Life Before Birth: How Experience in the Womb Can Affect Our Lives Forever

by Arthur Janov, Ph.D.

This article will be published in three parts. Part two will appear in the Summer issue of Inside Out 2010, part three will appear in the Autumn issue.

This article was first published in JAPPPH, The Journal of Prenatal and Perinatal Psychology and Health, Vol. 23, Number 3, Spring 2009.

Introduction

When I first wrote about how birth trauma and prenatal experience affected adult behavior decades ago, it was considered “New Agey.” Now, there are literally hundreds of studies verifying this proposition. There seems to be little question now that a pregnant woman’s mood and physiology can produce long-term effects on the offspring. That means us.

Here is a simple example of the new research. Dr. Daniel Schacter, psychologist at Harvard University, reported on a study where participants watched bits of a TV series and then had their brainwaves measured (Addis and Schacter, 2008). The researchers found when people remembered the TV event, the single brain cell signature was the same as in the first viewing. They reported that it seemed like a reliving; which of course, has been my position.

What do you call it when a memory brings up one’s exact history with its precise early physiology? When there are certain triggers, the brain conjures up its history, intact. That is why our behavior is so compulsive and unwavering; our history motivates us all of the time. We are largely victims of our deep unconscious brain. And that brain is a beehive of activity all of the time, even in a resting state. For years we have been measuring the brain when given a new task. Lately, work is going on with the brain in its resting state. What is it like? Well, it doesn’t rest much. Parts of the feeling/limbic brain (hippocampus) are hyperactive, chewing up a lot of energy, glucose and oxygen. It seems to me that as we rest or when we drop off to sleep, our feelings get relayed in order to be integrated with higher centers; the (medial) prefrontal cortex of the brain is also active. It would seem that when we have a good deal of repressed pain and feelings, the brain is required to keep constantly active. I have called that the reverberating circuits. Researchers now call that state the “default mode.” It works even in lieu of a task. Or, might the task of the hippocampus is to deal with submerged feelings that interfere with our sleep and rest? The default mode seems to be updating memories and turning short-term ones into long-term ones. Its job is to sort out what is important and eliminate the rest so that the brain is not overwhelmed with information.

It also can produce daydreaming where we are lost in mental images even while driving a car across the city. The hyperactive lower level has come up toward the top to replace or diminish our external focus. It may be that in default mode meditation is suppressing the active feelings, producing a spurious sense of calm.

Thoughts and beliefs are the final station of a process that can begin deep in the brain, very remote in history (personal and ancient, traveling upward and forward until feelings meet with their counterpart). In a way, then, we do every day what we do in sleep: we revisit our ancient phylogenetic past and also our ontogenetic past and then move forward in time to the present. We are clearly evolutionary creatures, creatures of needs, especially those that were not fulfilled. We are bedeviled by them all of our lives. In our therapy when we have a very disturbed patient, we may use tranquilizers for a time to block the deepest aspect of an imprint, thereby allowing the person to focus on the present and perhaps childhood. In our therapy, we also visit our ancient and remote past but in reverse order; current events first, childhood second and birth and gestation last. That order cannot be forgotten. It is sacred …

There is increasing evidence that real memory is organic; that is, recalling a memory invokes all of the identical neurophysiologic reactions. If there is an incomplete memory, I call it an abreaction; this can affect the healing process. A study by The Scripps Research Institute (2007) found that recalling early events did exactly that; brought forth the same neurons that existed in the learning or imprinting of the event. The investigators stated that “reactivated neurons were likely a component of a stable engram or memory trace.” (¶ 4) Let us not forget that those neural circuits affect a number of body/physiologic reactions, as well.

Although I have been writing about reliving for many years there is new evidence from University of Pennsylvania (2005) that “as you search for memories your brain progressively comes to resemble the state it was in when you initially experienced the event” The more fully an event is experienced the deeper and more lasting its effects. The same is true for reliving. The insights are broader and deeper. It is not the insights that make us well. The neurotic isn’t unwell because she lacks insights. They are the top-level aspect of a feeling and are integral to it. As one experiences deep feelings, one becomes conscious of what the feeling did to drive symptoms and behavior. It is a self-explanatory process. One then knows what the unconscious force is that gives one migraines or high blood pressure or irritability.

An event is registered at the highest level of brain function possible. So at four months of gestation, trauma will be registered at the brainstem level. There will be a highway with various detours going upward and forward informing higher levels about what is happening lower down, each level making a contribution in its own idiosyncratic language to the entire feeling.

According to a study by C. L. Lowery and colleagues, sensory fibers proliferate at 20 weeks of gestation. Thalamocortical projections mature at about 29 weeks, although the thalamus seems to be operational at around 20 weeks. Lowery and his team point out that “Evidence for the subconscious incorporation of pain into neurological development and plasticity is incontrovertible.” (Lowery, Hardman, Manning, Hall and Anand, 2007, p. 275) That important statement supports a position I have held for many decades; the unconscious is not a dark, evil place but rather, something that is inhabited by imprinted events very early in our lives that endure.

In normal situations there is a smooth interpenetration of each level. When there is colitis, we often know that the imprinted cause is very early. It is also telling us when and how the information was obtained. But when there is a constant trauma, during gestation, at birth and infancy and childhood, the barriers no longer work and the information from below surges to the top. That is why in our pre-psychotics we see them reliving birth in the first weeks in therapy. Their gating system is insufficient, damaged and cannot effectively hold back very early trauma. Their default mode is over the top. When we develop a therapy we need to keep all levels in mind so that we do not address the wrong one.

I want to go on with the notion of resonance; the idea that something in the present can trigger off or resonate with lower level imprints. I am positing the notion (still an assumption) that low level imprints have a distinct signature in terms of frequency. It may be that each level recognizes a relationship with one another in terms of a similar frequency. So that something we endured during womb-life, a mother heavily depressed and perhaps taking prescription medication, sends up through her nerve tracks nonverbal memories that then merge into what we undergo currently. That combined force then makes any reaction inappropriate. The problem thus far is that we have neglected deep brain imprints, focusing on knowable events and believing that the current situation is the one to concentrate on, when in reality it is but a fraction of the problem.

And indeed, in terms of Schacter’s research on epileptic surgery patients, the neurons involved in the memory may be the very same neurons involved in the original situation. Schacter threaded fine electrodes down in the brain of the patient. These electrodes could pinpoint small brainstorms at their origins. And they could make minute measurements during recall. The lesson? We can relive past events in their entirety precisely as they occurred. What is very new in all of this is how early an experience can affect our later life. Think of the implications: that old memories reside in the same neurons (nerve cells) as were involved originally. That is why the neurotic cannot distinguish between past and present and sees reality through the prism of the past. For a number of reasons we have had good luck with treating epileptics, rarely failing. (Full discussion in my book, Primal Healing.)

Epigenetics: The Inheritance of Acquired Characteristics

There is something we must add to the theoretical mix: epigenetics, or said other way, how very early events in the womb and at birth can alter the genetic unfolding. One genotype, a single genetic predisposition, can give rise to many phenotypes depending on what happens to those genes during gestation. So what we might imagine is genetic, is genetic-plus what happens to us in the womb. I was so surprised early on in my therapy when long-term patients reported that their wisdom teeth descended. Now I understand it better.

In the early nineteenth century, a French scientist named Jean Baptiste Lamarck decided that we acquired characteristics from experiences that our parents underwent. Russian communists applied this to agriculture but, no matter, it was a widely discredited theory … until recently.  Now this avowed Marxist position may have been resurrected a bit. There is a new field called epigenetics that states pretty much what Lamarck believed. So what is the evidence? And what exactly is it? What Lamarck said was that individuals acquire characteristics as a result of their environment, and now, these characteristics can be passed on to the offspring.

Much of the research work in epigenetics has to do with diet; a mother’s diet influences the offspring’s physiology. Epigenetics has to do with how genes are regulated and influenced by the experience of the baby. I believe it has more to do with the fetus who resides in the womb; that his experience is influenced forevermore by the mother’s diet but also by her moods, her anxiety and depression.

Has the genetic switch been delayed or was it premature? This can happen without making a radical change in the gene itself but rather in how it is expressed, whether it is shut off or on. What we are discussing is how a mother’s interaction with her environment can pass this on to her offspring. I think we need to understand that a fetus in the womb is always trying to adapt to his environment and that his genes will evolve and be expressed depending on that adaptation. For example, a mother who is anxious and who has depleted much of her serotonin supplies cannot fulfill the young fetal need for his own serotonin supplies (fully discussed in a moment). He may well grow up deficient in inhibitory or repressive capacities and be an anxiety/impulsive case forevermore; this can evolve into attention deficit in his youth. There may be a continued inability to have a cohesive cognitive ability. I think it is important that all this occurs while the fetal brain is rapidly developing and needs proper input to evolve normally. An anxious mother is so agitated that the neuronal input into the baby she is carrying is so extreme that he cannot adapt and integrate this input. Thereafter, this is the kind of person who cannot accept too much stimulation because the internal input is so great that anything from the outside, such as two term papers due immediately, can be overwhelming.

To get an idea of how early all this may begin, there is a study by the University of Miami School of Medicine that states that: “A review on (maternal) prenatal depression effects on the fetus and newborn suggests that fetal activity is elevated, growth is delayed, low birth weight common.” (Diego, et al., 2009, p. 70). Newborns of a depressed mother show a profile that mimics the mother’s prenatal state, including her physiologic state. This includes higher stress hormone levels, lower levels of dopamine and serotonin, and greater right frontal brain activity. What I think this means is that the right/feeling brain is forced to be hyperactive to deal with emotional push. It is, after all, the right prefrontal brain (orbitofrontal area) that maintains a history of our feelings and has a more internal focus.

To summarize: Higher resting levels of stress hormones in the carrying mother can already have an effect on the later life of the offspring. It already presages the constant need for tranquilizers because the early imprint has lowered levels permanently. Then with even minor setbacks later on, the resonance factor can compound the pain level so that taking painkillers is a matter of urgency.

The concept of epigenetics has import for diagnosis. For example, one of my patients was told that she had a genetic vulnerability, very much like her mother had. It led to a diagnosis of a “very serious autoimmune disease.” If it were seriously genetic, as the doctors believed, then any chance to change her state would be close to nil. What this does is prevent us from seeing or investigating beyond the inheritance to factors that may have been equally important; what happened to the baby while being carried? Further, if there was something that altered the immune state while in gestation, perhaps one can relive and connect to it, consequently affecting that imprint. Thus, it may be as a result of an experience, rather than a genetic inheritance, that is ultimately significant. This patient did relive her traumatic birth, and, perhaps, that helped her make some progress against the disease. This kind of change happens, again, because in reliving it is possible to gather up associated feelings and sensations that lie even below the later trauma but which may be related to it through frequency resonance.

There are some serious diseases that have been considered only in the domain of inheritance; muscular dystrophy is one of many. Perhaps the cures for these afflictions have been slow in coming because our emphasis has been on inherited factors rather than experience. If we don’t look at gestation as critical, our diagnoses are bound to be skewed.

Womb-life and Serotonin Output: The Origin for Later Mental Illness

What I shall be discussing is our life in the womb and how it affects the rest of our lives. Animal research sheds more light on all this. Let’s begin with the mouse and her womb-life. It is only after several months of gestation that the fetus produces adequate amounts of inhibitory/repressive chemicals such as serotonin. A mouse fetus does not make its own serotonin until close to the third trimester. It seems like the mother supplies what is needed until the baby can take over. But when the mother is low on supplies, she cannot fulfill what the developing baby lacks.

Now if we extrapolate a bit to human mothers … but first a caveat: It seems to me that the principles or laws of biology apply pretty much across many species, so that what is true in the physiologic evolution of mice might also be true in our own biologic evolution, as well, and as the following discussion indicates, it is true; the lag between the ability to experience pain and the ability to repress it can be considerable. Whereas the beginning of serotonin production in mice is sometime in the third trimester, in humans it seems to begin slightly earlier. Research on a fetus seems to indicate that it can experience pain after thirteen weeks from conception but that it really fully experiences pain after 20-24 weeks of gestation—about five months of life in utero. It is fully sensitive to adverse events at this time (Ranalli, 2000).

What is critical here is there is a time during gestation when the fetus cannot produce repressive/inhibitory chemicals and must “ask” for help physiologically from his mother. When the fetus does begin manufacturing its own neurochemicals it sends some of it to the mother. It says, “I can soothe myself now. Thanks for the help.” Above all, serotonin is a soother. Its function is to bolster the gating function so that pain does not slip across synapses in order to tell higher levels about its predicament. It enhances the unconscious; that is its job. It is merciful; that is, something in our brains has mercy and does its best to keep us out of pain. It is therefore a big part of our humanity. Although the pain-killing aspects of serotonin are well known, less is known about its role in affecting appetite, gastric symptoms and heart function. In short, it has a role in normal development and evolution. In particular, new evidence points to its role in actually shaping some brain structures early in fetal life (Côté et al., 2007).

Traumas very early on, before the secretion of serotonin is evident in the fetus, impact later serotonin output and can change who and what we are significantly. One reason we see serious mental illness arising during adolescence is that the hormonal turmoil going on and the weakening of defenses permits some of the fetal pain to rise and affect thought processes—hence: delusions and hallucinations.

Interestingly, in its early secretory life, serotonin functions to control and shape anatomic structure. When levels drop over time, we may expect changes in our body structure. Later on, it carries on as a pain controller. It too evolves and changes. Thus, we as humans may have a significant delay in secreting serotonin during gestation. And we rely on our mother to pitch in before we start making our own. She needs to have an adequate supply for both herself and her baby. If she is chronically depressed she is apt to have low levels of serotonin, used up in the fight against her pain. In this way, the mother cannot fulfill the fetal needs for a way to blunt the impact of adverse events (i.e., of pain). Thus, the fetus has developed a residue of unblocked, free-floating pain and terror early in his gestation. This makes him much more vulnerable to trauma at birth and in infancy. He has defective coping mechanisms. Any later trauma can have double the impact on the relatively undefended system.

The low serotonin output is an imprint that remains pretty much the same throughout our life, making us not up the task of everyday living. That is why we so desperately need serotonin enhancing medication later in life (Prozac, Zoloft). The medication is helping to block pain that may have happened before we set foot on this planet, and to bring the levels up to normal readings.

We know from current research that an imprint during gestation remains pristinely pure for all of our lives, whereas an imprint after birth can produce compensating secretions that blunt the impact of trauma during infancy. My very notion of the imprint means pre-birth events may create irreversible dislocations of function in the neurobiologic systems. The only way it can change is if we return to the origin of the dislocation and right the ship. It needs a push from below not a cry (an effort) from above. It seems to be another biologic law that whatever happens during gestation can alter basic physiologic set points, which is rarely the case after birth when there can be compensatory mechanisms to make up for the dislocation of function associated with the original trauma.

So we have a developing fetus who has no effective repressive mechanisms trying to borrow some of mother’s serotonin to help out, but to no avail. A completely naïve physical system has no frame of reference that tells it that basic physiologic processes are deviated. During gestation the system deviates and then considers that deviation as normal. So the baby is born with an inadequate serotonin/gating capacity and that deficiency follows him throughout life. But it is an already wounded organism, a wound that almost no one can see or even imagine. He will grow up chronically anxious, unable to concentrate or focus. He may well be ADD/ADHD and be unable to sit still because the activation goes on incessantly. It shows itself in the panic attacks that happen when the system is vulnerable and gating weak; the imprint from gestation rises to the top and shouts out its message, which almost no one can decipher. It is such a mystery because its origins are so arcane.

An example: A girl is born in wartime to a mother who is chronically anxious because her husband has been sent to fight, leaving her all alone. The anxious mother transmits some of that emotion to her baby who is then considerably weakened. She cannot fully repress to hold down pain. By the time infancy happens there is already a weak, vulnerable baby who is chronically agitated. This may be the beginning of serious mental illness. It is not obvious to the human eye, but the damage is done.

Too often this is ascribed to heredity because no one can imagine what has already happened in the womb. It is kind of a free-floating anxiety that seems to have no specific time of origin. Remember, this is a purely physiologic reaction which originated at a time when there was no higher brain center to process the event. To recapture it we must retreat to that primitive brain. What we may see many decades later are panic and anxiety attacks, and then much later a cerebral stroke. This imprint would militate against cancer because for some cancers to develop, we often need massive repression; and for that we need massive secretions of “neurojuices” such as serotonin.

What would exacerbate the risk of cancer are events later in infancy and childhood with unloving, stern parents. The result is a person who never had outlets for his pain. We have seen several epileptics who had that familial configuration. What further shuts down the person is growing up with a violent father or mother, or a strict religious household, with no one to turn to. The force of the imprint may well affect the brain when the person is in his sixties. How on earth can we access such remote experiences, back to a time when there were no ideas to help out?

Imipramine Binding Study

Through studying our patients, we learned that they were uniformly low in imipramine binding at the start of therapy but normalized after six months to one year of treatment. Imipramine is a serotonin analogue we believe can be a measure of a repressive system in action. We have done imipramine-binding studies (blind) of blood platelets. Blood platelets have a high degree biochemical resemblance to nerve cells, including neurotransmitter uptake and binding sites. We reasoned that we could measure through the blood, by surrogate, the serotonin production in the brain. Imipramine has a role as an antidepressant. It blocks the uptake of serotonin so that more of it remains to help repression. That is why it is important that levels normalized after one year of Primal Therapy (Briley, Raisman, and Langer, 1979).

Our informal analysis of a number of patients in Europe found that manic patients were low on binding. It is something we expected, as their frontal control mechanisms were faulty. We assumed that early trauma compromised the development of prefrontal brain tissue. Here is the report by Steven Rose, Professor Emeritus, Department of Life Sciences, Open University, England who led the research:

1. Self-referring individuals entering psychotherapy who a level of maximal specific binding of 3H imipramine binding to blood platelets about one-half that of a control group of self-defined normal subjects not in therapy.

2. Six months after beginning a course in Primal Therapy their average imipramine binding level had increased until it was indistinguishable from control levels, and this increase was maintained for a further six months.

3. Eleven of twelve subjects showed some improvement in score on a psychic assessment scale over this period, and this was a positive correlation between this improved assessment score and increased serotonin binding.

One important factor in this study was that the patients were able to increase their own level of inhibitory/repression and maintain it. We believe it to be the result of systematic reliving of early pain.

Michael Meaney of McGill University has experimented with mice and found that very early neglect by the mother results in lifelong alterations. In thirteen men who had committed suicide, all of whom suffered from child abuse, there were epigenetic effects. Abuse has many forms but to me those most deleterious is the abuse of a mother who smokes, drinks, or takes drugs during pregnancy (Mill, et al., 2008). Abuse means adversely affecting a child’s development. Meaney found the same changes in thirty-five people who suffered from schizophrenia. Here, several of the genes involved with the release of key neurotransmitters (which ordinarily help to repress pain or noxious stimuli) were affected.

What has been called the effects on epigenetic settings I call changing the set points of many biologic states; this includes the set points of the neurotransmitters that will later make us chronically comfortable or uncomfortable. Not feeling good in our skin is another way to state it. What is very new is that experiences of the mother could influence the sperm of the offspring, and that may affect how the grandchildren develop. It may be that smoking or taking in drugs while the embryo is just forming can later affect sperm production. The meaning of all this is that what happens in the womb while the organism is developing can affect the baby for a lifetime. It is so important that we not neglect this period when we attempt to understand and treat those with emotional problems. The more remote the imprint the more widespread the later effects, in my opinion. When a pregnant woman is under stress, her stress hormone level is high. When the levels remain high for a long time, the immune system is compromised, and that might well affect the immune status of the offspring. And as I note elsewhere, a strong immune system (natural killer cells) is needed to stay on the lookout for newly developing cancer cells. It is not that a deficient immune system can lead to cancer, it is that a weak maternal immune system does not impart a strong immune capability to the baby; and the same compromised physiology of the mother can also affect the fetus, setting the stage for later catastrophic disease. Womb-life has largely been neglected in the psychological literature. It is time to reorient ourselves.

Cold Feet, Cold Hands and a Hurting Heart

Most of us know someone who has chronically cold feet and hands (the extremities), and who are forever cold. We think, “That’s just their nature.” But what if it’s not? What if it is “nurture?” What if those cold hands and feet went with a certain kind of personality that got its start a few months after conception? Moreover, suppose we could change all of those tendencies at once? Well that is a tall order and it will need some explanation. My general philosophy is that most of us are normal, born normal and adapt normally. So when there is a deviation leading to changed anatomy or physiology early in life it means something went wrong. It is not normal for there to be serious illness or emotional problems after birth if something did not go wrong some time before.

I shall address this problem and try to explore what can go wrong that produces radical deviations in the first few years of our lives. (Some of the following information is described by the work of the German scientist, D. Singer [2004], who has done key research on the subject.) One of the constants I see in my practice is the reliving of oxygen deprivation at and before birth (hypoxia: meaning depleted oxygen, or anoxia: a total lack of oxygen). Many patients reliving birth lose their breath, struggle to breathe, sometimes turn red and are seemingly asphyxiating. It turns out that the literature is now filled with studies that indicate that a majority of babies are born with limited oxygen. This is often due to painkillers and anesthetics, which reduce oxygen input. The baby then has to adapt to this situation. It does this in many ways but one is to revert to the animal “diving reflex.” It redistributes oxygen to where it is most needed, namely, the key vital organs, lungs and heart. It deprives the extremities of oxygen so that there is set up a tendency to have cold hands and feet, not just for the moment of plus two days, but also for life/plus 80 years. Additionally, there is a reshaping of the personality, at the same time that also can last for those 80 years. Reduced oxygen (don’t forget the smoking mother or one who takes suppressive tranquilizers) also happens when a mother takes serious painkillers and/or tranquilizers during pregnancy. Involved in this is a long-term adaptation syndrome. The body needs to slow its metabolism (how fast it uses up nutrients), not for then only, but again for a lifetime. This adaptation I have called the parasympathetic one.

Dr. Arthur Janov is the Director of The Primal Center, Santa Monica, California. Creator of Primal Therapy (www.primaltherapy.com/) more than 40 years ago, 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: primalctr@mac.com or (310) 392-2003. Free access to Dr. Janov’s recent essays can be found on his blog at: http://www.arthurjanov.com/.

References

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.

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.

Côté, F., Fligny , C., Bayard, E., Launay, J. M., Gershon, M. D., Mallet, J., and Diego, M., Field, T., Hernandez-Reif, M., Schanberg, S., Kuhn, C., Gonzale Quintero

V. H., (2009). Prenatal depression restricts fetal growth. Early Human Development, 85(1), 65-70.

Mill, J., Tang, T., Kaminsky, Z., Khare, T., Yazdanpanah, S., Bouchad, L. et al, (2008). Epigenomic profiling reveals DNA-methylation changes associated with major psychosis. American Journal of Human Genetics, 82(3), 696-711.

Ranalli, P. (2000). The emerging reality of fetal pain in late abortion. National Right to Life News, 27(9). www.nrlc.org

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.