Obsessive–Compulsive Disorder is not simply a problem of “thoughts” or “behaviour.” It is a neurobiological pattern shaped by genetics, neurotransmitters, inflammation, trauma, sensory processing, gut–brain communication and the nervous system’s capacity to regulate threat. OCD arises when the brain becomes trapped in a cycle of perceived danger, intrusive thoughts and ritualised strategies to restore temporary relief. My work is to understand the roots of that cycle and help the system feel safe enough to step out of it.

Through Lifecode Gx testing, I assess the core genetic pathways involved in OCD. Variants in methylation genes (MTHFR, MTR, MTRR, SHMT1, BHMT) influence serotonin, dopamine and glutamate metabolism, all of which shape intrusive thoughts and compulsive patterns. COMT, MAOA and MAOB affect how quickly the brain processes adrenaline and stress hormones — when these pathways are slow, the system can become locked into hypervigilance, rumination or fear loops. GAD1 influences GABA production, the brain’s primary calming neurotransmitter; low GABA tone is often present in OCD. SLC6A4 (serotonin transporter) and SLC1A1 (glutamate transporter) variants are also important contributors, influencing rigidity, anxiety and the intensity of intrusive thoughts.

OCD is increasingly understood as connected to inflammation and immune dysregulation. For some individuals - especially children - infections, chronic inflammation, gut dysbiosis, high histamine, food sensitivities, or autoimmune activity can trigger or worsen obsessive–compulsive symptoms (as seen in PANS/PANDAS-type presentations). Genes such as IL6, TNF, IFNG, HLA subtypes and FUT2 influence these inflammatory and immune pathways, while detoxification genes (GSTs, SOD2, NQO1, CYP450 enzymes) affect the brain’s vulnerability to oxidative stress and environmental triggers.

Functional testing helps identify the real-time drivers beneath OCD: imbalances in serotonin, dopamine or glutamate metabolism; mitochondrial strain; gut infections or dysbiosis that produce neuroactive toxins; nutrient deficiencies (zinc, magnesium, B12, folate); elevated cortisol or adrenaline; poor sleep architecture; or signs of neuroinflammation. Rather than treating OCD as a purely psychological condition, I integrate these findings to understand why the brain is signalling danger so intensely.

However, biology is only one piece. OCD often emerges from a nervous system shaped by chronic stress, early hypervigilance, attachment wounds, medical trauma, perfectionism, shame or environments where emotions were not safe to express. Compulsions develop as protective strategies — attempts to reduce anxiety, regain control or neutralise a threat that feels overwhelming. My therapeutic work supports clients to understand these patterns with compassion, build emotional capacity, repair safety, and rewire the nervous system towards greater flexibility and trust.

Medication effects also matter. SSRIs, antipsychotics, stimulants, antihistamines, steroids and even some painkillers can influence neurotransmitters, inflammation and methylation. For individuals with genetic vulnerabilities, medication interactions may intensify OCD symptoms or destabilise mood. I help clients understand these patterns and work collaboratively with their medical team when adjustments are needed.

By bringing together genetics, functional medicine, gut–brain approaches, nutritional therapy, homeopathy, trauma-informed therapy and deep relational work, I create an individualised, root-cause roadmap for treating OCD. This approach stabilises the biochemical foundations, supports emotional resilience, and helps the brain and nervous system shift out of compulsive loops into greater clarity, safety and freedom.