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Low-dose ketamine stimulates neuroplastic changes by increasing brain-derived neurotrophic factor.

Ketamine reduces inflammation and protects neurons from damage by stimulating sigma-1 receptors.

Daily low-dose ketamine may be more effective than intermittent high-doses for sustained improvement.

Low doses of ketamine are inexpensive, safer, and do not cause severe dissociation like higher doses.

In my previous post, I shared my journey discovering that low-dose sublingual (LDSL) ketamine produces remarkable results in patients with treatment-resistant depression. Now, let's explore why lower doses may actually be more effective.

Understanding How Ketamine Works

After 3 years of observing my patients' amazing responses to treatment with low dose sublingual ketamine (LDSK), I wanted to understand more about how this medicine works. 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!

The Neuroplasticity........

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