Epigenetics and Mental Health Insights
Epigenetics and Mental Health Insights
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1
McDevitt, N. (2006, Fall). The nurture of things. Headway. Retrieved from
[Link]
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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)
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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.
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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)
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Leaves its Mark on the Brain.” ) 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.
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2
Childhood trauma leaves its mark on the brain. (2013, January 15). Ecole Polytechnique
Fédérale de Lausanne. Retrieved from
[Link]
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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 most
efficacious 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. Epigenetics modifies genetics. De-methylation undoes epigenetics. What
is left is a slightly modified gene. Being neurotic from a very young age shaped our
behavior in unhealthy directions. When we go back and re-live those imprints we do not
erase history, but we empty out the driving force that shaped and warped our early
behavior. In other words, life experience, neurotic though it may be, is still experience
that formed us. We can never go back and be pure again because neurosis has taken its
seat at the table. The real revolution lies in the possibility that people no longer have to
live with their genetic inheritance nor their epigenetic dictates, 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.
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coming years it will likely be one of most important areas of scientific research.
As I’ve mentioned, one reason for its preeminence is that many of the serious
diseases we think are genetic are actually epigenetic and, therefore,
environmentally caused, and possibly treatable. That is now an established fact in
human development. However, early discoveries in the field a short decade ago
were so startling that they even surprised the scientific world.
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3
Hoag, H. (2011, Summer). Are your genes your destiny? (Not if your mom has anything to
say about it). Retrieved from [Link]
genes-your-destiny-not-if- your-mom-has-anything-to-say-about-it/
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chemical reactions are taking place — hydrogen removal, methyl infusion, and so
on. Methylation leaves a heritable imprint, one that can be passed down even
from grandparents to their grandchildren, as research has shown. So what we
always thought was genetic may well be the result of very early experience
diverting the genetic legacy. In short, the experiences of our forbearers can
endure and be passed down the epigenetic chain – the inheritance of acquired
characteristics. This is something science thought impossible not long ago.
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furiously running here and there, avoiding dangerous or unhealthy situations. I
know of someone who did extreme heat/massage therapy while pregnant, never
realizing the possible harm to the baby.
Almost every animal form that is loved and licked has grown up pretty
healthy with no serious disease; and in my therapeutic experience, those children
who had bad and traumatic births with unhealthy gestations are the ones who
suffer the most as adults. Too often, catastrophic early life equals catastrophic
disease later in life.
To make sure that these changes in the rat pups resulted from experience
and not heredity, the researchers let normally stable rat pups raised by attentive
mothers be raised by neurotic negligent mothers. And the result was still the same
– unstressed babies. These babies had birth mothers who had normal amounts of
methylation in their genomes. Thus rats raised by loving mothers could pass it
onto offspring even when the adopted mother was not loving. The genes for stress
hormone output had minimal methylation; in other words love was passed down
the genetic chain. So normal babies raised by negligent and inattentive mothers
still had low methyl levels in their hippocampus. The babies started life one leg
up; a good start in life despite a bad childhood.
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acetylation, must occur very early as the whole neuronal system is evolving. So
before we can state what causes depression or anxiety, we need to observe the
early epigenetics at work. Again, pups born to bad mothers but reared by loving
mothers still seemed to be normal and relatively un-methylated.
Here is one more reason this research is important: the scientists found that
unloving mothers of rodents caused methylation of the estrogen receptors in
female offspring. Then, when they had offspring of their own, the offspring were
deficient in estrogen, which made them less attentive and loving to their own
babies. We as yet do not know how many key chemical processes can be affected
by lack of early love, and more, we have no idea how many hormones are
changed in neurotic (heavily methylated) mothers, and how that affects myriad
adult behaviors.
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living outside of Europe during the war.
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4
West, J. (2015, August 3). Holocaust survivors' grandchildren call for action over inherited
trauma. The Guardian.
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Although critics say the number of subjects in this study is too small –
reflecting the small number of Holocaust survivors still alive – the connection is
clear. "The gene changes in the children did not appear to be mediated by
adversity experienced during their own childhood but could only be attributed to
Holocaust exposure in the parents," said Yehuda, in a statement from the Max
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Planck Institute. "Environmental influences such as stress, smoking or diet can
affect the genes of our children.”
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5.
Holocaust survivors pass on trauma to their children’s genes. (2015, August 25). Retrieved
from [Link]
related and the great stressor seems to be a simple lack of love, meaning
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deprivation of basic need. Not surprising in the rat study was the fact that heavy
methylation occurred in the limbic/feeling structures such as the hippocampus
which has to do with feeling/memory. The upshot is that rat pups that are unloved
are more susceptible to later stress, while those that do get loved (licked) do much
better later in life, becoming more adventurous and curious.
Remember, when there is very early stress during womb-life, the genes can
be up-or-down-regulated, and here starts the origins of depression and anxiety. It
becomes the crucible for later disease. When we add later trauma – abuse in
infancy and childhood, given away to foster parents, a mother too sick to care for
the child, etc. – we can almost be sure that neurotic behavior and disease will
follow. That almost surely will involve ADD, lack of concentration and learning
disorders. The DNA has been chemically modified and it reroutes normal
reactions for behavior and disease. These changes are not neurotic; they are often
normal to the noxious intrusion of things like a mother’s smoking or drinking.
The fetus is trying to adapt as best she can. Neurosis is an adaptive reaction to
threat. It is in that sense, normal. So when we find a mother who is not loving we
need to know that she may be driven by her epigenes; she is a victim of those
changes. Her cortisol/stress hormone level militates against maternal instincts;
methylation shuts down a number of “natural” behaviors, including the maternal
instinct. One of the hormonal controls for love is oxytocin, which responds to our
therapy; it builds as pain descends and allows the person both to give and receive
love. Those new mothers who cannot give adequate
breast milk for their newborns are usually the ones with little love in infancy; they
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are often deficient in oxytocin. It is why I call it the hormone of love.
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for instance, indicates how this all might work— first by the imprint and then,
they suggest, by the methylation that carries on the imprint. Again, the imprint
changes how heredity manifests itself. Clearly, without an understanding of the
imprint there is no way to solve the mystery of mental illness which derives from
serious imprinted experience. And, in reality, it is never just “mental” illness. It is
neurophysiologic to the core. That is why to use intellectual methods such as
Cognitive Therapy to address deep-lying memories is a contradiction in terms.
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before birth and at the very beginning of life, methylation leaves the mark of that
trauma on the cells. The methyl chemicals seem to cling to the gene and control
whether the genetic switch is turned on or off, and whether it is on when it should
be off, such as in serious disease. In effect, it is methylation that is heavily
responsible for the imprint and its enduring affects.
Neurosis is Inherited
People exude who they are from every pore of their being. I mean that
literally. An uptight, tense mother radiates her repression. An angry father
radiates his rage. They don't have to “do” anything; just be. But it is worse than
that. When their underlying feelings show themselves, we instinctively sense we
should avoid them or be very careful around them. They distort our words, detour
our natural movements and disapprove of almost everything we do, not by words
but by those looks. And worse, when they show no emotion, we know that
feelings are what we keep to ourselves. The point is that even before we have
words a child is undergoing a lifetime of experience. And the earlier that
experience, the more impactful. It should be obvious; those early experiences that
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directly affect breathing, digestion and elimination are going to do a lot of
damage and will last a lifetime.
Our genes form the matrix of later life; that much we agree on. But our
epigenes, transformed by severe experiences, build a new “genetic” base that
changes or distorts the evolution of our genetic code. Those new altered traits
then become “inherited.” As I’ve noted, we too often confuse this with our
genetic heritage, which is largely impervious to later events. The person becomes
a meld of genes and epigenes, of genetics shaped by experience. Instead of
saying, “she looks and acts just like her mother,” we need to say, “her mother was
‘infected’ with neurosis, which got imprinted into the system of the offspring, and
now she is just as hyperactive and ADD as her distracted and hyperactive
mother.” In other words, the infant who is being carried has caught what could be
a fatal disease: neurosis, the same one lying inside the mother. The baby will
reflect the internal life of the mother and that is what will be imprinted inside him
and last a lifetime. Why? Because this is what had been learned in order to adapt
and adjust. No words, no reprimands, no social neglect, just who she is, does it
all.
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different audience – one approving, one neutral and one not approving. Guess
what? The 14-month old babies reflected what happened. There were differences
in heart rate and a greater stress response in those children of mothers who had
disapproval. The children “learned” through some kind of osmosis. They were
inculcated by the mother’s emotional state. As lead researcher Sara Waters stated
in an article on the website of the Association for Psychological Science, which
published the research: “Your infant may not be able to tell you that you seem
stressed or ask you what is wrong, but our work shows that, as soon as she is in
your arms, she is picking up on the bodily responses accompanying your
emotional state and immediately begins to feel in her own body your own
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negative emotion.” Now imagine that the baby and mother are one, where the
baby lives inside the mother. The influences are far more impactful.
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6
For Infants, Stress May be Caught, Not Taught. (2014, February 3). Association for
Psychological Science. Retrieved from
[Link]
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caught- [Link]
person eat so much?” We know that it is not current culture that is the sole cause;
it could also be because the mother was indulgent and ate compulsively. While in
the womb the baby is learning about his world and what to expect from it; hence
lots of food is to be expected from a mother who indulges. More evidence is
piling up to show how this early start can predict the early onset of disease and a
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shortened lifespan. The fetus is not only aware of certain tastes and smells in the
mother while she is carrying, but those memories can last a lifetime, and can
affect so much of our interests later on. Mothers ingesting carrot juice during
pregnancy, for example, had children who preferred it.
Researchers at Emory University in Atlanta, Georgia, found that even the
memory of a specific smell can be inherited (Dias & Ressler, 2013). The scientists
trained male mice to associate the smell of cherry blossom with an electric shock,
making them fearful of it. They then impregnated females with the sperm of these
mice and found that the pups were also fearful of the cherry blossom aroma. Even
the grand-pups inherited the fear of that specific smell. How did this olfactory
trait get passed down through generations? Researchers attribute it to epigenetics,
noting that DNA from the grandfather mice and their pups revealed epigenetic
marks on the gene encoding the receptor for that specific smell, known as M71.
In other words, this inheritance came through experience, not just genes. Like
their traumatized grandfathers, the grand-pups
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7.
See the work of Keith Godfrey, Professor of Epidemiology and Human Development, and
others at the University of Southampton in England.
[Link]
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y_r esearch_group.page
were more sensitive to the aroma of cherry blossom because their receptors were also
acutely attuned to it, more than control mice. The research “provides some of the best
evidence yet that memories or developed traits can be inherited,” according to a report
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on the experiment published in New Scientist.”
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8
Geddes, L. (2013). Fear of a smell can be passed down several generations. New Scientist,
220(2946), 10. doi:10.1016/s0262-4079(13)62827-4
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Mice can inherit learned sensitivity to a smell. (2013, December 2). Retrieved from
[Link]
10
[Link]
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still shaped your life. This should teach us something about memory; for
memories while being carried can last decades and drive and/or channel behavior.
We do not simply “grow out of it.”
Study after study has shown that a carrying mother’s stress can have long-
lasting effects on how the genes unravel and are expressed in the offspring, which
is the essence of epigenetics. Those brought up in abusive and unloving homes –
under condition of famine, violence, war, divorce, etc. – had lifelong changes in
their development, including chronically high levels of cortisol. Women who
were abused by their husbands had children with excessive methylation of their
gene. And this alteration was passed on to the baby just as if it were inherited. In
this way, and in many others, the anxiety and depression of the carrying mother
get translated into the baby. In short, he is born stressed. Later on, he will over-
react to tense events with higher stress levels.
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In that study, a team of Danish and American researchers interviewed a
group of 746 Danish soldiers before, during and after their deployment to
Afghanistan. The investigators, led by Dorthe Berntsen of Denmark’s Aarhus
University, wanted to trace the causes of PTSD and find out why some soldiers
developed the disorder while others did not. They found that the vast majority of
subject soldiers handled the war experience with little or no psychological harm.
Surprisingly, for those men who did develop serious stress symptoms, the cause
was not found to be connected to battlefield trauma. Instead, the strongest
predictor of PTSD was extreme childhood abuse, not combat experience.
Researchers found that the PTSD sufferers were more likely to have been victims
of severe beatings, burns and broken bones, or to have witnessed family violence
as children. In addition, these soldiers had past experiences that they were unable,
or unwilling, to talk about with the investigators.
“In other words, they showed improvement as soldiers only because they
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were in such poor psychological condition in civilian life,” concludes an article
about the research published in Scientific American. “Army life – even combat—
offered them more in the way of social support and life satisfaction than they had
ever had at home. These soldiers were probably benefiting emotionally from
being valued as individuals for the first time ever and from their first authentic
camaraderie – mental health benefits that diminished after they once again
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returned to civilian life.”
To cure the affliction of PTSD we need to deal with the trauma of combat
and also the adversity from childhood that set the stage for it. In other words,
there were antecedents for this affliction. Cure occurs when all the current and
antecedent factors are addressed and relived. So a soldier can be aware of his
combat trauma and unconscious of the traumas underlying it. It is what we can’t
see that does so much damage. Moreover, the most deleterious traumas are those
that occurred during the early critical period, when need is greatest and pain is at
its asymptote. It means that the sealed-in imprint is almost irreversible in its
effects (excluding Primal Therapy). War is such a powerful force that its effects
can be engraved just as during a critical period in childhood, when the brain is so
vulnerable. There is, therefore, a confluence of two traumas: one that is obvious
and the other that we cannot see. We must not only treat what is obvious if we
want to make sure that the PTSD does not linger on and on. To leave the basic
primeval imprint intact and untouched means always that we
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11. Herbert, W. (2012). Embattled Childhood: The Real Trauma in PTSD. Scientific American
Mind Sci Am Mind, 23(5), 74-75. doi:10.1038/scientificamericanmind1112-74
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must do something each day to handle the symptoms which never seem to go
away.
That is why we must always include the concept of the imprint in any
attempt to understand human behavior, whether it be PTSD or ADD or any
number of ailments. It may seem like one abuse cannot be that bad as to cause
such lasting damage; but it is one abuse among many, a series of traumas that are
encapsulated and imprinted with a force that lasts a lifetime. A mother who fights
with her spouse over time is setting up future behavior in the offspring. It not only
upsets the mother but it also upsets the baby for life by changing his genetic
inheritance. We have treated such cases and they are often punctuated by frequent
trips to the emergency room for allergy and asthma attacks.
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In order to suffer “mental illness” we need a “mental” component, the
cognitive apparatus that allows for mental deviation. Until that evolutionary step
in brain development, we will suffer physically from that same imprint.
Sometimes it is not different diseases we are dealing with, but different
evolutionary stages of our growing up; our ontology. It is not possible to develop
an “attention deficit” until we develop the cognitive capacity to pay attention and
concentrate. And then it is the impact of multiple imprints or one very strong
imprint that sends constant messages to the top level brain, the neo-cortex, trying
to inform it of the problems on deeper levels, and thus interrupting normal
thought. Those messages are importuning and unrelenting, and keep us from any
long-term focus. They are trying to inform us of priorities; what is urgently in
need of being dealt with.
Although the study of epigenetics can get fairly complex, one of the keys to
proper understanding lies in accounting how the brain develops during the fetal
period. The thalamo-cortical (thinking/feeling) circuits are established very late in
gestation. Only after they have developed and the amygdala-cortical circuits are
in place is it possible for us to have a mental appreciation of the pain we are in.
Before then, we can experience pain without acknowledging it. Thus, pain is laid
down unconsciously, without words to explain or clarify it. There was a study
reported in the British journal Nature, (Garcia, Vouimba,
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Beaudry & Thompson, 1999) in which the investigators noted that when babies
are under threat the amygdala sends a signal to the prefrontal cortex, triggering
the expression of fear in behavior. The cortex becomes the “decider,” as it were,
planning for action. As part of the study, the researchers trained mice to associate
a tone with an accompanying shock delivered whenever the tone was issued. Each
time the mice heard the tone, there was commensurate brain activity in the
prefrontal area, signaling a threat. But when the amygdala was surgically
removed there was no longer any prefrontal activity; the former could no longer
signal fear to the top level. The same is true when we drug that structure or
tranquilize it: we thereby diminish the force that mounts in the prefrontal area. As
we learned earlier, gating problems in the amygdala may be part of the reason so
many of us have trouble either falling asleep, staying asleep, or even
concentrating. Lower level imprints thrusting upwards and forward keep us from
traveling to a lower level of brain function by jolting us into a hyper-vigilant state
whenever we lie down to relax. There is simply too much activity in that deeper
level to permit sleep.
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form of SSRI’s, Selective Serotonin Reuptake Inhibitors. And what does that do?
Make up for what was depleted during brainstem dominance.
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If we had the ability to employ words at birth we would say, “Oh My, such
terror”. But we wait years to have those words, and then we call it anxiety. Why?
Because we lost the connection to the origin of it. Now it seems like a different
disease with no known cause. It is the same old imprint with a new title. Yet it is
a powerhouse, and when we begin our study into the development of cancer later
in life we expect to see strong correlations. Remember, terror – now called
anxiety – has a purpose: it is essential for memory to alert us to danger from
inside and out. We try to do away with anxiety with pills when it is a life-saving
mechanism and needs to be available.
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study’s lead researcher, Alicia Meuret, Associate Professor Of Psychology and
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Director of the Anxiety and Depression Research Center at SMU. ) Because the
terror is set down so early, in the beginning months of gestation, and imprinted so
deep in the brain, we have no idea where it comes from. Terror surely begins its
life in the brainstem and in archaic parts of the limbic system (amygdala). It is
only when the gates falter and the terror bursts through that we become aware of
it. Attention Deficit Disorder means that the gates have let through scattered pain
and terror, distracting our focus and attention. This means that we pay too much
to a multitude of inputs. It is not a deficit; our attentional processes are
overwhelmed. And what is the message it is trying to unravel? It is not one
message but a myriad of them, all shouting “I hurt.”
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.
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12. Meuret, A., Ph.D. (2011, July 26). SMU: Out-of-the-blue panic attacks aren't without
warning. Retrieved from [Link]
databases for panic disorders (Perna, Guerriero, Brambilla & Caldirola, 2014).
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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
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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.
Canadian group from the Douglas Mental Health University in Montreal that
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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
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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.
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smart. Somewhere, there are indelible and permanent marks on the sperm and
egg.
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offspring for a lifetime. Just that early exposure is enough to set up a child to be
revved up and jumpy for life. Of course this may stem from more than just drugs,
as we saw with the study of Holocaust survivors. I say that a better approach for
understanding and treating Attention Deficit Disorder is to trace its origins, back
to womb-life, as well as an individual’s ancestral history.
These critical experiences are left out of the usual psychotherapy, but they
are key motivations for how we behave, how we learn and how and if we make
love. It also plays a part in whether the offspring can have children or will be
sterile. It can also help determine if we become obese, to say nothing of mental
illness. In this period when the body and brain are rapidly developing, it is not a
surprise that adversity affects so much of us – body and brain.
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cannot. Thus, such afflictions as the herpes virus, which often lie latent, are more
likely to be activated in those who have poor immune control. In this case,
traumatized patients had higher levels of herpes antibodies, indicating their
immune systems were compromised against the herpes virus. Those later living in
a stable environment still showed higher levels of herpes antibodies.
There is little question now that stress and chronic anxiety of the mother
affects the baby’s HPA axis, as we have seen. Thus, stress sets the stage for later
anxiety in the offspring, partly accomplished by methylation. It heightens cortisol
levels, and chronically high stress hormones affect so many functions later in life,
not the least of which is thinking and memory (Radtke et al., 2011). Much further
down the road it may affect the development of both Alzheimer’s and Parkinson’s
disease. What is important here is that in-utero trauma sets the program for adult
behavior, especially afflictions such as heroin addiction. The person is trying to
calm something inside but has no idea it exists or what it is. Years later there may
be panic attacks that seem to come out of nowhere. But they come out of
somewhere; it is our job to find out where. If we ignore early womb-life
experience we will never discover origins, and we will keep looking into the
current environment for answers. What is clear now is that some get addicted to
heavy drugs to keep panic attacks from happening. That is, it may be the same
imprint involved in both the panic attack and the addiction, only the drug user has
found a way to block it. Addiction may be forever a mystery
because it comes from archaic imprints that share common cause with sharks.
How can anyone find that ancient cause? There is a way. Allow the patient, after
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a time in our therapy, to descend to deep-lying imprints organized millions of
years earlier. Patients are not led there nor are they forced there; the process of
resonance will accomplish it (which I explain more fully below in connection
with new research about how traumas get embedded in the system). To repeat: as
we evolve there are more and more neurons that take part. They evolve out of
earlier neuronal processes and are related to them. Thus there is an
interconnectedness so that they form a neuronal circuit. Each different level of
brain function has a link to yet other higher levels. It is what I call the chain of
pain. When we start with a patient about his current life, eventually, over months
he will descend automatically to lower connected levels. Until after at least a year
of therapy he may touch on brainstem imprints. Here lies the deepest and most
remote memories, also the most devastating in terms of the force of the imprinted
pain. It is later the most disruptive of imprints. It is ineluctably the neuronal chain
that will lead the patient there. When we look at mental illness and severe
physiologic afflictions we need to focus on these early memories. Here may lie
the origins of our mysterious maladies.
The study of twins provides fertile ground for demonstrating the far-
reaching impact of womb-life on who we turn out to be and what we suffer from
years later. In one study, researchers investigated the perplexing case of identical
twin girls born with vastly different physical conditions. One girl was normal
while the other had severe birth defects, born with two vaginas, two
colons and a spinal cord that split in two towards the bottom of her back. “So how
could twins who shared the same genes be so different?” asked the author of a
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report on the epigenetic research, “The Third Factor: Beyond Nature and
13
Nurture,” in New Scientist.
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13. Pilcher, H. (2013). The third factor: Beyond nature and nurture. New Scientist, 219(2932),
44-47. doi:10.1016/s0262-4079(13)62149-1
twin and not the other,” said senior author Dr. Jeffrey Craig of Australia’s
Murdoch Childrens Research Institute, in a press announcement from the research
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14
laboratory. So although twins share a womb, what happens to each of them can
be quite different. The study, published online in Genome Research, has “for the
first time shown that the environment experienced in the womb defines the
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newborn epigenetic profile.” And, no surprise, the authors believe that womb-
life events may have a more profound effect than previously thought. They claim
that this discovery is a powerful tool for managing future health and modifying
risk.
The lead author believes we can modify risk through dietary intervention
and other environmental approaches. He does not say what is crucial: how about
we intervene during womb-life and make it salubrious and salutary? How about
we make womb-life a great place to be? We can do it through education and we
can also do it by reliving those adverse womb events and reversing their
deleterious effects.