Review: Bupropion and SSRI-induced side effects

University Psychiatric Center KuLeuven, Campus Gasthuisberg, B-3000 Leuven, Belgium.
Journal of Psychopharmacology (Impact Factor: 2.81). 03/2008; 22(7):792-804. DOI: 10.1177/0269881107083798
Source: PubMed

ABSTRACT Selective serotonin reuptake inhibitors (SSRIs) are a first line treatment option for millions of patients, due to the positive balance between efficacy and tolerability. However, some side effects associated with their use, can impair quality of life and compliance with treatment. This paper reviews the prevalence of sexual dysfunction, weight gain and emotional detachment during SSRI treatment, the profile of bupropion for each of these events and the ability of bupropion to reverse them. Double-blind trials, open-label trials and anecdotical reports derived from Medline were included. First, there is robust evidence that SSRIs can induce sexual side effects and that bupropion causes less sexual dysfunction than SSRIs. There is limited, mainly open-label evidence that bupropion can reverse SSRI-induced sexual side effects. Second, there is good evidence that long-term treatment with some SSRIs can result in weight gain and that long-term treatment with bupropion can result in a small weight loss. There is only anecdotical evidence that bupropion can reverse SSRI-induced weight gain. Third, treatment with SSRIs has been associated with ;emotional detachment', although controversy exists about this concept. No data are available on the profile of bupropion for ;emotional detachment' or for the reversal of SSRI-induced ;emotional detachment' by bupropion-addition.

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    • "An early meta-analysis of studies with differing methodologies (including open-label, double-blind, cross-sectional, and retrospective investigations) indicates that " treatmentemergent sexual dysfunction " is no more common with agomelatine, amineptine, bupropion, moclobemide, mirtazapine , or nefazodone than it is with placebo, in contrast to the situation with other antidepressants [17] (Table 1): all other antidepressants were significantly more likely than placebo to be associated with sexual dysfunction, as a unitary category, and nearly all of these were significantly more likely to be associated with dysfunction in each stage of the normal sexual response. A meta-analysis of randomized controlled trials of the efficacy and tolerability of acute treatment of major depressive episodes with " second-generation " antidepressants indicates that bupropion is associated with a significantly lower rate of treatment-emergent sexual dysfunction than is seen with escitalopram, fluoxetine, paroxetine, or sertraline [18]: this is probably due to the nonserotonergic but predominantly noradrenergic-dopaminergic mechanism of action of bupropion [19]. A systematic review of the relative efficacy and tolerability of mirtazapine and comparator antidepressants in the acute treatment of major depression suggests that mirtazapine is significantly less likely than other antidepressants to cause adverse sexual effects [20], which is probably related to its antagonist effects at both the alpha-2 adrenergic receptor and the 5-HT 2C receptor [21]. "
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    ABSTRACT: Pleasurable sexual activity is an essential component of many human relationships, providing a sense of physical, psychological, and social well-being. Epidemiological and clinical studies show that depressive symptoms and depressive illness are associated with impairments in sexual function and satisfaction, both in untreated and treated patients. The findings of randomized placebo-controlled trials demonstrate that most of the currently available antidepressant drugs are associated with the development or worsening of sexual dysfunction, in a substantial proportion of patients. Sexual difficulties during antidepressant treatment often resolve as depression lifts but can endure over long periods and may reduce self-esteem and affect mood and relationships adversely. Sexual dysfunction during antidepressant treatment is typically associated with many possible causes, but the risk and type of dysfunction vary with differing compounds and should be considered when making decisions about the relative merits and drawbacks of differing antidepressants. A range of interventions can be considered when managing patients with sexual dysfunction associated with antidepressants, including the prescription of phosphodiesterase-5 inhibitors, but none of these approaches can be considered "ideal." As treatment-emergent sexual dysfunction is less frequent with certain drugs, presumably related to differences in their pharmacological properties, and because current management approaches are less than ideal, a reduced burden of treatment-emergent sexual dysfunction represents a tolerability target in the development of novel antidepressants.
    Depression research and treatment 02/2013; 2013(2):256841. DOI:10.1155/2013/256841
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    • "The present study findings are in line with efficacy trials that have demonstrated the weightgaining properties of antidepressants and antipsychotics (e.g., Allison et al., 1999; Demyttenaere & Jaspers, 2008; Fava et al., 2000; Sussman et al., 2001). Indeed, even after controlling for theoretically relevant variables, the obesity rate among persons taking antidepressants over the past 12 months was over one and a half times the rate observed among persons who did not take this medication; for antipsychotics this ratio was greater than two. "
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    ABSTRACT: Growing evidence points to a relationship between obesity and both mood and anxiety disorders, but the question of what accounts for this association remains unanswered. The present study examined the use of psychotropic medications as a mediator of the mood/anxiety disorder-obesity relationship. Data came from the public use dataset of the Canadian Community Health Survey Cycle 1.2 (age 15 years and older, N = 36,984). Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition psychiatric diagnoses of 12-month mood disorders (e.g., major depressive disorder, mania) and anxiety disorders (e.g., panic attacks, panic disorder, social phobia, agoraphobia) were examined as was use of psychotropic medications (e.g., antidepressants, antipsychotics, anxiolytics, hypnotics, mood stabilizers) and obesity (defined as body mass index ≥30). A series of multiple logistic regression analyses were completed to test study hypotheses. Covariates in these analyses included sociodemographic factors, physical activity, and physical illness burden. The use of two medication classes, namely antidepressants and antipsychotics, emerged as significant predictors of obesity as well as mediators of the psychiatric diagnosis-obesity relationship after evaluating all psychotropic medication classes simultaneously, while also controlling for other theoretically relevant variables. The use of these two medications accounted for 86% of the relationship between mood disorders and obesity and 32% of the relationship between anxiety disorders and obesity. The study findings guide advances in the theoretical conceptualization of the mechanisms involved in mood/anxiety disorder-obesity relations. Clinical implications are discussed.
    Journal of Psychiatric Research 04/2010; 44(15):1010-6. DOI:10.1016/j.jpsychires.2010.04.007 · 4.09 Impact Factor
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    • "These antidepressants have become a first-line treatment option for millions of patients due to their good balance between efficacy and tolerability. However, some adverse effects associated with their use such as, weight gain, sexual dysfunction, RLS, and emotional detachment, can impair the quality of life and compliance with treatment.5,6 Because it appears that these adverse effects are mainly associated with serotonin, many clinicians have moved toward the use of bupropion. "
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    ABSTRACT: Bupropion is a selective norepinephrine and dopamine reuptake inhibitor with no serotonergic activity, and is therefore an antidepressant with unique pharmacological properties. There are some reports that selective serotonin reuptake inhibitors (SSRIs) or mirtazapine can induce adverse effects including restless legs syndrome (RLS) and that bupropion can reverse these adverse effects. Here, we report about a patient with a major depressive disorder who exhibited RLS after being treated with pregabalin and mirtazapine. This adverse effect disappeared after having switched from mirtazapine to bupropion. Bupropion inhibits the reuptake of dopamine and increases dopamine neurotransmission in both the nucleus accumbens and the prefrontal cortex. This pharmacological profile can be effective in patients with RLS related to dopamine hypoactivity. However, the limitations of this single case report mean that further investigations with larger samples are needed.
    Psychiatry investigation 12/2009; 6(4):313-5. DOI:10.4306/pi.2009.6.4.313 · 1.15 Impact Factor
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