Why Cognitive Behavioral Therapy is Vital to the Success of Depression Treatment
About the Author Dr. Steven P. Levine is a board-certified psychiatrist internationally recognized for his contributions to advancements in mental health care. Though he is a psychiatrist who places great emphasis on the importance of psychotherapy, medication is often a necessary component of treatment, and he was dissatisfied with the relatively ineffective available options with burdensome side effects. Dr. Levine pioneered a protocol for the clinical use of ketamine infusions, has directly supervised many thousands of infusions and has helped establish similar programs across the country and around the world.
Why Do Most Psychologists Practice Cognitive Behavioral Therapy?
Study after study confirms that a combination of medication and psychotherapy is more effective than either one alone.1 The most frequently chosen approaches for these studies are selective serotonin reuptake inhibitors (SSRIs) and cognitive behavioral therapy (CBT). Is there something uniquely effective about either? Not necessarily – but SSRIs are the most popular first-line choice of antidepressant/antianxiety medication, and the fact that CBT has a manual-based structure makes it easy to study in research. For this reason, CBT is a widely practiced method for replacing the automatic negative thoughts of depression and anxiety with more balanced alternatives.
I’ll come back to this.
There are many options for the treatment of major depression and the spectrum of anxiety disorders, roughly lumped together because of their common co-occurrence and therapeutics. Biological interventions – treatments that directly affect body/brain chemistry as opposed to “talking treatments” – include prescriptions medications, nutritional supplements, brain stimulation technologies, and exercise. There are also hundreds of actively practiced styles of psychotherapy.
When we talk about the brain, we must necessarily oversimplify.
We are limited by our current knowledge and by the need to masticate something so dense and complex into a palatable form. In that spirit, the hippocampus is the putative center of memory and learning, a major component of the emotion regulation system, and the only site of lifelong neurogenesis, the production of new neurons. It may not be an accident that these significant functions take place within the same structure (hippocampus).
Perhaps human memory is similar to computer memory. Computer memory storage has a finite capacity. When filled, old memories must be deleted to make space for the new. But, we don’t lose all those memories (and I use the term “memory” loosely to include stored knowledge, feelings, thoughts, skills, etc). And, similar to computer memory, they are never completely erased – there are traces left that can be mined by those skilled at doing so. We retain a relatively select few, likely because of some special significance or because of stories told by family and others. Some may be so frequently repeated that they become “overlearned”, meaning that they are given so much space in the brain that they are highly resistant to forgetting.
The inability to forget negative memories may partly explain the difficulty in treating depression and anxiety, states in which depressive ruminations and anxious obsessions result in copy after copy after copy of destructive thoughts, memories, and feelings. One of the most notoriously treatment-refractory subtypes of anxiety is obsessive-compulsive disorder (OCD), a condition in which the process of making copies of obsessive thoughts occupies a significant portion of daily life – unchecked, the competition doesn’t stand a chance.
Having a good memory is generally considered a laudable quality. In consideration of the above, perhaps it is as, or more, important to be a “good forgetter”. This, of course, does not mean deleting one’s memory, but allowing for a diminished representation of negative, harmful memories over time by altering (re-framing) and re-copying them in a more useful way or by filling up the memory storage space with some other new material. This process is a common thread that runs through many of the hundreds of psychotherapy styles mentioned above.
Although an older theory of depression focused on brain chemicals such as serotonin, norepinephrine, and dopamine being “out of balance”, it is now believed that even medications that affect these chemicals as a first step (like SSRIs) ultimately promote brain plasticity. Plasticity is the capacity to repair, grow, and form new connections in the brain, helping it to recover from the damage of depression and anxiety. A medicine called ketamine, that was FDA approved in 1970 as an anesthetic, has been shown to very rapidly promote plasticity and potentially enhance new learning. Its rapid antidepressant effect has led to widespread off-label adoption around the world, and to serve as a model for new treatment development.
CBT Helps Train Your Brain to be Well
Psychotherapies like CBT capitalize on this fertile environment of plasticity that is primed for new, healthy learning. In this way, we have an explanation for why SSRI + CBT is more effective than either one alone.2 IV ketamine, the most exciting advance in the treatment of mood and anxiety disorders in decades, is an agent that is fairly unique in its capacity to very rapidly restore connections and promote new learning. In fact, a 2017 Yale study showed that CBT following ketamine helped extend the antidepressant benefit. So, when treatment is needed for depression or anxiety disorders, please consider a provider that values this combined and most effective approach.
- Wilkinson ST, Toprak M, Turner MS, Levine SP, Katz RB, Sanacora G. A survey of the clinical, off-label use of ketamine as a treatment for psychiatric Disorders. Am J Psychiatry. 2017;174(7):695-696. doi:10.1176/appi. ajp.2017.17020239.
- Morgan CJA, Riccelli M, Maitland CH, Curran HV. Long-term effects of ketamine: evidence for a persisting impairment of source memory in recreational users. Drug Alcohol Depend. 2004;75:301-308. doi:10.1016/j.drugalcdep.2004.03.006.