One of the most influential models in psychiatry’s history for understanding brain dysfunction is the monoamine hypothesis.  In short, it proposes that deficiencies or excess of certain neuromodulating agents, in particular the monoamines serotonin, dopamine, and norepinephrine (AKA noradrenaline) drive many psychiatric disorders.  The paper I will primarily reference is a publication by the same name in 2016 by Montoya, Bruins, Katzman, and Blier in Neuropsychiatric Disease and Treatment.  Its basic proposal is that, at the time of publication, there were at least 52 controlled clinical trials published that consistently showed a benefit of using SNRIs (like venlafaxine and duloxetine) and NERIs (like atomoxetine and reboxitine) for reducing anxiety in patients without the expected side effect of noradrenergic agents: to increase anxiety.  This is a paradox. 

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