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Wellbutrin withdrawal – How to taper Wellbutrin is fully described in How to Taper Psychoactive Medication. The full step by step process in detail. Free assistance is also available if needed.
When you do a Wellbutrin withdrawal, several things must be kept in mind. We have used DNA testing of Wellbutrin metabolism to formulate a few supplements to help with withdrawal. You do not have to use the supplements to do a Wellbutrin withdrawal, but your success rate will be higher.
As of April 2025, over 19 million people have used this information to become medication free.
Dr. Lester M. Crawford, Acting FDA Commissioner had this to say about this test on
Dec. 24, 2004. “Physicians can use the genetic information from this test to prevent harmful drug interactions and to assure drugs are used optimally, which in some cases will enable patients to avoid less effective or potentially harmful treatment choices,”
Wellbutrin uses three major pathways for metabolism. Roughly 50% of the population will have variations in these pathways used to metabolize Wellbutrin. A simple DNA test will show you and your physician if you are a poor metabolizer, ultra metabolizer, or normal metabolizer on these three pathways.
Your physician, with this information, will be able to predict if your dosage should be reduced, increased or if another medication should be prescribed which does not use either of the same pathways as Wellbutrin.
Bupropion
Brand name (Wellbutrin)
Description
Bupropion hydrochloride, an antidepressant of the aminoketone class, is chemically unrelated to tricyclic, tetracyclic, or other known antidepressant agents. Its structure closely resembles that of diethylpropion; it is related to phenylethylamines. It is designated as (±)-1-(3-chlorophenyl)-2-[(1,1-dimethylethyl)amino]-1-propanone hydrochloride. The molecular weight is 276.2. The emperical formula is C13H18CINO*HCl. Bupropion powder is white, crystalline, and highly soluble in water. It has a bitter taste and produces the sensation of local anesthesia on the oral mucosa.
Bupropion is supplied for oral administration as 75 mg (yellow-gold) and 100 mg (red) film-coated tablets. Each tablet contains the labeled amount of bupropion hydrochloride and the inactive ingredients: 75 mg tablet – D&C Yellow No. 10 Lake, FD&C Yellow No. 6 Lake, hydroxypropyl cellulose, hydroxypropyl methylcelluose, microcrystalline cellulose, polyethylene glycol, talc, and titanium dioxide; 100 mg tablet – FD&C Red No. 40 Lake, FD&C Yellow No. 6 Lake, hydroxypropyl cellulose, hydroxypropyl methylcellulose, microcrystalline cellulose, polyethylene glycol, talc, and titanium dioxide.
Clinical Pharmacology
Pharmacodynamics and Pharmacological Actions:
The neurochemical mechanism of the antidepressant effect of bupropion is not known. Bupropion does not inhibit monoamine oxidase. Compared to classical tricyclic antidepressants, it is a weak blocker of the neuronal uptake of serotonin and norepinephrine; it also inhibits the neuronal re-uptake of dopamine to some extent.
Bupropion produces dose-related CNS stimulant effects in animals, as evidenced by increased locomotor activity, increased rates of responding in various schedule-controlled operant behavior tasks, and, at high doses, induction of mild stereotyped behavior.
Bupropion causes convulsions in rodents and dogs at doses approximately tenfold the dose recommended as the human antidepressant dose.
Absorption, Distribution, Pharmacokinetics, Metabolism, and Elimination:
Oral bioavailability and single-dose pharmacokinetics:
In humans, following oral administration of bupropion, peak plasma bupropion concentrations are usually achieved within 2 hours, followed by a biphasic decline. The average half-life of the second (post-distributional) phase is approximately 14 hours, with a range of 8 to 24 hours. Six hours after a single dose, plasma bupropion concentrations are approximately 30% of peak concentrations. Plasma bupropion concentrations are dose-proportional following single doses of 100 to 250 mg; however, it is not known if the proportionality between dose and plasma level is maintained in chronic use.
The absolute bioavailability of bupropion tablets in humans has not been determined because an intravenous formulation for human use is not available.
However, it appears likely that only a small proportion of any orally administered dose reaches the systemic circulation intact. For example, the absolute bioavailability of bupropion in animals (rats and dogs) ranges from 5% to 20%.
Metabolism:
Following oral administration of 200 mg of 14C-bupropion, 87% and 10% of the radioactive dose were recovered in the urine and feces, respectively. However, the fraction of the oral dose of bupropion excreted unchanged was only 0.5%, a finding documenting the extensive metabolism of bupropion.
Several of the known metabolites of bupropion are pharmacologically active, but their potency and toxicity relative to bupropion have not been fully characterized. However, because of their longer elimination half-lives, the plasma concentrations of at least two of the known metabolites can be expected, especially in chronic use, to be very much higher than the plasma concentration of bupropion. This is of potential clinical importance because factors or conditions altering metabolic capacity (e.g., liver disease, congestive heart failure, age, concomitant medications, etc.) or elimination may be expected to influence the degree and extend of accumulation of these active metabolites.
Furthermore, bupropion has been shown to induce its own metabolism in three animal species (mice, rats, and dogs) following subchronic administration. If induction also occurs in humans, the relative contribution of bupropion and its metabolites to the clinical effects of bupropion may be changed in chronic use.
Plasma and urinary metabolites so far identified include biotransformation products formed via reduction of the carbonyl group and/or hydroxylation of the tert-butyl group of bupropion. Four basic metabolites have been identified.
They are the erythro- and threo-amino alcohols of bupropion, the erythro-amino diol of bupropion, and a morpholinol, metabolite (formed from hydroxylation of the tert-butyl group of bupropion).
The morpholinol metabolite appears in the systemic circulation almost as rapidly as the parent drug following a single oral dose. Its peak level is three times the peak level of the parent drug; it has a half life on the order of 24 hours; and its AUC 0 to 60 hours is about 15 times that of bupropion.
The threo-amino alcohol metabolite has a plasma concentration time profile similar to that of the morpholinol metabolite. The erythro-amino alcohol and the erythro-amino diol metabolites generally cannot be detected in the systemic circulation following a single oral dose of the parent drug. The morpholinol and the threo-amino alcohol metabolites have been found to be half as potent as bupropion in animal screening tests for antidepressant drugs.
During a chronic dosing study in 14 depressed patients with left ventricular dysfunction, it was found that there was substantial interpatient variability (two- to five-fold) in the trough steady-state concentrations of bupropion and the morpholinol and threo-amino alcohol metabolites. In addition, the steady-state plasma concentrations of these metabolites were 10 to 100 times the steady-state concentrations of the parent drug.
The effect of other disease states and altered organ function on the metabolism and/or elimination of bupropion has not been studied in detail. However, the elimination of the major metabolites of bupropion may be affected by reduced renal or hepatic function because they are moderately polar compounds and are likely to undergo conjugation in the liver prior to urinary excretion. The preliminary results of a comparative single-dose pharmacokinetic study in normal versus cirrhotic patients indicated that half-lives of the metabolites were prolonged by cirrhosis and that the metabolites accumulated to levels two to three times those in normals.
The effect of age on plasma concentrations of bupropion and its metabolites has not been characterized.
In vitro tests show that bupropion is 80% or more bound to human albumin at plasma concentrations up to 800 micromolar (200 mcg/mL).
Indications And Usage
Bupropion is indicated for the treatment of depression. A physician considering bupropion for the management of a patient’s first episodes of depression should be aware that the drug may cause generalized seizures with an approximate incidence of 0.4% (4/1000). This incidence of seizures may exceed that of other marketed antidepressants by as much as fourfold. This relative risk is only an approximate estimate because no direct comparative studies have been conducted.
The efficacy of bupropion has been established in three placebo-controlled trials, including two of approximately 3 weeks duration in depressed inpatients, and one of approximately 6 weeks duration in depressed outpatients. The depressive disorder of the patients studied corresponds most closely to the Major Depression category of the APA Diagnostic and Statistical Manual III.
Major Depression implies a prominent and relatively persistent depressed or dysphoric mood that usually interferes with daily functioning (nearly every day for at least 2 weeks); it should include at least four of the following eight symptoms: change in appetite, change in sleep, psychomotor agitation or retardation, loss of interest in usual activities or decrease in sexual drive, increased fatigability, feelings of guilt or worthlessness, slowed thinking or impaired concentration, and suicidal ideation or attempts.
Effectiveness of bupropion in long-term use, that is, for more than 6 weeks, has not been systematically evaluated in controlled trials. Therefore, the physician who elects to use bupropion for extended periods should periodically re-evaluate the long-term usefulness of the drug for the individual patient.
Contraindications
Bupropion is contraindicated in patients with a seizure disorder. Bupropion is also contraindicated in patients with a current or prior diagnosis of bulimia or anorexia nervosa because of a higher incidence of seizures noted in such patients treated with bupropion. The concurrent administration of bupropion and a monoamine oxidase (MAO) inhibitor is contraindicated. At least 14 days should elapse between discontinuation of an MAO inhibitor and initiation of treatment with bupropion. Bupropion is contraindicated in patients who have shown an allergic response to it.
Warnings
Seizures:
Bupropion is associated with seizures in approximately 0.4% (4/1000) of patients treated at doses up to 450 mg/day. This incidence of seizures may exceed that of other marketed antidepressants by as much as fourfold. This relative risk is only an approximate estimate because no direct comparative studies have been conducted. The estimate seizure incidence for bupropion increases almost tenfold between 450 and 600 mg/day, which is twice the usually required daily dose (300 mg) and one and one-third the maximum recommended daily dose (450 mg). Given the wide variability among individuals and their capacity to metabolize and eliminate drugs, this disproportionate increase in seizure incidence with dose incrementation calls for caution in dosing.
During the initial development, 25 among approximately 2400 patients treated with bupropion experienced seizures. At the time of seizure, seven patients were receiving daily doses of 450 mg or below for an incidence of 0.33% (3/1000) within the recommended dose range. Twelve patients experienced seizures at 600 mg per day (2.3% incidence); six additional patients have seizures at daily doses between 600 and 900 mg (2.8% incidence).
A separate, prospective study was conducted to determine the incidence of seizure during an 8-week treatment exposure in approximately 3200 additional patients who received daily doses of up to 450 mg. Patients were permitted to continue treatment beyond 8 weeks if clinically indicated. Eight seizures occurred during the initial 8-week treatment period and five seizures were reported in patients continuing treatment beyond 8 weeks, resulting in a total seizure incidence of 0.4%.
The risk of seizure appears to be strongly associated with dose and the presence of predisposing factors. A significant seizure, CNS tumor, concomitant medications that lower seizure threshold, etc.) was present in approximately one-half of the patients experiencing a seizure. Sudden and large increments in dose may contribute to increased risk. While many seizures occurred early in the course of treatment, some seizures did occur after several weeks at fixed dose.
Recommendations for reducing the risk of seizure:
Retrospective analysis of clinical experience gained during the development of bupropion suggests that the risk of seizure may be minimized if (1) the total daily dose of bupropion does not exceed 450 mg, (2) the daily dose is administered t.i.d., with each single dose not to exceed 150 mg to avoid high peak concentrations of bupropion and/or its metabolites, and (3) the rate of incrementation of dose is very gradual. Extreme caution should be used when bupropion is (1) administered to patients with a history of seizure, cranial trauma, or other predisposition(s) toward seizure, or (2) prescribed with other agents (e.g., antipsychotics, other antidepressants, etc.) or treatment regimens (e.g., abrupt discontinuation of a benzodiazepine) that lower seizure threshold.
Potential for Hepatotoxicity:
In rats receiving large doses of bupropion chronically, there was an increase in incidence of hepatic hyperplastic nodules and hepatocellular hypertrophy. In dogs receiving large doses of bupropion chronically, various histologic changes were seen in the liver, and laboratory tests suggesting mild hepatocellular injury were noted. Although scattered abnormalities in liver function tests were detected in patients participating in clinical trials, there is no clinical evidence that bupropion acts as a hepatotoxin in humans.
Precautions
General:
Agitation and Insomnia: A substantial proportion of patients treated with bupropion experience some degree of increased restlessness, agitation, anxiety, and insomnia, especially shortly after initiation of treatment. In clinical studies, these symptoms were sometimes of sufficient magnitude to require treatment with sedative/hypnotic drugs. In approximately 2% of patients, symptoms were sufficiently severe to require discontinuation of treatment with bupropion.
Psychosis, Confusion, and Other Neuropsychiatric Phenomena: Patients treated with bupropion have been reported to show a variety of neuropsychiatric signs and symptoms including delusions, hallucinations, psychotic episodes, confusion, and paranoia. Because of the uncontrolled nature of many studies, it is impossible to provide a precise estimate of the extent of risk imposed by treatment with bupropion. In several cases, neuropsychitric phenomena abated upon dose reduction and/or withdrawal of treatment.
Activation of Psychosis and/or Mania: Antidepressants can precipitate manic episodes in Bipolar Manic Depressive patients during the depressed phase of their illness and may activate latent psychosis in other susceptible patients. Bupropion is expected to pose similar risks.
Altered Appetite and Weight: A weight loss of greater than 5 pounds occurred in 28% of patients receiving bupropion. This incidence is approximately double that seen in comparable patients treated with tricyclics or placebo. Furthermore, while 34.5% of patients receiving tricyclic antidepressants gained weight, only 9.4% of patients treated with bupropion did. Consequently, if weight loss is a major presenting sign of a patient’s depressive illness, the anorectic and/or weight reducing potential of bupropion should be considered.
Suicide: The possibility of a suicide attempt is inherent in depression and may persist until significant remission occurs. Accordingly, prescriptions for bupropion should be written for the smallest number of tablets consistent with good patient management.
Use in Patients with Systemic Illness:
There is no clinical experience establishing the safety of bupropion in patients with a recent history of myocardial infarction or unstable heart disease. Therefore, care should be exercised if it is used in these groups. Bupropion was well tolerated in patients who has previously developed orthostatic hypotension while receiving tricyclic antidepressants.
Because bupropion HCl and its metabolites are almost completely excreted through the kidney and metabolites are likely to undergo conjugation in the liver prior to urinary excretion, treatment of patients with renal or hepatic, impairment should be initiated at reduced dosage as bupropion and its metabolites may accumulate in such patients beyond concentrations expected in patients without renal or hepatic impairment. The patient should be closely monitored for possible toxic effects of elevated blood and tissue levels of drug and metabolites.
Information for Patients:
Physicians are advised to discuss the following issues with patients:
Patients should be instructed to take bupropion in equally divided doses three or four times a day to minimize the risk of seizure.
Patients should be told that any CNS-active drug like bupropion may impair their ability to perform tasks requiring judgment or motor and cognitive skills. Consequently, until they are reasonably certain that bupropion does not adversely affect their performance, they should refrain from driving an automobile or operating complex, hazardous machinery.
Patients should be told that the use and cessation of use of alcohol may alter the seizure threshold, and, therefore, that the consumption of alcohol should be minimized, and, if possible, avoided completely.
Patients should be advised to inform their physician if they are taking or plan to take any prescription or over-the-counter drugs. Concern is warranted because bupropion and other drugs may affect each others metabolism.
Patients should be advised to notify their physician if they become pregnant or intend to become pregnant during therapy.
Drug Interactions:
No systematic data have been collected on the consequences of the concomitant administration of bupropion and other drugs.
However, animal data suggest that bupropion may be an inducer of drug metabolizing enzymes. This may be of potential clinical importance because the blood levels of co-administered drugs may be altered.
Alternatively, because bupropion is extensively metabolized, the co-administration of other drugs may affect its clinical activity. In particular, care should be exercised when administering drugs known to affect hepatic drug-metabolizing enzyme systems (e.g., carbamazepine, cimetidine, phenobarbital, phenytoin).
Studies in animals demonstrate that the acute toxicity of buproprion is enhanced by the MAO inhibitor phenelzine (see CONTRAINDICATIONS).
Limited clinical data suggest a higher incidence of adverse experiences in patients receiving concurrent administration of bupropion and L-dopa. Administration of bupropion to patients receiving L-dopa concurrently should be undertaken with caution, using small initial doses and small gradual dose increases.
Concurrent administration of bupropion and agents which lower seizure threshold should be undertaken only with extreme caution (see WARNINGS). Low initial dosing and small gradual dose increases should be employed.
Carcinogenesis, Mutagenesis, Impairment of Fertility:
Lifetime carcinogenicity studies were performed in rats and mice at doses up to 300 and 150 mg/kg/day, respectively. In the rat study there was an increase in nodular proliferative lesions of the liver at doses of 100 to 300 mg/kg/day; lower doses were not tested. The question of whether or not such lesions may be precursors of neoplasms of the liver is currently unresolved. Similar liver lesions were not seen in the mouse study, and no increase in malignant tumors of the liver and other organs was seen in either study.
Bupropion produced a borderline positive response (2 to 3 times control mutation rate) in some strains in the Ames bacterial mutagenicity test, and a high oral dose (300, but not 100 or 200 mg/kg) produced a low incidence of chromosomal aberrations in rats. The relevance of these results in estimating the risk of human exposure to therapeutic doses is unknown.
A fertility study was performed in rats; no evidence of impairment of fertility was encountered at oral doses up to 300 mg/kg/day.
Pregnancy: Teratogenic Effects:
Pregnancy Category B: Reproduction studies have been performed in rabbits and rats at doses up to 15 to 45 times the human daily dose and have revealed no definitive evidence of impaired fertility or harm to the fetus due to bupropion. (In rabbits, a slightly increased incidence of fetal abnormalities was seen in two studies, but there was no increase in any specific abnormality.) There are no adequate and well-controlled studies in pregnant women. Because animal reproduction studies are not always predictive of human response, this drug should be used during pregnancy only if clearly needed.
Labor and Delivery:
The effect of bupropion on labor and delivery in humans is unknown.
Nursing Mothers:
Because of the potential for serious adverse reactions in nursing infants from bupropion, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.
Pediatric Use:
The safety and effectiveness of bupropion in individuals under 18 years old have not been established.
Use in the Elderly:
Bupropion has not been systematically evaluated in older patients.
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