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Can seroquel get you high: Can Seroquel Get You High?

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Can Seroquel Get You High?

What Is Seroquel?

Seroquel is the brand name of the prescription drug quetiapine. This drug is available in brand-name and generic versions and has immediate-release and extended-release options. The brand name for the extended-release option is Seroquel XR. Both options usually come in the form of an oral tablet.

When an individual takes this atypical antipsychotic, the chemical activity in their brain is altered. Seroquel releases serotonin and dopamine in the brain, which improves symptoms in individuals with various mental health disorders.

Why People Use Seroquel

Doctors commonly prescribe Seroquel to treat or ease the symptoms of various mental health disorders including schizophrenia, bipolar disorder, and depression. It may be used in combination with therapy and may be prescribed in addition to another medication, like an antidepressant. When used correctly, Seroquel may prevent mood swings, decrease hallucinations (if applicable), improve concentration, increase confidence, and treat depressive or manic episodes. The Seroquel dosage depends on various factors like the specific mental health condition being treated, the age of the individual being treated, and others. 

Does Seroquel Get You High?

If Seroquel is misused, it can cause someone to feel an intense and potentially dangerous high. Abusing Seroquel to improve mood, increase pleasure, or reduce anxiety may result in unpleasant or even fatal side effects. When misused, Seroquel overdoses are possible and may include symptoms like drowsiness/sleepiness, increased heartbeat, dizziness, and fainting.

This prescription drug comes with a high risk of addiction, especially when combined with other medications and drugs. Some individuals who misuse Seroquel may mix it with cocaine, for example. Chances of addiction and dependence also increase when someone snorts or injects Seroquel instead of taking it as an oral tablet. When Seroquel is snorted, it enters the bloodstream more quickly, resulting it an intense high and can lead to a Seroquel overdose.

Side Effects of Seroquel

Seroquel, when misused, comes with complications. It’s still important to be careful when using Seroquel as prescribed, including the Seroquel dosage, while also considering the potential symptoms and risks that come with regular use.

Side effects of Seroquel may include:

  • Dry mouth
  • Drowsiness
  • Constipation
  • Stomach pain
  • Increased appetite
  • Weight gain
  • nausea/vomiting
  • Sore throat
  • Rapid heartbeat
  • Weakness
  • Trouble moving

Not only can this prescription drug potentially cause undesirable symptoms, but it can also have long-lasting side effects.

Risks of Seroquel Use

Individual risks of taking Seroquel vary from person to person based on their mental health condition, their age, etc., however, some possible risks to consider include:

  • Suicidal thoughts/actions

  • Increased cholesterol

  • High blood sugar

  • Low white blood cell count

  • Cataracts

  • Seizures

  • Changes in thyroid levels

  • Metabolism changes

  • Stroke

  • Allergies

  • Tremors

Although Seroquel does come with its possible dangers and risks, it’s usually harmless if used as prescribed and responsibly. If you experience any of the issues above while using Seroquel, it’s vital to talk to your doctor to discuss the best next steps.

Responsible Use of Seroquel

Seroquel can interact with other medications. For example, it shouldn’t be combined with anti-arrhythmic drugs, certain antibiotics, antipsychotic drugs, alcohol, or methadone. When mixed with specific drugs, the side effects may increase and become more intense. These drugs include benzodiazepines, muscle relaxants, certain pain medications, antihistamines, and sedatives.

If addiction occurs, residential addiction treatment, like the one we offer at Silver Pines, is likely the best solution. . Our residential addiction treatment program begins with detoxing, allowing individuals to experience the effects in Seroquel withdrawal in a comfortable and healthy environment. Due to the dangers of Seroquel withdrawal, it’s important to speak with your doctor if you’re thinking of stopping the drug.

If you have any questions about the effects of Seroquel and other prescription drugs and if you need to enter a drug detox program, like the one we offer at Silver Pines, call us today at 267. 719.8689. 

Sources

https://www.medicalnewstoday.com/articles/quetiapine-oral-tablet#alternatives

https://www.everydayhealth.com/drugs/quetiapine

The Dangers Of Snorting Seroquel (Insufflation)

Quetiapine Misuse and Abuse: Is it an Atypical Paradigm of Drug Seeking Behavior?

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Side effects of neuroleptics and excess weight

Author Masha Pushkina, psychoeducator Views 914 02 Antipsychotics and excess weight is a problem that worries many. As you know, antipsychotics affect weight gain. According to statistics, more than 80% of people with severe mental disorders are overweight. A patient taking olonzapine gains an average of 2. 3 kg per month, clozapine – 1.7 kg, quetiapine – 1.8 kg, zotepine – 2.3 kg.

Weight gain with antipsychotics

Weight gain is a very common side effect of many antipsychotics, especially some second-generation (newer) drugs.

This may be due to the fact that neuroleptics increase appetite, so you want to eat more than usual. They can also make you less active and feel tired, so you move less and burn fewer calories.

If you gain a lot of weight, it can increase your risk of developing diabetes and other health problems.

Changes in weight can have a negative effect on mood and self-esteem.

What can be done to keep from getting fat?

If the problem becomes significant, it should be discussed with your psychiatrist and possibly switched to another antipsychotic. You should also eat a healthy diet and increase your level of physical activity.

Weight gain often causes patients to resist taking pills, and it also creates additional psychological or physiological problems that then have to be sorted out. Weight gain due to psychotropic drugs is not the only reason why people with mental disorders gain weight, but let’s look at this problem.

What is considered overweight?

In clinical practice, to assess body weight, physicians are usually guided by the concept of body mass index (BMI), which was developed by the Belgian sociologist and statistician Adolphe Quetelet back in 1869. This is a value that allows you to assess the degree of correspondence between a person’s mass and his height, and thereby indirectly assess whether the mass is insufficient, normal or excessive.

Body mass index is calculated by the formula: body weight / height in meters squared (kg/m²).

BMI between 18.5 and 24.9 is considered normal, BMI between 25 and 29.9 indicates overweight, BMI between 30 and 39.9 indicates obesity of I and II degrees, BMI above 40 indicates morbid obesity, that is, condition of the body that interferes with the normal functioning of the body.

The interpretation of BMI indicators recommended by the World Health Organization does not take into account the sex and age of the person, and this is a flaw in the system, but the US Department of Health, for example, collects statistics on anthropometric data on BMI. These data show that BMI is generally higher in men than in women. In addition, BMI is higher in middle-aged people than in young and old people.

Which drugs make you gain weight. Whether only from neuroleptics?

There are a number of studies that have examined the relationship between weight gain and certain groups of drugs. Metabolic disorders are most often associated with the use of antipsychotics.

A patient taking olonzapine gains on average 2.3 kg per month, clozapine 1.7 kg, quetiapine 1.8 kg, zotepine 2.3 kg. Changes in weight during the course of the studies were also observed in those taking risperidone (1.0 kg per month) and ziprasidone (0.8 kg per month).

Also gaining weight are patients taking antidepressants and lithium, which is used in the treatment of mood disorders, in particular the manic and hypomanic phases of bipolar disorder, as well as in the prevention of its exacerbations and in the treatment of severe and resistant depression. Here, research data diverge, but if you measure the average values, then in the course of observations it turned out that people on antidepressants can add from 0.57 to 1.37 kg per month. With regard to lithium, 20% of patients on long-term treatment with this drug gain more than 10 kg of weight.

What is it about these medicines that causes weight gain?

There is no unequivocal opinion on this issue among scientists. However, this issue is being studied. Scientists at the National Institute of Mental Health in 2007 conducted an experiment on mice, during which they found that neuroleptics block the brain receptors responsible for controlling appetite. Another study, conducted already in 2012 by the staff of the Feinstein Institute for Medical Research, suggests that the problem of weight gain when taking antipsychotics is associated with a genetic predisposition in certain patients to gain excess weight in principle.

Are there drugs that don’t make you fat?

Yes, there certainly are. Not all psychotropic drugs lead to weight gain. There is evidence that taking some selective serotonin reuptake inhibitors even leads to a decrease in it during the first weeks after the start of administration. The same is written about the antiepileptic drugs felbamate and topiramate. But still, when prescribing drugs, the doctor is primarily guided not by the danger of gaining excess weight, but by improving your general well-being, because this, in any case, is more important than the number on the scales.

Sources:
  • Bodyweight gain with atypical antipsychotics, Wetterling, 2001
  • Weight gain and antidepressants, Fava, 2000
  • Lithium: a review of its metabolic adverse effects, Livingstone and Rampes, 2006
  • Weight Gain From Antipsychotics Traced to Appetite-Regulating Enzyme, Receptor, Science Update, 2007
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  • Interruption of selective serotonin reuptake inhibitor treatment, Michelson, 2000
  • Clozapine weight gain, plus topiramate weight loss, Dursun and Devarajan, 2000

The aim of the current publication is to review more recent clinical data on the use of trazodone for depression, focusing on the approved dose of 300 mg/day, and to discuss its place in current treatment strategies for depression and related conditions, as well as for off-label indications – insomnia and anxiety.

Trazodone is available in many countries around the world in a variety of formulations, including immediate release (IR) tablets, extended release tablets and, in some countries, even as oral drops and injection.

Recently, a new once-daily extended-release formulation of trazodone (150 mg and 300 mg halved tablets) has been developed. This patented delivery technology is able to control the release of trazodone within 24 hours and was developed in an attempt to improve patient adherence to therapy without loss of efficacy and improve tolerability by avoiding the early high plasma concentration peaks seen with conventional IR drugs. Trazadone extended release was approved in the US in early 2010 for the treatment of patients with depression and is in the process of being approved in many European countries.

Through combined serotonergic receptor antagonism and serotonin reuptake inhibition (SSRI), trazodone has also demonstrated unique therapeutic flexibility, leading to its potential use in a wide range of depression-related comorbidities as well as off-label indications including insomnia, anxiety, dementia, Alzheimer’s disease, substance abuse, schizophrenia, bulimia and fibromyalgia.

PubMed/MEDLINE searched the literature using the following keywords: “trazodone” and “major depressive disorder” as free text. The search was limited to fully published randomized controlled trials, in English only. Each article was assessed for relevance, and only articles published after 1981 (US approval date) were included. Separate searches have been made for the use of trazodone for other indications, including insomnia and anxiety. Again, only fully published randomized controlled trials were included.

Mechanisms of action and pharmacological properties of trazodone

Trazodone is a derivative of triazolopyridine. Although its pharmacological effects in humans are not fully understood, trazodone is believed to have more than one mechanism of therapeutic action, making it a multifunctional drug.

Trazodone: antidepressant, antagonist, serotonin reuptake inhibitor (SSRI)

Trazodone is the first antidepressant with a dual mechanism of action involving serotonin transporter (SERT) inhibition and serotonin type 2 (5-HT2) receptor antagonism (both 5-HT2A and 5-HT2C receptors). Preclinical evidence suggests that the antidepressant activity of SSRIs and SNRIs is most likely due to blockade of serotonin, whereby serotonin exerts its 5-HT1A receptor agonist action. However, this serotonin agonist effect also affects other serotonin receptor subtypes, such as the 5-HT2A and 5-HT2C receptors, which are thought to be responsible for the side effects often associated with SSRI and SNRI therapy, including insomnia, sexual dysfunction, and anxiety. Unlike SSRIs and SNRIs, serotonin antagonist/reuptake inhibitors (SSRIs) such as trazodone provide simultaneous inhibition of SERT and 5-HT2A and 5-HT2C receptor antagonism, thus avoiding the tolerability problems often associated with 5-HT2C stimulation. NT 2A/2C. In addition, there have been suggestions that concurrent 5-HT2A/2C antagonism and serotonin inhibition may have a synergistic effect that enhances the antidepressant activity of SARIs and may improve treatment tolerability.

Moreover, trazodone exhibits α1- and α2-adrenergic and histamine H1 receptor antagonistic properties with minimal anticholinergic effects. It is also well known that at low doses (25-100 mg) trazodone has therapeutic activity as a hypnotic. It is known that the action of several neurotransmitter systems, including serotonin, norepinephrine, dopamine, acetylcholine and histamine, are involved in the excitation mechanism. Thus, arousal can be effectively disrupted and sleep induced by inhibition of several of these neurotransmitter systems. The effectiveness of trazodone in this regard may be explained by its ability to inhibit H1 receptors, and the sleep-inducing effect of H1 receptor blockade may be enhanced by simultaneous antagonism of 5-HT2A and α-adrenergic receptors.

Dosage and method of administration

According to the relevant summary of the characteristics of the drug trazodone, therapy should be started with an evening dose (initial dose of 75-150 mg at bedtime). Subsequently, the dose can be increased every 3 days to 300 mg/day, administered in repeated doses after meals (trazodone IR), twice daily (extended release trazodone) or once daily, preferably at bedtime. In hospitalized patients, the dose may be further increased to 600 mg/day on repeated doses. For elderly patients, the initial dose should be reduced to 100 mg/day.

Extended release formulations

In the 1980s, extended-release tablets of trazodone (Roussel Laboratories Ltd., Guildford, UK) [75 and 150 mg tablets] were developed to limit the early and relatively high peak plasma concentrations that are observed with IR tablets. This high peak plasma concentration may be associated with side effects such as drowsiness or hypotension, especially during the first week of treatment. These side effects may limit treatment tolerability and adherence, thereby limiting the use of the therapeutic dose (up to 300 mg/day) in depressed patients.

As reported in the SPC, after a single oral dose of 100 mg of fast-release trazodone, a maximum plasma concentration (max) of 1.2 μg / ml of the drug is achieved, and the time to reach the maximum plasma concentration (t max) is 1 hour. With prolonged release of trazodone after a single oral dose of 75 mg, a maximum concentration of about 0.7 μg / ml is reached with a maximum duration of 4 hours. 4 hours after ingestion. The half-life is approximately 12 hours.

The half-life of trazodone IR is relatively short (6.6 hours after a single 100 mg dose), so repeated daily dosing is often used to achieve sufficient dose levels for depressed patients, but this dosing regimen can be inconvenient and may result in missed doses and decrease in compliance.

More recently, a new once-daily extended-release formulation of trazodone has been developed to further improve adherence to treatment at therapeutic doses and reduce peak plasma concentration and dosing frequency compared to the conventional fast-release formulation. Extended-release trazodone was developed in two doses (tablets scored at 150 and 300 mg) to ensure proper titration, starting at 150 mg/day, in increments of 75 mg every 3 days.

Efficacy and tolerability of trazodone in depression

Several direct studies have demonstrated comparable efficacy of trazodone with other drug classes, including TCAs (amitriptyline and imipramine), SSRIs (fluoxetine, paroxetine, sertraline, citalopram and escitalopram), SNRIs (venlafaxine and mirtazapine) and norepinephrine and dopamine reuptake inhibitors (bupropion). ) . Randomized controlled trials of trazodone in elderly people with depression published since 1981 years old

Trazodone versus tricyclic antidepressants (TCAs)

In a series of comparative trials conducted in the 1980s, short-term therapy (4–6 weeks) with trazodone (100–400 mg) was found to be comparable in efficacy to TCAs such as amitriptyline and imipramine. An early randomized, double-blind, placebo-controlled study of elderly patients with unipolar depression demonstrated that the therapeutic efficacy of trazodone was superior to placebo and comparable to that of imipramine after 4 weeks of treatment. A double-blind, randomized trial of trazodone in elderly patients with severe depression reported significant improvements in both the Hamilton Depression Rating Scale (HAM-D) and the Geriatric Depression Scale (GDS), which were similar to those observed in patients treated with amitriptyline and mianserin. In addition, HAM-D and visual analogue scale (VAS) scores were similar between trazodone and amitriptyline in a study of elderly depressed patients.

Trazodone (Trittico) versus second-generation antidepressants

There have been several direct trials of trazodone (dose range 150-450 mg) and second-generation antidepressants in patients with depression. An analysis of head-to-head trials comparing different second-generation antidepressants found that the relative benefit in terms of response was comparable between trazodone and other second-generation antidepressants, including SSRIs, SNRIs, and bupropion.

A small study (n = 27) comparing the antidepressant efficacy and safety of trazodone and the SSRI fluoxetine in elderly depressed patients reported similar improvements in HAM-D scores after 6 weeks of treatment. Significant improvement in HAM-D scores from baseline was also observed with trazodone IR (dose range 50-400 mg/day) and fluoxetine (dose range 20-40 mg/day) in a larger, randomized, double-blind study (n = 126) outpatients with depression – these improvements in clinical performance were similar in the two treatment groups, but HAM-D sleep disturbance scores improved significantly in the trazodone group than in the fluoxetine group (-2. 7 vs 1.6; p = 0.001).

More recently, two similar European multicentre, double-blind, randomized trials compared twice-daily long-acting trazodone with paroxetine and sertraline in patients with depression. Efficacy was assessed by measuring change from baseline in the HAM-D, Montgomery Osberg Depression Rating Scale (MADRS) and Clinical Global Impression Severity (CGI-S) after 6 weeks of treatment. The results of these two studies showed that extended release trazodone was as effective as paroxetine and sertraline in reducing depressive symptoms and promoting remission; trazodone may also be of benefit to patients with major depression who have difficulty sleeping or exhibit common sleep disturbances.

The efficacy of venlafaxine SNRIs was compared with that of trazodone in a double-blind, randomized, placebo-controlled trial in 225 patients with depression. Overall, both trazodone (dose range 150-400 mg/day after the titration phase) and venlafaxine (dose range 75-200 mg/day) were significantly more effective than placebo, as measured by changes in HAM-D scores. However, trazodone was associated with greater improvement in HAM-D-associated sleep disturbance factor than venlafaxine, while greater improvement in cognitive impairment and developmental delay was observed with venlafaxine.

In contrast to these results, a double-blind, randomized trial of patients with moderate to severe depression demonstrated that mirtazapine and SNRIs were associated with greater improvement in HAM-D scores compared with trazodone after 6 weeks of treatment.

Trazodone was compared with the norepinephrine-dopamine reuptake inhibitor bupropion in a double-blind, randomized study of outpatients with moderate to severe depression. After 6 weeks, overall efficacy in terms of HAM-D and CGI-S was similar between the trazodone IR and bupropion groups. However, improvements in HAM-D and CGI-S scores at day 7 were significantly greater with trazodone compared with bupropion due to the beneficial effects of trazodone on sleep. At the end of treatment, 46% and 58% of patients were considered to have improved significantly/very much in the trazodone and bupropion groups, respectively.

Trazodone extended release preparations

An extended release formulation (Roussel Laboratories Ltd.) was compared with standard trazodone IR in a double-blind, randomized study of 347 general practitioner patients with MDD. After 6 weeks of treatment (150 mg/day at bedtime for both treatment groups), both treatment groups showed significant improvements from baseline in overall severity, overall improvement, and HAM-D scores. The difference in these improvements was not statistically significant between extended-release trazodone and trazodone IR, but small differences in treatment response rates were in favor of patients receiving extended-release trazodone. Safety, tolerability, and compliance did not differ significantly between the two treatment groups, demonstrating that the new formulation was effective and safe.

The efficacy and safety of extended release trazodone was evaluated in a double-blind, randomized, placebo-controlled trial in 412 patients with MDD (treatment course 6 weeks, dose range 150 to 375 mg/day). The mean maximum daily dose of trazodone administered during the study was 310 mg. The improvement in HAM-D scores was significantly greater with trazodone than with placebo, a difference that was statistically significant after the first week of treatment and persisted throughout the study. Moreover, there was a higher percentage of HAMD-17 responders and a greater decrease in deviations from baseline on the HAMD-17 Depressed Mood Scale, CGI-S, and MADRS total score. In the HAM-D group, the greatest improvement was observed in insomnia, guilt, and depressed mood, while in the MADR group, the greatest improvement was seen in reduced sleep, internal tension, reports of sadness, and suicidal thoughts. Notably, the antidepressant efficacy of trazodone was independent of baseline severity of insomnia and improvement in insomnia. Trazodone was also well tolerated; The most common adverse events were headache and drowsiness. There were no serious treatment-related adverse events or clinically significant ECG or laboratory abnormalities. These results suggest that once-daily long-acting trazodone may be an effective monotherapy option in patients with DMD when administered at an appropriate therapeutic dose (up to 375 mg/day).

Trazodone in special patient populations

Trazodone has been studied for the treatment of depression in a variety of patient populations, including the elderly, pediatric patients, and patients with renal insufficiency.

In elderly depressed patients, comparable efficacy has been reported between trazodone and amitriptyline TCAs. Two double-blind, randomized trials comparing trazodone and the SSRI fluoxetine also reported similar antidepressant efficacy between the two treatments studied. In addition, fluoxetine was associated with a higher incidence of activating side effects (arousal, anxiety, nervousness, insomnia) compared to trazodone. In contrast, sedative effects were reported more frequently with trazodone than with fluoxetine.

Trazodone extended release (Roussel Laboratories Ltd. ) has been evaluated in depressed elderly patients. After 4 weeks of treatment, both trazodone controlled-release formulations and conventional formulations (both given at night as single daily doses starting at 100 mg and increased to 200 mg/day depending on tolerability) were similar in efficacy as measured by change from baseline on the HAM-D scale and the global assessment of the severity of depression. During the first week of treatment, fewer side effects were reported in patients treated with the controlled release drug.

Patients often experience their first episode of depression in early childhood, before the onset of puberty or adolescence. To date, there are no data on the use of trazodone in children and adolescents with depression. In a small open-label study of ten children with chronic tics and Tourette’s syndrome, the combination of haloperidol and trazodone was shown to be effective in improving clinical symptoms. At the end of the study, the Yale Global Tic Severity Scale score was significantly reduced from baseline, and no side effects were reported. However, it should be noted that trazodone is not recommended for use in children under 18 years of age.

Trazodone is extensively metabolized in the liver, but the effects of trazodone in patients with renal or hepatic insufficiency are not well understood. An early study in the late 1970s evaluated the effects of a 12-day treatment with trazodone (75 mg) in patients with mixed neurosis and normal or impaired renal function. Although higher serum concentrations of trazodone were observed in patients with impaired renal function compared with patients with normal renal function, these differences were not statistically significant. As a result, the authors concluded that impaired renal function is not a contraindication to treatment with low doses of trazodone. A recent case of severe liver toxicity leading to fulminant liver failure has been reported following treatment with venlafaxine and trazodone for 4 months.

Given the available data on the use of trazodone in patients with renal or hepatic impairment, the labeling of trazodone recommends careful dosing and regular monitoring in patients with hepatic impairment, especially in cases of severe hepatic impairment and severe renal impairment (usually in mild or moderate renal impairment, dose adjustment is not required).

Trazodone tolerance

Trazodone is generally well tolerated in the treatment of depression, with the most common side effects being drowsiness (hypnotics/sedation), headache, dizziness, and dry mouth.

Drowsiness is the most common side effect of trazodone, with incidence in depressed patients ranging from 5.6% to 22.5% (last estimate shown in the figure).

Trazodone has minimal anticholinergic activity. However, an increased risk of orthostatic hypotension may be associated with trazodone, especially in elderly patients or patients with pre-existing heart disease. This effect, due to the blockade of adrenergic α 1 receptors, is temporary and is associated with the plasma concentration of the drug.

At toxic plasma levels, trazodone may be associated with prolongation of the corrected QT interval (QTc) and torsades de pointes. Even at therapeutic doses, several cases of life-threatening cardiac arrhythmias, including ventricular tachycardia, have been reported in clinical and preclinical studies. Evidence suggests that QT interval prolongation is due to the interaction of trazodone with hERG potassium channels. Concomitant use of trazodone with drugs known to cause cardiac toxicity or prolong the QT interval should be avoided as this may increase the risk of ventricular arrhythmias, including torso de pointe arrhythmia.

Trazodone may also be associated with rare cases of priapism. For this reason, trazodone should be used with caution in men with conditions that may predispose them to priapism (eg, sickle cell anemia, multiple myeloma, leukemia, autonomic nervous system dysfunction, and hypercoagulable states) or in men with an anatomical deformity of the penis (eg, angulation, cavernous fibrosis or Peyronie’s disease).

Drug interactions have been reported with inhibitors of the cytochrome P450 (CYP) 3A4 enzyme, such as erythromycin, ketoconazole and ritonavir, resulting in increased plasma concentrations of trazodone; conversely, carbamazepine may reduce plasma concentrations of trazodone. Concomitant use with other antidepressants such as TCAs, MAOs or fluoxetine should be avoided due to the risk of serotonin syndrome and cardiovascular side effects. Interactions between trazodone, citalopram and fluoxetine have been studied in 97 patients with depressive syndrome within 1 year. The results showed that the use of citalopram and fluoxetine in combination with trazodone did not significantly affect the concentration of trazodone in the blood serum, and no cases of headache, daytime sedation, fatigue or serotonin syndrome were reported during the study.

Antidepressants increase the risk of suicidal ideation and behavior (suicidality) in children, adolescents, and young adults compared with placebo in short-term studies of MDD and other psychiatric disorders. Cases of suicidal thoughts and suicidal behavior have been reported during trazodone therapy or shortly after cessation of treatment.

Side effects of the antidepressant Trittiko

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