For the last five decades, the prevailing theory for the origins and development of depression and anxiety has pointed to low levels of certain neurotransmitters in the brain as the culprit. Consequently, targeting these key neurotransmitters – such as serotonin, norepinephrine, dopamine, and GABA – became a major focus in the development of treatments for these disorders.
As a result, medications thought to help correct this “chemical imbalance” — such as SSRIs and benzodiazepines — have dominated psychiatry for decades. While these medications have long been the gold standard of treatment, they’ve garnered considerable criticism for their unsatisfactory rates of effectiveness, long delays before patients feel a positive impact, and unpleasant side effects. Studies report that between 30% and 50% of patients with depression treated with traditional antidepressants experience no improvement in their symptoms, while only about 50% of patients with anxiety respond to conventional treatments. So while these medications have offered relief for countless people, they’ve failed to do the same for innumerable others, leaving millions without adequate treatment for their mental illnesses.
Research has established that the factors underlying disorders like depression and anxiety are far more nuanced than the previous cut-and-dried presumption of a deficiency in serotonin or norepinephrine. A growing number of scientists are endorsing a broader view that points to abnormalities in higher-level neuron circuit functioning, connections between neurons, and neuron growth.
This view is supported by the finding that both depression and anxiety disorders are marked by a loss of neurons and a reduction in connectivity within particular regions of the brain, such as the prefrontal cortex and the hippocampus.5 These powerful higher brain centers coordinate a range of fundamental cognitive processes, regulating our thoughts, moods, and emotions.
A loss of connections in these regions, as is seen in conditions like depression and anxiety, interferes with the ability of these structures to function properly, leading to impaired cognition and disruptions in normal mood and emotional control. The association between depression and anxiety disorders and these structural abnormalities has spurred a surge of interest in finding treatments that could potentially reverse this damage, such as through supporting the generation of new neurons and the growth and strengthening of connections between nerve cells and circuits.
Those processes fall under the umbrella of a phenomenon known as neuroplasticity, which refers to the brain’s remarkable ability to change, adapt, and reorganize itself throughout life. Neuroplasticity is a crucial function of a healthy brain, and includes processes like neurogenesis (the formation of new neurons), synaptogenesis (the formation of new connections between neurons), and the strengthening – or weakening – of existing connections between neurons and neural circuits. The brain’s ability to rewire and reprogram itself is its innate superpower, one that lies within all of us.
We’ve come to understand that this high level of activity observed in the brain during idle periods is a product of what we now call the default mode network. We can think of the DMN as our internal dialogue – it becomes active when we think about ourselves or about others or about the world, when we reflect on the past or imagine the future, and when we engage in activities like contemplation, reflection, daydreaming, and emotional processing.
The DMN is most active when the brain is not focused on the external world and is instead engaged in introspective thought, but this network never fully “turns off.” It remains active in the background of all we do, consciously or unconsciously, in our daily lives.
We know from studies imaging the brains of meditation practitioners that mindfulness and other forms of meditation have been shown to reduce DMN activity. We also know that the same seems to be true for psychedelics, which regulate the connectivity between the DMN and areas of the brain active in task behavior, while also decreasing within network DMN activity.
Ketamine specifically has been shown to modulate the functional connectivity and activity of the DMN, allowing for regulation of previously dysfunctional processes involved in depression and anxiety. During a ketamine session, connectivity within the frontal regions of the DMN decreases, essentially “turning down the volume” on our default thought patterns and providing space to reflect on these repetitive scripts with renewed perspective.
Via Wondermed
Below is the protocol that ALL VA's Mental Health Providers are supposed to follow when a patient that has Treatment Resistant Depression and/or Severe Suicidal Ideations, requests Ketamine.
If you are a ketamine provider interested in helping Veteran's access Ketamine Therapy, please sign up to be a community care provider with your local VA here
Seeking care outside of the VA? Providers like Wondermed & Mindbloom provide Ketamine Therapy virtually with mental health providers in the privacy of your own home. If you're a Veteran and choose to use Wondermed use code VETERANS80 to get 20% off.
Comments