as a child, his offspring have a much greater chance of being fat and developing diabetes.

Clearly, we need to change our focus in order to understand who we are. Our idea of what is heredity is rapidly changing. There are all kinds of intriguing possibilities. In one recent experiment, some animals that were raised in an enriched environment and appeared smarter had offspring who seemed to inherit that intelligence (finding their way through mazes more easily) even though they were not raised in an enriched milieu. Let’s be clear: when the parent had a chance to develop intellectually his offspring had a better shot at being smart. Somewhere, there are indelible and permanent marks on the sperm and egg.