Many doctors are hesitant to put people with bipolar disorder on antidepressants because of possibly cycling into the mania. While doctors treat the manic phase of the mood disorder, they are often remiss in treating the depressive side for fear they will trigger the manic side. Lately in the news one is hearing more and more warnings for instance about Paxil and bad side effects on teenagers. Makes one wonder if some of these teenagers are actually bipolar and are suffering bipolar depression and are being given an antidepressant without a mood stabilizer and creating worse symptoms...What a way to get diagnosed! What a way to get misdiagnosed! What a tragic way for more doctors to become more careful about investigating bipolar disorder and not assuming that an antidepressant is all that is needed.
Advances are being made. Less reliance is being placed on the standard and relatively inexpensive lithium and movement is toward the anticonvulsants..the crossover drugs that are primarily used for epilepsy. As they appear to be helping many bipolar suffers, some researchers are beginning to believe there is a connection between the two disorders.
This page simply refers to the research abstracts in pubmed on bipolar disorder and the well known antidepressants Effexor and Wellbutrin to see what the findings were...especially in triggering manic episodes...Please skim the articles or show them to your psychiatrist.
The more one reads about these drugs, the more one realizes how one needs a very patient and "gifted" psychopharmocologist to find the right cocktail or mixture of drugs.
Please click here for research for antidepressants and sexual dysfunction and which antidepressants have less side effects such as Wellbutrin.
http://www.dr-bob.org/babble/ is a very active message board called psycho babble where people discuss their reactions to medications to pyschopharmaceuticals
Brain Talk Communities
The safety profile of the selective serotonin reuptake inhibitor, fluvoxamine, has been assessed in clinical and post-marketing studies. Post-marketing surveillance provides the opportunity to assess a drug's safety in every day clinical conditions in a much greater patient population than in clinical trials and therefore serves as a useful tool to detect signals for adverse effects with an incidence of less than 1 : 10,000. The safety profile of fluvoxamine was evaluated based on data from 17 years of global post-marketing surveillance in an estimated 28 million patients exposed to fluvoxamine. A total of 6,658 adverse drug reaction reports received from world-wide sources were reviewed and analysed. Post-marketing surveillance data confirmed the favourable safety profile already observed in clinical and post-marketing studies. A remarkably low level of suicidality, switch to mania, and sexual dysfunction was found. Serotonin syndrome appeared to be a very rare complication of fluvoxamine treatment. No signals for drug interactions unknown so far were identified. Withdrawal symptoms were observed in everyday clinical conditions, which were generally mild and resolved spontaneously. However, no cases suggestive for drug dependence have been reported. In conclusion, the data presented underlined that fluvoxamine offers a safe and well-tolerated option in the treatment of depression and obsessive-compulsive disord
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Int J Neuropsychopharmacol. 2002 Jun;5(2):147-51. : Emotional blunting associated with SSRI-induced sexual dysfunction. Do SSRIs inhibit emotional responses?
Opbroek A, Delgado PL, Laukes C, McGahuey C, Katsanis J, Moreno FA, Manber R.
Anecdotal and published case reports suggest that some patients taking selective serotonin reuptake inhibitors (SSRI) experience diminution in emotional responsiveness. This study aims to define the individual components of emotion disturbed in these patients. Fifteen patients reporting SSRI-induced sexual dysfunction completed the Laukes Emotional Intensity Scale (LEIS), a questionnaire about various emotions. Compared to controls, patients reported significantly (p&0.05) less ability to cry, irritation, care about others' feelings, sadness, erotic dreaming, creativity, surprise, anger, expression of their feelings, worry over things or situations, sexual pleasure, and interest in sex. Total score on the LEIS did not correlate with total score on the Hamilton Depression Rating Scale. In our sample, 80% of patients with SSRI-induced sexual dysfunction also describe clinically significant blunting of several emotions. Emotional blunting may be an under-appreciated side-effect of SSRIs that may contribute to treatment non-compliance and/or reduced quality of life.
Familial concordance of fluvoxamine response as a tool for differentiating mood disorder pedigrees.
Concordance to antidepressant response in members of the same family is a common observation in clinical practice. However, few published data support this view; moreover families with affected members responder to the same antidepressant have been poorly studied. We have analyzed 45 pairs consisting of one mood disorder fluvoxamine double-responder proband and one first-degree relative with known outcome to fluvoxamine treatment. Among 45 pairs 30 (67%) were concordant for good response to fluvoxamine. In family pedigrees of concordant pairs we found a significantly higher distribution of bipolar forms in secondary cases than in families of non concordant pairs (14.9% vs 3.9% P = 0.039) suggesting that concordance to antidepressant therapy could select families with higher genetic loading.
Int Clin Psychopharmacol. 2003 May;18(3):133-41. : A randomized, double-blind, 24-week study comparing the efficacy and tolerability of mirtazapine and paroxetine in depressed patients in primary care.
Wade A, Crawford GM, Angus M, Wilson R, Hamilton L.
Community Pharmacology Services Ltd (CPS), Clydebank, Glasgow, UK.
cps@cpsresearch.co.uk
Primary care patients with a major depressive disorder and 17-item Hamilton Rating Scale for Depression (17-HAM-D) score >18 were randomized to 24 weeks of treatment with mirtazapine 30-45 mg/day (n=99) or paroxetine 20-30 mg/day (n=98). Both treatments were efficacious in improving depressive symptomatology, as assessed by group mean 17-HAM-D scores, percentages of HAM-D responders and remitters and Clinical Global Improvement responders. The mirtazapine group showed statistically significantly larger decreases from baseline in group mean 17-HAM-D scores at weeks 1, 2 and 4, and the difference with the paroxetine group reached the level of clinical relevance at weeks 2 and 4. Antidepressant efficacy was maintained throughout both the acute and continuation phase of treatment. Both treatments were well tolerated. The only adverse event with a statistically significantly higher incidence in the mirtazapine group was fatigue. Statistically significantly more paroxetine-treated patients complained of increased sweating, headache and nausea. The results demonstrate that both mirtazapine and paroxetine were efficacious and well tolerated when used for 24 weeks in depressed patients treated in primary care. An observed difference in efficacy favouring mirtazapine between weeks 1 and 4 indicates that mirtazapine patients had improved earlier compared to those on paroxetine, and corroborates similar findings in other comparisons of mirtazapine versus selective serotonin reuptake inhibitors.
Neurosci Lett. 2003 Jul 17;345(2):105-8. : High platelet-serotonin uptake activity is associated with a rapid response in depressed patients treated with amitriptyline.
Franke L, Schewe HJ, Uebelhack R, Muller-Oerlinghausen B.
Department of Psychiatry, Laboratory of Clinical Neurobiology, Humboldt University (Charite), Schumannstrasse 20-21, D-10117 Berlin, Germany.
leonora.franke@charite.de
Based on the assumption that there is a biological basis behind the individual differences in the speed with which an antidepressant produces its therapeutic effects, we compared initial serotonin (5HT) uptake characteristics in platelets of rapid (2 weeks), slow (4 weeks) and non-responders in a group of 47 depressed patients who were treated with amitriptyline for at least 4 weeks. A response was defined as a reduction in the Hamilton Depression Rating Scale score of > or =50% from baseline. In 16 rapid responders, a significantly higher mean 5HT uptake efficiency (Vmax/Km) corresponded with a significantly higher 5HT uptake activity at a low, physiological substrate concentration in comparison with the 15 non-responders or the 16 slow responders (33.1+/-7.8 versus 25.5+/-7.7 versus 24.1+/-5.8 pMol [3H]-5HT/10(9) plat. x 5 min, respectively). The findings indicate that pre-treatment 5HT uptake activity contributes to the individual variability in response time to amitriptyline treatment.
EFFEXOR
BACKGROUND: The treatment of depressive episodes occurring in bipolar patients taking mood stabilizers is an understudied area of research with outstanding clinical consequences. This study was aimed to assess and compare the efficacy and safety of 2 different antidepressant drugs, paroxetine and venlafaxine, in this indication. METHOD: Sixty DSM-IV bipolar patients. each presenting with a major depressive episode while receiving mood stabilizers, were randomly assigned to either paroxetine (N = 30) or venlafaxine (N = 30) for 6 weeks in a single-blind manner. They had to score higher than 17 on the 17-item Hamilton Rating Scale for Depression (HAM-D-17) and have their mood stabilizer blood levels within the therapeutic range. Efficacy was measured by the HAM-D. Reports of side effects were collected at each visit; switch to mania or hypomania was specifically assessed by the Young Mania Rating Scale at 5 of 7 visits. RESULTS: Significant improvements in HAM-D scores were observed in both paroxetine- and venlafaxine-treated patients (Wilcoxon p < .0001). There were no significant differences in either efficacy or safety measures between the 2 drugs. By intention-to-treat analysis, 43% (N = 13) of patients taking paroxetine and 48% (N = 14) taking venlafaxine were considered to be responders. Only 3% (N = 1) of patients switched to hypomania or mania in the paroxetine group, whereas 13% (N = 4) switched in the venlafaxine group. CONCLUSION: Paroxetine and venlafaxine are both effective and safe in the treatment of depressive breakthrough episodes in bipolar disorder. There was a suggestion of a slightly higher risk for switch to mania or hypomania with venlafaxine
Mirtazapine is a new antidepressant with a specific pharmacological profile which is different from all other currently available antidepressants. It is a so-called noradrenergic and specific serotonergic antidepressant (NaSSA). 46 in-patients were treated with mirtazapine. The mean dose was 56 mg mirtazapine per day (SD: 23; range: 15 to 90). The duration of treatment was 3.6 weeks (SD +/- 3.4). Patients presented with following diagnosis: 29 (= 63%) were diagnosed as having a unipolar depression, 26% (n = 12) suffered from a depression in the course of a bipolar disorder. 37% (n = 17) were moderately depressed, 52% (n = 24) were severely depressed. 2 patients (= 4%) met ICD-10 (international Classification of Diseases) criteria for a schizoaffective disorder, 2 patients (= 4%) suffered from dysthymia. 1 patient suffered from an organic depressive disorder. The efficacy of the treatment was evaluated with CGI (Clinical Global Impression), when patients were discharged from hospital. 68% of the patients were in partial or full remission (CGI 2, 3 and 4), 17% were unimproved (CGI 5 and 6), in 15% of the patients the treatment was stopped before. Our observations are indicative that mirtazapine is effective in the treatment of moderately and severely depressed patients and therefore confirm the data obtained in phase III-trials. Furthermore we found mirtazapine in either mono- or combination-therapy with various other antidepressants to be tolerated well. Side effects did not cause in a single patient a discontinuation in treatment.
Does intolerance or lack of response with fluoxetine predict the same will happen with sertraline?[zoloft]
BACKGROUND: The purpose of this study was to determine whether sertraline would be well tolerated and effective in patients who had failed fluoxetine therapy or were unable to tolerate the medication. METHOD: Hospital records were reviewed for 88 consecutive patients started on sertraline treatment at McLean Hospital from February 11, 1992 to August 28, 1992. Forty-two patients were identified who had received sertraline treatment and who had had previous trials of fluoxetine. Patients were contacted after discharge to determine sertraline efficacy and side effects. A variety of patient characteristics and outcome measures were compared. RESULTS: Thirty-nine subjects (93%) were available for follow-up interviews. The DSM-III-R diagnoses at discharge were as follows: major depression (N=25), bipolar depression (N=6), schizoaffective disorder (N=4), and obsessive-compulsive disorder (N=4). The sertraline discontinuation rate was 64% (25/39) by a mean +/- SD of 2.3 +/- 2.1 months. In patients with major depression (N=25) and bipolar depression (N=6) discharged on sertraline, only 13 (42%) were considered responders to sertraline therapy, and at follow-up, only 8 (26%) of 31 were considered responders to sertraline therapy. Patients who had previously discontinued fluoxetine because of side effects were significantly more likely to have side effects during sertraline treatment (p = .027), and to have discontinued sertraline at follow-up (p = .018). CONCLUSION: Sertraline was found to be modestly efficacious and associated with numerous side effects and discontinuation rates in patients who had previously discontinued fluoxetine.
OBJECTIVE: The notion that antidepressant treatment-associated hypomania or mania being pharmacologically induced has been challenged. To determine whether selective serotonin reuptake inhibitors (SSRI) induced hypomania is secondary to medication effects, we examined the dose-response relationship of SSRI-induced hypomania in two patients with depressive disorder. METHOD: Case study. RESULT: Hypomanic symptoms emerged during treatment with sertraline at the dose of 300 mg per day in a 45-year-old male with major depression. Paroxetine treatment at the dose of 80 mg per day induced hypomania in a 37-year-old female with dysthymia and trichitillomania. These patients have no family or personal history of bipolar disorder. Hypomania resolved when sertraline was decreased to 200 mg per day and paroxetine to 40 mg per day. No hypomanic switch was observed during 18-24 months follow-up. CONCLUSION: In the absence of risk factors for manic switch, SSRI-induced hypomania may be dose-dependent medication effects
BACKGROUND: Women with bipolar (BP) disorder have more depressive episodes and drug-induced manic switches compared to men. Current guidelines suggest treating BP type I and type II major depressive episode (MDE) with both a mood-stabilizer and antidepressant. In a post hoc analysis, we examined the safety and efficacy of venlafaxine monotherapy in women with BP II MDE. METHODS: 15 women with BP II MDE (mean+/-SD age: 37+/-12 years) were compared to 17 women with unipolar (UP) MDE (41+/-12 years). Patients were randomized to double-blind treatment with once versus twice daily venlafaxine up to 225 mg for 6 weeks. Efficacy was measured using the HAM-D(21), MADRS and CGI scales. Drug-induced manic switch episodes characterized by agitation, irritability, euphoria or mood lability were assessed at each visit. RESULTS: No episodes of drug-induced hypomania or rapid cycling were observed during 6 weeks of venlafaxine monotherapy. Similar efficacy was observed in BP and UP depressed women (p=ns). LIMITATIONS: This study was retrospective in nature and limited in patient number. Only BP II women were included in this study, and it is possible that efficacy and the manic switch rate might have differed if BP I women were included. CONCLUSION: Short-term venlafaxine monotherapy may be a safe and effective antidepressant treatment in women with BP II MDE
WELLBUTRIN
Bupropion as add-on strategy in difficult-to-treat bipolar depressive patients.
Bupropion, a selective norepinephrine and dopamine reuptake inhibitor, has been suggested for the treatment of bipolar depression, not only because of its efficacy, but also because of a probably lower risk of inducing switches to hypomania or mania. Most studies on bupropion treatment in bipolar patients have been performed in moderately ill out-patients. In contrast, we report on a sample of difficult-to-treat, predominantly severely ill, co-morbid, psychotic or therapy-refractory bipolar depressive in-patients. In this open and prospective study, 13 patients were treated with bupropion as an add-on strategy mainly to other antidepressants and to various mood stabilizers. Our data support the idea that bupropion is a first-line antidepressant in the treatment of severe bipolar depression. Eight of 13 patients showed a >50% reduction of Montgomery-Asberg Depression Scale ratings within 4 weeks. Co-medication with drugs commonly used in treatment-resistant bipolar disorder including venlafaxine, clozapine, lithium, topiramate and sodium valproate was safe in our small sample. While adhering to the suggestion of Goren and Levin not to exceed a daily dose of 450 mg of bupropion when treating bipolar depressed patients, we did not observe any switch from depression to hypomania or mania.
Mania with bupropion: a dose-related phenomenon?
OBJECTIVE: To report a case in which bipolar depression was resistant to usual therapies, requiring dosages of bupropion >450 mg/d and to review the literature on mania associated with bupropion and propose a potential theory of a dose-related threshold associated with bupropion and mania. CASE SUMMARY: A 44-year-old white man with a 25-year history of bipolar affective disorder presented with depression resistant to usual therapies. Bupropion therapy was initiated and the dosage was titrated to 600 mg/d. After exceeding the maximum recommended daily dose (450 mg/d), he experienced a manic episode attributed to high-dose bupropion. DISCUSSION: Due to increased risk of seizures, current prescribing guidelines state that the total daily dose of bupropion is not to exceed 450 mg/d. Since bupropion is the agent least likely to cause a manic switch in bipolar disorder, this agent seemed a logical choice to treat the patient's depression. Due to a lack of response, the bupropion dosage was titrated to a maximum of 600 mg/d. Since the patient did not switch into mania until the dosage exceeded 450 mg/d, we speculate that this adverse reaction is a dose-related phenomenon. Scientific literature supports this theory. CONCLUSIONS: A switch into mania is a potential risk associated with antidepressant drug use in bipolar affective disorder. Bupropion is believed to be associated with a decreased risk compared with other antidepressant therapies. However, our case report as well as others support the theory that this decreased risk may be due to dosages not exceeding the recommended daily dose (450 mg/d). Doses of bupropion >450 mg/d should be used with caution in depressed patients with bipolar affective disorder.
Bupropion-induced isolated impairment of sensory trigeminal nerve function
Bupropion is increasingly used for nicotine withdrawal and in the treatment of major depression, especially in bipolar patients. We present the case of a 38-year-old female schizoaffective, rapid-cycling patient treated with bupropion for a depressive episode. After 4 weeks of successful treatment (300 mg/day), the patient developed a circumscribed unilateral impairment of sensory trigeminal nerve function. Symptoms completely recovered after discontinuation of bupropion. When re-exposed to bupropion, mild symptoms reappeared, leading to final discontinuation of bupropion. With this natural on-off-on-off design, a causative role of bupropion for trigeminal impairment in this patient can be assumed. To our knowledge, a similar side-effect of bupropion has not been described to date
The treatment of bipolar depression.
BACKGROUND: The treatment of bipolar depression represents a relatively understudied area in clinical psychiatry. The depressive phases of bipolar disorder can be very disabling, with significant associated comorbidity and suicide risk, impairment in functioning, and infringement on quality of life. We review the current evidence for the management of bipolar depression. METHOD: References for this review were obtained through MEDLINE searches of the medical literature on subjects pertaining to the treatment of bipolar depression. Search terms included bipolar depression, antidepressants, and bipolar disorder. Only publications in English are reviewed here. RESULTS: Lithium is currently the gold standard and most appropriate initial treatment for the depressive phase of bipolar disorder. Other mood stabilizers have demonstrated preliminary efficacy. Of the antidepressants, bupropion and the selective serotonin reuptake inhibitors may be associated with less risk of inducing hypomania, mania, and rapid cycling compared with tricyclic antidepressants. Monoamine oxidase inhibitors should be considered for patients with anergic bipolar depression. Electroconvulsive therapy has been shown to be highly efficacious. Other treatment modalities, including psychotherapy, sleep deprivation, phototherapy, and newer medications, require further research. CONCLUSIONS: Although the treatment of bipolar depression can be a complicated clinical task, the treatment armamentarium is expanding. Further research, especially in the form of randomized controlled trials, is warranted. Clinicians should be familiar with general guidelines for the use of psychopharmacologic agents for treating bipolar depression.
A double-blind study comparing idazoxan and bupropion in bipolar depressed patients
BACKGROUND: There is a small body of evidence indicating that idazoxan, a potent and selective alpha-2 antagonist, may be effective in treating bipolar depressive disorder. The purpose of this prospective controlled study is to compare idazoxan to bupropion, an antidepressant which has been suggested to have some advantages over other antidepressants in treating bipolar depressed patients. METHODS: Bipolar I depressed patients were randomly assigned in this 6-week double-blind out-patient study to receive either idazoxan, titrated to 240 mg/day and placebo bupropion, or bupropion, titrated to 450 mg/day and placebo idazoxan. These doses were achieved after 2 weeks. Depression severity was assessed with the Hamilton Depression Rating Scale and possible psychosis with the Brief Psychiatric Rating Scale. Side effects, heart rate, weight, and orthostatic blood pressure were also monitored. RESULTS: Fourteen patients completed this study (seven in each group). Both idazoxan and bupropion demonstrated significant improvement over time with reductions in Hamilton scores of 50%. LIMITATIONS: Limitations of this study include lack of a placebo group and small sample size. CONCLUSION: In light of our preliminary findings suggesting the usefulness of idazoxan in bipolar depression, larger more rigorous studies are indicated.
Use of bupropion with SRIs and venlafaxine.
Because of reported efficacy of combining classes of antidepressants, 25 patients were treated with bupropion in combination with SRI's and venlafaxine. Fifteen patients inadequately responsive to monotherapy received combination treatment; ten patients without residual symptoms received adjunctive bupropion to treat SRI- or venlafaxine-induced side effects. Fourteen subjects (56%) responded, 11 (44%) did not. Twelve of 15 subjects receiving combination treatment to boost the effects of monotherapy responded, while only 2 of 10 subjects receiving combination treatment for side effects responded. Combination therapy was well tolerated even by geriatric and "medically frail" patients
Bupropion and anticonvulsant drug interactions
The use of bupropion (BUP) involves a higher seizure risk than the use of other antidepressants, limiting its dose and widespread use. The two reported cases document anticonvulsant-BUP drug interactions through plasma levels. Carbamazepine appeared to decrease the plasma BUP to nondetectable levels, while hydroxybupropion was found at very high levels. Data presented suggest that BUP may increase sodium valproate levels. Conclusions from these case reports are tentative, pending further study. Monitering of BUP and its metabolites may ultimately prove useful in guiding clinicians dosing decisions, especially when mood stabilizers are combined with other psychotropic drugs in refractory bipolar patients
J Clin Psychiatry 1990 Nov;51(11):450-5-Bupropion as a promising approach to rapid cycling bipolar II patients.
Bupropion was added to lithium and/or levothyroxine in four female and two male bipolar II patients who had established baselines of at least 2 years of rapid cycling that had not responded to several of the most commonly used anticycling interventions. Although all six patients improved significantly, the response was dramatic in four (three female, one male) and is still sustained after an average of 2 years of continued treatment. Furthermore, unlike what happened in their prior course with more conventional antidepressants, none developed hypomania nor was rapid cycling observed during the course of continued pharmacotherapy. These findings, based on open but systematic clinical observation, suggest that bupropion may have special merit for rapid cycling, predominantly depressed bipolar patients and that, under close clinical vigilance, combining bupropion with appropriate doses of lithium is both efficacious and safe.
| Medication Name | Strength | Quantity | Price | |
| Wellbutrin SR (bupropion) | 100mg | 60 | $47.99 | |
| Wellbutrin SR (bupropion) | 150mg | 60 | $48.99 |
Clinical efficacy of bupropion in the management of smoking cessation.
Nicotine addiction is a chronic relapsing condition that can be difficult to treat. Until recently, pharmacological options for the treatment of tobacco dependence were primarily limited to nicotine replacement therapy (NRT). Sustained-release bupropion (bupropion SR) is the first non-nicotine pharmacological treatment approved for smoking cessation. Bupropion SR is recommended for first-line pharmacotherapy alongside NRT in the updated US Clinical Practice Guidelines and the UK Health Education Authority Guidelines. The UK National Institute of Clinical Excellence recommends NRT and bupropion SR for smokers who have expressed a desire to quit smoking. This review presents evidence that bupropion SR is an effective first-line therapy for smoking cessation in a wide range of patient populations. It is associated with significantly higher smoking cessation rates compared with placebo in patients with or without a history of prior bupropion SR or NRT use, and its effect is independent of gender. Bupropion SR treatment is effective in the prevention of relapse to smoking in those patients who have successfully quit, and re-treatment is effective in smokers who recommence smoking after a previous course of bupropion SR. Bupropion SR treatment relieves the symptoms of craving and nicotine withdrawal, and attenuates the weight gain that often occurs after smoking cessation. Data collected from motivational support programmes and employer-based studies provide strong evidence of the effectiveness of bupropion SR as an aid to smoking cessation in 'real life' situations, and confirm the efficacy seen in clinical trials.
Use of sustained-release bupropion in specific patient populations for smoking cessation.
Smoking cessation trials of sustained-release bupropion (bupropion SR) were initially conducted in a general population of smokers who were motivated to quit smoking. Bupropion SR has also been found to be a useful treatment of tobacco dependence in various special populations of smokers who often experience difficulty in overcoming tobacco addiction. Point-prevalence quit rates at 6 months were higher in those treated with bupropion SR than in those receiving placebo in studies on smokers with chronic obstructive pulmonary disease (23% vs 16%) and in those with cardiovascular disease (34% vs 12%). Abstinence from smoking after treatment with bupropion SR was not affected by a history of major depression or alcoholism. Women treated with bupropion SR were just as likely as men to abstain from smoking. Approximately one-third of a study population who were initially unwilling or unable to quit smoking were able to reduce their smoking by 50% or more during therapy with bupropion SR; 14% of these went on to achieve abstinence. Bupropion SR was well tolerated in these trials; importantly, it had no clinically significant effect on mean blood pressure in smokers, including those with hypertension, and attenuated the weight gain associated with smoking cessation, particularly in women.
Sustained-release bupropion for pharmacologic relapse prevention after smoking cessation. a randomized, controlled trial.
BACKGROUND: Smoking relapse is common after successful pharmacologic treatment for smoking cessation. No previous studies have examined long-term drug therapy used expressly for prevention of smoking relapse. OBJECTIVE: To evaluate the efficacy of bupropion to prevent smoking relapse. DESIGN: Randomized, placebo-controlled trial. PARTICIPANTS: 784 healthy community volunteers who were motivated to quit smoking and who smoked at least 15 cigarettes per day. INTERVENTION: The participants received open-label, sustained-release bupropion, 300 mg/d, for 7 weeks. Participants who were abstinent throughout week 7 of open-label treatment were randomly assigned to receive bupropion, 300 mg/d, or placebo for 45 weeks and were subsequently followed for an additional year after the conclusion of the medication phase. Participants were briefly counseled at all follow-up visits. At the end of open-label bupropion treatment, 461 of 784 participants (58.8%) were abstinent from smoking. MEASUREMENT: Self-reported abstinence was confirmed by an expired air carbon monoxide concentration of 10 parts per million or less. RESULTS: The point prevalence of smoking abstinence was significantly higher in the bupropion group than in the placebo group at the end (week 52) of drug therapy (55.1% vs. 42.3%, respectively; P = 0.008) and at week 78 (47.7% vs. 37.7%; P = 0.034) but did not differ at the final (week 104) follow-up visit (41.6% vs. 40.0%). The median time to relapse was significantly greater for bupropion recipients than for placebo recipients (156 days vs. 65 days; P = 0.021). The continuous abstinence rate was higher in the bupropion group than in the placebo group at study week 24 (17 weeks after randomization) (52.3% vs. 42.3%; P = 0.037) but did not differ between groups after week 24. Weight gain was significantly less in the bupropion group than in the placebo group at study weeks 52 (3.8 kg vs. 5.6 kg; P = 0.002) and 104 (4.1 kg vs. 5.4 kg; P = 0.016). CONCLUSIONS: In persons who stopped smoking with 7 weeks of bupropion treatment, sustained-release bupropion for 12 months delayed smoking relapse and resulted in less weight gain.
BACKGROUND: Patients with depressive disorders smoke tobacco more often than the population at large and find quitting more difficult. Furthermore, when they quit smoking, they are more likely to suffer a relapse of depression. We evaluated the addition of bupropion sustained release (SR) for smoking cessation among patients with a history of depressive disorders being maintained in a euthymic state with selective serotonin reuptake inhibitor (SSRI) antidepressants. METHOD: Twenty-five adults with DSM-IV major depressive disorder or depressive disorder NOS currently receiving SSRI maintenance treatment and smoking > or = 15 cigarettes per day participated in the 9-week study. Bupropion SR, 150 mg/day, was added to SSRI treatment and increased to 300 mg/day. Subjects were counseled on smoking cessation measures and chose a target quit date 2 or 4 weeks after the initiation of bupropion SR. Self-reported smoking status, expired carbon monoxide (CO) measurements, Hamilton Rating Scales for Depression and Anxiety scores, and weight were measured at each visit. Subjects were abstinent if they reported not smoking during the prior 7 days, confirmed with an expired-air CO value of < or = 10 ppm. RESULTS: Eight (32%) of 25 subjects were abstinent after 9 weeks. At 3-month follow-up, 3 subjects remained abstinent, 3 relapsed, and 2 were lost to follow-up. Eleven subjects (44%) were nonresponders, and 6 (24%) dropped out prior to 3 weeks of treatment due to side effects (N = 3) or were lost to follow-up (N = 3). Mean weight gain was approximately 0.5 lb (0.2 kg) for those completing 9 weeks of bupropion SR treatment. During the 9-week study and the 3-month follow-up, there was no evidence of emergent depression in any subject. Four subjects (16%) spontaneously reported an improvement in SSRI-associated sexual dysfunction. CONCLUSION: These open data suggest modest effectiveness for and the safety of bupropion SR as a smoking cessation agent in individuals with depression maintained on treatment with SSRIs. Minimal weight gain, lack of emergent depressive episodes, and improvement of SSRI-associated sexual dysfunction are added advantages.
Bupropion for weight loss: an investigation of efficacy and tolerability in overweight and obese women
OBJECTIVE: On the basis of the clinical observations that bupropion facilitated weight loss, we investigated the efficacy and tolerability of this drug in overweight and obese adult women. RESEARCH METHODS AND PROCEDURES: A total of 50 overweight and obese (body mass index: 28.0 to 52.6 kg/m(2)) women were included. The core component of the study was a randomized, double-blind, placebo-controlled comparison for 8 weeks. Bupropion or placebo was started at 100 mg/d with gradual dose increase to a maximum of 200 mg twice daily. All subjects were prescribed a 1600 kcal/d balanced diet and compliance was monitored with food diaries. Responders continued the same treatment in a double-blind manner for an additional 16 weeks to a total of 24 weeks. There was additional single-blind follow-up treatment for a total of 2 years. RESULTS: Subjects receiving bupropion achieved greater mean weight loss (last-observation-carried-forward analysis) over the first 8 weeks of the study (p = 0.0001): 4.9% +/- 3.4% (n = 25) for bupropion treatment compared with 1.3% +/- 2.4% (n = 25) for placebo treatment. For those who completed the 8 weeks, the comparison was 6.2% +/- 3.1% (n = 18) vs. 1.6% +/- 2.9% (n = 13), respectively(p = 0.0002), with 12 of 18 of the bupropion subjects (67%) losing over 5% of baseline body weight compared with 2 of 13 in the placebo group (15%; p = 0.0094). In the continuation phase, 14 bupropion responders who completed 24 weeks achieved weight loss of 12.9% +/- 5.6% with fat accounting for 73.5% +/- 3.7% of the weight lost and no change in bone mineral density as assessed by DXA. Bupropion was generally well-tolerated in this sample. DISCUSSION: Bupropion was more effective than placebo in achieving weight loss at 8 weeks in overweight and obese adult women in this preliminary study. Initial responders to bupropion benefited further in the continuation phase.
Pharmcentral has an excellent writeup on antidepressants and goes into great detail
It describes Wellbutrin as
:"
Wellbutrin enhances dopamine and norepinephrine function and has a stimulating profile, inducing seizure in high doses. Like the
amphetamines, it may act as a dopamine releaser, but it is only a very mild reuptake inhibitor at noradrenergic and serotonin amine
pumps. It could also act as a partial agonist at dopamine and/or norepinephrine terminals. Appending a bulky moiety like the tert-butyl
group to a molecule which would otherwise be an agonist is a standard means of obtaining a partial agonist/ antagonist (see the
narcotics page).
Wellbutrin (bupropion) is the only antidepressant without antisexual side effects (with the possible exception of reboxetine): most
antidepressants inhibit orgasm. Coadministering Wellbutrin with other antidepressants (usually an SSRI; never an MAOI) reduces this
antisexual effect.
Wellbutrin is currently being marketed as Zyban as an aid in smoking cessation. The rationale is to replace one dopamine-enhancing drug (nicotine) with another. The sustained-release form of this drug (Wellbutrin SR) is generally preferred since the half-life is relatively short.
Prescribing trends of antidepressants in bipolar depression.(1995)
BACKGROUND: This study utilizing pharmacoepidemiologic methods was undertaken to determine the prescribing patterns of antidepressants particularly in bipolar depression. METHOD: From pharmacy records of the McLean Hospital, the number of patients receiving antidepressants and given electroconvulsive therapy (ECT) from June 1, 1987, to May 8, 1993, was determined. We later linked these data bases with patients who were diagnosed with DSM-III-R bipolar depression (296.5) during the same period of time. RESULTS: During the 6-year period, it was determined that 3829 inpatients had received tricyclic antidepressants (TCAs), 2981 fluoxetine, 2603 trazodone, 809 bupropion, 743 monoamine oxidase inhibitors (MAOIs), 592 stimulants, 588 sertraline, 48 paroxetine, and 894 ECT. There were significant increases over time in prescriptions of MAOIs compared with fluoxetine (chi 2 = 14.36, p = .006), and bupropion compared with TCAs (chi 2 = 6.45, p = .04). There was a trend for bupropion to be prescribed more over time compared with fluoxetine (chi 2 = 5.09, p = .08). There were no significant changes in the prescribing of other antidepressants or in the use of ECT. CONCLUSION: At our center, prescribing of bupropion and MAOIs in bipolar depression has increased significantly. This may be related to the reports in the literature of the low switch rates to mania with the use of these drugs.
Here is a list of antidepressants in alphabetical order:
*supplied by independent psychologist who happens to be both bipolar and on Wellbutrin. Rxbyfax not responsible for what is included. Just for your educational information.