by Arthur Janov
This article has been published in three parts. Part 1 was published in Inside Out, Spring 2010 and Part 2 was published in Inside Out, Summer 2010. This issue contains the complete list of references for this article.
This article was first published in JAPPPH, The Journal of Prenatal and Perinatal Psychology and Health, Vol. 23, Number 3, Spring 2009.
To summarize so far
There seems to be a time in gestation when pain or noxious stimuli impinge, but we are not yet able to produce our own gating chemicals, such as serotonin and endorphin, resulting in un-gated pain. When I refer to gating, I refer to electrochemical process that blocks the transmission of the pain message across the synapse. This residue will continue and may lead to bouts of anxiety later on in life. It becomes free-floating, unbound fear or terror. It can then be focused on elevators and a phobia is born. This is not due to heredity but rather to experience in the womb. Part of our in utero life, therefore, takes on hurt at a time when the system can do nothing about it; nevertheless, it affects all later development. At 30, we may suffer from panic attacks that began life in the very early months of our mother’s pregnancy. It is pristine, ready to spring forth whenever we are vulnerable. No talk therapy can affect it because it involves a vegetative, primitive nervous system that was only adequate to register pain and terror during womb life. This is a nervous system impervious to words; so insights leave it absolutely indifferent. That is why new experiences do not change the neurotic. She goes on having the same experience, the imprint, over and again. It is a sealed-off feeling that remains as part of a survival function.
The womb experience leaves us fragile for a lifetime so that any insult or lack of love in infancy and childhood weakens us all the more. And the imprint can dictate chronically low levels of serotonin. That is why we need drugs that work on lower brain centers below the intellectual in order to suppress these imprints for a time. So much severe mental illness has its causes early in our lives; and then nature later provides us with unusable intellectual tools to address them. All we have to do is let the primitive nervous system take charge and lead the way. It knows the path to liberation.
The hypothalamus controls many hormone secretions. It also controls two different nervous systems—the sympathetic, managing our aggressive, active tendencies, as well as the parasympathetic, managing the more reposeful, healing ones. A trauma such as low oxygen at birth can produce a dominant parasympathetic predilection that encompasses many biological parameters and also psychological ones, as well. In short, we have the makings of a depressed, passive, unassuming, held back personality; someone who is always reacting to the imprint of low oxygen input. Thus, everything becomes a problem, everything is too much, and there is a tendency to give up easily because there is a not a prolonged and continued aggressive, assertive response. These are the shallow, slow breathers, cold in the extremities, reluctant of personality, diffident and not a self-starter. We think we can change these individuals? Remember that the ensemble of all these biologic/psychologic responses are involved in survival strategies; not things picked at random because they were simply convenient.
We begin to understand a bit about later drug addiction, which always seems like such a mystery. We are slowly become aware that pain can be installed in the foetal system before she is born. It still needs quelling. It is generally of such high valence, to witness our patients reliving early trauma, that it is logical that one uses painkillers later on. Until we re-direct our focus earlier we shall never solve these human problems.
The University of California, Irvine is important in this research. Gary Lynch, a well-known neurobiologist and his colleagues (2008) there found that with very early trauma there was a later likelihood of memory problems. After years and years of suppressing feelings there seems to be a “caving in” of the externally oriented prefrontal area as neurons under constant pressure from the imprint begin to die. That is one reason why in early stress a memory structure in the brain, the hippocampus, tends to diminish in size. Mice that have their hippocampus surgically tampered with are much more excitable and prone to anxiety states. They do not adapt well. In short, one’s personal history, one’s neurobiologic memory, is a significant factor in what happens to her brain.
An experiment by Cirulli, Bonsignore, Venerosi, Valanzano, Chiarotti, and Alleva (2003) investigated neonatal rat pups born with reduced oxygen. Those females who were born with limited oxygen; rats delivered by cesarean section with reduced oxygen, were less loving to their offspring; slow to retrieve puppies and did much less licking. The author believes that this hypoxia results later in an “arousal deficit.” It seems that the animals had less energy and that possibly there were reduced dopamine levels in their systems. They were simply not aggressive or energetic. The traumatic birth of insufficient oxygen produced that. Though it was animals that were being researched, clearly, there are implications for humans. Too many of us, some report up to fifty percent do not get born with adequate amounts of oxygen. Depletion of energy, then, is one way that birth hypoxia shows its effects. It becomes an imprint. And that imprint can and does produce neglectful mothers; mothers who were not alert or watchful of their babies.
Research on dopamine has discovered important new information. Tiffany Field and her colleagues (2007) have studied dopamine levels in depressed mothers. Two groups were divided by high and low levels of dopamine. It was found that the babies they were carrying mirrored almost exactly the levels of dopamine and serotonin in the mother. Depressed mothers, in general, have higher stress hormone levels (cortisol) which means that pain/stress is a major component of the affliction. So it is no wonder that painkillers help alleviate depression in many cases. And it is also clear that those depressives with low dopamine levels do not fare as well in life. There is a biochemical send-off when babies are born with deficient dopamine levels. In short, there may later be vulnerabilities to depression in them, as well. And depending on life circumstance it will flower into full-blown depression when there is a repressive atmosphere in the home. This is why one child responds with depression and another does not. It depends on the chemical send-off. This notion of the send-off also helps explain some addictions in adulthood. Mothers who take tranquilizers or other painkillers are forcing the foetus to adapt to the input. Often a dose for an adult enters the foetal system, and is much too much to allow for adaptation. Later on, in adverse events, the now grown-up adult will seek out drugs; this time voluntarily (Nyberg, Buka, and Lipsitt, 2000).
Clearly, we cannot alter hormones in human for research on ethical grounds, but animal experiments show that over-stimulation of the foetus can alter its growth hormone output. Sedatives given to the mother during pregnancy increase the chance of later drug addiction in the offspring. Anand (2007) has concluded that imprinting at gestation or birth is far more predictive of later addiction problems than the socioeconomic status of the person. His view is that the critical window for trauma is just before and just after birth. Here adverse events leave an indelible mark for a lifetime. The field of psychology is coming around to the notion of imprint. Once that is accepted it will lead us back in history to when and how the event was sealed into the nervous system. We will no longer focus on the here-and-now to understand the human condition.
The concept of the imprint is critical to my theory, for it means that very early preverbal events control our destiny. It means alterations in the biologic system even down on the molecular level. And when later there is catastrophic illness we should be alert to possible molecular origins. Generally, the more catastrophic the imprint is, the more catastrophic the illness. The symptoms will occur deeper in the system in accordance with where deep-lying imprints are stationed. My rule is: a brainstem imprint results in a brainstem reaction/symptom, hence major disease; dangerously high blood pressure, for example.
And we should not forget the concept of the critical window, the time when the input is most needed to fulfill basic need, oxygen, for example, and the time when deprivation engenders the most widespread effects. That window cannot be changed. It is evolutionary and biological, predetermined in our DNA. We get one shot at fulfillment, not several. It cannot be made up for. The greatest painkiller that exists for us is parental love. When that is missing we hurt—for a lifetime.
Perinatal insult has lasting results, particularly in the dopaminergic (alerting/vigilance) system. This is often involved in learning disorders and attention deficit disorder. It is also a factor in later schizophrenia. Children of women, who undergo an extremely stressful event during the first month of pregnancy, are more likely to develop serious mental illness later on (a death of a close relative, for example; JAMA, 2008). The time when the baby is getting organized as a human being is when even slight disruptions in development can have catastrophic effects later on. One of the possible results is autism. (See the work of the Dutch investigator, Annemie Ploeger). It would seem that stress provokes the increase of stress hormones in the pregnant woman. This is not a benign event because that may alter the baby’s developing brain, as well. It is clear that there are different critical windows during gestation so that a trauma to the mother/foetus in the first month will have different effects than a trauma in the last month of gestation.
For example, birth weight reduction is most severe when steroids are administered in the late stages of pregnancy. And birth weight change usually indicates problems in foetal evolution (i.e., trauma). It is known in animal research that stress hormones given during pregnancy will elevate blood pressure in the offspring. There is evidence, as well, that this happens in human evolution. When stress is evident in the last month of gestation there is a good chance of high blood pressure later on. At the risk of “drowning the fish” it has become clear that life before birth is paramount in later behavior and symptoms; so much new information and research continually points in this direction. When we have inexplicable symptoms or behavior deviations later in life we need to search out prenatal events to see what impact they had. This is truly the new frontier.
A study by Finnish scientists Huttunen and Niskanen (1978) investigated children whose fathers died either while the mother was carrying them or during the first year of the child’s life. The offspring were examined over a thirty-five year period using documentary evidence. Only those who lost their father while the child was in the womb were at increased risk of mental diseases, alcoholism/addiction, or criminal behavior. Clearly, the emotional state of the mother was affected and that possibly had lifelong deleterious affects on the child. The results of this study suggest that the emotional state of the pregnant mother has more long-term effects on the child than the emotional state of the mother during the years following birth.
And when we are investigating addiction, we must pay attention to womb-life. We know from animal experiments that those deprived of touch and love right after birth tend to consume alcohol later on when offered, versus those normal, loved animals who refuse it. A study with monkeys by Barr, Newman, Becker, Champoux, and Lesch, et al. (2003) demonstrates this point. Those more stressed early on were more likely to drink alcohol. Eighty rhesus monkeys were investigated; half were separated from their mother at birth. This group responded to any later stress with 25% more stress hormone release. Later both groups were offered drinks with alcohol in it. One fifth drank nothing. Among those who did consume alcohol, those with the higher levels of cortisol before the experiment were the heavy drinkers. Those monkeys weren’t saying any irrational things to themselves; they reacted in terms of their history. We may ascribe alcoholism to genetics, but this study makes clear that those who were unloved early in life took to alcohol.
The point I have been making for the last forty years is that traumas while being carried and at birth create new set points for important chemical/hormone release. These may well be accompanied by long-term changes in the feeling/limbic system so that there may already be a tendency to overreact because there is a resonance factor where a current event can enter the brain at a certain frequency and trigger off similar feelings within the same frequency in the limbic system (helplessness, for example); and also because the bar for reaction is already quite low due to the imprint which has compromised the nervous system.
Supporting evidence for our theory has come from D. I. W. Phillips and Alexander Jones (2006) who researched fetal programming. They presented their results to the Journal of Physiology Symposium. They use the term “set points,” and maintain that early trauma can permanently alter basic physiologic set points. This means deviations in our physiology and psychology. Studies are coming in quite fast now confirming this point, specifically, that anxious pregnant mothers set up higher than normal levels of stress hormones in the baby. And this high level can be the predictor of later serious illness.
The foetus has an environment—his mother; and he is reacting to that environment, having key experiences just as he would after birth. He is learning. Just because we don’t see it doesn’t mean it doesn’t exist. But because we don’t see it, and because we never perfected the tools to observe it, we have fashioned psychotherapies that ignore it. Because we do now have the tools, we are able to observe this first hand. When we understand that feelings of hopelessness and helplessness underlie many of the deep depressions we can then understand how deep the base of it all is. Those feelings can occur to the foetus before birth when the input to the baby from an anxious mother cannot be stopped so that he is overwhelmed before he sets foot on this earth. That feeling, not yet articulated, shapes both physiology and psychology, and is shaped by it. We therefore cannot undo what heretofore was called “endogenous depression” with a current focus. We need to address origins of feelings. Suppose we learn that in many cases of acute anxiety there is not enough residual serotonin in the person’s system. So we add chemicals that boost serotonin (Prozac) and the person feels better, somehow normalized. We now need to roll back the clock to see why that serotonin level was so low, and we may find grave traumas in the sixth month of gestation when serotonin production in the fetus was being organized. When the patient relives those kinds of traumas there is again a normalization (see our research on imipramine binding as discussed in my book, Primal Healing).
We need to understand how deep “deep” is, because otherwise we shall be skimming the top in depression, leaving the basis to continue its destructive path. That means not changing the critical set points. I am suggesting that nothing can alter those set points, which may be too high or too low, except for fully addressing and reliving origins. The adult system is now adequate to tolerate critical levels of pain involved in those early systems. Current psychotherapeutic tools simply cannot go deep enough to touch origins. It is no accident that many studies now show that in recalling a memory the same neurons are reactivated as originally involved. As I noted earlier, in reliving we are attacking the same memory neurons. Many of these neurons are located in the limbic system, and the hippocampal cells where memories are created and stored is heavily involved. This is the area of the brain where Alzheimer’s disease is concentrated. Memory formation and retention relies on this structure (as well as others).
What is current in science is the tendency is to avoid any leap of faith, from the facts to possibilities. For the most part I agree. However, there has to be a middle ground; there has to be a space for leaps of faith but as well as observable truths. This is uncertain territory, I know. But we need to make an effort to both have those leaps into imagination coupled with what we know in science. Observation is still a valid mode in science.
My thesis is that there are predictable long-term effects of prenatal, neonatal, and infancy experience. This is not the “shoemaker sees only shoes in the world,” but a need to emphasize a neglected aspect of the human condition. If we are to fashion a truly scientific psychotherapy we need both; I mean if we did not do research into cortisol levels or imipramine binding (measuring levels of serotonin in the system) we would not know exactly how a therapy can change the human being. We would not know what aspects of a psychotherapy are valid and which are not. For example, thirty-five years ago I thought that forced heavy breathing was essential to our therapy. Now, as a result of research and the refining of our techniques we know that deep breathing as a therapeutic option is not necessary, and can be dangerous—the same with forcing patients or subjects to delve into reliving a birth-event when the neurologic system is not ready.
But with a bit of a scientific background, one would know that we cannot breech evolution and hope to succeed; that integration is the be-all and end-all; connection (bottom-to-top; right- brain-to-left), is the goal. We cannot integrate massive pains unleashed prematurely; it is simply not possible. Sometimes the patient is getting worse while the therapist and patient swear they are making progress. As therapists we should never trump evolution in our work.
My patients have been reliving birth traumas for a very long time. These events are often minutely measured by us. We used an electronic rectal thermistor and blood pressure cuff fixed during the session to observe the rises and drops in body temperature, which were often significant; beyond what a physician might see except in cases of extreme illness. I had trouble believing what I saw originally to the point of threatening to discharge patients who continuously fell into reliving birth. The UCLA neurology department told me it was not possible. Well, it is! And not only is it possible but the birth trauma lays on an already heavy substrate of adverse events during gestation. And this substrate can determine a good part of our adult life, including how long we live.
The problem has been that we have equated memory with what we remember cerebrally, when there is an important physiologic memory that exists before we have thoughts or words to explain the memory. But what do we call it when heavily depressed patients enter a session with two degrees less in their body temperature; and after a session the readings (and the her body) normalize? When we see this month after month and year after year we are building an objective case. The problem, then, is to find out why this is so; and then further to find out how to treat and normalize this problem.
Our UCLA Pulmonary Laboratory Study
At the UCLA Pulmonary Laboratory we wired two patients to a number of instruments, oxygen levels, carbon dioxide, and blood samples every three minutes while they relived, as it turned out, oxygen deficit at birth, something we had not planned at all. Again, we had no preconceived notion of where the participants had to go. Neither patient observed the other so we had a rather pure experience on the part of both men. After the reliving, we did another experiment where each patient mimicked the Primal in every way with the same movements and breathing except for being in the past. Both almost fainted after three or four minutes in what was clearly a hyperventilation syndrome (clawed hands). While in the past feeling they breathed very deeply, I call this “locomotive breathing” because that is what it sounds like and seems to emanate from the brainstem––medulla, for about twenty minutes with no hyperventilation. What the researchers from the pulmonary laboratory found was that when the patient was back in the old feeling and its context of anoxia at birth the body needed oxygen; the patient was “back there” in every way, not the least of which was physiologically. It was evidence of the veracity of reliving; that patients can and do go back in time. And they not only go back psychologically but in a complete biologic state. The corollary to this is that the early need for love stays the same and does not change throughout our lifetime. We seek symbolic, substitute fulfillment but it is never fulfilling and compels us to go on seeking more and more, always in vain. The critical time when need must be fulfilled has past.
What we found at UCLA was that despite the heavy prolonged breathing the acid-alkaline balance did not change. The conclusion of the investigators, who were not Primal based, was that no other factor other than memory could account for the results. In short, the life-and-death memory was real. It was imprinted. Despite the fact that the blood oxygen was normal in the room the brain was sending signals of a great lack of oxygen, and the heavy breathing ensued. There was no hyperventilation syndrome because the whole system was back in history re-experiencing a key trauma and urgent need.
This is important because it can open up a whole universe to us about the depths of man’s unconscious. It confirms that very early experience is impressed into us; not just as a memory but also as a wound that needs healing. It endures. We can directly observe anoxia and hypoxia. Reliving is a real event; the baby cries during a session can never be repeated by the patient after it. Again, that is because his entire neurophysiology is in the past, in a specific time and place and undergoing a specific experience. The marks that originally appeared during the birth trauma may again appear in a later session. It is clearly not a simulation. In other words, the past and its neurobiology remain encapsulated inside of us. This is exactly what can account for a number of lingering diseases in adult life. What is remarkable is that it never changes; it is impervious to experience. No matter how much approval an actor gets he always needs more. It is why I maintain that only being in the context of an old traumatic memory can be curative. Consider, in the session, despite the adequate oxygen in the room the brain is signaling a serious lack of it and the body responds accordingly, gasping for air, all to do with the memory and not reality. Therein lies the tale. We are continually responding to old imprinted memory despite current reality.
The body smokes to kill the pain of anoxia or it takes drugs beyond all control of the upper reaches of the cortex. It is reacting to internal events. That is why lectures on smoking do very little good. The little girl inside the woman is taking drugs to kill her pain, something we never see. Something the person never sees, being disconnected as he/she is. We must understand that resonance is a two-way street. At first there is the imprint, followed by compounding events that reinforce and seal it in. Then later there are ideas to resonate with the original imprint. If the original imprint produced a physiologic deviation, as it nearly always does, then when we have the ability to develop ideas, those ideas will follow suit; that is, they too will be deviated so that perceptions are askew. In brief, the traumatic information from below will resonate higher up and will distort those thinking processes, as well. So it is not just that ideas are warped or bent. It is that those ideas and perceptions continue on from the imprint. The whole neural circuit is “off,” or deviated. On an emotional level we often see the sex drive distorted, as well. An example of this resonance is found in a young man who was suicidal when he came to us. His girlfriend left him for his best friend while his closest male friend was killed in battle. He felt hopeless and helpless; there was nothing he could do about either situation. This current situation with its feelings left him in great anxiety and too weak to do anything about it; all he could think of was killing himself. That resonated down the chain of pain to the deepest brain levels and dredged up the same feeling with a great deal more emphasis and power.
Originally, there was nothing he could do to get born; the odds were insurmountable because his mother was heavily anesthetized, and of course, so was he. Biologically he was helpless and hopeless, as yet completely unarticulated feelings. But feelings don’t have to be articulated to exist physiologically. They can only be articulated when we have the brain capacity for it; that is, when the prefrontal neocortex is sufficiently developed. But there it was—the resonated part of the whole feeling. Further, what was also dredged up was the notion that the only way to end the agony was death (i.e., suicide). His method of choice: painkillers. It was most certainly the only way out of the pain originally, a biologic memory which was whisked up with the feeling of hopelessness. None of this was thought out—but was inescapable, nevertheless. So the current situation left him with no alternative forms of behavior, duplicating the original situation where there were, indeed, no alternate forms of behavior. That is why he could not think of anything else to do. Resonance is what makes us behave redundantly, and causes us to duplicate our earlier trauma over and over again.
In the case of anxiety, imagine a current situation where someone refuses to honor an application, and it sets off inordinate anxiety. Why? The situation resonated with very early terror, which is dredged up and inserts itself into the person’s current situation. Anxiety is the lower level aspect, the primal aspect, of the overall feeling of, “I can’t get through … to you.” It is current, resonates with parents whom could not be reached emotionally, and finally to the birth where the baby could not get through. The essential part of this is, “I can’t get through.” That is the base. Later on, we add whatever circumstances compounds the feeling. It gets to be anxiety when the gating system is inadequate to stem the access to lower brain levels. It is very much like need. At first there is pure need for love, for touching and holding, for caressing and warmth. When that is deprived very early on the need becomes the “need for.” It can be the need for drugs or food or gambling. But that is derivative of basic need; so when we treat these afflictions we must keep in mind that it is at bottom a real need we are dealing with.
Getting straight with oneself, as a result of reliving the very early imprints, generally will correct strange ideas and perceptions, not the least of which are psychotic notions. I have seen a psychotic relive a deep trauma and come out of it with an explanation for her delusions. “Those devils that I thought were pursuing me were my deep, bad thoughts and fears of my parents.” In this case we used tranquilizers for a time to allow her to feel and experience aspects of the imprint without being overwhelmed by the totality of it all. What we do with medication is use it sparingly in order to feel. What conventional therapy does with medication is use it to block and suppress feelings, a very different approach.
Research reported in the Sept. 26, 2000, Proceedings of the National Academy of Sciences, indicates that when a memory is activated, the visual cortex is busy when a memory includes visual scenes, just as auditory memories light up the auditory cortex. Those with heavy emotional content activate limbic structures. In other words, memory is total and needs to be when we go back and visit our past. Too often recall is an intellectual exercise bereft of the emotional connection that would make for personality change. The report indicates that parts of the frontal brain recruit these secondary areas to integrate the totality as a memory. It is the assembly point where aspects of our history join to become whole and to make sense of disparate aspects of our history. If one goal of psychotherapy is make a person whole, then memory must be complete and connected.
Without proper cortical connection the energy is not dissipated and is rerouted back into the system creating one symptom or another from tendencies to hypothyroidism to asthma. Though there may well be genetic components, I submit that the symptoms may not become manifest without a residue of trauma. One way we know this is that reliving these traumas often rids the person of troubling symptoms. One of the most important by-products of this connection is that stress hormone/cortisol levels are reduced permanently. When we consider that high stress hormone levels impact so many symptoms from nightmares to depression, from palpitations to hypertension, this finding is of some import. Cortisol levels do not drop over time without deep feeling.
What is curative is that repression is lifting and the system is again reacting, as it should have originally. The pain is finally traveling to its proper destination––connecting with frontal cortical structures producing conscious-awareness. It is not simply cortical awareness, lacking in feeling, but conscious-awareness derived from feeling. Thus, it is unconsciousness that is the culprit, and consciousness that is the savior––and that unconsciousness is the result of repression; and that repression is a function of pain; all an automatic process.
As our patients’ defenses weaken, great pain begins its march to prefrontal areas. And when the feelings lock-in and connect the system can finally relax. All vital signs fall below baseline readings. Until there is this lock-in, the cortex may continually ruminate about this danger or that until sleep becomes impossible. Low-lying imprinted terror in the brainstem can activate cortical centers creating outbursts of unusual thoughts: “There’s no space for me.” “I am stuck and no one is helping.” These often are birth statements, emanating from the birth imprint that is consciously unknown to the person. The latest evolving cortex must deal with the input in some fashion or another. It must make it “ego-syntonic,” comfortable and not alien to the self. What we do in our therapy is take away the rerouting symbolism, “I am stuck––in my job, marriage, etc.,” and help the patient place it in direct context, “I am stuck in the canal and I’m in danger of dying.” And as I write this I am aware of how strange and perhaps unbelievable all of this seems. But this is not an intellectual proposition stemming from some ideas of mine, but rather the result of careful observation and measurement over 40 years.
Returning to our research at the UCLA Pulmonary Laboratory, one of the young men, after reliving a birth sequence, suddenly went into apnoea and stopped breathing for a full minute. This was not a voluntary act. He replicated what happened to him at birth. It was a wordless reliving which achieved some kind of awareness that was not totally verbal. In fact, it was a connected sensation that heretofore played out in his sleep where he suffered from periodic apnea. If we relive an early terror before we have words to wrap around it, it still can be a connected event. It has entered awareness. Afterward, it is no longer a vague, inexplicable anxiety. It is what it was—terror.
We are still those primates, but with a cortex added on: we’ve put on a thinking cap permanently. If monkeys can be neurotic without words, so can we. If they can be addicted, so can we. Because these monkeys were deprived of love early on, they later felt the need to comfort their pain, and did so with alcohol. The basic pain and physiology of two primates, humans and monkeys, are pretty much the same. We hurt in the same way with basically the same physiological equipment. It is clear from so many similar animal experiments, and there are literally thousands of them, dating from the early work of Harry Harlow to the present, that words do not matter and cannot permanently ease the pain.
Ideas arrived hundreds of millions years after our instincts and feelings. Ideas are not the problem; they signal the problem, providing the words for it all. Changing ideas is not as important as feeling feelings in psychotherapy. It is those hidden feelings that so often drive us. Let us not abandon the past in an effort to modernize current practice. Memory is medicine. Let us not eschew critical medicine in order to cure our afflictions.
In sum, there is a qualitative difference between events that happened to us while being carried in mother’s womb, and those events that happened after birth. It is a matter of irreversibility. What happens to us during gestation imprints a now-print memory that endures as if that were our genetic legacy. The physiology and later psychology revolve around this imprint. There are little or no compensating mechanisms that will right the ship. It adjusts to the imbalance and goes on from there. If the imprint includes a general passivity then the vital signs, temperature and blood pressure will accommodate themselves to this new state. After birth there is often the possibility to correct the imbalance. So, accommodations, which the body makes while we are in the womb, take on a genetic focus because it seems to occur so early in life and remains such a force.
Thus far we have been talking to the non-verbal brain! This brain is one that contains our history, our pain and our feelings, and ultimately, the one that can finally liberate us. We need to speak that language—one without words. We have to convince the brain that spouts words and ideas that it is necessary to go back to early life and relive—that lack of love—feelings that were too much to feel at the time. We have to convince that thinking brain to let go, let the lower brain systems emerge and breathe the air of freedom. It can be done. A cure is possible.
Dr. Arthur Janov is the Director of The Primal Center, Santa Monica, California. Creator of Primal Therapy (www.primaltherapy.com/) Dr. Janov is a prolific author, educator and clinician, whose recent works focuses on the prenatal and perinatal periods. This article is a portion of an upcoming book. Contact information: email@example.com or (310) 392-2003. Free access to Dr. Janov’s recent essays can be found on his blog at: http://www.arthurjanov.com/.
Addis, D. R., and Schacter, D. L. (2008). Constructive episodic simulation: Temporal distance
And detail of past and future events modulate hippocampal engagement. Hippocampus, 18, 227, 237.
Anand, K. J. S. and Scalzo, F. M. (2000). Can adverse neonatal experiences alter brain development and subsequent behavior? Biology of the Neonate, 77(2), 69-82.
Barr, C. S., Newman, T. K., Becker, M. L., Champoux, M., Lesch, K. P., Suomi, S. J., Goldman,
D., and Higley, J. D. (2003). Serotonin transporter gene variation is associated with alcohol sensitivity in rhesus macaques exposed to early-life stress. Alcoholism Clinical and Experimental Research, 27(5), 812-7.
Briley, M. S., Raisman, R., and Langer, S. Z. (1979). Human platelets posses high-affinity binding sites for 3H-imipramine. European Journal Pharmacology, 58(3), 347-348.
Bygdeman, M. and Jacobson, B. (1998). Obstetric care and proneness of offspring to suicide as adults: Case control study. British Medical Journal, 317(7169), 1346-9.
Cannon, T. D., Yolken, R., Buka, S., and Torrey, E. F. (2008). Decreased neurotrophic response to birth hypoxia in the etiology of schizophrenia. Biological Psychiatry, 64(9), 797-802.
Canoy, D., Pouta, A., Ruokonen, A., Hartikainen, A. L., Saikku, P., and Järvelin, M. R. (2009).
Weight at birth and infancy in relation to adult leukocyte count: a population-based study of 5619 men and women followed from the fetal period to adulthood. Journal of Clinical Endocrinology and Metabolism. Retrieved March 2009 from: http://jcem.endojournals.org/
Cirulli, F., Bonsignore, L. T., Venerosi, A., Valanzano, A., Chiarotti, F., and Alleva, E. (2003).
Long-term effects of acute perinatal asphyxia on rat maternal behavior. Neurotoxicology and Teratology, 25(5), 571-578.
Côté, F., Fligny , C., Bayard, E., Launay, J. M., Gershon, M. D., Mallet, J., and Vodjdani, G. (2007). Maternal serotonin is crucial for murine embryonic development. Proceedings of the National Academy of Sciences of the United States of America, 104(1), 329-34.
Diego, M., Field, T., Hernandez-Reif, M., Schanberg, S., Kuhn, C., Gonzalez-Quintero, V. H., (2009). Prenatal depression restricts fetal growth. Early Human Development, 85(1), 65-70.
Fendt, M., Lex, A., Falkai, P., Henn, F. A., and Schmitt, A. (2008). Behavioural alterations in Rats following neonatal hypoxia and effects of clozapine: implications for schizophrenia.
Pharmacopsychiatry, 41(4) 138-45.
Field, T. (2001). Targeting adolescent mothers with depressive symptoms for early intervention.
Sage Family Studies Abstracts, 23(3), 275-407.
Field, T., Diego, M., Hernandez-Reif, M. and Fernandez, M. (2007). Depressed mothers’ newborns show less discrimination of other newborns’ cry sounds. Infant Behavior and Development, 30(3), 431–435.
Field, T., Diego, M., Dietera, J., Hernandez-Reifa, M., Schanbergb, S., Kuhnb, C., Yandoc, R.
And Bendelld, D. (2004). Prenatal depression effects on the fetus and the newborn. Infant Behavior and Development, 27(2), 216-229.
Huttunen, M. O. and Niskanen, P. (1978). Prenatal loss of father and psychiatric disorders. Archives of General Psychiatry, 35(4), 429-31.
Hoffman, E. and Goldstein, L. (1981). Hemispheric quantitative EEG changes following emotional reactions in neurotic patients. Acta Psychiatrica Scandinavica, 63(2), 153-64.
Huot, R. L., Brennan, P. A., Stowe, Z. N., Plotsky, P. M., and Walker, E. F. (2004). Negative affect in offspring of depressed mothers is predicted by infant cortisol levels at 6 months and maternal depression during pregnancy, but not postpartum. N.Y. Academy of Science, 1032, 234-236.
Jacobson, B. and Bygdeman, M. (1998). Obstetric care and proneness of offspring to suicide as adults: Case-control study. BMJ, 317, 1346-49.
JAMA and Archives Journals (2008, February 5). Severe stressful events early in pregnancy may be associated with schizophrenia among offspring. ScienceDaily. Retrieved January 22, 2009, from http://www.sciencedaily.com /releases/2008/02/080204161433.htm
Kaplan, L., Evans, L., and Monk, C. (2008). Effects of mother’s prenatal psychiatric status and postnatal caregiving on infant biobehavioral regulation. Early Human Development, 84(4), 249, 256.
Lowery, C. L., Hardman, M., Manning, N., Hall, R., and Anand, K. (2007). Neurodevelopmental changes of fetal pain. Seminars in Perinatology, 31(5), 275-282.
Lynch, G., Rex, C. S., Chen, L. Y., and Gall, C. M. (2008). The substrates of memory: Defects, treatments and enhancement. European Journal of Pharmacology, 585, 2-13.
Mill, J., Tang, T., Kaminsky, Z., Khare, T., Yazdanpanah, S., Bouchard, L. et al, (2008).
Epigenomic profiling reveals DNA-methylation changes associated with major psychosis. American Journal of Human Genetics, 82(3), 696-711.
Nyberg, K., Buka, S. L., and Lipsitt, L. P. (2000). Perinatal medication as a potential risk factor for adult drug abuse in a North American cohort. Epidemiology, 11(6), 715-716.
Phillips, D. I. W., and Jones, A. (2006). Fetal programming of autonomic and HPA function: do people who were small babies have enhanced stress responses? Journal of Physiology, 572(1), 45-50.
Ponirakis, A., Susman, E.J., and Stifer, C.A. (1998). Negative emotionality and cortisol during adolescent pregnancy and its effects on infant health and autonomic nervous system reactivity. Developmental Psychobiology, 33, 163-174.
Ranalli, P. (2000). The emerging reality of fetal pain in late abortion. National Right to Life
News, 27(9). www.nrlc.org
Singer, D. (2004). Metabolic adaptation to hypoxia: Cost and benefit of being small.
Respiratory Physiology and Neurobiology, 141(3), 215-228.
Singer, D. (1999). Neonatal tolerance to hypoxia: a comparative-physiological approach.
Comparative Biochemistry And Physiology. Part A, Molecular and Integrative Physiology, 123(3), 221-34.
Scripps Research Institute (2007, September 6). Specific neurons involved in memory formation identified. ScienceDaily. Retrieved 1/20/2009.
Seckl, J. R. and Meaney, M. J. (2006). Glucocorticoid “programming” and PTSD risk. Annals of the N.Y. Academy of Science, 1071, 351-378.
Thompson, P. (2007). “Down will come baby”: Prenatal stress, primitive defenses and gestational dysregulation. Journal of Trauma and Dissociation, 8(3), 99-113.
University of Pennsylvania (2005, December 25). Researchers know what you were about to say; fMRI used to detect memory storage. Science Daily. Retrieved 1/18/2009.