More on Low-Dose Sublingual Ketamine

"The standard explanation is that ketamine blocks NMDA receptors. These receptors bind glutamate, which is a chemical messenger found throughout the brain and body. By blocking NMDA receptors, ketamine increase "brain-derived neurotrophic factor" (BDNF), a protein which I refer to as "Miracle-Grow for the brain." BDNF promotes neuroplasticity-which is the growth of new connections (synapses) in the brain. This has traditionally been viewed as the primary mechanism responsible for ketamine's therapeutic benefits. But ketamine does so much more!"

"You can think of neuroplasticity as your brain's ability to rewire itself. Depression, anxiety, and trauma are disorders of brain connectivity- neural networks become rigid or break down. Ketamine "repairs" these networks. These neuroplastic changes don't require high doses. High-dose intermittent treatment can produce dramatic immediate effects, but may not provide the sustained stimulation needed for lasting change."

Low-dose sublingual ketamine produces marked improvement in treatment-resistant depression by blocking NMDA receptors, increasing BDNF, and promoting neuroplasticity. Neuroplasticity restores connectivity compromised by depression, anxiety, and trauma by growing new synapses. Ketamine also stimulates sigma-1 receptors, reducing inflammation and protecting neurons. Daily low-dose administration may provide sustained stimulation superior to intermittent high doses. Low doses are inexpensive, safer, and cause less dissociation than higher doses. Multiple mechanisms beyond NMDA antagonism contribute to ketamine's therapeutic effects. Sustained low-dose protocols optimize long-term neuroplastic adaptation without inducing severe dissociative side effects. Accessibility and safety profiles favor broader clinical implementation.

Read at Psychology Today