What is Neuroplasticity
Neuroplasticity is the brain's ability to reorganize itself by forming new neural connections during its lifetime.
As the fundamental units of the brain, neurons function to integrate and transmit a myriad of signals across complex networks. Neurons by definition are continually forming, eliminating, and modulating connections in response to the constant flow of information.
Neuroplasticity plays the main role in the brain's adaptation to stress, and dysregulation or disruption in neuroplasticity may cause various psychiatric disorders, such as depression, anxiety, post-traumatic stress disorder (PTSD), etc.
The Neuroplasticity Theory of Depression and Anxiety
The neuroplasticity theory of depression and anxiety is usually supported by findings of decreased neuroplasticity in certain areas of the brain and low concentration of neurotrophic factors, such as Brain-Derived Neurotrophic Factor (BDNF) in patients with depression, anxiety, and PTSD.
BDNF is involved in multiple levels of neuroplasticity like:
- Synaptic modulation (neuronal communication)
- Adult neurogenesis (growth of new neurons from neural stem cells)
- Dendritic growth (protoplasmic extension of a nerve cell)
The Role of Medicine in the Neuroplasticity Theory
Ketamine and psychedelics are suggested to increase levels of BDNF to normal levels. They also moderate glutamate levels, which multiple clinical studies suggest play an important role in the pathophysiology of depression.
Comparing to the Current Pharmaceutical Model (Monoamine Theory)
The Monoamine theory of depression was developed in the 1950s and has been the golden standard for psychiatric treatments for over 50 years.
The monoamine hypothesis of depression and anxiety states that the pathophysiologic basis of these disorders is a deficit in the levels of monoamines (serotonin, norepinephrine, and/or dopamine) in the central nervous system.
Limitations of the “monoamine hypothesis of depression” emerged in the 1990s, since it was proven that decreased levels of monoamines don’t induce depression in healthy people, nor do they cause worsening of symptoms in depressed patients.
Pharmaceutical Antidepressants on the Brain
Current treatments for depression primarily focus on targeting monoaminergic processes in the brain, but studies report that between 30-50% of patients treated with antidepressants experience no improvement in their symptoms, leaving a large population without adequate treatment for their depression.
Patients who do eventually respond to pharmaceutical antidepressants experience a delay in the improvement of their symptoms due to the fact that these antidepressants take weeks or even months before becoming effective.
Adverse effects of antidepressant drugs can increase non-compliance and delay recovery. Side effects associated with antidepressant use include sexual dysfunction, nausea, diarrhea, constipation, changes in appetite, weight gain, dry mouth, anxiety, insomnia, headaches, dizziness, restlessness, and an increased risk of suicidal thoughts and behaviors.
A monoamine imbalance in the brain must be permanently treated by a pharmaceutical intervention.
Neuroplasticity can be increased and maintained using advanced medicines and non-medicinal therapeutic modalities. Medicinal interventions may be impermanent.
Ketamine, Psychedelics, and Neuroplasticity
Multiple clinical studies suggest that the glutamatergic system plays an important role in the pathophysiology of depression.
Glutamate is a powerful excitatory neurotransmitter that is present in over 90% of all brain synapses. Glutamate plays an essential role in normal brain functioning and its levels must be tightly regulated.
Glutamate acts via stimulation of glutamate receptors (e.g., NMDA, AMPA or Kainate receptors). NMDA is a major glutamate receptor in the brain. By modulating NMDA we can directly increase neuroplasticity levels in the brain. We can prime the mind to respond more positively to stimuli that may otherwise trigger negative emotions and thought patterns.
Ketamine blocks the NMDA receptor, which causes antidepressant effects as rapidly as 24 hours after administration. These effects have been found to last days or even weeks.
Psychedelics are a class of hallucinogenic drugs whose primary effect is to trigger non-ordinary states of consciousness. Classic psychedelics produce mind-altering effects through agonism of the serotonergic receptors (5-HT).
Clinical studies suggest that by inducing brain neuroplasticity, psychedelics can be helpful in stress-related disorders.
Non-Medicinal Paths to Increase Neuroplasticity
In addition to ketamine and psychedelics, neuroplasticity can also be enhanced through non-medicinal modalities. Wondermed uses some of these additional self-healing modalities alongside their treatment protocol to encourage patients to create lasting changes in their mental health.
Try New Skills
Trying and practicing new and challenging skills, like learning to play an instrument or speak a new language. Novel experiences, such as traveling and exploring a new place, can also drive neuroplastic gains.
Exercise enhances brain function and health. Aerobic exercise has been shown to increase neurogenesis and influence the survival and maturation of neurons in humans.
Meditation enhances neuroplasticity and increases levels of BDNF. Meditation disrupts negative thinking patterns associated with stress, anxiety, and sadness and replaces them with more positive thoughts and emotions.
Regular meditation results in continual reinforcement of these positive pathways, strengthening them over the long term and leading to greater brain health and overall well-being.
Sleep is another important component of maintaining healthy brain plasticity. Chronic sleep deprivation has been shown to decrease BDNF levels in the brain and decrease neurogenesis. Adequate, healthy sleep has been shown to reverse these impairments.
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