The Mystery Known as Depression, Part 5/12

5. THE KEY ROLE OF EPIGENETICS

Although genetics may be partly responsible for depression in rare cases, by and large it is early life experience (including experience in the womb and birth trauma), that is the root cause. What we see at work is epigenetics, the altering of gene function without changes in the underlying DNA sequence (Booij et al., 2013). Those alterations, or deviations, if you will, often involve a biochemical process known as methylation. And it is through methylation that psychological trauma is imprinted. Thus the trauma – which can be as simple as a lack of caring and love by the mother – becomes “fixed” in the system and endures. It is the imprint, the linchpin of depression. The biochemistry, and ultimately the brain have been rerouted, sealing in depressive tendencies. It is this imprint that ultimately must be addressed and resolved.

What the scientific evidence shows more and more is that gestation and birth events are critical for later disease. In a 2010 study conducted at the Hannover Medical School in Germany,researchers concluded that “epigenetics is of considerable interest for the understanding of early life stress in depression.” The study, published in the journal Current Opinion in Psychiatry, found, among many other things, that unloved and untouched children had a predisposition to depression. (Schroeder, Krebs, Bleich, & Frieling, 2010). Recent work by a team of Canadian researchers also pointed to the critical role played by epigenetics. (Booij et al., 2013) 
The following passage is from their article:
“The functioning of the hypothalamic–pituitary–adrenal (HPA) axis and serotonergic (5-HT) system are known to be intertwined with mood. Alterations in these systems are often associated with depression. However, neither (is) sufficient to cause depression in and of themselves. It is now becoming increasingly clear that the environment plays a crucial role, particularly, the perinatal environment. In this review, we posit that early environmental stress triggers a series of epigenetic mechanisms that adapt the genome and program the HPA axis and 5-HT system for survival in a harsh environment. We focus on DNA methylation as it is the most stable epigenetic mark. Given that DNA methylation patterns are in large part set within the perinatal period, long- term gene expression programming by DNA methylation is especially vulnerable to environmental insults during this period. We discuss specific examples of genes in the 5-HT system (serotonin transporter) and HPA axis (glucocorticoid receptor and arginine vasopressin enhancer) whose DNA methylation state is associated with early life experience and may potentially lead to depression vulnerability. We conclude with a discussion on the relevance of studying epigenetic mechanisms in peripheral tissue as a proxy for those occurring in the human brain and suggest avenues for future research.”
It seems that the fastest changes in methylation occur early in our lives, at the very least in the neonatal period, though this thesis is subject to further study. What is important now is that certain genes which should not be silenced, are. Thus, certain means of expression are suppressed, which is often the case in depression. None of this means that methylation “causes” the affliction but rather, there are adverse events very early in life that increase its production.

Though the Canadian researchers emphasize the perinatal period, we have found the imprint to lie earlier, as well. If the neonate is especially sensitive to environment insults, it surely is possible that those insults can occur earlier and form the primordial imprint that later gives rise to depression. Methylation, in brief, offers the primordial event that sets the prototype for later inhibition and repression; thus, high methylation may be a predictor for later depression. It means that certain key genes which should find expression are silenced, especially due to modification of the genes promoter region. The tendencies for no or difficult expression are imprinted.

My opinion is that some of these changes in physiology occur during our life in the womb, when the set-points of so many hormones are being established, including thyroid hormone. Indeed if we give a small does of thyroid medication to depressive patients there is a transient improvement. One may think that such deficiencies are genetic but there are events that can cause them that are not always obvious. They are only obvious when the patient in therapy descends down to the far reaches of the unconscious where the crucial explanation of one’s depression lies. One again relives the birth experience, the suffocation, strangulation, the hopeless battle to get out – the unutterable and ineffable despair. Of course, it is not given a name until years later but the feeling is there engraved in the nervous system. We can feel hopeless without giving it a label. In the face of adult adversity, the old imprint – wanting to give up – appears and is now called depression.

We give it that name because we have not seen the generating sources of deep imprinted despair, something we have observed many times. We name it depression because we do not know the hopelessness inside that makes us miserable. We give depression the name of the defense instead of its cause – pain.