Anxiety is the everyday stuff that blocks you from doing what you want. Approaching someone you're attracted to. Going on a first date. Giving a presentation. Creating content. Making a sales call. Having the hard conversation and it links all of it is the same dysregulated stress response: too much glutamate, too little GABA, overactive sympathetic nervous system, chronic cortisol. Different interventions can help us dampen that activation and building parasympathetic tone.

What drives anxiety

• GABA is the brain's main calming, inhibitory neurotransmitter, the "slow down" signal. It works through two different receptor types that produce different effects. Low overall GABA tone produces a wired, restless, hyper-alert baseline.
  • GABA-A is the fast switch. When activated, it produces rapid calm within minutes, less mental chatter, muscle relaxation, and at higher doses sedation. This is what benzodiazepines, alcohol, kava, and apigenin work on. The classic anxiolytic feel.
  • GABA-B is the slow, mood-shifting dial. When activated, it produces a longer-lasting state that's less about sedation and more about feeling good: pro-social, talkative, emotionally open, sometimes mildly euphoric. This is what phenibut and baclofen work on. The pro-social, feel-good profile is exactly what makes them more addictive and dangerous than GABA-A compounds, withdrawal can be severe.
• Glutamate is the main excitatory neurotransmitter (the "go" signal). Too much glutamate signalling produces anxiety, racing thoughts, and difficulty winding down. Magnesium gates the NMDA glutamate receptor, which is why magnesium deficiency commonly shows up as anxiety.
• The HPA axis and cortisol. Cortisol is your main stress hormone. It spikes during stress, then should drop. When stress is constant, cortisol stays elevated, and the brain reads this as "we are still in danger," keeping you hypervigilant and anxious. The anxiety itself keeps the cortisol up, creating a loop. Adaptogens (herbs like Ashwagandha and Rhodiola) work by modulating this system, bringing elevated cortisol back toward normal
• Noradrenaline is the alertness signal. In acute anxiety (the moment before you go on stage, before the date, behind the wheel), it's overactive, producing the racing heart, sweating, shaking, and "on edge" physical symptoms. Beta-blockers like propranolol work by blocking peripheral noradrenaline, which is why they're so effective for performance situations specifically.
• Serotonin influences emotional regulation and impulsivity. Low serotonin shows up as irritability, restlessness, and difficulty tolerating discomfort. SSRIs work by raising it, slowly.
• The vagus nerve and parasympathetic tone. Your nervous system runs two opposing branches automatically in the background. The sympathetic branch is fight-or-flight (racing heart, fast breathing, tense, alert). The parasympathetic branch is the opposite, the "we're safe, calm down" mode. The vagus nerve runs the parasympathetic system. When it fires, it releases acetylcholine to your heart and organs (slowing them down), and the brain reads that calm body state and responds by raising GABA, dropping cortisol, and reducing noradrenaline. This is how deep breathing, cold water on the face and humming calms you down.
• MAO (Monoamine Oxidase) is the enzyme your body uses to break down dopamine, serotonin, and noradrenaline after they've done their job.
  • MAO-A preferentially breaks down serotonin and noradrenaline. Inhibiting it raises serotonin and noradrenaline. This is what classical antidepressant MAOIs target.
  • MAO-B preferentially breaks down dopamine. Inhibiting it raises dopamine specifically, which is why selective MAO-B inhibitors (Selegiline, 9-Me-BC) are used for motivation, focus, and Parkinson's-related dopamine preservation.

Tier 0 — Cookie cutter lifestyle and behaviour advice

• Gradual exposure. For any anxiety that's situation-specific, exposure works trough fear extinction learning: when you encounter a feared situation repeatedly without the bad outcome happening, the prefrontal cortex learns to inhibit the amygdala's fear response.
• Sleep. 7-9 hours, consistent timing. Sleep deprivation hits anxiety through the amygdala (fear centre) becoming more reactive, and the prefrontal cortex's brake on it weakens. GABA is replenished during sleep, so loss leaves the brain's calming signal underpowered. And the cortisol curve inverts (high at night, low in the morning), which drives more anxiety.
• Aerobic exercise. 30-45 minutes daily. Reduces anxiety acutely (lower for hours after) and chronically (resets HPA axis tone over weeks). Comparable to SSRIs for mild-to-moderate anxiety in head-to-head trials.
• Breathwork. Specifically the physiological sigh (double inhale through nose, long exhale through mouth) for acute panic, or box breathing (4-4-4-4). Longer exhale than inhale activates the parasympathetic system directly. do 5 min before any acute situation.
• Cut caffeine if you’re sensitive. Caffeine raises noradrenaline and cortisol. Cut it for two weeks and see what your real baseline is.
• Sunlight in the morning. Anchors circadian rhythm and regulates cortisol's natural curve. Morning sun supports the right cortisol pattern (high in the morning, low at night).
• Time in nature. Urban environments bombard the nervous system with low-level sensory threats that keep the sympathetic system activated. Nature has less of this, the parasympathetic system takes over by default.
• Cold exposure. Acute discomfort followed by sustained parasympathetic activation. Also useful as exposure training for tolerating physical anxiety symptoms.