What is New About the Imprint?

It seems that new research is confirming much of the Primal position. This is especially true of the work of Michael Meaney and Moshe Szyf (McGill University,Canada). (see for example http://publications.mcgill.ca/headway/magazine/the-nurture-of-things/ or http://publications.mcgill.ca/mcgillnews/2011/06/01/are-your-genes-your-destiny-not-if-your-mom-has-anything-to-say-about-it/ or http://epigenome.eu/en/2,68,1181 ) They are critical work on epigenetics, and how imprints through methylation can be passed down from one generation to another.

They don’t call it an imprint but that is what it is……a key repressed memory that endures and persists throughout our lives; it drives behavior and symptoms. It turns out that imprints can be passed down from parents to baby and from grandparents to baby. Methylation depends on the work of the chemical methyl group which is recruited when there is a traumatic event, and helps embed that memory. . It seems that when there is a surge of methylation part of it attaches to one element of the gene known as cytosine. It is now part of the DNA and turns on or off certain hormones and other neuro-chemical processes.. Once that happens methyl is recruited and the genetic unfolding is thereafter altered.

In short, methylation can be an agent of repression. A study at Duke University showed that when female mice were fed a diet rich in methyl it completed altered the fur pigment of the offspring. In other words, it acted like a genetic inheritance when it was not. It was the result of experience and that is the linchpin of our theory… epigenetics.

As a result of this study the two scientists from Canada, (Meaney and Szyf) thought, if that is true why shouldn’t it be true of other experiences such as bad mothering or negligent parenting? Well, it was and epigenetics research exploded. Think of that: traumatic events in very early childhood leave a mark or tag on a gene that affects us just about forever. They found that even grandparents affected the imprints of the grandchildren, which we will get to in a moment. But suffice to say that the experiences of our forbearers can endure and be passed down the genetic chain, the inheritance of acquired characteristics. This is something science thought impossible decades ago.
 What the scientists found is that the right amount of licking and grooming early on left offspring with less chronic stress hormone output as adults. It is what we all know; that early love makes us stronger and less anxious. But it turns out that if the mothers were licked and groomed early on in their lives, that experience could be passed on. The genes could be modified by the methyl group (and also other chemicals) in a beneficent way. Good history in the mother, good childhood for the children. And more loving by the mother the less methylation in the child . And with less chronic stress hormone production there is far less chance of serious diseases later on such as Alzheimer’s.

To make sure that these changes in the rat pups resulted from experience and not hereditary, they let normally stable rat pups be raised by neurotic negligent mothers. And the result was still the same,; unstressed babies. These babies had mothers who had normal amounts of methyl in their systems. 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. I believe that changes in the genes, methylation and 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 unloving mothers were handed over to loving mothers, and those born to bad mothers reared by loving mothers still seemed to be normal and relatively un-methylated.

Here is one more reason this research is important: they found that unloving mothers of rodents causes 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 mothers (heavily methylated) and how that affects myriad adult behaviors. Is depression inherited? There may be precursors for it which is never manifested if there were plenty of love later in childhood. Is some of the tendency to methylation inherited or epigenetically passed on? And does that form the basis for depression? It seems from the research just cited that that neurotic mothers (methylated), are ineluctably forced to be unloving, thus laying the groundwork for depression in the offspring later on. And what other hormones are depleted by this scenario? Are we born with a tendency to anxiety? Possibly but then the imprint is not methyl so much as acetyl., in this case. With acetylation there are more faults in the repressive system and “holes” in the gating system. Acetylation (recruiting acetyl) pretty much produces the opposite of methylation, a tendency to open rather than close.

Early trauma produced heavy methylation in those children who grew up in orphanages. And that process then affected much more in terms of brain and neuronal development. So when we find a mother who is not loving we need to know that she may being 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. In neurosis we cannot be natural and appreciate nature because we are disconnected and alienated from our own nature.. We cannot rely on our feelings to guide us because they have effectively been shut down; we are alienated from them. Literally, the feelings are aliens. We have found that patients on the verge of these feelings in sessions often run a fever. The body treats the feelings as a menace, a danger and something to be avoided; yet it is also what can liberate us.

Can we reverse or undo methylation? The research informs us that with rats who had been damaged, and raised by unloving mothers, when they were infused with trichostatin did not show evident damage. As though the trauma never occurred. This drug removes methyl from the system. It did, in brief, undo history. This is what I think may be happening with our patients. In the reliving there must be a change in methylation so as to reverse history; this is what we shall study in our future research projects. It seems to me the natural way provides far less possibility for collateral damage to the system. Since we already have found that chronically high cortisol levels have been reversed in our therapy, it would perhaps follow that methylation could also be reversed. In a way, the levels of methylation can be a marker for having been loved early on or not having been loved. We could tell more than the statements by the person who claims he was loved in his childhood if he were indeed not loved. How much denial is there?

Neurochemistry may be better relied on because it has no reason to lie and wouldn’t know how to do it even if possible. It can be a marker for post traumatic stress or how much repression exists in ADD. Or how much pain/repression is there in Alzheimer’s disease? We already have some information in this regard because autopsies on depressive/ suicides found them to have been heavily methylated in the hippocampal area. The more abuse as a child in these cases the more methylation produced. When we add this to our future research on telomeres and cortisol we will begin to have precise measures of the pain in us. And we will know when a drug is too dangerous for us, particularly the drugs like marijuana that tend to open us to ourselves; to our feelings and pain. Finally we will have a marker for the efficacy of certain psychotherapies.  Does the therapy undo the past? Does it help relieve repression and therefore depression? Is there great first line pain in anxiety states? What seems to be the case is that love obviates methylation and produces normal souls.

More on Telomeres

I have written about telomeres before, and it is something we plan to study with our patients. But it is worth another look as it pretty much determines how long we live, but more importantly whether we fall ill prematurely. The research on it is largely about outside stress, never on internal forces. So it is a matter of war, poverty, strikes and parental fights. Yet the key chronic stressor is the imprint that carries forth those parental fights as a fixed memory that follows us for the rest of our lives. And they say that we have to eliminate stress in order to live longer. So how do we do that? We can move to a new city or country but the imprint follows us assiduously and never lets up. We can go to cognitive therapy and talk our feelings to death, or we can attack the imprint at its origin, relive the trauma and finally be rid of it. I know of no other way to do it. The imprint is tenacious and it must be because it is there to guide our lives and control our reactions. It was lifesaving originally and the system remembers and carries it on.


It is clear that stress and its handmaiden, cortisol, the stress hormone does shorten telomeres. Or beginning patients were high in cortisol until one year of therapy; then it reduced significantly. We assume that since cortisol and telomeres work in see-saw fashion: cortisol high, telomeres short; cortisol low, telomeres longer. That is why we will do this research because I am convinced that since we lower cortisol we may also lengthen telomeres. Or at least keep them from shortening. When telomeres get too short so do our lives. There is an article by Elizabeth Blackburn and Elissa Apel about all this in Nature (11 Oct. 2012) (See a short preview:http://www.readcube.com/articles/10.1038/490169a ). Worth a read. They report on a number of studies of telomeres: in 2004 that compared white blood cells of mothers with chronically ill children with those mothers with healthy children. Clearly, mothers of ill children had shorter telomeres. Again, stress is a factor. And that means increased cortisol levels. And that means shorter telomeres. It is not short term stress that is the culprit but enduring stress; and what could be more enduring than the imprint? If only that could be accepted by the scientific
community.


What cortisol may do, inter alia, is increase the action of telomerase which affects the function of telomeres. To be clear: what that enzyme may do is get busy fighting deterioration taking place with the input of primal pain. This, it seems, is happening to prevent further neuro-biologic damage to the system. A research team led by Owen Wolkowitz of the University of California, San Francisco, has been studying telomeres and depression. (May 23, 2013, “Depression linked to telomere enzyme”) (See for example http://www.sciencedaily.com/releases/2013/05/130523004558.htm). What telomerase does ordinarily is help maintain the length of the telomeres, even lengthen them. They are protective. And they go up when depressives take antidepressants; they also go up in animals where it is associated with increased nerve cells in the hippocampus. It appears that the hippocampus deals with the facts of feeling and the memory of it. It is seriously affected by depression. The longer the depression the shorter the telomeres, and it becomes a life-or-death matter. They have found, for example, the very serious pancreatic cancer, is associated with shorter telomeres in blood cells. These people were also studied before the onset of cancer so we cannot say that telomeres shortened because of shorter telomeres. Telomeres maintain the stability of genes; my view is unstable individuals, unstable telomeres. There are other cancers associated with shorter telomeres. We do indeed plan to study them in our therapy. The point is made, but not by the researchers: imprinted pain has a lot to do with depression and with later serious illness. We need to study this among our patient population.


Much of the research on telomeres seems to confirm our hypothesis, that it is the very early experience that stamps in the most forceful and enduring imprints. The work quoted above found that stress in infancy “and even before” erodes telomeres. Children who spent a lengthy time in orphanages had shorter telomeres.


Telomeres are shorter in chronic depressives, and that fact is crucial. Why? We have to assume that there is an imprint of early trauma to set up the depression, in the first place. That means pain. There is a great amount of imprinted pain in depressives, something we have seen over and over again in our patients. And we see depression lift as patients relive very early pain. This seems to be also true with immune disorders, as depression affects the immune system adversely. Chronic depressives have shorter telomeres. That can mean premature serious illness and early death. I believe that our therapy is life-saving, and we are beginning to see why. One problem we have is that when patients get to earlier imprints the pain is painful; but if they stay with it, it does not last, and makes for great changes throughout the system. It is indeed tempting to want to quit when pain arrives but for every pain experienced there is that much less to feel.


And when cortisol is chronically high and telomeres short, there is a much greater chance of suffering from certain cancers, including the deadly pancreatic cancer. What causes this cancer? Early trauma that is imprinted and endures. Another effect is the appearance of dementia in those with shorter telomeres. Again, we need to look at very early trauma, even in gestation, to find the answer to the question, what causes cancer? What causes dementia?


Doesn’t this make sense? When you have a constant pressure and tension on the organs due to the imprint it makes sense that they will give in and break down, The organs are saying, I can’t hold on any more. It is more than I can handle, all too much. It is surprising to me that they do continue to hold their integrity as long as they do.


There is an article in July issue of Brigham and Women’s Hospital, Boston, Mass., 2012 that underlines the importance of anxiety to damaging the telomeres.(See http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0040516). It is an important study in which they took blood samples from 5200 women ages 42-69. It is known as the Woman’s Health Study. They analyzed telomere length among them. Those who reported frequent anxiety attacks (phobias) had significantly shorter telomeres. They implied that it would deduct six years from their lives. They conclude that chronic anxiety in childhood leads to premature aging and, of course, a shorter life. Anxiety will kill us; which is why it is so important not to leave the imprint untouched in psychotherapy. Telomeres will soon be the key marker for not only how how long we live but how many years a key psychotherapy can add to our lives. If we leave it untouched and unchanged the therapy is a failure.


Stress erodes telomeres very early on, according to late research. So children who spent time in orphanages from birth on had shorter telomeres. I think the evidence is there in so many dimensions; early trauma damages the system in every way possible. We need to pay attention when we carry a baby in the womb and we need to pay real attention to our birth practices which are deleterious too often.


The research emphasizes that the early stress carries on into adulthood. Those women in a study in England who had early abuse also had shorter telomeres We can run but cannot hide from our imprint. It follows us everywhere and anywhere until we acknowledge it and relive the damage. Here is supporting evidence for the imprint even if not stated. Why else does it endure and shorten telomeres? Why cannot they make the equation that early trauma stays fixed in the system and drives behavior while shortening our lives? I believe that the earlier the stress, the carrying mother smoking early in pregnancy, the more harmful it will be later on. Let’s teach about pregnancy in school so that adolescents understand what pregnancy means for a human life.