PTSD is often described in psychological language, yet the lived experience is profoundly chemical. It is a state in which the nervous system has learned “danger” so deeply that the body continues to run threat biology long after the original threat has passed. In this state, the brain’s alarm circuitry becomes easier to activate and harder to deactivate. Stress-hormone feedback loses precision, adrenaline signalling remains elevated, sleep and digestion shift into survival mode, and inflammatory chemistry rises quietly in the background.

Nervous system genetics matters because these same pathways - stress hormones, adrenaline receptors, neurotransmitter clearance, and immune activation - are strongly shaped by inherited genetic variants as well as trauma-driven epigenetic changes. Trauma does not only influence thoughts or emotions; it alters how genes are expressed under stress, recalibrating the biological systems that govern safety, threat, and recovery.

A useful way to understand PTSD is to imagine a body that is constantly sampling its environment for danger. Central to this process is the amygdala, which rapidly tags sensory input as safe or unsafe and recruits the stress response before conscious thought has fully engaged. Research consistently shows altered amygdala activity in PTSD, alongside disrupted communication with regulatory regions such as the medial prefrontal cortex and changes in memory and context processing systems, including the hippocampus. When the amygdala becomes over-responsive, it does not simply generate fearful thoughts; it initiates full physiological mobilisation, increasing heart rate, altering breathing, tightening muscles, suppressing digestion, and biasing learning toward avoidance and threat.

From here, the hypothalamic–pituitary–adrenal (HPA) axis and the sympathetic nervous system take over. Cortisol is designed to rise in response to stress, mobilise energy, and then feed back to the brain and immune system to terminate the stress response. In PTSD, this feedback loop often becomes unreliable. One of the most influential genetic regulators in this system is FKBP5, which codes for a co-chaperone protein that alters glucocorticoid receptor sensitivity to cortisol. Increased FKBP5 expression is associated with reduced receptor efficiency, distorting cortisol’s feedback signal and increasing the likelihood that the stress response remains active for longer than necessary.

FKBP5 is particularly important in trauma research because it exemplifies gene–environment interaction. Exposure to trauma, especially chronic or early-life adversity, has been associated with long-lasting epigenetic changes around FKBP5 that influence how strongly it is expressed. These changes can recalibrate stress physiology over time, increasing vulnerability to prolonged activation even when immediate danger is no longer present.

Adrenaline and noradrenaline biology add another layer. PTSD is strongly associated with heightened noradrenergic tone, driven by increased signalling from the locus coeruleus–norepinephrine system. This creates a body primed for startle, vigilance, scanning, insomnia, and sudden surges of panic. In this context, adrenaline and noradrenaline receptor genetics become clinically relevant, as receptor variants influence both the intensity of response to catecholamines and the speed at which the nervous system returns to baseline. Variations in beta-adrenergic receptors, particularly ADRB2, have been studied in relation to PTSD risk when combined with trauma exposure, supporting the role of inherited sensitivity in shaping hyperarousal patterns.

Sustained noradrenergic activation also strengthens fear-based learning and reinforces trauma memory encoding. When memories are laid down in a biochemical state of emergency, they are more likely to feel immediate and present rather than contextualised as past events. This contributes to intrusive memories, flashbacks, and the sense that danger is ongoing.

Clearance pathways further shape how PTSD is expressed. COMT (catechol-O-methyltransferase) is responsible for breaking down catecholamines such as dopamine and norepinephrine. Common genetic variants influence how quickly this enzyme works. Slower COMT activity can result in prolonged stress signalling, experienced as heightened sensitivity to stress, increased rumination, stronger somatic activation, and a slower physiological recovery after triggers. In PTSD research, COMT variants have been linked to differences in stress reactivity and cortisol response under repeated or chronic stress.

MAOA (monoamine oxidase A) plays a parallel role in breaking down monoamines including serotonin, norepinephrine, and dopamine. Variations in MAOA activity influence emotional regulation, frustration tolerance, threat sensitivity, and escalation under perceived danger. The most consistent findings again point to gene–environment interaction, where MAOA variation moderates outcomes in the presence of maltreatment or severe adversity. In PTSD presentations characterised by irritability, agitation, or volatility alongside fear or shutdown, MAOA-related differences in monoamine tone become particularly relevant.

These biological pathways converge in the everyday chemistry of PTSD symptoms. Hypervigilance and insomnia often reflect sustained noradrenergic dominance combined with insufficient inhibitory signalling, where GABA does not adequately dampen glutamatergic activation. Intrusive memories are reinforced by adrenaline-enhanced encoding and amygdala-driven threat tagging. Emotional numbing and dissociation can emerge as protective counter-responses when activation remains too high for too long, shifting the system into conservation mode. Alongside this, chronic inflammation frequently rises, as stress signalling alters immune tone. Inflammatory mediators feed back into the brain, intensifying fatigue, low mood, pain sensitivity, and cognitive fog, further reducing resilience and increasing sensitivity to triggers.

Taken together, these mechanisms help explain why PTSD varies so widely between individuals. Differences in stress-hormone feedback, receptor sensitivity, neurotransmitter clearance, inflammatory tendency, and epigenetic imprinting shape whether a nervous system remains hyperaroused, oscillates between activation and collapse, or moves toward shutdown and dissociation. These patterns are not random, nor are they signs of weakness; they reflect the biological logic of a system adapted for survival under threat.

From this perspective, PTSD is not a failure to cope or an inability to “move on,” but the predictable outcome of threat biology that has not yet been able to stand down. Recovery depends not only on cognitive understanding, but on restoring balance across stress hormones, neurotransmitter systems, immune signalling, circadian rhythms, and nervous system feedback loops. When the chemistry of survival softens, the brain becomes capable of learning safety again, and integration becomes possible.

This reframing places PTSD firmly in the domain of neurobiology shaped by experience, genetics, and physiology. It shifts the narrative away from judgement and toward understanding, recognising symptoms as meaningful expressions of a nervous system doing exactly what it learned to do in order to survive.

This understanding shapes how I work with PTSD and complex trauma. When stress chemistry, nervous system signalling, inflammation, and genetic sensitivity are taken into account together, symptoms begin to make sense rather than feeling chaotic or inexplicable. This allows regulation to be approached with far more precision and care, reducing the risk of interventions that unintentionally push an already over-activated system further into threat.

My work brings together trauma-informed therapy, mindscaping, nervous system regulation, functional medicine, and genetics-led insight. By exploring how an individual’s stress system mobilises, how efficiently stress hormones and neurotransmitters are cleared, and how sensitive threat circuitry may be, I can support regulation at the level the body is actually operating. This often includes addressing biological contributors such as methylation strain, inflammatory load, blood sugar instability, micronutrient depletion, and circadian disruption alongside therapeutic work that supports meaning-making, emotional safety, and integration.

Rather than asking a survival-adapted nervous system to think its way out of distress, this approach supports the body to gradually stand down from emergency physiology. As stress chemistry settles and regulation increases, the nervous system becomes more capable of learning safety again. From this place, insight, emotional processing, and relational repair can land more deeply, allowing healing to unfold at a pace the system can tolerate.

I am right here….