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How to Avoid Weight Gain When Taking Antidepressant Medication

With Sean Wharton, MD, PharmD, Michael McGee, MD, and J. Michael Gonzalez-Campoy, MD, PhD

Are you among the nearly one in eight adults in the United States) who should be or is already taking an antidepressant to address a mood disorder,1 or an antipsychotic medication for other mental health conditions such as obsessive compulsive disorder or bipolar disorder—but your hesitate out of worry about gaining weight?  

Taking an antidepressant or antipsychotic medication often produces the added worry of possible weight gain but starting a formal weight loss program can prevent it. Photo: 123rf

While these medications are very effective, they often come with a major downside for many patients—undesirable and often significant weight gain.2  For anyone who may benefit from a psychiatric drug but fears the prospect of obesity and its related complications, there is now a good answer.

As simple as it may sound, the best chance of avoiding, or lessening further, undesirable weight gain when taking a prescribed antidepressant or antipsychotic medication, is to simultaneously participate in a formal weight management program. This is true regardless of the psych medication you are taking,according to the experience of patients who were treated at the Wharton Medical Clinics in Toronto, Canada.

Effect of Formal Weight Loss Programs with Psych Medication

Even if you are already taking one of these psych-related medications and you’re stressed about weight gain, or if your doctor has recently suggested that you consider taking one of these drugs but you’re stalling due to concerns about weight gain—this study points to an effective way forward—to enroll in a structured weight loss program.2

After evaluating the experience of more than 17,000 men and women, comparing medical data of those who were on psychiatric medications to those not taking such medication, the researchers found that an organized weight management plan helped everyone—overall and on average—to lose weight. 2

Sean Wharton, MD, PharmD, an internal medicine specialist and director of the Wharton Medical Clinics, which is devoted to weight and diabetes management, in Toronto, Canada, and his team, reports that individuals who are taking a prescribed medication for a mental illness and following a structured weight loss program avoid weight gain based on their analysis.

In all, 4094 patients, or about 1 in 4 of those in the study, were taking at least one psychiatric medication. Most were taking an antidepressant, although about 11% took both. The aim of the study was to compare weight loss for those taking the medications and those not taking them. Data was collected from 2008 to 2017.2

The men and women were, on average, in their late 40s or early 50s. Their average body mass index or BMI was about 39 or 40.2 The program stresses effective, personalized lifestyle changes, Dr. Wharton says. Patients answered questions about family medical history, weight management history, and other health information. Then, a trained weight management educator gave suggestions regarding eating and physical activity to help avoid weight gain.2

In general, participants were taught to cut out 500 calories a day from their usual intake, and they returned to the clinic for ongoing dietary guidance every 3-4 weeks.2

Over the average of 16 months of clinic attendance, on average, patients lost about 7.5 pounds, or 2.9% of their body weight. That translated to 27.6% of patients losing 5% or more of their baseline weight and 10.1% losing twice that amount or more.2

You may be saying….a 2.9% weight loss is not such a big deal…but according to Dr. Wharton, these results correlate with those of other weight loss interventions and, this number indicates an average, meaning some lost more, some lost less.

More importantly, Dr. Wharton tells EndocrineWeb, contrary to past beliefs, the findings from this study suggest that weight gain is not inevitable when taking psychiatric medications. Also, weight loss is achieved in direct contrast to the expectation that everyone would gain weight when taking an antidepressant or antipsychotic medication.2

Men who were taking antidepressants lost slightly less than people in the other groups, but it wasn’t a big difference,2 says Ms. Christensen. While the researchers can’t explain the reason for this finding, they believe it could be that the other patients were feeling better mentally so they were a bit more successful with their weight loss goal but this would require further testing to gain a clear answer.

Weight Gain—Causes Added Worry with Psych Meds

You are not alone in gaining benefit from psychiatric medication—and you aren’t the only one who stresses about the weight gain linked with many of the drugs. As such, this challenge inspired Ms. Christensen to test for a solution that would address this vexing problem. She tells EndocrineWeb that concern about weight gain is both a real and almost universal experience among the patients in her clinic that are prescribed psychiatric medications. 2

“The fear of weight gain is sometimes so powerful that people will stop taking their [mental health] medication,” says Dr. Wharton who is the senior investigator of the study that shows that participating in an organized, medical weight loss programs work.

As if to confirm how common this conundrum is, Michael McGee, MD, chief medical officer at The Haven at Pismo, an addiction treatment center near San Luis Obispo in California, says that he frequently hears about the anxiety linked with medication-related weight gain.

 “My patients fear and complain about weight gain, particularly the women, who often do gain weight, but it is not a given,” he tells EndocrineWeb. With years of practice, Dr. McGee has seen many patients who have experienced weight gain, increasing about five to 10% of their starting weight. That means, for example, a 150-pound woman would be facing up to a 15-pound gain in body weight.

Balancing Mental and Physical Health is Often Complicated

Even when not taking a psychiatric medication, some people with mental health disorders may already be battling overweight or obesity, says Dr. Wharton and his colleagues. Research has shown that those with mental health disorders seem to have up to 1.5 times greater odds of having obesity. 2,3

In addition, the weight gain linked with antidepressant and antipsychotic drugs has been well recognized, although the experience varies and is not the same for everyone.4-7

So how much weight gain are we talking about? In another recent study,7 researchers looked at the weight status of 362 patients taking an antidepressant medication for six to 36 months. More than half of them gained weight, with 40% of individuals gaining at least 7% of their starting weight. The only drug of the eight psych medications evaluated in the study not linked with weight gain was fluoxetine (ie, Prozac). The study did not have funding from pharmaceutical companies.7

The links between weight gain and medications have been shown to differ by medication type, says J. Michael Gonzalez-Campoy, MD, PhD, FACE, medical director and CEO of the Minnesota Center for Obesity, Metabolism and Endocrinology.

“In general, the use of antipsychotic medications are most often associated with weight gain,” Dr. Gonzalez-Campoy tells EndocrineWeb “In general, the use of antidepressants is associated with more modest weight gain—with the exception of fluoxetine and bupropion (Wellbutrin, others), which appear to be weight neutral.”

Steps to Avoid Weight Gain When Starting a Psych Medication

Asking for a referral to a qualified weight loss program in your area is a good idea, says Dr. McGee.  What else?

  • Focus on what (ie, choose a Mediterranean approach to eating) and how you eat (eg, seated at the table, with other people, chewing slowly and mindfully)
  • Don’t eat for gratification, boredom, or self-soothing or overeat to punish yourself
  • Discuss whether weight loss medicines, in addition to the structured weight loss program, may be appropriate, at least to start.

According to Dr. Gonzalez-Campoy, ”along with a prescription for antipsychotic medications and most antidepressants, a concomitant prescription for weight management should be provided [for patients who already have overweight or obesity].

And for those on antipsychotics, you should be made aware of the health risks that come with significant weight gain such as the development or worsening of high blood sugar, high blood pressure, and high cholesterol, he says. These are medical issues that should be monitored as well, he says.

The bottom line—For anyone who is taking an antidepressant or antipsychotic medication: “Taking these medications [to manage a mental health issue] is very important,” Ms. Christensen says. “Don’t be concerned about the potential weight gain because that can be mitigated [ie, managed].”

None of the healthcare practitioners had relevant financial conflicts with regard to this study.


Last updated on 09/19/2019

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Antidepressants That Cause Weight Loss

If you have any medical questions or concerns, please talk to your healthcare provider. The articles on Health Guide are underpinned by peer-reviewed research and information drawn from medical societies and governmental agencies. However, they are not a substitute for professional medical advice, diagnosis, or treatment.

If you’ve been prescribed an antidepressant, you may be curious about its potential effect on weight, particularly if it causes weight gain or weight loss. Here’s what the research says about how antidepressant use can affect what you see on the scale.

There are more than a dozen antidepressant drugs that are popularly prescribed. But only one has been consistently associated with weight loss in studies: bupropion (brand name Wellbutrin).

A 2019 meta-analysis of 27 studies on antidepressants and weight gain found that antidepressant use can increase  body weight by an average of 5%—except bupropion, which was associated with weight loss (Alonso-Pedrero, 2019).


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Another study from 2016 looked at the long-term weight loss effect of various antidepressants and found that non-smokers who took bupropion lost 7.1 pounds over two years. (This effect was not seen in smokers.) Users of the other antidepressants in the study gained weight (Arterburn, 2016).

Bupropion also seems to help with weight loss maintenance. A 2012 study found that adults with obesity who took bupropion SR (standard release) in 300mg or 400mg doses lost 7.2% and 10% of their body weight, respectively, over 24 weeks and maintained much of that weight loss at 48 weeks (Anderson, 2012). 

In fact, bupropion is part of the popular weight loss drug naltrexone-bupropion (brand name Contrave), which is FDA approved for the treatment of overweight or obesity. 

Experts aren’t exactly sure. Antidepressant drugs’ effect on weight is, in the words of one study, “only partially understood” and “poorly described” (Gafoor, 2018).  

In very broad terms, antidepressants act on a variety of chemicals, neurotransmitters and receptors in the brain. This changes the level of the impact of these neurotransmitters in the brain. Ideally, that improves mental health issues like depression and anxiety. Less-than-ideally, in some cases, these effects seem to cause metabolic changes that lead to weight gain.

For example: Bupropion is a medication known as an NDRI (norepinephrine-dopamine reuptake inhibitor). It prevents the brain from absorbing free-floating norepinephrine (a.k.a. adrenaline) and dopamine (otherwise known as the feel-good hormone). When they aren’t reabsorbed quickly, adrenaline and dopamine stick around and act on the brain longer. This may have an effect on metabolism and appetite, resulting in weight loss. 

Some antidepressants affect histamine and serotonin, which regulate appetite (Gill, 2020). Others act on neurotransmitters and receptors that are connected to weight gain (David, 2016). Some of these drugs, mainly the early first-generation tricyclic antidepressants, may change the way the body metabolizes lipids (fats) and glucose (blood sugar)  (Hasnain, 2012; David, 2016). 

However, weight gain or weight loss is far from guaranteed when you take antidepressants.

Fear of weight gain shouldn’t keep you from taking antidepressants if you need them. Talk with your healthcare provider if you’re bothered by weight gain—adjusting your diet, increasing exercise or, in some cases, switching medications can be effective solutions.

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The latest Diagnostic and Statistical Manual of Mental Disorders (DSM 5) defines major depressive disorder (MDD) as “two or more weeks of five of the following symptoms that cause problems with social, occupational, or other areas of functioning:”

  • Depressed mood
  • Decreased interest or pleasure in doing things
  • Weight loss or weight gain, or increased or decreased appetite
  • Insomnia or sleeping too much
  • Moving slowly or being fidgety or restless
  • Fatigue or loss of energy
  • Feelings of excessive guilt or worthlessness
  • Difficulty concentrating or making decisions
  • Recurrent thoughts of death or suicide (DSM, 2013)

Don’t hesitate to seek medical advice if you or someone you know may be suffering from depression.

In some cases, depression can have a medical cause, such as hypothyroidism, vitamin B12 deficiency, low testosterone, or side effects of medication. A healthcare provider can diagnose and treat these.

Unfortunately, most cases of depression aren’t caused by medical issues. For depression that doesn’t have a medical cause, the main treatments are medication and psychotherapy.

The most common antidepressant medications are selective serotonin reuptake inhibitors (SSRIs), which include fluoxetine (brand name Prozac), sertraline (brand name Zoloft), paroxetine (brand name Paxil), and escitalopram (brand name Lexapro). 

Serotonin-norepinephrine reuptake inhibitors (SNRIs) are also frequently prescribed, including venlafaxine (brand name Effexor), duloxetine (brand name Cymbalta), and desvenlafaxine (brand name Pristiq). 

Talk with your healthcare provider to find the right medication for you.

Research shows that antidepressants and cognitive behavioral therapy (CBT) are about equally effective for the treatment of depression. However, CBT may have more long-lasting effects and prevent relapse (Hollon, 2005). During CBT, therapists encourage patients to replace negative, unhelpful thoughts with more positive ones. 

Both aerobic and resistance exercises have been found to be effective at relieving depression (Craft, 2004). Some studies indicate that the Mediterranean diet is associated with a lower rate of depression (Sánchez-Villegas, 2009). 

Other things that might improve depression include getting better sleep, increasing social interaction, and avoiding excessive use of alcohol and tobacco. 

If you are feeling depressed, it’s important to seek out the help you need. Speak with your healthcare provider or a mental health professional to figure out if antidepressants, therapy, or a combination thereof are right for you. If you are concerned about weight gain on antidepressants, be sure to discuss that with your healthcare provider as well. 

  1. Alonso‐Pedrero, L. , Bes‐Rastrollo, M., & Marti, A. (2019). Effects of antidepressant and antipsychotic use on weight gain: A systematic review. Obesity reviews : an official journal of the International Association for the Study of Obesity20(12), 1680–1690. doi: 10.1111/obr.12934. Retrieved from https://pubmed.ncbi.nlm.nih.gov/31524318/
  2. Craft, L. L., & Perna, F. M. (2004). The Benefits of Exercise for the Clinically Depressed. The Primary Care Companion to The Journal of Clinical Psychiatry, 06(03), 104–111. doi: 10.4088/pcc.v06n0301. Retrieved from https://pubmed.ncbi.nlm.nih.gov/15361924/
  3. David, D. J., & Gourion, D. (2016). Antidépresseurs et tolérance : déterminants et prise en charge des principaux effets indésirables [Antidepressant and tolerance: Determinants and management of major side effects]. L’Encephale, 42(6), 553–561. https://doi.org/10.1016/j.encep.2016.05.006. Retrieved from https://pubmed.ncbi.nlm.nih.gov/27423475/
  4. DSM-5 (2013). Depressive disorders. Diagnostic and Statistical Manual of Mental Disorders. doi:10.1176/appi.books.9780890425596.dsm04. https://dsm.psychiatryonline.org/doi/book/10.1176/appi.books.9780890425596
  5. Gafoor, R., Booth, H. P., & Gulliford, M. C. (2018). Antidepressant utilisation and incidence of weight gain during 10 years’ follow-up: population based cohort study. BMJ (Clinical research ed.), 361, k1951. https://doi.org/10.1136/bmj.k1951. Retrieved from https://pubmed.ncbi.nlm.nih.gov/29793997/
  6. Gill, H., Gill, B., El-Halabi, S., Chen-Li, D., Lipsitz, O., Rosenblat, J. D., et al. (2020). Antidepressant Medications and Weight Change: A Narrative Review. Obesity, 28(11), 2064–2072. doi: 10.1002/oby.22969. Retrieved from https://onlinelibrary.wiley.com/doi/abs/10.1002/oby.22969
  7. Hasnain, M., Vieweg, W. V., & Hollett, B. (2012). Weight gain and glucose dysregulation with second-generation antipsychotics and antidepressants: a review for primary care physicians. Postgraduate medicine, 124(4), 154–167. https://doi.org/10.3810/pgm.2012.07.2577. Retrieved from https://pubmed.ncbi.nlm.nih.gov/22913904/
  8. Hollon, S. D., Derubeis, R. J., Shelton, R. C., Amsterdam, J. D., Salomon, R. M., O’Reardon, J. P., et al. (2005). Prevention of Relapse Following Cognitive Therapy vs Medications in Moderate to Severe Depression. Archives of General Psychiatry, 62(4), 417. doi: 10.1001/archpsyc.62.4.417. Retrieved from https://pubmed.ncbi.nlm.nih.gov/15809409/

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Wellbutrin vs. Prozac: Main differences and similarities

Main differences | Conditions treated | Efficacy | Insurance coverage and cost comparison | Side effects | Drug interactions | Warnings | FAQ

Wellbutrin (bupropion) and Prozac (fluoxetine) are medications that can treat depression. Specifically, these drugs are prescribed to treat major depressive disorder. Symptoms of major depressive disorder may include feelings of sadness or hopelessness, loss of interest in daily activities, and problems with sleep.  

Wellbutrin and Prozac are only available with a prescription from a doctor or healthcare provider. Although they have similar uses, Wellbutrin and Prozac work in different ways and have different side effects. Continue reading to learn more about the similarities and differences between Wellbutrin and Prozac. 

What are the main differences between Wellbutrin and Prozac?

Wellbutrin is an aminoketone antidepressant that is also known by its generic name, bupropion. The exact way in which Wellbutrin works is not well understood. However, it is believed to increase levels of certain neurotransmitters called norepinephrine and dopamine in the brain. Individuals with depression may have an imbalance of these neurotransmitters. Unlike other commonly prescribed antidepressants, Wellbutrin has no effect on serotonin levels. 

Wellbutrin is available in three different formulations: immediate-release (IR), sustained-release (SR), and extended-release (XL). Depending on the dosage form, Wellbutrin can be taken once, twice, or three times daily. The active ingredient in Wellbutrin, bupropion, is also marketed as Zyban to support smoking cessation. 

Prozac is one of the most commonly prescribed antidepressants. It is also known by the generic name fluoxetine. Prozac belongs to a class of drugs called selective serotonin reuptake inhibitors (SSRIs). These drugs work by increasing levels of the neurotransmitter serotonin to ease symptoms of depression. 

Prozac comes as a daily oral capsule. The exact dosage depends on the condition being treated. Prozac is also available as a delayed-release capsule that is taken once per week.

Differences between Wellbutrin and Prozac
Drug class Aminoketone  Selective serotonin reuptake inhibitor
Brand/generic status Brand and generic available Brand and generic available
What is the generic name? Bupropion Fluoxetine
What form(s) does the drug come in? Oral tablet Oral capsule, Delayed-release
What is the standard dosage? 100 mg three times daily
Dosage dependent on condition
20 mg once per day
Dosage dependent on condition
How long is the typical treatment? Long term depending on the condition being treated Long term depending on the condition being treated
Who typically uses the medication? Adults Adults; children 8 years and older (depression)

Conditions treated by Wellbutrin and Prozac

All forms of Wellbutrin are approved by the Food and Drug Administration (FDA) to treat major depressive disorder, also known as major depression. Wellbutrin XL, the extended-release form of Wellbutrin, is also approved to prevent seasonal affective disorder (SAD), a type of depression that develops during seasonal changes. Wellbutrin is sometimes used off-label to treat bipolar disorder. 

Prozac is FDA approved to treat major depressive disorder. It is also approved to treat obsessive-compulsive disorder (OCD) and panic disorder, as well as an eating disorder called bulimia nervosa. When used along with an antipsychotic called Zyprexa (olanzapine), Prozac is used to treat depressive episodes in those with bipolar disorder. Some individuals with depression may not respond to other medications and thus, they may be prescribed Prozac and Zyprexa (olanzapine). Prozac is marketed under a different brand name called Sarafem to treat premenstrual dysphoric disorder. 

Wellbutrin and Prozac have also been studied for the treatment of ADHD. One study found that Wellbutrin helped improve symptoms of ADHD compared to placebo.

Major depression Yes Yes
Depression associated with seasonal affective disorder Yes Off-label
Depression associated with bipolar I disorder Off-label Yes
Obsessive-compulsive disorder (OCD) No Yes
Panic disorder No Yes
Bulimia nervosa No Yes
Premenstrual dysphoric disorder (PMDD) No Yes
Attention-deficit hyperactivity disorder (ADHD) Off-label Off-label

Is Wellbutrin or Prozac more effective?

Wellbutrin and Prozac are effective prescription medications for treating depression. The best antidepressant will depend on a number of factors such as cost, individual response to treatment, and potential side effects. Consult a healthcare provider on the best treatment options for your condition.  

According to one double-blind comparison study, bupropion and fluoxetine were found to be similar in effectiveness for the treatment of depression. The study was conducted over seven weeks and utilized the Hamilton Rating Scale for Depression among other tools to assess treatment efficacy. Both bupropion and fluoxetine helped relieve depression symptoms with no severe adverse effects. 

One systematic review found that Wellbutrin is an effective and safe medication compared to other antidepressants. Wellbutrin may have less side effects compared to SSRIs. It also causes less sexual side effects and weight gain than other antidepressants. 

A systematic review found that Prozac is an effective medication for several mental health conditions, including depression, bulimia, and OCD. Prozac was found to be more effective than placebo in some studies within the review. It was also found to be as effective as Anafranil (clomipramine) for treating OCD.

Coverage and cost comparison of Wellbutrin vs.


The average cost of Wellbutrin XL without insurance is around $194. Wellbutrin XL is available in a generic form that is usually covered by most Medicare and health insurance plans. With a SingleCare prescription discount card, you may be able to lower the cost of the generic Wellbutrin XL to around $5, depending on the dosage and quantity prescribed. 

Prozac is available in a generic form. It is usually covered by most insurance plans. The average cash price of Prozac is around $300. However, the price can vary depending on the dosage and quantity prescribed. A SingleCare prescription discount card for generic Prozac is available, which can help lower the cost to $4. 

Typically covered by insurance? Yes Yes
Typically covered by Medicare Part D? Yes Yes
Quantity 30 tablets 30 capsules
Typical Medicare copay $0–$2 $12
SingleCare cost $5 $4–$20

Common side effects of Wellbutrin vs.


The most common side effects of Wellbutrin are dry mouth, nausea, dizziness, insomnia, stomach upset, anxiety, palpitations, and sweating. Wellbutrin may also cause muscle aches, rash, and itching. Weight changes have also been reported while using Wellbutrin. However, Wellbutrin is more likely to cause weight loss than weight gain. 

The most common side effects or Prozac include sexual dysfunction, decreased sex drive, diarrhea, indigestion, nausea, fatigue, dizziness, and drowsiness. Prozac may also cause rash, flu-like symptoms, and tremors. Weight changes have also been reported with Prozac. 

Severe side effects of Wellbutrin and Prozac include worsened depression and suicidal thoughts or behaviors. Seek immediate medical attention if you experience worsened depression symptoms. You should also seek medical attention if you experience an allergic reaction to Wellbutrin or Prozac. Symptoms of an allergic reaction include hives, trouble breathing, or swelling of the face or throat.  

Side effect Applicable? Frequency Applicable? Frequency
Nausea Yes 13% Yes 22%
Indigestion Yes 3% Yes 8%
Dry Mouth Yes 17% Yes 9%
Constipation Yes 10% Yes 5%
Diarrhea Yes 5% Yes 11%
Muscle pain Yes 2% No
Anxiety Yes 5% Yes 12%
Rash Yes 5% Yes 4%
Dizziness Yes 7% Yes 9%
Somnolence Yes 2% Yes 12%
Tremor Yes 6% Yes 9%
Insomnia Yes 11% Yes 19%
Decreased libido No Yes 4%
Palpitations Yes 2% Yes 1%

Source: DailyMed (Wellbutrin SR), DailyMed (Prozac)

Drug interactions of Wellbutrin vs.


Wellbutrin should not be combined with a monoamine oxidase inhibitor (MAOI), such as selegiline or phenelzine. Taking Wellbutrin with an MAOI can increase the risk of high blood pressure. Prozac should also be avoided with an MAOI. Combining Prozac with an MAOI can increase the risk of serotonin syndrome, a condition that may require hospitalization. Wellbutrin or Prozac should also not be taken within 14 days of stopping an MAOI. 

Dopaminergic drugs like levodopa and amantadine can interact with Wellbutrin. Using these medications with Wellbutrin can increase the risk of adverse effects, such as restlessness, dizziness, and tremors. 

The use of nonsteroidal anti-inflammatory drugs (NSAIDs) or warfarin should be avoided or monitored while taking Prozac. This drug interaction may lead to an increased risk of bleeding.

Prozac can also interact with other serotonergic drugs like certain opioids, tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors (SNRIs), seizure medications, and mood stabilizers. Taking these medications with Prozac may increase the risk of serotonin syndrome. 

MAOIs Yes Yes
Dopaminergic  Yes No
Antipsychotic Yes Yes
Opioids Yes Yes
Tricyclic antidepressant Yes Yes
SNRIs Yes Yes
St. John’s Wort Herbal Yes Yes
Antiepileptic Yes Yes
Lithium Mood stabilizer Yes Yes
Warfarin Anticoagulant No Yes

*Consult a healthcare professional for other drug interactions

Warnings of Wellbutrin and Prozac

Both drug labels for Wellbutrin and Prozac contain black box warnings about suicidal thoughts and behaviors. There may be an increased risk of worsened depression while taking Wellbutrin or Prozac. Seek immediate medical attention if your symptoms don’t improve or you experience suicidal thoughts and behaviors. 

There may be an increased risk of seizures while taking Wellbutrin, especially in higher doses. The use of Wellbutrin is also associated with an increased risk of high blood pressure, mania, psychosis, and glaucoma in certain people. Consult a healthcare provider if you have had a history of these conditions before taking Wellbutrin. 

Like Wellbutrin, Prozac also carries a risk of seizures, mania, and glaucoma. In addition, the use of Prozac can also increase the risk of serotonin syndrome. Signs and symptoms of serotonin syndrome include confusion, rapid heart rate, and muscle stiffness, among others. Low sodium levels (hyponatremia), heart rhythm problems (QT prolongation), and abnormal bleeding have also been reported with Prozac in certain people. 

Seek medical advice from a healthcare provider prior to starting treatment with Wellbutrin or Prozac.  

Frequently asked questions about Wellbutrin vs. Prozac

What is Wellbutrin?

Wellbutrin is an aminoketone antidepressant that is FDA approved to treat major depressive disorder. It comes in an immediate-release, sustained-release, and extended-release form. In addition to treating major depressive disorder, Wellbutrin XL is also approved to prevent seasonal affective disorder. The generic name of Wellbutrin is bupropion. 

What is Prozac?

Prozac is a selective serotonin reuptake inhibitor (SSRI) that is FDA approved to treat major depressive disorder. As an SSRI antidepressant, Prozac can also treat depression associated with bipolar disorder. Prozac is also approved to treat other mental health conditions, including OCD, panic disorder, bulimia, and premenstrual dysphoric disorder (as Sarafem). Prozac comes in a daily or weekly oral capsule. The generic name of Prozac is fluoxetine. 

Are Wellbutrin and Prozac the same?

Both Wellbutrin and Prozac are antidepressant medications but they work in different ways. Wellbutrin is an aminoketone that works by increasing the levels of norepinephrine and dopamine in the brain. Prozac is an SSRI that works by increasing the levels of serotonin in the brain. A doctor who specializes in psychiatry may prescribe these prescription drugs to treat various mental health conditions, primarily depression. 

Is Wellbutrin or Prozac better?

Wellbutrin and Prozac are similarly effective for treating depression. The best antidepressant is the one that causes the least side effects and is more cost effective, depending on the situation. Wellbutrin causes less sexual side effects and weight gain than SSRIs like Prozac. Other SSRIs include Paxil (paroxetine), Zoloft (sertraline), Lexapro (escitalopram), and Celexa (citalopram). Prozac may be more appropriate than Wellbutrin to treat depression in an individual with bipolar disorder, bulimia, or OCD. Antidepressant medications often work better in combination with psychotherapy. 

Can I use Wellbutrin or Prozac while pregnant?

Wellbutrin may be prescribed to treat depression during pregnancy. However, there may be a risk of birth defects and miscarriage while using Wellbutrin during pregnancy. Prozac is not recommended during late pregnancy due to the risk of pulmonary hypertension, respiratory distress, and other problems in the infant. Wellbutrin and Prozac may pass into the breast milk. Consult a healthcare provider before taking an antidepressant while pregnant or breastfeeding. 

Can I use Wellbutrin or Prozac with alcohol?

It is not generally recommended to drink alcohol while taking Wellbutrin or Prozac. Combining alcohol with antidepressants can increase the risk of side effects such as drowsiness and dizziness. Therefore, alcohol consumption should be monitored or minimized while taking Wellbutrin or Prozac. 

Managing the Adverse Effects of Antidepressants

Primum non nocere

-Hippocratic Oath


Antidepressants are among the most widely prescribed drugs. Both in Europe and the US, 6% to 10% of the population are treated with antidepressant medications. 1 Most, if not all, antidepressants can cause bothersome adverse effects in a substantial number of patients, with nonadherence as a likely consequence. Nonadherence rates are high, estimated to be between 31% and 60%, and are probably governed by a trade-off between perceived benefits and drawbacks.1,2 Adverse effects are dramatically underestimated by the prescribing physicians: more than 80% of patients experience at least one and, on average, patients experience 4 different adverse effects, most of which pose substantial bother, sometimes to the extent that the patient’s daily functioning is affected.3 Not surprisingly, for about 20% of (primary care) patients, the benefits of antidepressants do not outweigh the adverse effects.1

Modern antidepressants held the promise of reducing the adverse-effect burden of the older TCAs. This did not, however, prove to be true. The burden might have changed, but it did not diminish. The most frequently experienced adverse effects, according to a recent survey in 225 primary care patients using different types of antidepressants, are shown in the Figure. Patients seem to be bothered the most by GI complaints, dizziness, weight gain, and decreased libido.

Jitteriness syndrome

Jitteriness is a poorly defined syndrome of early worsening of anxiety, agitation, and irritability. It is estimated to occur in up to 65% of patients immediately after starting therapy with a serotonergic or noradrenergic antidepressant.4 Its importance lies in the fact that it might cause patients to discontinue treatment if they become convinced that it will worsen their condition. A slower titration, especially in patients with anxiety symptoms, might prevent the syndrome. Since jitteriness is time-limited, waiting for tolerance to develop or temporarily combining the antidepressant with a benzodiazepine or propranolol may be helpful.


Peter is 36, is depressed, and suffers from panic attacks. He is referred by his primary care physician because “things got worse” after starting therapy with escitalopram. He reports having had occasional panic attacks before he started taking the medication, but after beginning the treatment, he was “freaking out all day, couldn’t sit still, and felt restless all the time. It made everything worse.” Even after his physician explained that these effects were likely temporary, Peter refused to continue taking the medication. Eventually he consented to try another SSRI, which was started at the lowest dose and slowly titrated.

Other adverse effects

GI problems. Complaints such as nausea emerge in about 25% of patients, soon after initiating modern antidepressants. Such complaints are more frequent with venlafaxine and SSRIs than with bupropion, mirtazapine, or reboxetine.5 In most cases, nausea wanes after 2 or 3 weeks, but it persists in about one-third of patients. Dividing doses, taking medication with some food, or administering more of the dose at bedtime can help; ginger may be beneficial when tak-ing ranitidine or omeprazole. 5 Add-ing low-dose mirtazapine to the antidepressant regimen may also help.6

Diarrhea develops in about 15% of patients. Antidiarrheal agents may be helpful, although in patients in whom diarrhea persists, a switch to another agent should be considered. Constipation, an adverse effect described as bothersome in about 5% of patients, can be managed by physical activity, fluid and fiber intake, or laxatives.7

Weight gain. Another frequent adverse effect of long-term antidepressant treatment is weight gain. Several antidepressants cause an initial but transient weight loss, followed by weight gain during maintenance treatment. The majority of antidepressants cause only slight weight gain, except for mirtazapine, amitriptyline, and paroxetine. Bupropion is the only antidepressant that induces weight loss.

Various strategies are suggested, such as nutritional counseling and physical exercise, but most often, antidepressants need to be switched. If a switch is not an option, the addition of bupropion or a psychostimulant can be considered. In any case, patients with a high risk of weight gain should be advised to avoid low-volume, high-calorie foods when they begin treatment with an antidepressant.

Sweating. As many as 20% of patients taking antidepressants experience excessive sweating.8 It is commonly prominent in the scalp, face, neck, and chest and usually occurs with episodic bursts, often persisting throughout treatment. Reboxetine, venlafaxine, and bupropion increase susceptibility, whereas paroxetine and mirtazapine might decrease susceptibility. Several agents have been proposed to treat excessive sweating, based on hypotheses about its pathophysiology: serotonin antagonists, such as cyproheptadine; antiadrenergic agents, such as clonidine; and anticholinergic agents, such as benztropine and glycopyrrolate.

Sexual dysfunction. Antidepressants can affect every aspect of sexual functioning and cause decreased libido, problems with arousal, ejaculatory delay, anorgasmia, and erectile dysfunction. Prevalence rates up to 80% have been reported.9 SSRIs are more likely to cause sexual adverse effects than are noradrenergic drugs. In some patients, sexual adverse effects will disappear spontaneously or improve after dose reduction. Taking a drug holiday, ie, stopping the antidepressant for a few days, has been shown to improve sexual function and satisfaction in approximately half of the patients taking an SSRI with a short half-life, such as sertraline or paroxetine.10

The addition of sildenafil or tadalafil is an effective strategy for men with antidepressant-induced erectile dysfunction.11 In women, transdermal testosterone increases the frequency of satisfactory sexual events12; adding a higher dose of bupropion (300 mg/d) also seems to improve sexual function.11 Although generally considered to resolve on cessation of the drug, SSRI- and SNRI-emergent sexual adverse effects may persist after drug discontinuation in some patients. 13 Psychological processes probably play a role in the persistence of these sexual dysfunctions, and they should be addressed.

Sedation. Often wanted but frequently annoying, sedation is more commonly associated with TCAs and mirtazapine than with SSRIs and SNRIs. In the event that dose reduction or bedtime dosing does not help, switching to a less sedating alternative, such as bupropion, an SSRI, or an SNRI, can be considered. In the case of excessive sleepiness and fatigue, adjunctive modafinil can be considered to improve wakefulness.

A dose-related and reversible decrease in motivation and emotional responsivity or detachment, also referred to as apathy or emotional blunting, has been reported, mainly in case reports and predominantly associated with the use of SSRIs.14 In these cases, reducing the dose or switching to another antidepressant, preferably bupropion, may help.

The discontinuation syndrome

A final hurdle to overcome is the discontinuation syndrome, which develops in some patients (5% to 86%) 1 to 7 days following dose reduction or discontinuation of an SSRI or SNRI. 15 Typically, patients describe electric shocks in the brain, visual flashes, and headaches. Other symptoms are dizziness, lethargy, light-headedness, insomnia, fatigue, anxiety, agitation, and nausea.

This syndrome has been linked to the half-life of a given SSRI; paroxetine has been involved more often than other SSRIs.16 Tailoring tapering to the individual patient and to the specific antidepressant should reduce the likelihood of experiencing discontinuation symptoms. In some cases, prescribing an SSRI with a longer half-life (eg, fluoxetine) while discontinuing the antidepressant might be helpful.


Maria, who is 58, was treated for depression and anxiety. She has been referred by her primary care physician because her symptoms relapsed during tapering of venlafaxine. She reports, “Two days after tapering, I felt electrical twitches in my head; I have headaches and feel nervous and agitated. I think I am relapsing and will have to take my pills forever.

Maria is experiencing discontinuation symptoms. Gradual tapering of venlafaxine, taking 37.5 mg every other day, does not prevent severe discontinuation symptoms. Fluoxetine 20 mg/d is prescribed, and venlafaxine is discontinued without any problem. Fluoxetine is then gradually tapered, but about 2 weeks after the final dose, Maria experiences mild discontinuation symptoms (“feeling nervous”). These disappear after another week.

Serious adverse effects

Apart from the annoying and bothersome adverse effects described above, the clinician should be aware of several serious adverse effects that can be associated with modern antidepressants. In a small subgroup (4% to 14%) of younger patients, suicidal ideation can emerge in the first weeks following treatment initiation and dose adjustments.17

Even after short-term use of an SSRI or venlafaxine, the risk of upper GI bleeding is slightly higher than with the older TCAs, especially in higher-risk situations such as alcohol use. Although depression is associated with the metabolic syndrome and some antidepressants may induce weight gain, there may not necessarily be a correlation between the two. However, in young adults, long-term antidepressant use may increase the risk of type 2 diabetes mellitus.

Although more often associated with TCAs, cardiovascular adverse effects, seizures, and agranulocytosis are also possible adverse effects of other antidepressants. Treatment decisions based on identifying risk factors, carefully reviewing all appropriate antidepressants, and patient preferences, as well as careful monitoring, will help keep adverse effects to a minimum (Table).


Clinicians will be confronted with bothersome and sometimes severe adverse effects in their patients when prescribing antidepressants. Before the initiation of antidepressant treatment, patients should be informed about potential adverse effects and encouraged to contact the physician with any concerns, so that these can be managed adequately. As a rule, begin with an antidepressant that has shown better tolerance at the lowest dose, then titrate slowly.

Careful monitoring should focus on tolerance as well as on symptom alleviation. It is important to distinguish adverse effects from depression symptoms, such as fatigue and carbohydrate craving. Should bothersome adverse effects emerge, watchful waiting is often a reasonable option, since most adverse effects diminish over time. Either reducing the dose or adjusting the dosing schedule can be tried before switching to another antidepressant. If this strategy is not successful, the (off-label) addition of other pharmacological agents can be considered.


Dr Sienaert is Assistant Professor at the faculty of medicine, Catholic University of Leuven (KU Leuven) and psychiatrist in the department of mood disorders at the University Psychiatric Center KU Leuven in Kortenberg, Belgium. He reports that in the past 5 years, he has been an independent speaker (no product-related lectures) for AstraZeneca, Bristol-Myers Squibb, Lanssen, Eli Lilly and Company, and Lundbeck, and a consultant for AstraZeneca, Janssen, Eli Lilly and Company, Lundbeck, and Servier, for which he has received honoraria.


1. Wouters H, Van Dijk L, Van Geffen EC, et al. Primary-care patients’ trade-off preferences with regard to antidepressants. Psychol Med. 2014 Jan 7:1-8; [Epub ahead of print].

2. Demyttenaere K, Enzlin P, Dewé W, et al. Compliance with antidepressants in a primary care setting, 1: beyond lack of efficacy and adverse events. J Clin Psychiatry. 2001;62(suppl 22):30-33.

3. Hu XH, Bull SA, Hunkeler EM, et al. Incidence and duration of side effects and those rated as bothersome with selective serotonin reuptake inhibitor treatment for depression: patient report versus physician estimate. J Clin Psychiatry. 2004;65:959-965.

4. Sinclair LI, Christmas DM, Hood SD, et al. Antidepressant-induced jitteriness/anxiety syndrome: systematic review. Br J Psychiatry. 2009;194:483-490.

5. Kelly K, Posternak M, Alpert JE. Toward achieving optimal response: understanding and managing antidepressant side effects. Dialogues Clin Neurosci. 2008;10:409-418.

6. Uguz F. Low-dose mirtazapine added to selective serotonin reuptake inhibitors in pregnant women with major depression or panic disorder including symptoms of severe nausea, insomnia and decreased appetite: three cases. J Matern Fetal Neonatal Med. 2013;26:1066-1068.

7. Wouters H, Bouvy ML, Van Geffen EC, et al. Antidepressants in primary care: patients’ experiences, perceptions, self-efficacy beliefs, and nonadherence. Patient Prefer Adherence. 2014;8:179-190.

8. Marcy TR, Britton ML. Antidepressant-induced sweating. Ann Pharmacother. 2005;39:748-752.

9. La Torre A, Giupponi G, Duffy D, Conca A. Sexual dysfunction related to psychotropic drugs: a critical review-part I: antidepressants. Pharmacopsychiatry. 2013;46:191-199.

10. Rothschild AJ. Selective serotonin reuptake inhibitor-induced sexual dysfunction: efficacy of a drug holiday. Am J Psychiatry. 1995;152:1514-1516.

11. Taylor MJ, Rudkin L, Bullemor-Day P, et al. Strategies for managing sexual dysfunction induced by antidepressant medication. Cochrane Database Syst Rev. 2013;5:CD003382.

12. Fooladi E, Bell RJ, Jane F, et al. Testosterone improves antidepressant-emergent loss of libido in women: findings from a randomized, double-blind, placebo-controlled trial. J Sex Med. 2014;11:831-839.

13. Bahrick AS. Persistence of sexual dysfunction side effects after discontinuation of antidepressant medications: emerging evidence. Open Psychol J. 2008;1:42-50.

14. Demyttenaere K, Jaspers L. Review: bupropion and SSRI-induced side effects. J Psychopharmacol. 2008;22:792-804.

15. Zajecka J, Tracy KA, Mitchell S. Discontinuation symptoms after treatment with serotonin reuptake inhibitors: a literature review. J Clin Psychiatry. 1997;58:291-297.

16. Renoir T. Selective serotonin reuptake inhibitor antidepressant treatment discontinuation syndrome: a review of the clinical evidence and the possible mechanisms involved. Front Pharmacol. 2013;4:45.

17. Menke A, Domschke K, Czamara D, et al. Genome-wide association study of antidepressant treatment-emergent suicidal ideation. Neuropsychopharmacology. 2012;37:797-807.

Prozac Weight Loss and Gain

Prozac is the brand name product of fluoxetine, an antidepressant that belongs to the class called the selective serotonin reuptake inhibitors, or SSRIs. You will need a doctor’s prescription for this medication, used for treating depression, panic disorder and obsessive compulsive disorder. Your doctor might also prescribe Prozac to treat binge-eating and vomiting in patients who have moderate to severe bulimia, an eating disorder. In some cases, Prozac can cause either weight gain or weight loss.


Prozac increases the amount of serotonin, which a chemical found in the brain, by blocking its reabsorption into the body. This normalizes the level of serotonin in the body and promotes mental balance, according to PubMed Health.

Weight Loss

Bad Side Effects From Wellbutrin

Significant weight loss, especially in underweight depressed or bulimic individuals, may be an unwanted effect of treatment with Prozac. About 2 percent of patients may experience weight loss, according to eMed TV. This weight loss seen in some patients may be due to other side effects, including loss of appetite, nausea and dry mouth. Nausea is the most common gastrointestinal side effect, which may be present in up to 15 to 21 percent of individuals, Drugs.com explains.

Weight Gain

Prozac may also lead to an increased appetite and weight gain in about 1 to 10 percent patients, according to the “Drug Information Handbook.” Significant weight gain may lead to health concerns, such as the development of high blood pressure, high cholesterol and diabetes. Weight gain can also lead to increased depression and poor self-esteem.


Ambroxol Hydrochloride Side Effects

If you experience gastrointestinal side effects, take the medication with a meal. You may also chew gum or suck on hard candy to avoid dry mouth and nausea. Don’t skip meals to avoid losing too much weight. If you lose 10 lbs or more without trying, speak with your physician right away. Weight gain can be prevented by eating a healthy diet and being active. Managing your caloric intake and exercising regularly can greatly reduce your risks of gaining weight. Your physician can help you develop a well-balanced diet and determine what exercises are right for you.


See your physician regularly to ensure proper monitoring of gastrointestinal side effects and weight loss or gain while taking Prozac. If weight loss or gain persists, your physician can determine if you need to to stop taking the drug or modify the dose.

Bupropion Only Antidepressant Linked to Weight Loss

Bupropion is the only antidepressant associated with modest long-term weight loss, but only among nonsmokers, according to a new retrospective cohort study published recently in the Journal of Clinical Medicine.

“We found that bupropion is the only antidepressant that tends to be linked to weight loss over 2 years,” study leader David Arterburn, MD, Group Health Research Institute, Seattle, Washington, said in a Group Health Research Institute news release. “All other antidepressants are linked to varying degrees of weight gain.”

“Our study suggests that bupropion is the best initial choice of antidepressant for the vast majority of Americans who have depression and are overweight or obese,” he added.

Only Nonsmokers Lost Weight With Bupropion

Dr Arterburn and colleagues studied the relationship between antidepressant choice and weight change over 2 years among adults with a new prescription for antidepressant therapy.

“Because one of the most commonly prescribed antidepressants, bupropion, is also used as an adjunct to smoking cessation, and smoking cessation is strongly associated with weight gain, we sought to examine the effects of this antidepressant on weight gain among smokers and nonsmokers separately,” the authors write.

They conducted a retrospective electronic health record–based cohort study of adult patients who began monotherapy with second-generation antidepressant treatment between 2005 and 2009. They used fluoxetine as the reference treatment and included citalopram, bupropion, paroxetine, sertraline, trazodone, mirtazapine, venlafaxine, and duloxetine.

The researchers adjusted for potential confounders present at baseline, including age, sex, history of anxiety disorder, bipolar disorder, sleep disorder, schizophrenia and schizoaffective disorders, and smoking status at the time of beginning antidepressant treatment.

Bupropion was the only medication associated with a significantly different estimate of weight loss at 2 years when compared with fluoxetine, and this finding was seen only in nonsmokers.

After adjustment for confounders, nonsmokers who began treatment with bupropion lost, on average, 7.1 pounds compared with nonsmokers who used fluoxetine (P < .01).

The results were different in those who smoked, however. Smokers who used bupropion gained, on average, 2.1 pounds compared with smokers who used fluoxetine, although this difference was not significant (P = .33).

Those who used mirtazapine gained, on average, an estimated 11.6 pounds compared with those who used fluoxetine (P = .12). This difference was not statistically significant, probably because of the small number of patients who began mirtazapine.

And with the exception of sertraline, the remaining antidepressant-drug weight-change estimates did not differ significantly from fluoxetine. Those who used sertraline gained, on average, 5.9 pounds compared with those who used fluoxetine (P = .02).

Choose Bupropion for Nonsmokers With Obesity and No Contraindications

“Obesity and depression…commonly occur together, and adults with both conditions may have even greater health risks. The causal pathway is probably bidirectional — obese adults are at greater risk of depression and vice versa,” the authors write.

But bupropion is not appropriate for all patients, including those with a history of seizure disorder, they note.

“In conclusion, we find that bupropion is the only antidepressant associated with long-term weight loss (although this effect is limited to nonsmokers).”

“Given similar efficacy for improvement in depressive symptoms across bupropion and other second-generation antidepressants, bupropion may be considered the first-line drug of choice for overweight and obese patients unless there are other existing contraindications,” they surmise.

Coauthor Gregory Simon, MD, Group Health, Group Health Research Institute, and University of Washington School of Medicine, Seattle, agrees, commenting in the news release: “A large body of evidence indicates no difference in how effectively the newer antidepressants improve people’s moods.

“So it makes sense for doctors and patients to choose antidepressants on the basis of their side effects, costs, and patients’ preferences — and, now, on whether patients are overweight or obese,” Dr Simon concluded.

The authors have disclosed no relevant financial relationships.

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J Clin Med. Published online April 13, 206. Article

90,000 SIDE EFFECTS OF ANTI-DEPRESSANTS (SSRI) | Clinical Center “Psychiatry – Narcology”

The most frequently prescribed antidepressants are currently drugs from the group of selective serotonin reuptake inhibitors (SSRIs). For most, these medicines are safe and effective, but like any medicine, they can cause side effects. According to statistics, about 40% of patients taking antidepressants also experience side effects, in about 25% of cases they are quite unpleasant. Two of the most common effects (sexual dysfunction and weight gain) are often the reason for not taking these drugs.

Listed below are the 7 most common antidepressant side effects that the patient should be aware of:


When medication for depression is first prescribed, the most common physical symptoms are headache, nausea, joint pain, muscle pain, rash, and diarrhea.These symptoms, most often, are mild and temporary. The results of clinical studies have shown that nausea and headache are the most common. As a rule, these symptoms are adaptive in nature, as a rule, they go away on their own, without requiring discontinuation of the drug.


Many patients, when they are first prescribed antidepressants, report problems with sleep: difficulty falling asleep or shallow sleep with frequent awakenings.Also, while taking SSRIs, nightmares and sleepwalking can be observed. Studies have shown that about 22% of people taking antidepressants experience sleep problems.


Drowsiness during the day may result from poor nighttime sleep, or the direct sedative effect of an antidepressant. In the case when this is a sedative effect, the problem can be solved by postponing the drug intake in the evening.


Due to the fact that people prone to depression also often suffer from migraines, you need to be careful when taking combined medications. Medicines; Used to treat migraines, triptans, like SSRIs, increase serotonin levels in the brain. If these drugs are used together, it can lead to the development of serotonin syndrome, which manifests itself in the form of headaches, palpitations, hot flashes. It is imperative to discuss with your doctor how to avoid the development of serotonin syndrome if both groups of drugs are prescribed.


Weight gain is a late side effect of antidepressant medication and is one of the most common reasons for refusal or indication for drug change. Moderate exercise (for example, a 30-minute workout every other day) is a good prevention of this side effect. The likelihood of weight gain also depends on the drug that is prescribed. According to clinical trials, when taking paroxetine, about 25% of patients gain 7% of their weight.


The risk of suicide while taking antidepressants is being extensively researched. In most studies, compared with a placebo, taking SSRIs or other antidepressants doubles the likelihood of suicidal ideation. The overall risk of this side effect when taking antidepressants in adolescents and adults is 2 to 4 percent. One of the reasons for suicide while taking antidepressants is that medications increase activity, giving energy to implement the suicidal plan.Regular medical supervision can reduce the risk of this side effect.


Sexual dysfunction is one of the most common long-term side effects of SSRIs. These include decreased sexual desire, delayed ejaculation in men, and inability to achieve orgasm in women. Up to 60% of people taking SSRIs experience one of these side effects. And these are the side effects that patients are not willing to tolerate.

If you have any side effects, discuss them with your doctor.Usually, you can find a solution for any of them. It is not recommended to stop taking medications on your own.

90,000 What they are treating us with: Prozac. From depression to bulimia

Fluoxetine is readily absorbed into the bloodstream, can bind to plasma proteins and accumulate in body tissues. It also penetrates the blood-brain barrier, which protects the nervous system and the brain from many substances circulating in the blood. There, in the nervous system, it works in the already mentioned synaptic cleft, preventing the excess serotonin neurotransmitter released from the synapse from returning back. Because of this, serotonin remains in the synaptic cleft longer and can bind to receptors. How exactly fluoxetine achieves this effect is not clear even to manufacturers, but it is known that it has little effect on the work of other neurotransmitters. However, in high doses, fluoxetine increases levels of adrenaline and dopamine in rat brain tissue studies.

Fluoxetine and its metabolite (the substance into which it is converted in the body) norfluoxetine can inhibit each other’s action.Because of this, according to scientists from the Institute for Research Medicine in Barcelona, ​​a constant concentration of fluoxetine in the blood is achieved only after four weeks of taking the drug. Likewise, the consequences of taking the medication do not go away immediately. This is also associated with difficulties in selecting the required dose for a particular patient.

Serotonin itself, which is absolutely wrongly called the “hormone of happiness” (hormones are produced in one organ of the body, and perform their function in another, while serotonin in this context simply conducts nerve impulses in the brain regions responsible for a good mood, and is produced there same), in fact, performs much more functions. Yes, it affects mood, sleep and appetite, so some cases of depression, bulimia nervosa, and OCD can be caused by inadequate production of this neurotransmitter and corrected by serotonin reuptake inhibitors. But in addition, platelets can actively capture it and affect blood clotting. Also, serotonin is involved in the processes of memorization and learning. Moreover, it can be produced not only by vertebrates: according to a study by Chinese and American scientists, the pain from an insect bite is largely associated with the presence of serotonin in the venom, and dysentery amoeba, according to an article in Science, can cause diarrhea by secreting serotonin in our intestines.

The lists (not) included

But all these are only mechanisms, moreover, not studied to the smallest detail. To understand how this works in real people and how often it helps, let’s turn to clinical trials. However, anyone who scores a combination of “fluoxetine depression double blind randomized controlled” in the PubMed scientific article database and selects a clinical trial filter will see more than 558 articles, up to and including work comparing the effectiveness of Prozac and homeopathy.

Unexpected side effects of drugs


What is not really there can be seen, heard or felt by taking the usual sleeping pill Lunesta (eszopiclone). The drug for depression Lexapro (escitalopram), unfortunately, can cause the same side effect.

Discoloration of urine

The urine can turn pink due to the fact that you have eaten beets, orange, if you overdo it with vitamins. This is not dangerous and has happened to you at least once.But what if the urine turns green or blue? This is most likely a side effect of antidepressant Elavil (amitriptyline) or pain reliever Indocin (indomethacin). The antibiotic Flagil (metronidazole) may turn your urine black.

Vivid dreams, blackouts

If you decide to quit smoking with Chantix (varenicline), dreams can become very vivid and exciting. Do you need to see a doctor, even if you are leading a more interesting life in a dream than in reality? Sure. Sleeping pills Ambien (zolpidem) may cause sleepwalking symptoms. A person can get up at night, drive a car, talk on the phone and even have sex, and in the morning he does not remember anything about it.


Preparations against constipation containing lactulose or sorbitol, as well as antacids , which include calcium carbonate, can cause bloating (flatulence). The problem is unpleasant, especially when it manifests itself not at home, but in the office or in a public place.For example, Prilosec (omeprazole), a drug used to treat heartburn or GERD, causes bloating.

Weight gain

You can add 10 kg in just 3 months by taking antipsychotic Zyprex (olanzapine), aimed at treating bipolar disorder. Antidepressants such as Paxil (paroxetine) can cause the same side effect. Other medicines that can affect weight: steroids, birth control pills, hormone replacement therapy, diabetes medications.

Decreased libido

Basically, a decrease in sexual desire is caused by antidepressants – selective serotonin reuptake inhibitors: Prozac (fluoxetine), Celexa (citalopram), Zoloft (sertraline). Another side effect of these drugs can be priapism, a painful erection that lasts more than 4 hours and is not associated with sexual arousal. An example is the antidepressant Desyrel (trazodone).

Visual impairment

Distortions of visual perception (fog, halos, bifurcation of objects) can cause antihistamines , drugs for lowering blood pressure , drugs against malaria and tuberculosis .You can also see everything through blue or green “glasses” – by taking Viagra (sildenafil). But better not.

Hair loss / abnormal hair growth

Hair loss can be caused by the cancer treatment , but there are several common medications that can cause this side effect. These include blood thinners , birth control pills , antidepressants and gout drugs .Sometimes medications provoke excessive hair growth in the most unexpected places. It can be steroid drugs or a drug for treatment of endometriosis in women – Danocrin (danazol).

Tendon rupture

Fluoroquinolone antibiotics *** may damage the Achilles tendon. If you have been prescribed fluoroquinolone Cipro (ciprofloxacin) or Levaquin (levofloxacin), keep this in mind.

If strange symptoms appear that do not cause discomfort, but are still frightening, discuss this with your doctor.In any case, even if treatment or withdrawal of the drug is not required, it will not hurt to know what is happening to your body.

*** The US Food and Drug Administration (FDA) has issued a Side Effects Bulletin fluoroquinolone antibiotics aimed at treating infections of the genitourinary system, intestines, nasopharynx, eyes, ears, lungs and bronchi. It is reported that fluoroquinolones can cause significant decreases in blood sugar levels as well as adversely affect the functioning of the central nervous system (CNS).The bulletin specifies that a sudden drop in blood sugar (hypoglycemia) can cause coma . And disorders of the central nervous system can manifest itself in the form of decreased attention and memory, disorientation, excitability, nervousness, confusion.

If the attending physician has prescribed a fluoroquinolone antibiotic, the patient with diabetes must inform him about his illness and list the medications he is taking. If the appointment remains in effect for one reason or another, it is necessary to carefully monitor the blood sugar level and know the symptoms of hypoglycemia.Early signs include: confusion, rapid heart rate, heart palpitations, dizziness, pale skin, sweating, unusual hunger, tremors, headache, irritability.

Physicians, when prescribing fluoroquinolones, should take into account the increased risk of hypoglycemia (and coma) in elderly diabetic patients and in diabetic patients who are prescribed oral hypoglycemic (antidiabetic) drugs or insulin. If the patient reports the appearance of side effects associated with a dysfunction of the central nervous system or characteristic of hypoglycemia, it is advisable to change the treatment regimen for the infection.

Physicians should not prescribe fluoroquinolones to patients for whom other treatment options are available for acute bacterial sinusitis, acute bacterial exacerbation, chronic bronchitis, and uncomplicated urinary tract infections, since the risks outweigh the benefits of .

Fluoroquinolones – broad-spectrum antibiotics capable of suppressing the activity of gram-positive (staphylococci, streptococci, clostridia, corynebacteria, listeria; diseases of the nasopharynx, eyes, ears, lungs, bronchi) and gram-negative bacteria (Escherichia coli, Salmonella, Shigabella, Moraine ; diseases of the intestines and genitourinary system).

Broad-spectrum antibiotics are prescribed when the pathogen cannot be identified as a result of tests or it is impossible to conduct a bacterial culture analysis.

Fluoroquinolones banned during pregnancy and breastfeeding. In young children, fluoroquinolones slow bone growth and are therefore prescribed only if the benefits of antibiotic therapy outweigh the harm. Oxolinic and nalidixic acids are toxic to the kidneys and are therefore not recommended for patients with kidney disease.

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90,000 Generation Prozac. How the truth about antidepressants was hidden from us – Snob

Today, a widespread version is that depression is the result of biochemical disorders of the brain. In fact, this is just one of the hypotheses that is so often replicated in the scientific community that it began to be perceived as a proven truth.

This happened because in medical science psychiatry had no weight for a long time and, as a rule, was associated with the theory of Hippocrates about four types of temperament and phrenology (a pseudoscience about the connection between the psyche and the shape of the skull). Freud’s psychoanalytic theory was not convincing to doctors either. Under these conditions, the hypothesis that mental illness is a consequence of organic disorders of the brain sounded very attractive. This version was most often discussed as the main one, but no significant studies confirming it have appeared.

Prozac (fluoxetine) was one of the first drugs that “capitalized” the hypothesis of mental illness as a result of biochemical disorders of the brain. The drug appeared in American pharmacies 30 years ago, and we still do not know how it works and whether it is really effective in treating depression.

Psychiatrists, who benefit from the claim that depression is a brain disease and not a mental illness, insist on medication. Various social factors are left behind, which can also provoke depression: isolation, poverty, tragic events in life and much more.Psychotherapy as a method of treatment is secondary to pills. This distorts not only our understanding of depression, but even our experience of depression.

Various types of depressive disorders * are described today. For example, major depressive disorder, drug-induced depressive disorder, organic mood disorders resulting from organic disease. They all differ in etiology and duration, but the symptoms described are generally the same.Patients with different depressive conditions are treated with the same drugs, although there are no talk of the same violations of the biochemical processes of the brain.

In the 1950s and 1970s, rather dangerous drugs could be bought in the American pharmacy for the treatment of depressive conditions. Even a minor overdose of these drugs – Butisol (barbiturate) and Valiuma (diazepam) – could be fatal, which frightened off many buyers. The appearance of Prozac on the market changed the situation a lot, because it was a new generation antidepressant – safer and with fewer unpleasant side effects.

The antidepressants that exist today work more or less in the same way. So says Anthony Rothschild, professor of psychiatry at the University of Massachusetts School of Medicine. Moreover, over the three decades of using Prozac in the treatment of depression, the choice of antidepressants in pharmacies has grown significantly. However, nothing more effective than imipramine, the main drug of tricyclic antidepressants, has not been created.

All this time, antidepressant manufacturers had nothing to stop them from claiming that depression was a brain disorder that could be corrected with pills: both Paroxetine and Zoloft (sertraline) were marketed as “chemical balance-restoring” drugs.Meanwhile, there are still no convincing, scientifically proven versions of the causes of depression.

According to modern research, 37 percent of cases of depression are inherited , which means that genetics and biology obviously play a significant role. But since neuroscientists still don’t have a precise way to determine which brain function is considered “normal” and which is not, it is impossible to test some of the hypotheses.

If the cause of depression was a violation of serotonin levels, then SSRI drugs would work instantly, and not require a long cycle of administration **. In addition, a decrease in the level of serotonin in the brain should have provoked depression, but research shows that this is not the case. This is not to say that antidepressants aimed at restoring serotonin levels are not working. But we do not know if they ultimately influence the root cause of depression or only fight its consequences.

Our understanding of diseases and their nature influences their course. For example, the symptoms of anorexia in Hong Kong patients changed as people in the region became more aware of how the disease is progressing in Western countries.Perhaps our current understanding of depression and the medical approach leads to the fact that the disease affects more people: psychiatry calls mental illness even those conditions that were previously considered stress or emotional decline.

According to this study, the placebo effect in treating depression is almost as good as taking antidepressants. The difference is so small that it practically does not affect the clinical picture. Study author Irwin Kirsch, director of the placebo program at Harvard Medical School, is a staunch proponent of drug-free treatment for depression.Studies have shown that pills combined with psychotherapy are effective in the short term, but patients who receive psychotherapy without taking medication feel better over longer periods of time and have a significantly lower relapse rate. Kirsch, of course, is full of opponents who, on the contrary, are convinced that drugs are necessary.

The truth, as often happens, turned out to be somewhere in between: patients with severe depression who do not have the strength to go to psychotherapy should be prescribed medications.Those who are able to undergo psychotherapy should definitely do this, especially since drug treatment does not help all patients. Cognitive-behavioral psychotherapy, which is more expensive than drugs, but whose effect will be more stable, has also proven itself well in the treatment of depression.

Depression has become a global epidemic and today affects one in four people in the world. Obviously, the reasons are not only in biology, but also around us: poverty, unemployment, sexual violence – it is impossible to stop the epidemic if you do not fight all the causes, many of which, alas, cannot be defeated with pills.

* DSM-5 – 5th Edition of the American Diagnostic Manual for Mental Disorders

** SSRIs – Selective serotonin reuptake inhibitors – a group of third-generation antidepressants

Outpatient Antidepressant Therapy Practice | Internet edition “News of Medicine and Pharmacy”

The use of antidepressants has become widespread in the practice of not only psychiatrists, but also doctors of other specialties.The main target of drugs from the group of antidepressants is affective pathology in the form of depressive disorders of various origins and varying degrees of severity. Long-term clinical experience has proven the effectiveness of antidepressant treatment for conditions from the range of neurotic and neurosis-like. We are talking in these cases about anxiety manifestations in phobic and obsessive-compulsive disorders, as well as in somatoform disorders.

In recent decades, the recognition of depressive disorders has improved not only in psychiatric but also in general medical practice.Early detection of depression has been made possible by intensive clinical development in this area. Population studies have provided a more accurate understanding of the frequency of depressive disorders in different social and age groups of the population. To date, the prevalence of depression in the population is estimated at 3-6%. The annual incidence of depression reaches 1%. It has been established that 20% of the population suffers a depression at least once in their life. It is known that women are susceptible to depression several times more often than men.

As a result of clinical and epidemiological studies, the idea of ​​the frequency ratio of severe psychotic forms of depression and less pronounced depressive disorders has significantly changed, among which atypical forms of affective pathology occupy a significant place. A targeted study of the clinic and psychopathology of atypical depression made it possible to identify a variety of somatic “masks” of depression. These conditions were found to be widespread among patients in general somatic practice.The results of the clinical and epidemiological program for the study of depression in the practice of general physicians have confirmed these ideas [20]. It turned out that almost half of the patients seen by cardiologists, therapists and neurologists show depressive symptoms, while every 4th patient has clinically expressed depression and needs antidepressant therapy. Somatic illnesses and depression are often combined. In these cases, the manifestations of somatic pathology are often aggravated.According to existing estimates, 30-60% of patients with somatic diseases have symptoms of anxiety-depressive disorder. Depressed mood is characteristic of most patients with somatic diseases. It is necessary to distinguish between true depression, requiring adequate treatment with antidepressants, from a psychological reaction. It has been shown that among hospitalized young patients, major depressive disorder is more common, in old age, symptoms of minor depression are more common.

The growing awareness of doctors of different specialties (not only psychiatrists) about the entire clinical variety of manifestations of depression and the possibilities of effective antidepressant therapy has determined the trend of earlier recognition and treatment of these disorders.This was facilitated by the expansion and optimization of the work of outpatient psychiatric institutions and services, the introduction of consultative psychiatric care in inpatient and outpatient units of general medical practice.

The significance of the problem of depression was reflected not only in special medical publications, but also in the popularization of this information by the media, which contributed to the growth of psychiatric literacy of the population, the awareness of patients suffering from somatized depression, and an improvement in their appeal for help.

The successes achieved in the neurochemistry of depressive disorders led to the clarification of individual links in the pathogenesis of these conditions and the determination of the key role of neurotransmitter systems and the state of receptors, which, in turn, justified the development of entire classes of modern antidepressant drugs.

A significant number of different antidepressants are currently available to the practitioner, including selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs) and related compounds, monoamine oxidase inhibitors (MAOIs) and other new generation antidepressants.

Taking into account the idea of ​​most depressions as recurrent diseases, the stages of their treatment have been developed [13], a therapeutic algorithm [20]. At the first stage, stopping therapy is carried out, aimed at reducing the symptoms of depression. At the second stage, follow-up treatment is carried out in order to stabilize the achieved improvement and go into remission. The tasks of the third stage of antidepressant therapy include the prevention of the return of painful manifestations, the prevention of relapse of depression.It is recognized that the greatest effectiveness of antidepressant therapy is achieved when it is started in the initial stages of depression.

Each of these stages of treatment requires adherence to certain rules and methodological techniques.

1. A thorough psychopathological assessment of depressive disorder contributes to a more correct and adequate choice of antidepressant.

2. The choice of the drug, taking into account the previous experience of successful treatment of a similar condition in this patient.

3. Avoid prescribing antidepressants with a high risk of side effects.

4. Compliance with the therapy regimen with adequate doses not lower than recommended, taking into account the patient’s age and comorbid somatic pathology.

5. The duration of taking the selected antidepressant should be at least 4-6 weeks to be able to assess the effectiveness or lack thereof, when it is required to replace one antidepressant with another.

6. The total duration of antidepressant therapy is currently set for a period of at least 6-12 months without changing the doses of the drug.

The search for ways to optimize the pharmacotherapy of depression, increase its effectiveness, conduct pathogenetically and clinically justified therapy with an individual approach to the choice of one or another antidepressant are at the present stage the most important conditions for successful medical practice.

Modern ideas about the pathogenesis of depression include changes in the neurotransmission of serotonin and norepinephrine to the main link. The main result of numerous studies of the state of the serotonergic system in depression was the creation in 1987.the first class of drugs with specific pharmacological activity, called selective serotonin reuptake inhibitors (SI-OZS). This group of drugs was the ancestor of the third generation of antidepressants. This new generation includes fluoxetine, fluvoxamine, sertraline, paroxetine and citalopram. The clinical effects of these drugs are primarily determined by their thymoanaleptic activity with an effect on the actual depression of mood. The spectrum of their action includes stimulating, sedative, anxiolytic and antiphobic activity.The severity of these individual components of the antidepressant effect differs somewhat among the representatives of this group and forms the characteristics of their selective action.

A distinctive feature of antidepressants from the SSRI group is a high degree of safety of their use, associated with the absence of cardiotoxic and anticholinergic effects. The speed and selectivity of the onset of the clinical effect are no less important. The combination of these properties makes it preferable to choose drugs from the SSRI group for the treatment of non-psychotic forms of depression on an outpatient basis.For the treatment of depression with somatoform disorders, they have become the drugs of choice. The use of tricyclic antidepressants with their pronounced anticholinergic effects in these cases aggravates vegetative and somatized manifestations, worsening the already low quality of life of depressed patients and causing frequent refusals from treatment due to its poor tolerance or the inability to achieve adequate therapeutic doses. The advent of SSRIs has significantly expanded the age range of safe antidepressant therapy.This applies primarily to elderly patients with their multiple somatic pathology and the frequency of contraindications to TCAs caused by the presence of prostate adenoma, glaucoma, cardiac arrhythmias, etc.

The known high risk of suicidal attempts in depressed patients is often associated with the use of drugs, including antidepressants, for the purpose of poisoning. When SSRIs are used as antidepressants, the risk of death when trying to use them as a method of suicide is minimized or practically absent, which also accounts for their certain advantages.It should nevertheless be noted that when SSRIs are prescribed in the first week of their intake, suicidal thoughts may become actualized, which makes it reasonable at the beginning of therapy to combine SSRIs with tranquilizers.

The main ability of antidepressants is to reduce mood depression, that is, the thymoanaleptic property itself, is associated with the potentiation of the serotonergic structures of the brain. Currently, serotonergic properties also explain the anti-anxiety, or anxiolytic, activity of antidepressants.The influence on the psychomotor sphere, the increase in mental activity is addressed to the effect of drugs on the noradrenergic receptor systems. In the mechanisms of the development of the clinical effect of antidepressants, an important role belongs to a gradual change in the sensitivity of receptors during therapy, which explains the delay in time of their visible effect by 2-3 weeks.

All of the above indicates that the thymoleptic effect of antidepressants is the result of a complex effect on most of the neurotransmitter and receptor systems of the brain.The clinical effects of antidepressant therapy are an expression of interactions between various monoaminergic systems in the brain. The success of antidepressant therapy, individual choice of the drug is impossible without taking into account the psychotropic, neurotropic and somatotropic effects of the antidepressant. It is necessary to be aware of the relationship between these different components of antidepressant action.

Paroxetine is the leader in the SSRI group in terms of the strength of the blocking effect on serotonin reuptake [13].The blockade of serotonin reuptake leads to a weakening of the main depressive symptoms (low mood, anhedonia, diurnal-vital manifestations), a decrease in the manifestations of anxiety and obsessive-phobic symptoms, an increase in control over impulsive-compulsive actions, suppression of aggressive and auto-aggressive behavior, suppression of craving for toxic substances , weakening of pain syndrome due to antinociceptive action. Paroxetine is a blocker of presynaptic uptake of predominantly serotonin.At the same time, it has a weak effect on the norepinephrine and dopamine re-drink, does not affect histamine receptors, very weakly binds to α 1 , – and α 2 -receptors, moderately blocks muscarinic receptors. The absence of active metabolites in paroxetine reduces the risk of side effects in drug interactions. Paroxetine actually belongs to the second generation SSRIs, as it contains one enantiomer and is most complementary to receptors.

In terms of its clinical effects, paroxetine is classified as a balanced antidepressant [13].It is devoid of sedative properties, but has a pronounced anxiolytic effect. Like all antidepressants from the SSRI group, paroxetine does not surpass the strength of the antidepressant effect of the classical TCAs of the first two generations. However, it was found that, in contrast to tricyclic antidepressants, SSRIs are equally effective in the pathology of a circle of positive (vital, anxiety and senestopathic symptoms) and negative (apatoadynamic and depersonalization symptoms) affectivity in the structure of depression [20].Paroxetine, possessing undoubted anti-anxiety properties, does not cause sedation, does not show pronounced anticholinergic properties, does not lead to orthostatic hypotension, which determines the high safety of its use.

The appointment of paroxetine is indicated for a wide range of non-psychotic depressive conditions with anxiety, hypochondriacal, obsessive-phobic symptoms [2, 12]. The undoubted effectiveness of the treatment of depression of mild and moderate severity is affirmed.Compared to TCAs, the use of paroxetine for the treatment of severe melancholic depression does not pay off.

Foreign studies have shown the high efficacy of paroxetine, comparable to the antidepressant activity of traditional drugs of this group, and in resistant cases, sometimes even exceeding it, the absence of anticholinergic side effects characteristic of TCAs was noted. A balancing component of the action of paroxetine was found in the presence of anxiety disorders and lethargy.

The antidepressant properties of paroxetine have been studied in the outpatient treatment of endogenous depression in the context of cyclothymia and schizophrenia [7]. The dose of the drug was 20-40 mg per day. The average duration of treatment was 1 month. A good therapeutic effect was noted in 77% of cases. It has been shown that paroxetine is an effective antidepressant drug with a fast and harmonious manifestation of its own antidepressant, mild stimulating and distinct anxiolytic effect. The drug not only has a positive effect on the reverse development of depressive symptoms, but at the same time affects the improvement of social functioning and the quality of life of patients, which is especially important when carrying out outpatient therapy.

A comparative study of the therapeutic efficacy of a new generation of antidepressants from the SSRI group has been carried out [18]. 129 patients with endogenous depression (melancholic, anxious and apatoadynamic variants) received one of 4 antidepressants (fluoxetine, fluvoxamine, paroxetine, sertraline) for one month. By the end of the course of treatment, a significant improvement was noted in 89.3% of patients receiving paroxetine, and this indicator exceeded that of other comparable antidepressants.Paroxetine ranked first in the rate of onset of the antidepressant effect; by the end of the study, the signs of depression had disappeared almost completely (by 78%). Attention was drawn to the fact that the therapeutic effect of paroxetine was practically the same in the treatment of both severe depressive disorders (84.6%) and moderate depression (80%). Already in the early stages of therapy, the actual thymoleptic and tranquilizing effect of the drug was clearly revealed. Subsequently, an increase in these effects was noted, while the stimulating effect of paroxetine lagged somewhat.A conclusion was made about a balanced spectrum of antidepressant action of paroxetine with a relative predominance of the thymoanaleptic effect.

In 2002, the results of a multicenter study of the clinical efficacy of paroxetine, conducted by an open method in the treatment of depression in the context of an affective disease, were published [14, 15]. The drug was prescribed to 65 patients at a dose of 20 mg per day, in some cases with an increase in the dose to 50 mg per day. Patients with moderate depression predominated.It was concluded that paroxetine has a distinct thymoanaleptic, anxiolytic and activating effect, that is, its belonging to antidepressants of balanced action was confirmed. It is noted that paroxetine is quite effective and quickly eliminates sleep disorders associated with depression. Clinically, this is manifested by a gradual increase in the duration, and then an improvement in the quality of sleep in the absence of a hypnotic effect. The study showed the possibility of effective use of paroxetine both in a hospital setting and on an outpatient basis.The advantages of paroxetine are indicated regarding its good tolerability and high patient compliance during the period of treatment with this drug.

In a recent comparative study of the results of treatment of adolescent depression [3] with various antidepressants from the SSRI group, it was convincingly shown that paroxetine gives the best results in terms of the degree of improvement achieved. The reduction in the mean total score for depression on the Hamilton scale after 6 weeks of taking paroxetine reached 76.4%.The number of responders was 84.2%, while 42% achieved remission within 6 weeks of treatment with paroxetine. Paroxetine showed a high degree of thymoanaleptic (80.9%), stimulating (73.1%) and anxiolytic (70.8%) effects in the treatment of depression in adolescent patients. The best response to paroxetine therapy was found in patients of this age group with depression, whose clinical picture was dominated by melancholy and anxious affect. The universality of the antidepressant action of paroxetine and the validity of the indications for prescribing this drug for various types of depression in adolescence have been shown, that is, paroxetine is, in fact, considered as the drug of first choice in these clinical situations.

The possibility of effective and safe use of paroxetine in antidepressant therapy in adolescent patients has been proven [10]. The study of the clinical action of paroxetine was carried out in adolescents 13-15 years old suffering from depressive disorders of various origins (schizophrenia, socialized behavior disorder, organic mood disorder, mental behavioral disorders as a result of the use of volatile solvents). The therapeutic dose of paroxetine was 10 mg per day.It was found that in the treatment of endogenous depression in schizophrenia, paroxetine provided rapid positive dynamics with a long-term stable effect. In delinquent behavior, the target of paroxetine action was dysphoric affective disorder. There was a reduction in dysphoric manifestations, excitability and aggressiveness, the emergence of a critical assessment of one’s behavior and condition, an improvement in social and school adaptation. Depressive disorders in early organic lesions of the central nervous system (anxiety-dysphoric, dysthymia, sensitive with dyssomnia) were also treated with paroxetine at a dose of 5 mg per day.Not only stabilization of mood was noted, but also the possibility of compensating for mild cognitive dysfunctions. The positive effect of taking paroxetine at a dose of 5-10 mg per day was also noted in adolescents with toxic behavior. It should be emphasized that long-term (at least three to four months) therapy with paroxetine did not lead to the development of adverse events, which is extremely important when conducting psychopharmacotherapy at this age.

Data on the use of paroxetine in outpatient practice in adolescents with suicidal depressive mood disorders [6] indicate that in the overwhelming majority of cases it is possible to achieve deactualization of suicidal experiences and prevent their recurrence.The success of paroxetine therapy is explained by the tropism of the drug to anxiety symptoms, since it is anxiety and fear in the structure of depression that predetermine life-threatening behavior in adolescents.

The relative safety of SSRI antidepressants has significantly expanded the age range of their use not only in young men and adolescents, but also in elderly patients. For depressions of late age, antidepressants of this class are considered the drugs of choice due to their good tolerance.Indications for the prescription of antidepressants from the SSRI group have been developed not only for endogenous depressions of late age, but also for depressive disorders of organic genesis. A specially conducted study [11] compared the efficacy of paroxetine in endogenous and organic depression in elderly patients. Depressive disorders were regarded as manifestations of cerebrovascular disease. It was noted that in the structure of the depressive syndrome, hypothymia was always combined with symptoms of anxiety and asthenia, as well as manifestations of overvalued hypochondria.During treatment with paroxetine, a uniform reduction of hypothymia, symptoms of anxiety and lethargy was observed, while maintaining over a longer period of overvalued fixation on somatic complaints and ailments. It is extremely important that there were practically no side effects of antidepressant therapy with paroxetine, in contrast to what is usually observed in depressed elderly and senile patients during treatment with TCAs, when it is often impossible to achieve therapeutic doses or, in general, the appointment of TCAs is undesirable due to the risk of anticholinergic effects. aggravating somatic complaints or the severity of cognitive dysfunctions.Thus, paroxetine can be recommended for the treatment of both endogenous and organic depressions of late age.

An independent problem is the treatment of depressive disorders in patients with somatic diseases. The proportion of such patients in a multidisciplinary hospital is 19.1-25.8%, which is not much less than the same indicator for a psychiatric hospital – 25.4% [8, 9]. In the outpatient department, depressive states are detected in 34.3% of patients.The need for the introduction of antidepressant therapy in this situation is not in doubt, given not only the high prevalence of depression in these contingents, but also in connection with the known facts of aggravation of somatic suffering and worsening prognosis in combination with depression. While antidepressant therapy with TCAs has significant somatic limitations, SSRI drugs appear to be the preferred treatment for depression in these settings. Paroxetine is one of the most popular antidepressants in this group among internists.

The efficacy, safety and tolerance of paroxetine in the treatment of depressive conditions in patients of a somatic hospital were studied [9]. Paroxetine was prescribed to 40 patients at a dose of 20 mg per day (1 tablet in the morning) for a course of 4 weeks. Half of 40 patients were treated in the cardiology department, the rest were examined in the clinic for propaedeutics of internal diseases with pathology of the gastrointestinal tract. The obtained data indicate a high antidepressant activity of paroxetine, regardless of the nosological nature of depression with somatized and anxious manifestations.It has been noted that paroxetine is better tolerated by patients with cardiovascular disease. The administration of paroxetine to patients with diseases of the digestive system requires greater caution due to the risk of dyspeptic adverse events. The rarity of clinically significant interactions of paroxetine with somatotropic drugs is emphasized.

TCAs have traditionally been used in the treatment of depression in the dermatological clinic. However, at present, SSRIs are recommended for use in general practice, including paroxetine from first-line antidepressants, which has a favorable spectrum of clinical effects [12].

A comparative study of paroxetine and TCA was carried out in a neuropsychiatric dispensary [19]. The drug was prescribed to patients with affective and anxiety disorders. A 4-week course of therapy with paroxetine 20 mg per day led to an improvement in the condition of more than two-thirds of the patients. The advantages in the effectiveness of the use of paroxetine in patients with a short duration of the disease and the absence of deficient symptoms, i.e. in patients with anxiety-phobic disorder.Reduction of the anxiety component was noted, followed by a weakening of the severity of vegetative symptoms and somatic sensations accompanying the “panic attack”. The drug also had an activating effect in rather severe endogenous patients with persistent depressive, neurosis-like disorders against the background of a personality defect with a long history of the disease. The authors noted an improvement in the quality of life during treatment with paroxetine and in this heavy contingent of dispensary patients.

Paroxetine has proven itself not only as an effective antidepressant, but also as a drug with a powerful anti-anxiety effect in the treatment of generalized anxiety disorder with panic attack syndrome [2, 12]. Paroxetine is the first SSRI drug approved for use in panic disorder. Such conditions in Russian psychiatry are usually considered within the framework of borderline neuropsychiatric disorders, mainly neuroses. In accordance with the ICD-10, panic disorder is separated into a separate nosological heading.

In a multicenter study conducted in Russia [16], the overall efficacy of paroxetine in panic disorder, agoraphobia with panic disorder was 77% on the Overall Clinical Impression Scale. A decrease in the frequency of panic attacks was achieved in 75% of patients. A harmonious effect on all components of the syndrome of panic disorder, including the antiphobic effect of the drug, was noted. Most often, the minimum effective dose of paroxetine in these cases is 40 mg per day, it is quite justified to increase the daily dose to 60 mg, less often the success of therapy is achieved with the use of lower doses.

The advantages of paroxetine over benzodiazepine and TCAs, which have been used to treat panic disorder, have been established [4]. They boil down to the following points:

– a wide range of actions with a rapid reduction of the mental and somatic components of anxiety, as well as an effect on comorbid disorders;

– a significant improvement in the social functioning of patients, which contributes to productive cooperation with the doctor;

– effective prevention of disease recurrence;

– good tolerability of the drug;

– no risk of developing dependence on paroxetine.

Paroxetine has been used with success for the monotherapy of neurotic anxiety disorder with a phobic component. Depression comorbid in panic disorder is very common, which leads to the choice of therapy with this antidepressant as the primary treatment for both of these conditions. However, anticipatory anxiety and avoidance behaviors are known to be most torpid to antidepressant monotherapy after the disappearance of panic attacks. Additional cognitive-behavioral therapy after the disappearance of panic attacks serves to overcome these persistent disorders and the lack of antidepressant therapy for anticipatory anxiety.

Like other SSRIs, paroxetine is recommended for use in the treatment of alcohol and substance abuse. The indications for the appointment of paroxetine are depressive disorders within the framework of dipsomania, as well as withdrawal depressive states [12]. Along with this, there has been a beneficial effect of paroxetine on weakening the pathological craving for alcohol and drugs. It is possible to carry out treatment with paroxetine for these indications not only in a hospital, but also on an outpatient basis. The multivalence of paroxetine action, its good tolerance determine a wide clinical field for its use.Short-term administration of paroxetine is useful for dysphoria in conditions of premenstrual tension.

One of the advantages of antidepressant therapy with SSRI drugs, in particular paroxetine, is the possibility of prescribing a drug, as a rule, once a day, which is especially convenient for outpatient treatment. This medication regimen is of no small importance in geriatric practice, making it easier for the elderly to comply with medical recommendations. Along with the efficacy and safety of use, this is one of the arguments in favor of the preferable prescription of paroxetine to elderly patients.

For all indications, paroxetine treatment begins with 20 mg per day. In old age, in adolescents and in somatically burdened patients, it is advisable to start therapy with a dose of 10 mg per day. If necessary, it is also possible in these cases to slowly increase the dose to 20 mg with good tolerance and stability of the somatic state. It is recommended that the initial dose of paroxetine (20 mg per day) be maintained for at least 4-6 weeks. The first signs of mental improvement with depression treatment may appear 1-2 weeks after starting the drug.In the absence of a therapeutic effect after 4-6 weeks of treatment, the dose of paroxetine can be increased to 40 mg per day in the elderly and up to 50 mg in young and middle-aged patients.

Treatment of anxiety-phobic disorders, panic disorder and obsessive-compulsive disorders requires the administration of higher doses of paroxetine (up to 60 mg per day) with an increase in dosage by an average of 10 mg per week.

In most cases, paroxetine is given in the morning, but when the drug shows sedation, the single dose can be rescheduled in the evening.When the dose is increased, it may be advisable to divide the daily dose into 2 doses – in the morning and in the evening. In some cases, the dose increased to 40 mg can be taken only once a day – in the morning or in the evening.

Paroxetine antidepressant therapy is usually given with this drug alone. However, in the initial period of treatment, a combination with the use of benzodiazepine tranquilizers is often required in connection with a possible increase in anxiety, activation of suicidal thoughts, disturbed sleep depth or aggravated difficulty falling asleep.This combination therapy should be short-term with a gradual withdrawal of the tranquilizer and a transition to monotherapy with paroxetine.

The success of antidepressant therapy with paroxetine, even with complete recovery from depression, should not serve as a reason for discontinuation of the drug. An exception is made by patients with an exit into a manic state, requiring the appointment of other psychotropic drugs. The post-treatment phase of depression with paroxetine should last 4-6 months. Dose reduction is carried out gradually to avoid withdrawal syndrome.It is most advisable not to cancel the treatment with paroxetine, but to recommend the continuation of its use for prophylactic purposes for at least a year to prevent relapse of depression. In anxiety-phobic disorders, the duration of effective use of paroxetine increases to 2-3 years.

The need for a combination of paroxetine with other psychotropic drugs arises in the management of patients with schizophrenia with depressive manifestations. Prescribing neuroleptic or atypical antipsychotics does not lead to drug interactions with paroxetine and is safe even with long-term use of these drugs.In the presence of organic brain disease, the following are possible: the combined use of therapy with paroxetine, nootropic and vasoactive drugs, basic therapy of somatic diseases, as a rule, if there are no restrictions or contraindications if it is necessary to conduct antidepressant therapy with paroxetine.

An indication for transfer to treatment with paroxetine may be the lack of effect from the use of other representatives from the SSRI group. Such a therapeutic approach is justified and advisable, since each of the antidepressants of this group, despite the general mechanism of antidepressant action, has individual properties.

On the other hand, if the effect of long-term administration of paroxetine in adequate doses is insufficient, it is possible to add a second antidepressant in order to potentiate the antidepressant effect of paroxetine. In these cases, combinations with tricyclic antidepressants in low doses (up to 75 mg), the addition of bupropion (100 mg per day) are recommended, including to reduce the severity of sexual dysfunction. The combination with mirtazaline can lead to an increase in the antidepressant effect of paroxetine treatment, improvement of sleep and sexual function.Paroxetine should not be combined with MAOIs and clomipramine.

When compared with first-generation antidepressants, treatment with paroxetine is reasonably safe. But the doctor needs to know about the possible side effects of paroxetine and explain to the patient the features of these manifestations. Adverse events that occur when taking paroxetine, like all antidepressants from the SSRI group, are associated with hyperstimulation of the central and peripheral serotonergic systems. Severe serotonin syndrome (arterial hypertension, profuse diarrhea, tremor) is extremely rare.The most frequent are dyspeptic disorders (nausea, anorexia, increased stool frequency). Drowsiness and sedation are very rare. There is no orthostatic hypotension. Due to the secondary anticholinergic effect, paroxetine is more likely than other SSRIs to cause constipation and weight gain, but this is very rare. The most specific undesirable effect of the use of paroxetine, as with all SSRIs, is disorders of the genital area in the form of delayed ejaculation or anorgasmia.The ability of paroxetine to cause delayed ejaculation is used in urological practice to treat premature ejaculation. Side effects are more likely to occur with combined treatment with tricyclic antidepressants and antipsychotics than with paroxetine monotherapy.

The appointment of antidepressant treatment after the diagnosis has been established should be preceded by a very important section of medical work, which is often omitted due to a misunderstanding of its meaning or simply due to a banal lack of time at the doctor.It is not enough to call the condition a depression and prescribe an antidepressant. It is necessary to very thoroughly and clearly explain the painful nature of all symptoms. It is useful to draw the patient’s attention to the typicality and regularity of some manifestations of depression (for example, daily fluctuations in well-being with morning worsening). It is necessary to provide the patient with as complete information as possible about the course of the disease, drawing the attention of patients, especially those who have fallen ill for the first time, to the fundamental reversibility of a depressive disorder, its temporary nature, and a generally favorable prognosis.It is worth explaining to the patient that it is impossible to accurately predict the individual duration of the painful state in advance.

Patient’s consent to treatment, adherence to medical recommendations and adherence to therapy (compliance) largely depend on the efforts and time that the doctor spends on explanatory work with the patient [17]. The prescription of antidepressant therapy with medication also requires the same thoroughness in explanations. It is not superfluous to explain to the patient in advance the modern attitudes to carry out, first of all, drug therapy, followed by the addition of methods of psychotherapy or psychological correction.A very important point is an open discussion with the patient of the objectives of treatment with antidepressants, which consist in achieving significant relief of the condition, reducing the severity of symptoms of depression, followed by a recovery period after some time. It is advisable to outline the stages of treatment already at the beginning of therapy, and in the process of follow-up, to focus the patient’s attention on the specific tasks of each of the stages. The physician should keep in mind that only 50-60% of patients respond satisfactorily to the initial antidepressant therapy regimen, and complete remission is achieved only in a small proportion of patients with a satisfactory response to the first stage therapy [1].

When prescribing antidepressants, the patient needs to be told about the expected clinical effects of the drug, the approximate timing of the appearance of the first signs of changes in the state in connection with the treatment. It is necessary to warn about the possibility of intensifying individual symptoms in the first week of taking the medication, explain the temporary nature of these manifestations and the possibility of stopping an exacerbation when prescribing a tranquilizer for a short time. In some cases, it is advisable to combine the intake of an antidepressant and a tranquilizer from the very beginning of therapy, without waiting for an exacerbation of anxiety symptoms.

The doctor is obliged to warn the patient about the possible side effects of treatment, doing it in a calm manner and explaining the optional occurrence of undesirable phenomena, their transient nature during the period of adaptation to treatment and the possibility of overcoming these manifestations over time. The main task of the doctor before starting treatment is not only to reach an understanding of the need for treatment, but also to encourage the patient to cooperate in the treatment process. Explanatory work should continue throughout the entire period of treatment with a shift in emphasis in setting goals depending on the dynamics of the condition and the stage of therapy.It is very important to convince the patient not to discontinue treatment when a therapeutic effect is achieved, even with a complete recovery from depression, which often happens when the patient feels a rapid onset of improvement and interrupts the antidepressant intake, not seeing the need for further treatment. The return of depressive symptoms as soon as possible from the start of treatment discredits antidepressant therapy. On the other hand, subtle signs of only partial improvement also raise doubts in patients about the effectiveness of the drug.It is necessary to patiently and methodically explain the need to continue treatment in order to achieve therapeutic remission, emphasizing the role of the drug in preventing the return of painful symptoms of depression.

Compliance, that is, patients’ adherence to therapy, is determined primarily by the nature of the interaction between the doctor and the patient and largely depends on the doctor’s enthusiasm, his age and experience, and the total time of conversations with the patient. If patients feel that they have been “heard” and have been “fully discussed” with them about their condition and treatment, compliance is more likely to reach the required level.Authoritarian treatment is often detrimental to adherence to treatment. Patients who have comprehensive information about their disease, the main effect of drugs and their side effects, obtained from various sources, are much less likely to interrupt therapy.

The problem of refusal of treatment is considered one of the most important aspects of antidepressant therapy [5]. The variability of the manifestations of this phenomenon in relation to treatment allows us to distinguish between “complete” and “incomplete” refusal, as well as primary refusal (that is, even before the start of treatment) and secondary – in the process of drug therapy.In depressed patients, there are early secondary refusals and late ones after a long period of taking antidepressants. A number of patients have only occasional refusal to take medications. Some patients experience recurrence of these behavioral manifestations in the form of recurrent treatment refusals.

Among patients with depressive disorders, refusal of treatment or interruption of antidepressant medication occurs, according to various sources, in 8-50% of cases. In clinical trials of antidepressants, the failure rate is significantly lower than in their subsequent use in medical practice.It has been shown that the inconstancy of contact with the doctor, the factor of the duration of treatment and the need for fractional medication during the day have an adverse effect on the compliance of patients. Most refusals from antidepressant therapy are recorded by the third month of treatment. It has been noted that women with depression and elderly patients with depressive disorder are more likely to stop taking medications over time. 30% of patients with therapeutically resistant depression do not fully comply with the regimen of administration or dosing of drugs.Personal and psychological characteristics of patients have a significant impact on the risk of refusal from treatment. Surprising as it may seem, treatment refusals are common in patients with anxious and hypochondriacal personality traits. However, this is explained by the fact that in about half of depressed patients who refuse to take medications, this is due to aversion of side effects. At the same time, according to some, the clinical features and the severity of depression do not matter. Others note a higher failure rate in mild depression.

Side effects often determine the risk of failure early in treatment. The fact that the side effects of an antidepressant drug often appear earlier than the therapeutic effect and worsen the general well-being causes anxiety in patients with regard to drug intervention. In these situations, the more intact the personality, the greater the demand for therapy, primarily in terms of minimizing side effects that negatively affect everyday life.Such patients may refuse to take medications even with a full understanding of the need for treatment. It should be borne in mind that the attitude to side effects in half of patients changes with a positive dynamics of the mental state, that is, with its improvement, tolerance to unwanted side effects of therapy decreases [1]. The cautious attitude of patients about the need for long-term administration of drugs is now increasingly motivated by fears of drug dependence.With regard to modern antidepressants, the economic factor, the costly nature of long-term (up to a year or more) treatment, is also gaining importance.

Modern SSRI antidepressants are much better tolerated than tricyclic antidepressants. Treatment refusals are less likely due to side effects, but not excluded. The reason may be the actual mental state with the experience of apathy, feelings of hopelessness, hypochondriacal mood, a feeling of collapse in connection with the rejection of the usual way of life.Among the somatic undesirable effects, the most significant for patients and influencing the decision to stop taking the drug are disorders of the genital area that occur during treatment with SSRIs. Confidence in the therapy is increased with the desire of the doctor to inform the patient as much as possible, with the individual selection of the tone of the conversation and the style of communication. Achieving interaction with the patient in the course of treatment, planning consultations, attention to the manifestations of side effects, advice on adapting to them help to prevent non-compliance and refusal of treatment.Correction and maintenance of compliance are considered as an essential element of the overall system of patient management [5].

Currently, a new antidepressant, Reksetin (paroxetine), has entered the practice of psychopharmacotherapy. The drug belongs to the first-line antidepressants from the SSRI group. Indications for the appointment of Reksetin cover a wide range of syndromes of the affective and neurotic registers. The use of the drug is effective for a wide variety of anxiety disorders of varying severity and generalization.It is justified to prescribe adequate high doses of Reksetin for anxiety-phobic manifestations in the form of so-called panic attacks, as well as for obsessive-compulsive disorders within the framework of obsessive-compulsive syndrome. An unconditional indication for the use of Reksetin are depressive states of various structures, primarily with manifestations of anxious affect. The effect of Reksetin therapy is found not only in stress-induced disorders and endogenous affective diseases, but also in the complex therapy of neurosis-like and depressive disorders of a schizophrenic nature.Good tolerance and safety of the drug use make it possible to recommend the appointment of Reksetin to elderly and senile patients in accordance with the indicated indications and to carry out treatment on an outpatient basis. The drug is intended for long-term maintenance and anti-relapse therapy. The availability of purchase is an argument for the economic feasibility of choosing Reksetin, which is relevant for both service managers and patients. In the arsenal of a practicing physician, the drug can be one of the main antidepressants from the SSRI group, the use of which must be mastered and widely prescribed on an outpatient basis, taking into account the indications and characteristics of the action.

instructions for use, analogs, composition, indications

The drug is taken orally, regardless of the time of the meal.
Major depressive episodes / disorders. The initial dose for depression for adults is 20 mg once a day in one morning intake. This dose is sufficient to achieve an antidepressant effect. If clinically necessary, after 3-4 weeks from the start of therapy, the dose can be increased to 20 mg per day; Although dose escalation may increase side effects, for some patients with insufficient response to treatment with a 20 mg dose, the dose may be gradually increased to 60 mg per day.
Increase the dose individually and with caution; therapy should be started with the minimum effective dose.
Patients with depressive disorders should be treated for a sufficient period of time, at least 6 months, to ensure that they are asymptomatic.
Obsessive-compulsive disorder. The usual recommended dose is 20 mg per day. Although dose escalation may increase side effects, for some patients with insufficient response to treatment within 2 weeks, the 20 mg dose can be gradually increased to 60 mg per day.
If there is no clinical effect within 10 weeks of treatment, fluoxetine therapy should be reconsidered.If a positive therapeutic effect was obtained from the treatment, fluoxetine therapy should be continued with an individually selected dose of the drug. Increase the dose individually and with caution; therapy should be carried out with a minimum maintenance dose. The patient’s need for drug treatment should be periodically reviewed.
Prolonged pharmacotherapy (more than 24 weeks) in patients with obsessive-compulsive disorder has not been studied.
Bulimia nervosa. For adults and elderly patients, the dose is 20 mg per day.Long-term pharmacotherapy (over 3 months) in patients with bulimia has not been studied.
General recommendations. The usual recommended dose is 20 mg per day, which can be increased if necessary. The maximum daily dose is 80 mg. Doses greater than 80 mg per day have not been studied. If it is necessary to use a single dose of less than 20 mg, it is necessary to use another form of the drug in the appropriate dosage. Fluoxetine can be prescribed 1-2 times a day, regardless of the meal time.After stopping the drug intake, the active substance circulates in the body for another 2 weeks, which should be taken into account when prescribing other drugs or stopping treatment.
Supportive care. As with other antidepressants, it may take 3–4 weeks for fluoxetine to fully respond.
The dose of the drug for patients with renal or hepatic insufficiency, for elderly patients with concomitant diseases, as well as for patients taking other drugs, should be reduced.
Elderly patients: Increase the dose with caution . Usually the daily dose does not exceed 40 mg. The maximum daily dose is 60 mg.
A reduced dose or intermittent administration of the drug (for example, every second day) can be recommended in patients with hepatic disorders or in concomitant therapy with drugs that may interact with fluoxetine. Abrupt cessation of fluoxetine therapy should be avoided. To discontinue the drug, the dose should be gradually reduced over 1 to 2 weeks to avoid withdrawal symptoms.If symptoms of deterioration appear during dose reduction or discontinuation of drug treatment, treatment with a previous effective therapeutic dose of the drug should be returned. After a while, the doctor may continue to gradually reduce the dose.
Children. The drug is contraindicated for use in children.

General disorders: hypersensitivity reactions (anaphylactoid reactions, vasculitis, serum sickness, angioedema), chills, excessive sweating, feeling cold or hot, serotonin syndrome, abnormal sensations, neuroleptic syndrome, photosensitivity, erythema multiforme, which can progress to Steve syndrome -Johnson or toxic epidermal necrolysis (Lyell’s syndrome), anorexia.
From the digestive tract: diarrhea, decreased appetite, nausea, vomiting, dyspepsia, dysphagia, pain in the esophagus, change in taste, dry mouth, liver dysfunction, dyskinesia; cases of idiosyncratic hepatitis, weight loss.
From the nervous system and sensory organs: headache, bruxism, sleep disturbances (pathological dreams, nocturnal delirium, insomnia), sedation, weakness, dizziness, fatigue (drowsiness, hypersomnia), euphoria, impaired coordination of movements (twitching, ataxia , tremor, psychomotor hyperactivity, dyskinesia, imbalance, myoclonus, buccolosal syndrome), epileptic seizures, psychomotor agitation / akathisia, impaired memory and attention, hallucinations, manic reactions (hypomania, mania), abnormal orgasm (incl.anorgasmia), confusion, agitation, anxiety and associated syndromes (nervousness), dysfemia, impaired concentration and thinking processes (depersonalization), panic attacks, hot flashes, suicidal thoughts and attempts (these symptoms may be due to the underlying disease). Cases of suicidal thoughts and suicidal attempts have been reported during fluoxetine therapy or immediately after discontinuation of treatment.
From the immune system: anaphylactoid reactions, serum sickness, anaphylactic shock, angioedema.
Skin and subcutaneous tissue disorders: skin rash, pruritus, urticaria, purpura, Stevens-Johnson syndrome, toxic epidermal necrolysis, alopecia, ecchymosis.
From the urinary system: urinary retention, frequent urination, pollakiuria, dysuria.
Reproductive system disorders: sexual dysfunctions, decreased libido, including loss of libido, erectile dysfunction, impaired or absent ejaculation, anorgasmia, priapism, galactorrhea, hyperprolactinemia.
From the cardiovascular system: postural hypotension, vasodilation, palpitations, hot flashes, ventricular arrhythmia, including polymorphic ventricular tachycardia “torsade de pointes”, prolongation of the QT interval.
From the side of the organs of vision: blurred vision, mydriasis, photosensitivity reaction.
From the musculoskeletal system: arthralgia, myalgia.
Blood disorders: thrombocytopenia, hemorrhagic manifestations, gynecological hemorrhages, gastrointestinal bleeding, other subcutaneous or mucous hemorrhages, epistaxis, bruising tendencies.
Metabolic disorders: cases of hyponatremia (including sodium levels below 110 mmol / L) have been rarely reported, which disappears when fluoxetine is discontinued. Some cases are possible with inadequate secretion of antidiuretic hormone. Most of these reports were about older patients and patients taking diuretics or other medications.
Respiratory system: pharyngitis, shortness of breath, yawning. Inflammation or various histopathological changes and / or fibrosis have been reported rarely.
Fluoxetine Withdrawal or Discontinuation Syndrome: Withdrawal of fluoxetine treatment results in a withdrawal syndrome. Dizziness, sensitivity disorders (including paresthesias), sleep disorders (including insomnia and heavy dreaming), asthenia, agitation or agitation, nausea and / or vomiting, tremors and headache.
An increased risk of bone fractures has been reported in patients aged 50 and above receiving SSRIs and TCAs. The mechanism leading to the risk is unknown.

Symptoms : nausea, vomiting, convulsions, arrhythmias, heart attacks, respiratory distress, agitation of the central nervous system, coma, hypomania.
Overdose cases of fluoxetine alone are usually mild, and death was extremely rare.
Treatment : provoking vomiting or gastric lavage, taking activated charcoal, sorbents, symptomatic and supportive therapy. There is no specific antidote. Forced diuresis or dialysis is ineffective in case of drug overdose.
Monitoring of cardiac and respiratory activity is recommended.

Epidemiological studies have shown that the use of fluoxetine in the first trimester of pregnancy increases the risk of congenital malformations of the cardiovascular system in the fetus.The mechanism is not known. When using fluoxetine in the first trimester of pregnancy, the risk of congenital malformations of the cardiovascular system is 2 cases per 100 pregnancies, compared with the expected level of development of this defect of 1 case per 100 pregnancies in the general population. Epidemiological data have shown that the use of selective serotonin reuptake inhibitors, especially in late pregnancy, may increase the risk of persistent pulmonary hypertension in newborns.The observed risk was almost 5 per 1000 pregnancies. In the general population – 1-2 cases per 1000 pregnancies. Application during pregnancy is possible only in exceptional cases for health reasons, if the expected benefit to the woman outweighs the potential risk to the fetus. In newborns whose mothers took fluoxetine during pregnancy, anxiety, tremors, hypotension, incessant screaming, impaired sucking, and sleep disturbances were observed. Perhaps these symptoms were associated with the action of fluoxetine and its active metabolite, norfluoxetine.
Fluoxetine and norfluoxetine are excreted in breast milk. If necessary, use during lactation, breastfeeding should be discontinued.
Animal studies have shown that fluoxetine can affect sperm quality. The effect on sperm quality in humans is reversible when using this drug. So far, no changes in human fertility have been identified with fluoxetine.

There are reports of skin rashes, anaphylactic reactions and progressive systemic disorders involving the skin, lungs, liver, and kidneys in the pathological process in patients taking fluoxetine.If skin rashes or other allergic reactions occur, the etiology of which cannot be determined, fluoxetine should be discontinued.
When taking fluoxetine, mydriasis may develop, so the drug should be prescribed with caution to patients with high intraocular pressure or those at risk of acute attacks of angle-closure glaucoma.
As with other antidepressants, fluoxetine should be used with caution in patients with a history of seizures and seizures.
With the simultaneous use of the drug fluoxetine and electroconvulsive therapy, the development of prolonged epileptic seizures is possible.
Fluoxetine, like other antidepressants, can cause mania or hypomania.
Fluoxetine is extensively metabolized in the liver and excreted by the kidneys. Low doses, as alternative daily doses, are recommended for patients with impaired liver function. When taking 20 mg per day for 2 months in patients with severe renal impairment (creatinine clearance <10 ml / min) and patients requiring hemodialysis, plasma levels of fluoxetine or norfluoxetine are the same as in patients with normal renal function.
Cardiovascular effects. Treatment with fluoxetine is known to be associated with prolongation of the QT interval and ventricular arrhythmias, including polymorphic ventricular tachycardia “torsade de pointes”. Thus, fluoxetine should be used with caution in patients with long QT syndrome, patients with a family history of QT prolongation, or clinical conditions that cause cardiac arrhythmias (eg, hypokalemia, hypomagnesemia, bradycardia, acute myocardial infarction, or decompensated heart failure).
In patients with concomitant stable cardiac diseases, ECG monitoring should be performed before treatment with fluoxetine. If arrhythmias occur during treatment with fluoxetine, it is necessary to stop taking the drug and perform an ECG.
Weight loss may occur in patients taking fluoxetine.
When using fluoxetine, hyponatremia may develop.
This is mainly typical for elderly patients and for patients receiving diuretics, due to a decrease in the BCC.In patients with diabetes mellitus, hypoglycemia was observed during treatment with fluoxetine, and after discontinuation of the drug, hyperglycemia. At the beginning and after the end of treatment with fluoxetine, it may be necessary to adjust the doses of insulin and / or hypoglycemic drugs for oral administration.
Serotonin syndrome. The development of potentially life-threatening serotonin syndrome has been reported with the use of only selective serotonin reuptake inhibitors and selective norepinephrine reuptake inhibitors, including fluoxetine.The risk increases with the concomitant use of serotonergic drugs (including triptans, tricyclic antidepressants, fentanyl, lithium, tramadol, tryptophan, buspirone, St. linezolid and methyl blue for intravenous use).
Serotonin syndrome can include changes in mental status (eg, agitation, hallucinations, delirium, and coma), autonomic instability (eg, tachycardia, blood pressure instability, dizziness, sweating, hot flashes, hyperthermia), neuromuscular abnormalities (eg, tremors, numbness, myoclonus, hyperreflexia, discoordination), convulsions and / or gastrointestinal symptoms (nausea, vomiting, diarrhea).The condition of patients should be monitored for the occurrence of possible symptoms and signs of the development of serotonin syndrome.
Suicide / suicidal ideation or clinical worsening. Depression associated with an increased risk of suicidal thoughts, suicide attempts. The risk exists until a certain remission occurs. Improvement may not occur for several weeks or more of treatment, and patients should be closely monitored until improvement occurs. General clinical experience suggests that the risk of suicide may increase in the early stages of recovery.
Patients with major depressive disorders and other mental illnesses should be monitored continuously.
Patients, especially those at high risk, should be closely monitored at the start of treatment or when the dose is changed.
If clinical deterioration, suicidal attempts or behavior change occurs, appropriate action should be taken.
Akathisia / psychomotor dysphoria. The use of fluoxetine is associated with the development of akathisia, which is subjectively characterized by the need to move, often with the inability to stand or sit.This is especially true in the first weeks of treatment. Patients who develop such symptoms are not advised to increase the dose.
Withdrawal symptoms. Withdrawal symptoms often occur if treatment is suddenly stopped. The risk of developing withdrawal symptoms depends on many factors, including duration, treatment dose, and level of dose reduction. Dose reduction titration should be performed for 1 or 2 weeks according to the patient’s needs.
Hemorrhages. The occurrence of subcutaneous hemorrhages such as ecchymosis or purpura has been reported.Ecchymosis is rare with fluoxetine. Other hemorrhagic manifestations (gynecological bleeding, gastrointestinal bleeding, and other cutaneous or mucous hemorrhages) were also rare. The drug should be used with caution in patients who are simultaneously taking oral anticoagulants and drugs that affect platelet function (atypical antipsychotics such as clozapine, phenothiazine, most tricyclic antidepressants, acetylsalicylic acid, nonsteroidal anti-inflammatory drugs), or other drugs that may increase the risk bleeding, patients with a history of bleeding.
Suicidal thoughts and hostility (mainly aggression, oppositional behavior and anger) were more often noted in children from 8 years of age: fluoxetine can be used in this age group exclusively for the treatment of moderate to severe depression and should not be used for other indications. If, based on clinical need, a decision on treatment is still made, the patient’s condition should be monitored for suicidal thoughts. Only in isolated cases can long-term treatment be prescribed, despite the safety of the drug, given the effects on growth, puberty and cognitive, emotional and behavioral manifestations.There is evidence that children treated with fluoxetine experienced a decrease in height and weight. Growth retardation during puberty cannot be ruled out. Monitoring of pubertal development (height, body weight and developmental stages) should be carried out during treatment and after treatment. If there are any deviations, you should definitely consult a doctor. In studies of the use of the drug, children were often reported to have mania and hypomania. Therefore, you should monitor the condition of patients regarding the appearance of mania / hypomania.The benefit / risk for both children and adults should always be assessed.
Sunset yellow component FCF (E 110), which is part of the capsule shell, can cause allergic reactions.

The combined use of fluoxetine with tryptophan can lead to an increase in the serotonergic effects of fluoxetine.With simultaneous use with lithium, there have been reports of the development of serotonin syndrome, therefore, simultaneous use requires caution and more frequent monitoring of the patient’s condition.
With the simultaneous use of fluoxetine and lithium, the level of the latter in the blood plasma may increase or decrease.
The interval between the end of therapy with MAO inhibitors and the start of treatment with fluoxetine should be at least 14 days. The interval between the end of treatment with fluoxetine and the start of treatment with MAO inhibitors should be at least 5 weeks.
Severe, sometimes fatal reactions (hyperthermia, rigidity, myoclonus, autonomic instability, rapid changes in vital signs and cerebral dysfunctions, including excessive agitation, delirium and coma) have been reported in patients who took fluoxetine in combination with MAO inhibitors, as well as in those who stop taking fluoxetine and then begin therapy with MAO inhibitors.
Fluoxetine can potentiate the effects of alprazolam, diazepam and alcohol, so they should be used with caution.
Fluoxetine enhances the effect of hypoglycemic drugs, increases the concentration of cyclic antidepressants, phenytoin in the blood.
Fluoxetine inhibits the CYP2D isoenzyme. Therefore, treatment with drugs that are metabolized by this isoenzyme and have a narrow therapeutic index (for example, flecainide, carbamazepine and tricyclic antidepressants) should be started with the lowest doses if the patient is simultaneously receiving fluoxetine or has taken it within the previous 5 weeks.If fluoxetine is included in the treatment regimen of a patient who is already taking a similar drug, a reduction in the dose of this drug should be provided.
With simultaneous use with fluoxetine, there is a change in blood concentrations of carbamazepine, haloperidol, clozapine, diazepam, alprazolam, lithium, imipramine and desipramine, and in some cases, manifestations of toxic effects are observed. When taking fluoxetine with these drugs, the conservative selection of the drug dose should be reviewed and the patient’s condition should be monitored.
Since fluoxetine is a potent inhibitor of CYP2D6, its use can lead to a decrease in the concentration of endoxifen (a metabolite of tamoxifen). Therefore, the combined use of fluoxetine and tamoxifen should be avoided whenever possible. Thioridazine should not be given concomitantly with fluoxetine and for at least 5 weeks after stopping fluoxetine. Simultaneous administration can lead to a significant increase in the plasma concentration of thioridazine due to the suppression of the SSRI activity of the metabolizing isoenzyme CYP2D6.The ability of thioridazine to prolong the QT interval is dose-dependent, and therefore the risk of this complication increases with simultaneous administration with fluoxetine. Fluoxetine binds tightly to blood plasma proteins, therefore, when fluoxetine is prescribed with another drug that tightly binds to blood plasma proteins, changes in plasma concentrations of both drugs are possible.
With the simultaneous use of fluoxetine with warfarin, an increase in bleeding time was noted.Changes in the anticoagulant effect when taking oral anticoagulants (laboratory parameters and / or clinical signs and symptoms) were inconsistent. As in the case of treatment with warfarin together with other drugs, before the start of use or if treatment with fluoxetine is discontinued during therapy with warfarin, a thorough check of blood coagulation parameters should be carried out. If it is necessary to prescribe other drugs after discontinuation of fluoxetine, the long half-life of fluoxetine and its active metabolite norfluoxetine should be taken into account and, therefore, possible drug interactions.Occasionally, there have been cases of increased duration of seizures in patients taking fluoxetine during electroshock therapy.
Concomitant administration is contraindicated with drugs that prolong the QT interval, such as: IA and III classes of antiarrhythmic, antipsychotic (for example, phenothiazine derivatives, pimozide, haloperidol), tricyclic antidepressants, some antimicrobial (for example, sparfloxacin, erythifloxacin) antimalarial (especially halofantrine), and antihistamines (astelizole, mizolastine).While special studies to determine the interaction of fluoxetine and the above drugs have not been carried out, concomitant administration is prohibited due to the potential for drug interactions with prolongation of the QT interval.
Use with caution in conjunction with St. John’s wort preparations, due to the risk of increased serotonergic effects (such as serotonin syndrome), as well as with an increased risk of adverse reactions.

90,000 Taking Fluoxetine for Weight Loss: Opportunities and Risks | Madame Georgette

There are many indications for the use of a drug such as Fluoxetine.For example, this drug has antidepressant properties. But what’s especially interesting is that Fluoxetine can also be used for weight loss. This is possible due to the fact that the drug also has an anorexigenic effect. But still, its action needs to be considered in detail in order to understand what can be encountered.

How Fluoxetine works

This drug is not prescribed for such weight loss, but in order to stop bulimia nervosa. It is this action of Fluoxetine that is most important.Unequal bulimia is a mental disorder in which a person experiences bouts of hunger and cannot control them. The consequence of this is the rapid development of obesity.

Similar conditions can be observed in depression, when people also cannot control food intake. It is the antidepressant effect of the pills that allows you to achieve weight loss. Thanks to its active substances , part of the nerve impulses is blocked, as a result of which appetite decreases .This allows you to achieve weight loss. It is also possible to stimulate weight loss with the help of this drug in women and men with hysterical inclinations. By itself, reducing the feeling of hunger and, as a result, losing weight with the help of Fluoxetine cannot be achieved.

When is it wise to take Fluoxetine for weight loss

As already mentioned, this type of drug primarily has antidepressant properties. This means that in the absence of depression, there is no point in accepting it.It will not be able to give an incentive to lose weight for those who are in a normal emotional state. Only a doctor can make the decision that Fluoxetine is needed to suppress hunger. If you make a decision about this on your own, you can not only not get the effect of losing weight, but also make yourself much worse.

Side effects when taking Fluoxetine

There are many negative effects of Fluoxetine. Moreover, they arise at once in many areas.There are violations of the heart, the work of blood vessels, gastrointestinal tract, respiratory and genitourinary systems, metabolism. Various rashes may appear on the skin. Allergies are relatively common.

Instead of losing weight, you can get headaches, anxiety, suicidal thoughts, stomach ulcers, decreased sex drive and even complete impotence in the case of men … Such a set of side effects far outweighs the rather small likelihood of losing weight. Therefore, before using Fluoxetine, you need to think very carefully whether such a risk is justified.

The use of Fluoxetine for weight loss

If the drug is prescribed by a doctor, then usually along with the prescription, a description of the way of its use is obtained. In general, taking Fluoxetine to obtain the effect of weight loss should be taken from small doses, gradually increasing them. Usually, the first week, 10 mg of the drug is used in the morning and in the evening. The maximum dose possible with weight loss is 40 mg per day. More serious doses may be prescribed, but not for weight loss, but, for example, in order to get rid of manic-depressive psychosis.