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Johns Hopkins Health Alert

Antidepressant Medication “Poop Out”

Comments (3)

A reader from Roswell, Georgia asks: “I have been taking 20 mg/day of Celexa (citalopram) for about a year and a half for depression. It was the first medication I tried, and it worked great. For the past two months or so, however, I haven't been feeling great. I have been sleeping a lot, crying a lot, and feeling antisocial. Is it possible for Celexa to "poop out" and just stop working over time? Should I talk to my doctor about increasing my dosage or changing medications? Or maybe this bout with depression is just extra bad and I should tough it out?” Here’s our advice.

Antidepressant tachyphylaxis -- known less formally as the "poop out" effect -- was first described in 1984 when researchers observed that some patients experienced relapse of mood symptoms on antidepressants that had previously been effective therapies. There is some suggestion that serotonin reuptake inhibitors, or SSRIs, such as Celexa, are more prone to tachyphylaxis than other antidepressants, such as tricyclic medications like nortriptyline and serotonin norepinephrine reuptake inhibitors (SNRIs) like Effexor.

When antidepressants appear to "poop out," there are four options available to the physician and patient. The first is to increase the medication dosage in an effort to boost the antidepressant effect, assuming the maximum dose is not already prescribed. For example, the maximum dose of Celexa is 60 mg daily. A common pattern with SSRIs is for there to be an initial response to a lower dose that is not sustained, requiring titration over time to higher doses. Increasing the dosage alone may be sufficient to jumpstart recovery.

The second option is to switch antidepressant medications, either to another medication within the same class or to a different class. This method has the benefit of simplicity, in that it continues to be a single medication regimen.

The third and fourth options involve augmentation of the current antidepressant, either with the addition of a second antidepressant or a non-antidepressant augmentation drug. If a second antidepressant is chosen, it is common to add a medication with a different mechanism of action. For example, if someone is already taking an SSRI, the physician might add a tricyclic antidepressant. Non-antidepressant augmentation strategies include lithium, low-dose atypical neuroleptics such as Zyprexa or Risperdal, thyroid hormone, the blood pressure medication Pindolol, or the anti-anxiety drug Buspar (buspirone).

Bottom line: In most cases like yours, the simplest intervention is to increase the dosage of the antidepressant medication you're already taking, particularly because it has been effective in the past and you're not currently taking the maximum dosage. The key to successful treatment of depression is ongoing communication between you and your physician and not settling for partial recovery or resigning oneself to "toughing it out."

Posted in Depression and Anxiety on November 11, 2009
Reviewed January 2011


Medical Disclaimer: This information is not intended to substitute for the advice of a physician. Click here for additional information: Johns Hopkins Health Alerts Disclaimer


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Health Alerts registered users may post comments and share experiences here at their own discretion. We regret that questions on individual health concerns to the Johns Hopkins editors cannot be answered in this space.

The views expressed here do not constitute medical advice, and do not represent the position of Johns Hopkins Medicine or Remedy Health Media, LLC, which has no responsibility for any comments posted on this site.


All antidepressants are "addictive," in the sense that they fairly quickly induce the features of substance dependence. According to the DSM-IV, these features include tolerance, withdrawal, unsuccessful efforts to cut back, continued use for longer periods of time than originally intended, and continued use despite known adverse effects.

Once tolerance has emerged in an antidepressant consumer [and in my clinical experience, it always does], the correct intervention is usually not in the direction of dose increase [animal studies have shown that drug use results in the down-regulation of SERTs, downregulation of serotonin turnover, and damage to nerve endings], nor is it in the direction of "chemical augmentation" [since the "new" agents are often equally neurotoxic and depressogenic]. Rather, patients must be helped with gradual detoxification off the offending agent, followed by careful neurorehabiliation.

Posted by: Grace E. Jackson MD | November 11, 2009 10:26 AM

And the fifth response is to send the client to a psychologist, cognitive-behavioral therapist or other mental health specialist who has expertise in the social, contextual, and environmental aspects of chronic depression in order to assess and treat the root cause(s) rather than continue to feed and, very possibly, to sustain them with medication. A possible sixth response would be for those responding to questions on this site to become more familiar with the extensive treatment literature that focuses on cognitive behavioral assessment and intervention for chronic depression since depression can be triggered by and/or very actively sustained as a result of errors in thinking and attributional deficits (among other social-contextual variables) both of which are correctable without medication. In fact, the persistent use of medication may only be further solidifying and reinforcing these 'errors in thinking' as the person becomes increasingly disempowered and less able to understand their own role in a return to mental health while being led to believe that the medication will somehow 'correct' their depression and those conditions/triggers which have lead to and sustained the depression. All too often, those conditions leading to chronic depression lie outside of the individual rather than deep inside like a cold or flu Medication can have relevance in the treatment of depression. But it should hardly be viewed as a means to the end and, as extensive treatment literature recognizes, should be part of an integrated behavioral-pharmacological approach. Simply changing the script or adding additional scripts to somehow 'enhance' the efficacy of the first script is problematic in general and especially so if these other therapeutic models have been overlooked or otherwise minimized.

Posted by: bfs46 | November 14, 2009 5:14 PM

A promising non-pharmacological alternative therapy for depression could be Neurofeedback (aka EEG Biofeedback). While there have been no double-blind studies done as yet, clinical reports and case studies have noted a positive response in reactive, endogenous, and cognitive depression. A fuller report may be found in Chapter 14, by Neurologist Jonathan Walker: in The Handbook of Neurofeedback, Dynamics and Clinical Applications, James Evans, PHD, Editor. Haworth Medical Press, 2007.

Posted by: michael sitar phd | November 16, 2009 3:57 PM

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