In our last post, we introduced one of two prevailing theories in medicine as to how neurotransmitter imbalances occur.  Recall that our approach to eliminating the urge to pull is based on premise that trichotillomania, along with many other disorders, often results from imbalances in neurotransmitter levels.  By reestablishing these levels, we can eliminate the urge to pull.  Now to further introduce the Monoamine Theory:

The monoamine theory of depression has long been the major framework against which the treatment of depression has been examined and developed due to the fact that the theory attempts to provide an explanation for depression and the actions of antidepressants. The central premise of the monoamine theory states that it may be possible to restore normal function in depressed patients by targeting the catecholamine and/or serotonin systems with antidepressants. This theory is based on evidence that depression symptoms can be improved by administering compounds that are capable of increasing monoamine concentrations in the nerve synapses.

Early research focused on deficits in the catecholamine system with specific emphasis on noradrenalin as a potential cause for depression. With further research, the theory was expanded to include the serotonin system as a cause for depression. This research has led to the use of drugs for treatment of depression that affect changes in monoamine uptake and enzymatic metabolism.1

While many of the depression treatments based on the monoamine theory appear to be initially useful, many of them lack the short-term and long-term efficacy needed for relief of symptoms in most patients. In several studies of reuptake inhibitors administered only 8% to 13% of subjects obtained relief of symptoms greater than placebo. 27,28,29,35,50,51,52,53,54,55

Let me repeat that so that it sinks in – studies show that reuptake inhibitors (including these) only work for about 8-13% of people taking them over placebo!

Treatment with reuptake inhibitors is based on the monoamine theory, which does not explain why most subjects studied achieve results no better than placebo and why treatment is much less efficacious in the elderly. Neither does it explain the efficacy of treating other conditions, including trichotillomania. In sum, the mechanism and corresponding medication for the treatment of depression suggest there may be more to the underlying pathophysiology. This has led to the development of the Bundle Damage Theory which we will present in the next post.