Why Ketamine Isn’t the Escape It Seems

Ketamine was first developed (or synthesised) in the 1960s, derived from its parent drug “phencyclidine” in the pursuit of an anaesthetic with fewer hallucinogenic effects. Ketamine still has a powerful effect on the brain’s perception of pain and reality. 

Ketamine works by blocking NMDA receptors, which are involved in the regulation of mood, memory and cognition. This is what gives ketamine its well-known dissociative and “out-of-body” effects, with sensations of being detached from your surroundings, or even your own body.

The disruptions these effects cause are profound if ketamine is abused over the long term. Research on extended ketamine risks found that repeated misuse can lead to neurochemical instability, as the brain’s glutamate and dopamine systems become impaired, affecting mood balance, appetite and emotional stability.

Beyond the brain, recreational ketamine dangers can affect many areas in the body, sometimes permanently. Ketamine-induced cystitis is common in chronic users, leading to persistent bladder pain, frequent urination, or potential incontinence. These outcomes become harder to reverse when abuse develops into full-blown dependency, often setting the stage for life-threatening ketamine risks.

The dangers when relief gives way to dependency

The shift from “escape” to dependence can happen more quickly and quietly than most people expect. Every time the drug is taken, the brain learns to adapt, and the original effects become dulled. More is needed in subsequent uses to achieve the same effects, so that eventually, the pathways between the brain and body that process pleasure and stress become impaired. 

With time, emotional flatness becomes common, and ketamine seems to offer the only relief. This is the treacherous cycle that keeps so many trapped, wherein a moment of freedom from pain soon becomes another form of imprisonment, both physically and emotionally.