truth2heal

While preparing for a seminar on this topic that I will be giving in Kyrgyzstan at the end of the month, I am once again struck by the fact that the symptoms of these three disorders have so many similarities and overlaps.

The stress response to trauma is mediated by the HPA axis (hypothalamic-pituitary-adrenocortical axis), also known as the stress axis, and by the noradrenergic system (norepinephrine system) in the brain. The goal is survival. Adrenaline and norepinephrine are released, and then cortisol secretion is inhibited to restore balance. People with (complex) PTSD have a hyperactive HPA axis and are constantly overstimulated and hypervigilant. They have a permanently elevated level of norepinephrine. This leads to poor impulse control and hyperactivity, as well as constant fatigue and possibly muscle and joint pain. Early trauma also has a strong influence on, among other things, attachment development, social and emotional development, concentration and attention, and executive functions such as decision-making and planning.

Hormones also play a crucial role in bonding. The so-called “bonding hormone” is oxytocin. It is primarily released during labor before birth, but also during breastfeeding and skin-to-skin contact after birth. Oxytocin reaches many different areas of the brain via neural pathways and therefore influences numerous brain functions, including anxiety regulation, memory formation, the reward system, well-being, and much more – as well as the HPA axis, or stress axis! Oxytocin reduces stress by lowering cortisol levels.

In a normal delivery, the newborn has higher oxytocin levels than the mother, as the newborn produces oxytocin on its own. A cesarean section or a planned delivery affects oxytocin levels. And people with an insecure attachment style have lower oxytocin levels than those with a secure attachment. People with insecure or disorganized attachment styles struggle with self-regulation, cannot rely on others, and have difficulty – or are unable – to accept help; they often exhibit controlling behavior. If an infant was unable to develop a secure attachment style because there was no reliable and caring caregiver present, then that in itself is an early childhood trauma—and, I would argue, one of the worst traumas imaginable, because it fundamentally shapes the perception of the self and the world, and trust was never able to be established.

Finally, ADHD affects very similar areas, such as self-regulation, executive functions, social and emotional development, and attachment development. The brain structures involved include the right prefrontal cortex (where executive functions are located), the striatum, and the nucleus accumbens, which serves as a link between the limbic system (emotions) and motor function. The striatum primarily has inhibitory functions and is part of the brain’s reward system, as is the nucleus accumbens, where, among other things, the dopamine systems governing motor function and motivation converge. Dopamine is important for regulating motor function, learning, memory, motivation, and cognition. Dopamine is therefore the key neurotransmitter here. The availability of sufficient dopamine is a prerequisite for the use of executive functions. Dopamine increases drive, but in people with ADHD, dopamine is reabsorbed too quickly. Hyperactivity can then be understood as a compensatory mechanism. People with ADHD attempt to compensate for the insufficient stimulation caused by a lack of dopamine through increased activity. Anything that is experienced as rewarding can promote the release of dopamine.

The hypothesis, then, is that ADHD is a multifactorial condition caused by complex gene-environment interactions. And among the most significant environmental factors is likely the mother’s well-being during pregnancy. If the mother has unresolved trauma and/or experiences excessive stress (including violence) during pregnancy, her stress hormones influence gene expression in the unborn child’s brain. This is because the HPA axis develops during pregnancy and continues to develop during the child’s first year of life. When the unborn child’s stress axis is activated, it leads to the release of cortisol, which can affect the child’s memory functions, alertness, and attention. This can permanently alter the child’s stress axis as well as the levels and distribution of neurotransmitters (such as dopamine, norepinephrine, etc.).

And so a multifactorial model of ADHD emerges, in which both genetic variants and environmental factors – such as unresolved trauma in the mother (and later in the child as well) and attachment disorders in both the mother and the child – together with the child’s brain development, particularly in relation to the stress axis, can lead to ADHD. And I would argue that all of this could also lead to autism.

Well… so what do we do with this now? First, we need to carefully consider treatment approaches for children with ADHD in light of this multifactorial model of development. First and foremost, therefore, a psychodynamic relational approach is needed, offering positive attachment experiences, followed possibly (and likely?) by trauma resolution, and finally by training in skills such as improved stress regulation, affect and impulse control, and strengthening empathy and mentalization abilities. Based on these facts, children with ADHD, as well as children with attachment disorders and/or early childhood trauma, need first and foremost a continuous, benevolent, acknowledging, and appreciative relationship with a reliable attachment figure. Are we prepared to provide this, or is it easier to simply sedate them with medication without addressing the root cause of their behavioral problems?

Many thanks to Monika Dreiner (Licensed Psychologist; Psychoanalyst (DGIP); Psychotherapist for Children, Adolescents, and Adults) and the Swiss Institute for Psychotraumatology in Winterthur for this very insightful presentation!