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Sedating or activating antidepressants that cause


Prescribing of antidepressant treatment ADT for major depressive disorder MDD has increased in quantity and popularity over the last two decades. This is likely due to the approval of safer medications, better education of clinicians and their patients, direct-to-consumer marketing practices, and Sedating or activating antidepressants that cause stigma associated with those taking ADT.

This trend has also been met with some controversy, however, as the ongoing safety and effectiveness of these treatments have at times been called into question.

This paper discusses the differing levels of evidence that support the use of ADT based on A Food and Drug Administration approvals, B data from randomized controlled trials or meta-analyses and, where these are not available, the authors discuss and apply, C theoretical pharmacodynamic principles to justify antidepressant choice in the treatment of MDD patients.


The final section discusses standard psychopharmacology guideline approaches to better alert the reader as to which practices are commonplace compared with those which are more outside of the standard of care.

This ultimately incentivized pharmaceutical companies to develop antidepressant treatments ADTs specifically targeted to correct these neurochemical imbalances. Their unprecedented success and popularity heralded prescription therapy as a clear standard of care for MDD of any severity; byADTs were the third-most prescribed medication in the USA [ 1 ]. As scientific knowledge of the neurobiological basis for MDD continues to increase, so too, in apparent lockstep, does the arsenal of drugs used to treat it.

In addition to the wide array of ADT classes available on the market today, each modulating one or more of the relevant biogenic amines serotonin, norepinephrine, dopaminethere exists a panoply of diverse compounds per class, all with distinct pharmacokinetic and pharmacodynamic properties affecting drug potency and efficacy. The abundance of pharmaceutical alternatives over the years has engendered both Sedating or activating antidepressants that cause and skepticism from those in the psychiatric community.

On the one hand, a mixed bag of options means Sedating or activating antidepressants that cause opportunity for individualization i. The fact that one in ten citizens is currently prescribed an ADT may reflect overtreatment of patients with subsyndromal MDD or adjustment disorders [ 2 ].

However, data also suggest that only half of the MDD patient population is accurately diagnosed and that only half of the accurately diagnosed MDD population is adequately prescribed [ 3 ].

Thus, two distinct problems—overprescribing and inadequate prescribing—need to be addressed, in part by increasing awareness of the proper ADT treatment guidelines. What poses perhaps a bigger problem to the advancement of MDD Sedating or activating antidepressants that cause is failure to recognize the importance of illness heterogeneity no less than ADT heterogeneity. As part of a fluid spectrum of mood disorders, MDD may manifest very differently in some patients than in others, defying nosological convention or straightforward syndromal classification.

As an example, melancholic depression presents very differently from an atypical depression or a seasonal one.

generally more sedating than citalopram,...

This paper seeks not only to challenge this assumption and emphasize the need for personalized MDD treatment, but to offer a brief, synthesized compendium of information on available ADT that may guide the general clinician through the lesser-known subtleties and complexities of psychopharmacological practice. In clinical research, randomized controlled trials RCTs represent the gold standard by which the overall quality of drugs, treatments, and other therapeutic interventions can be assessed and compared.

Furthermore, to judge ADT efficacy based largely on this arbitrary benchmark, set across all MDD trials, would appear to assume homogeneity of the MDD patient population with regard to symptom type and severity. This assumption, however, rarely holds, and, if taken for granted, can lead to underpowered RCTs and to the inaccurate interpretation that all antidepressants are equal. Clinical practice, which often renders apparent those subtle patient differences obscured in clinical trials, is a constant rebuke to that "Sedating or activating antidepressants that cause" [ 1011 ].

Such a difference can be expressed with the standardized term effect size referred to as d. In this case, the effect size d would equal 0. This would be considered a large effect size, suggesting a high likelihood that the ADT is very effective in treating MDD. If smaller treatment differences d are to be observed, then RCT sample sizes would need to be greatly increased to ensure good Sedating or activating antidepressants that cause power.

This approach, or this type of large study, is relatively unheard of in psychiatric trials and may explain why no clear RCT literature exists to definitively show superiority of one ADT over another. Type 2 bias errors in antidepressant clinical trials have increased over time as well [ 10 ].

Intent-to-treat principles in analyzing study results, decisions to conduct longer trials, and completing trials in less severe patients and ambulatory settings all have resulted in higher attrition rates [ 815 ]. These older trials often included more severe, more chronic, and more melancholic MDD patients as well. The net result is to have all ADTs appear to be equally effective. Meta-analyses are also used to better delineate ADT efficacy differences.

There are two types of meta-analyses: The former method is more widely used, as it is easier to obtain these data through literature searches than it is to obtain raw rating scale data from many different corporate trials. Meta-analyses may be biased depending on which studies are included or excluded and what data Sedating or activating antidepressants that cause utilized or discarded, and are often open to greater controversy post hoc than RCT.


Meta-analyses are often met with controversies that result in conflicting editorials in journals and lay press about how to interpret the initial results.

These two classes of compounds comprise the earliest specific ADT. Their clinical introduction in the s following fortuitous discovery of their antidepressant properties marked the advent of psychopharmacotherapy as an indispensable tool in the treatment of MDD and spurred the first monoaminergic theories in the etiopathogenesis of depression. TCAs, which take their name from the basic three-ring chemical structure common to them, act primarily by elevating serotonin and norepinephrine levels via uptake inhibition similar to the later developed serotonin norepinephrine reuptake inhibitors [SNRIs] mechanistically.

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