Epigenetics and Primal Therapy: The Cure for Neurosis (Part 3/20)

The Urgency of Early Love

What is important is that we can begin to zoom in on a specific answer to the question that eludes so many in the study of mental illness – why? Granted, damage means heavier methylation. But what is that great damage? The answer is simple – early lack of love. It takes many forms in humans: poor nutrition, abuse, neglect, lack of touch (licking in animals). Methylation seems to be an important marker for lack of early love, both in animals and in humans. The new research is finding that so many diseases are affected by methylation, including multiple sclerosis, diabetes and heart disease. Again, these are stress-related and the great stressor seems to be a simple lack of love, meaning 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 are often deficient in oxytocin. It is why I call it the hormone of love.

As it turns out, love is not as ephemeral as we might have thought. Love means having a proper birth, without heavy anesthetics to shut down the oxygen supply to the newborn. Most important, it means a mother fairly free of anguish and depression; for her physiologic and emotional state is more or less the offspring’s state, not just momentarily, but for a lifetime. In fact, when we see the documentation we discover that how we’ve been nurtured in the womb and our first years is at least as important, if not more so, than heredity; when love is absent, there are enduring physical consequences. And therein lies the rub; we are dealing with errors of omission, an absence not a presence — which is why it is so hard to pin down.

Animal experiments have shown that separating a baby sporadically and unpredictably from its mother causes severe stress, and the same applies to a human baby who is not touched right after birth and in the first weeks of life, as we find in babies raised in incubators. Another study showed that early trauma produced heavy methylation in those children who grew up in orphanages (Drury et al., 2011). And that process then affected much more in terms of brain and neuronal development. The effects of this stress become heritable from the epigenome. This imprint then affects many aspects of our biology, including the memory system. That may mean that a condition such as Alzheimer’s disease may get its start from birth, and not show up for another sixty years. Research by D.K. Lahiri and B. Maloney (2010), at the Indiana University School of Medicine, 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.

So what is the imprint? It is a memory, an ensemble of all the circumstances surrounding a key adverse event; a memory of an early trauma encapsulated. But it is not just a “memory” in the usual sense of recall or actively going back to purposefully retrieve something forgotten in the past. It is an event sealed-in biochemically and which affects us forevermore. The reason it is so important is that it determines personality, illness, longevity and many other facets of our lives. It drives our behavior and the kind of sickness we will suffer from, whether Alzheimer’s disease or cancer. Once we understand the nature of the imprint we understand that no basic change in personality can take place in therapy without altering the imprint. But you cannot get there from here; you cannot willfully try to retrieve the memory because “willful” is the opposite of what is needed. One needs to let go of high-level cortical processes and descend down the levels of consciousness where the imprint exists. And there we find that we cannot reach out to it because it is encapsulated, surrounded by aspects of the methyl chemical group, which helps encase it and makes it unreachable. Thus, when an infant suffers trauma during the critical period 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.

One example: when a patient relives a traumatic birth, we sometimes see the reappearance of the doctor’s fingerprints on the arms of the newborn. We have photographed this, as it is unmistakable to the eye. And at the same time, so difficult to understand, until we realize that memory is far more than cerebral. Hoping to cure by cerebral methods while ignoring the imprint is but a fantasy that ignores reality.