Psychosis is one of the most misunderstood states in mental health, often reduced to a set of symptoms that sit on the surface without any real appreciation of what is happening underneath. In clinical language, it is described through hallucinations, delusions, and disorganised thinking, but those descriptions are simply the visible expression of something far more complex. What is actually occurring is a loss of integration within the nervous system, a point at which the brain, body, and biochemical terrain can no longer maintain a coherent relationship with reality. When I see psychosis, I do not see something that has appeared out of nowhere, and I do not see a mind that has broken in isolation. I see a system that has been under increasing pressure, gradually losing its ability to regulate, filter, and interpret experience in a stable way.

If we begin with the architecture of the brain, the picture starts to make more sense. The prefrontal cortex, which allows us to reflect, reason, and test reality, begins to lose its regulatory influence. This part of the brain is essential for creating distance between a thought and a belief, for questioning whether something is true, and for holding multiple perspectives at once. When its function becomes reduced, that capacity begins to fade. At the same time, deeper and more primitive structures, particularly within the limbic system, become more dominant. The amygdala, which is constantly scanning for threat and emotional significance, and the hippocampus, which shapes memory and contextual meaning, begin to drive perception more strongly than the rational brain. This shift is not subtle. It changes the entire way the world is experienced. Things that would normally be filtered out as irrelevant begin to feel charged, meaningful, and personal, and internal thoughts can start to feel as though they are coming from outside.

Running through this shift in brain dominance is a very specific set of chemical changes, most notably within the dopaminergic system. Dopamine is not simply about pleasure or reward, it is fundamentally about salience. It is the mechanism through which the brain decides what matters and what does not. In psychosis, dopamine activity within the mesolimbic pathway becomes heightened, which means that the brain begins to assign importance in a way that is exaggerated and dysregulated. A passing comment can feel significant, a coincidence can feel orchestrated, and an internal thought can feel as real as a spoken voice. At the same time, dopamine activity within the mesocortical pathway, which supports the prefrontal cortex, is often reduced. This creates a very particular imbalance where meaning is amplified but the capacity to evaluate that meaning is diminished. The system is effectively generating intensity without providing the grounding needed to interpret it.

Alongside dopamine, glutamate and GABA are deeply involved in shaping this state. Glutamate is the primary excitatory neurotransmitter and is central to how neurons communicate and synchronise. When glutamatergic signalling becomes unstable, particularly through dysfunction in NMDA receptors, the coordination between different brain regions begins to break down. Information is no longer processed in a smooth, integrated way, and instead becomes fragmented, disjointed, and difficult to organise. GABA, which provides inhibitory control within the brain, acts as a necessary counterbalance to this excitation. When GABAergic function is reduced, the brain loses an important stabilising force. Neural activity becomes louder, faster, and less contained, which contributes to the sense of overwhelm, intrusion, and loss of control that often accompanies psychotic states.

When we move beneath these neurotransmitter systems into the genetic and biochemical terrain, the picture becomes even more layered, and this is where it aligns very strongly with the way you already work. There is no single gene responsible for psychosis, and there never will be, because what we are dealing with is a network of interdependent systems rather than a single pathway. Genes involved in dopamine regulation, including COMT, MAOA, MAOB, DRD2, DRD3, DRD4, and transporters such as SLC6A3, influence how dopamine is produced, broken down, and received. Variations here can affect how quickly dopamine is cleared from the system, how sensitive receptors are to stimulation, and how reactive the salience network becomes under stress. These differences do not cause psychosis on their own, but they shape the baseline sensitivity of the nervous system.

The glutamate system has its own genetic influences, particularly through genes involved in NMDA receptor function, such as those within the GRIN family. When these systems are less efficient, the brain’s ability to synchronise activity across networks becomes more fragile, making it harder to maintain coherent perception and thought under pressure. This is where fragmentation begins to emerge, not as a random symptom, but as a reflection of disrupted communication at a cellular level.

Methylation sits underneath all of this as a foundational process that supports neurotransmitter synthesis, detoxification, and cellular repair. Genes such as MTHFR, MTR, MTRR, and again COMT influence how effectively the body can regulate these processes. When methylation is not running efficiently, neurotransmitters can become more volatile, oxidative stress can increase, and the nervous system has less capacity to buffer against internal and external demands. This is not a small detail, it is part of the underlying resilience of the entire system.

Inflammation brings another dimension that is often overlooked in more traditional models of psychosis. The brain is in constant communication with the immune system, and inflammatory signals can directly alter neurotransmitter function and neural connectivity. Genetic tendencies towards a more reactive immune response, including those involving cytokine signalling pathways such as IFNG, can predispose individuals to higher levels of neuroinflammation when triggered. Environmental factors such as infections, gut dysbiosis, and exposure to mould or toxins can amplify this further. When the brain is inflamed, its ability to regulate itself changes. The blood-brain barrier can become more permeable, neurotransmitter systems can shift, and the overall stability of perception and cognition can be affected.

Energy metabolism is another crucial layer that cannot be separated from this picture. The brain requires a constant and substantial supply of energy to function coherently, and this depends on mitochondrial efficiency. Genes involved in oxidative stress management and mitochondrial function, including SOD pathways, influence how well the brain can cope with metabolic demand. When these systems are under strain, whether through genetic vulnerability, nutrient depletion, or chronic stress, the brain becomes more susceptible to dysregulation. Psychosis, in this sense, can be understood as a state in which the brain no longer has the metabolic capacity to maintain integrated processing.

Minerals form part of this terrain in a way that is both practical and often underestimated. Zinc plays a key role in modulating NMDA receptors and supporting immune balance, and low zinc levels can directly affect glutamate signalling. Magnesium acts as a natural calming agent within the nervous system and helps regulate excitatory activity. Copper, particularly when elevated relative to zinc, can shift neurotransmitter balance and increase excitability within the system. These imbalances are not theoretical, they are measurable, and they can significantly influence how stable or unstable the nervous system becomes over time.

When someone moves into a psychotic state, what we are often seeing is the culmination of all of these layers interacting over time. It can appear sudden, but it rarely is. There is usually a history of increasing load, whether that is emotional, physiological, environmental, or a combination of all three. Chronic stress, trauma, sleep disruption, substance use, hormonal changes, inflammatory burden, and genetic sensitivity all contribute to a gradual lowering of the system’s resilience. The nervous system becomes more reactive, more sensitised, and less able to regulate itself. At a certain point, the threshold is crossed, and the system can no longer maintain coherence.

In that moment, the boundaries that usually allow us to distinguish between internal and external reality begin to dissolve. Thoughts can be experienced as voices, perceptions can become distorted, and meaning can be assigned in ways that feel entirely real to the individual but are no longer shared by others. This is not a failure of will, and it is not a conscious choice. It is the nervous system reaching a point where it can no longer integrate the information it is receiving.

In my work, this understanding shifts the focus completely. Rather than seeing psychosis as something to be suppressed or controlled in isolation, it becomes something to be understood within the wider terrain of the individual. The question is no longer just what symptoms are present, but what has brought the system to this point, and what is needed to restore stability. That involves working across multiple layers, including sleep, nutrition, inflammation, mineral balance, neurotransmitter support, and relational safety. It involves recognising that regulation comes before insight, and that a nervous system that feels unsafe or overwhelmed cannot simply think its way back into balance.

Psychosis, when viewed through this lens, becomes less about pathology and more about threshold. It is the point at which the cumulative load on the system exceeds its capacity to integrate. Understanding it in this way does not reduce its seriousness, but it does open the door to a more compassionate and more comprehensive approach, one that honours the complexity of the brain, the body, and the lived experience that sits between them.

I am right here…