If anybody says he can think about quantum physics without getting giddy, that only shows that he has not understood the first thing about them.
We make no excuse for re-using Niels Bohr’s warning, but equally do not imply that what follows will be bewildering! We hope only that it will be thought-provoking. A systemic therapist’s need to know about findings now emerging from these disciplines, rests upon the relevance of better understanding the interaction between environment and family members as individuals. These interactions provide some explanation of the considerable individual variation observed in resilience and vulnerability to stress, which is not addressed by any of the other four domains that contribute to the Integrated model. This will be examined in relation to chronic stress and traumatic experiences.
The Human Genome: in just the same way our physical characteristics became established, it is likely that most human innate behavioural, emotional, and cognitive responses developed over a long period of evolution, where the range of each shaped by multiple gene-environment influences. The many abrupt changes in DNA-coding over this long period (affecting any one of the 20,000 genes located on our 23 pairs of chromosomes) would have occasionally conferred some minor environmental advantage, which became heritable, or some disadvantage that – if extreme – disrupted heritability. However, just like most of the daily damage and repair to our DNA now, most evolutionary changes would have made a silent gradual contribution to the Genome material still ‘conserved’ from our earliest days on earth.
It is misleading to base any understanding of genetic influences on behaviour upon such physical health problems as cystic fibrosis, Down’s syndrome, or Huntington’s Chorea. All these well-known but quite unusual conditions result from the multiple consequences of a single chromosomal anomaly, which prevents ‘healthy’ coding. Except for the specific effect of an X or Y chromosome, our physical attributes and most genetically-determined ill-health are almost certainly polymorphic i.e. the result of multiple genetic factors – the reason why modern genetic studies require very large samples in order to identify the small effects of each.
Epigenetics: less than 2% of our DNA is responsible for the DNA-coding which directly influences heritability; epigenetics involves the study of most of our DNA that is not directly involved in passing on our genetic inheritance. Much of it is quiescent, but the remainder is involved in regulating gene-expression, which can be subject to considerable environmental influence. So the study of epigenetics concerns any change in inheritability that does not involve actual changes to DNA-coding i.e. studying the impact of the environment on the expression of genes, how some are activated and others are suppressed.
For example, under the impact of a toxic substances (e.g. a chemical like benzene, or an inhaled material such as a carcinogen or cannabis, or some food contaminant), part of a DNA protein may wrap around a histone, resulting in the genes on that part of the DNA being unable to code (i.e. transmit their influence). Even a brief exposure can result in a permanent change: that is, it can have a very long-term effect (positive or negative) if the modification is handed on, without further change, from one generation to the next.
This was illustrated in the famous study of Swedish grandparents who were exposed to famine conditions in the mid-19th century before reaching they reached adolescence. Some epigenetic adaptation occurred which, in the case of men, resulted in their grandsons dying later than their contemporaries of cardiovascular disease, having acquired from their paternal grandfather some protection from metabolic disease. In contrast, the granddaughters of women who had been exposed to the famine before adolescence died before their contemporaries; mediated, it is now believed, by an adverse epigenetic effect in the developing eggs of these women.
The Neuroscience of Stress: psychological trauma acts a bit like a geological hammer which tests material built up over years, generations (or millennia in the case of rocks obviously), the response varying according to the composition of each. Even without a mind or memory, a rock can still demonstrate something of its history and origin under geological stress (e.g. limestone, formed of calcified animal matter, performs very differently to ancient continental plate, and different still to stones made of the cooled magma pushed up semi-molten from below the earth’s oceanic crust, which itself is still continually recycling (in the geological story oceanic crust is somewhat comparable to DNA, composed of many different constituents that had crystallised at different pressures and temperatures).
The main stress response in the human story is outwardly less complicated and has long been recognised: the HPA axis (under the influence of the glucocorticoid receptor gene), which supports a linear relationship between stress, hypothalamic activity in the mid-brain (part of the limbic system), and – adjacent to the kidneys – the adrenal glands under its control, which secretes cortisol.
Brain-imaging studies have contributed much more to understanding how this occurs. The outer part of the brain, the ‘grey matter’ (i.e. cortex), plays the main role in processing all observed sensations and (in the orbito-frontal cortex) social experiences. It has a two-way connections with the mid-brain (amygdala in particular), where together with the anterior cingulate gyrus (in front of it) and the hippocampus (below it), emotive memories and mood are mainly located. Past trauma or chronic stress lead to prolonged activation of the amygdala connectivity network, which may at first increase in size before a long-term reduction in its volume occurs. Either way, any new presentation of stress triggers an abnormal response, with a downstream effect on the HPA axis. Chronic high arousal may produce a continuous state of high cortisol levels, which have adverse effects on health, directly changing mid-brain structures in turn i.e. with mental consequences (e.g. seemingly ‘minor’ additional stress now precipitates feelings of helplessness or depression, memory impairment, etc.) as well as distant physical ones (e.g. re-kindling inflammatory responses and accelerating heart disease).
In summary, stress results in hyper-secretion of cortisol, which alerts the individual (fight/flight responses, etc.) but can become permanent (as in PTSD where, rather than fight/flight alone, ‘freezing’ in response to hyper-arousal can occur, even to ‘flop’ i.e. disassociation). We provide two further examples of how epigenetic influences are involved:
1. high maternal antenatal stress and perinatal low mood can up-regulate the glucocorticoid receptor gene responsible for HPA activity in their infant, but it is now known that the presence of particular gene-alleles can heighten the risk (and their absence observed to significantly reduce the risk);
2. preventing or allowing facial licking of new-borne small mammals by their mothers has been found to alter the expression of this gene: prevention of licking results in increased DNA-methylation, but the receptor-gene can ‘re-set’ (and the high cortisol levels reduce) if facial licking is finally allowed – providing it is not unduly delayed.
This illustrates a common observation from epigenetic studies: the longer or greater the change under epigenetic influences, the more irreversible the effect. There are examples from ordinary human growth and development (e.g. stem cells are pluripotent before they become liver, lung or bone marrow cells, but they can’t change back). The effect has also been observed in identical twins, where minor differences become more apparent over the years, especially if their lives become lived apart, all presumably under the influence of epigenetic factors (e.g. arising from their differing relationships, positive and negative life-experiences, etc.).
The Neuropsychology of Stress: we have described the effect of severe episodic or chronic stress on the HPA axis (e.g. early sustained abuse, relapsing depression, living under wartime conditions) and how it may result in lasting brain changes, observable by brain imaging many years later. This may explain why seemingly ‘minor’ additional stress can re-kindle feelings of helplessness or depression, and induce dissociative defence mechanisms.
The meaning attributed to the earlier trauma seems to influence the severity of its impact, mediated by frontal cortex functioning (where thinking, reflection, and mean-meaning is particularly located) which in turn influences mid-brain responses. The possible reversal of what had recently been considered perhaps ‘irreversible’ changes in brain structure and function is now being explored, not just through psychotherapy, mindfulness training, etc., but also by the pharmaceutical industry (whether for example an SSRI may have a protective role or can weaken long-lasting fear memories).
After the bombing of Guernica, Picasso’s preparatory drawings for his famous painting sought to capture how witnessing the atrocity was experienced, wordlessly seared in one woman’s memory as emotion and images, beyond any words – albeit witnessed (and portrayed by Picasso) using higher executive (cortical) functioning.
In traumatised individuals, psychotherapy CBT DBT and mindfulness training are all, to varying degree, addressing non-verbal aspects of the mind. To succeed, all approaches must avoid any early problem-saturated work, in order that thinking can remain clear, a strong relationship established between therapist and the individual, and the work commenced by a strengths-based approach (for further reading, see ‘Treatment of Complex Trauma: a sequential relationship-based approach’ by Christine Courtois and Julian Ford).
The therapist met Mandy on her own without David, her 12-year-old son, being present. Mandy used the time to reflect on some of the stressors she had experienced as a young child. She made a link between stressors in her relationship with her son activating similar feelings of helplessness that she had experienced at times before, when her birth father had been absent from the family home and she felt abandoned by him. By also exploring the strengths in herself and in other close relationships that assisted her to cope with this difficult period in her life, Mandy was able to think about supportive relationships in her life now and how she might access them in a different way.
The Neuroscience of Attachment: studies on the epigenetics of the glucocorticoid receptor gene squarely place attachment at the heart of the human story about stress.
Famously studied by Konrad Lorenz (whose parentless geese became very attached to him and his boots) and Mary Ainsworth (observing mother-infant interactions under laboratory conditions), the scientific story of attachment began from direct observation of behaviour, to inferences about the inner mental state either driving it or resulting from it. The scientific story has developed from attachment as care-giving and protective (or the opposite: deprivation, inadequacy, or insecure), to how attachment may influence an individual’s sense of themselves, their part in relationships, and their capacity to problem-solve and look after themselves – attachment styles, described as ‘inner working models’ in the psychoanalytic literature which may persist into adult life (as secure, anxious, avoidant, or disorganised).
The cortex of geese and humans are quite unlike (geese are impulsive and can only quack!), but much of the hypothalamus and other mid-brain structures (such as the amygdale and anterior cingulated gyrus) implicated in attachment and other emotional responding are shared in common.
As described above, the hypothalamus is responsible for synthesising and releasing chemicals that affect distant sites; much of its input (via the thalamus above it) comes from the cortex, particularly pre-frontal. This is far more developed in humans than any other animal (so small in geese that any of its key role in humans for planning, impulse control, and social responding is rarely evident as you run from an angry one).
The discovery of ‘mirror neurons’ brought neuroscience in the world of mother-infant intersubjectivity and how attachment becomes established. Touch (as in licking, breast feeding), sight (reciprocal gazing) and sound (reciprocal vocalisation) all contribute to the development of attachment, providing cortical input (particularly to the right cortical hemisphere), from where emotional learning becomes embedded in the mid-brain.
David and Mandy, the therapist noticed when meeting with them both together again, presented as equally flat and with low motivation after having had a challenging week. Observing similar feelings of hopelessness within herself at this point, the therapist recognised the role of mirror neurons in communicating the difficulties. The therapist verbally acknowledged the struggle with a reframe that despite overwhelming feelings of despair, both Mandy and David had committed to attending the appointment. This brought a lighter feeling of hope to the interaction, setting off a chain-reaction of mirror neurons that carried optimism instead of despair. Mandy and David were then able to articulate how hard they were working and how determined they were to find a resolution to the challenges.
The Neuropsychology of Learning: several very different types of memory have been identified e.g. short-term, long-term/autobiographical, procedural memory (where someone with dementia might still be able to play golf, etc.). Apart from the opportunities for re-exposure and rehearsal, what most new learning has in common is that it is most effective if it is emotionally embedded. Mirror neurons, the capacity to understand how others are feeling (and identifying with them), clear thinking rather than feeling overwhelmed, etc., all play a part. Memory and emotion are very closely related, both anatomically and functionally, from the earliest days of life (recent studies have demonstrated this arises during foetal life).
That process may be disrupted if intense emotional disturbance, deprivation or abandonment predominates. It explains the persistence into adult life of early attachment styles, and how challenging the establishment of a secure attachment may be if either infant or mother have an impaired capacity for ‘theory of mind’ relating. For example, if either have profound social-communication difficulties (as may occur with Asperger’s) or the mother incapacitated by depression or psychoactive substances.
The perception of distress in an infant or child for whom the adult is responsible might re-kindle profound distress in the adult, triggering memories acquired very early in their own lives, perhaps embedded without words and recalled as bodily experiences.
Other sources of individual difference: we have described some of the most influential biopsychosocial sources of variation between family members as individuals. There may in addition be interaction between one or several of these with ordinal position. For example, a complicated pregnancy and inexpert parenting of a first-born; or increasing family debt and maternal depression associated with the last born. The outcome of each may also considerably depend upon the infant’s innate particular temperament.
Although these may seem somewhat extreme examples, it is common for siblings who do not dispute the core facts of their early family-life to nevertheless recall their family experience in different ways. In some families the shared-experiences may be outweighed by non-shared aspects; that most obviously might occur if only one child is on the autistic spectrum, suffers from lasting physical disability after an accident or serious illness, or another had become the focus of abuse.
Equally, it may result from a less ‘visible’ complex interaction between ordinal position and unresolved parental issues that a hurried family history-taking would be likely to overlook. For example, a last-born, breast-fed for a long time by a depressed mother who has been increasingly bullied by her husband: the passive temperament of the infant may have increased the likelihood of continued oral dependence (and early inception of a role-reversal about ‘who was nurturing who’) and also the likelihood of subsequent mother-child emotional over-involvement and introjective identification of ‘bad’ feelings.