Posts Tagged SSRIs
Prozac and Zoloft are both selective serotonin reuptake inhibitors (SSRIs). This class of medication is among the first options for treating major depressive disorder, which people usually call depression.
In this article, we discuss the differences between Prozac and Zoloft.
What do they treat?
- major depressive disorder (MDD)
- obsessive-compulsive disorder (OCD)
- panic disorder
- premenstrual dysphoric disorder
In addition, the FDA have approved Prozac for the treatment of:
Other SSRIs include:
- escitalopram (Lexapro)
- vortioxetine (Trintellix)
- citalopram (Celexa)
- fluvoxamine (Luvox)
- paroxetine (Paxil)
- vilazodone (Viibryd)
Both Prozac and Zoloft are available in the forms of a liquid oral solution, a tablet, and a capsule.
The following table lists the different forms of each drug along with the available dosages in milligrams (mg) and milligrams per milliliter (mg/ml).
|Capsule||10 mg, 20 mg, 40 mg, 90 mg||25 mg, 50 mg, 100 mg|
|Tablet||60 mg||25 mg, 50 mg, 100 mg|
|Liquid||20 mg/5 ml||20 mg/ml|
How to take and dosage
When a person first starts taking antidepressants, they will typically begin on a smaller dosage and increase this over time. Doing this makes it possible to test how well the drug works and monitor its side effects, as the effectiveness and adverse effects can differ among individuals.
American Psychiatric Association guidelines report the following starting dosages and the usual effective dosages when treating MDD:
|Starting dosage||20 mg/day||50 mg/day|
|Usual effective dosages||20–60 mg/day||50–200 mg/day|
Some people may see improvements in their symptoms in the first 1–2 weeks of treatment, whereas it may take 2–4 weeks for others to notice changes.
Some studies have shown that all antidepressants require at least 4–6 weeks before they reach their maximal clinical effectiveness.
There are three phases of MDD therapy:
- The acute phase. The goal of the acute phase is for the person to recover from depressive symptoms and return to their baseline of functioning. This phase will last about 6–12 weeks.
- The continuation phase. During the continuation phase, doctors will recommend that people continue treatment for 4–9 months to prevent symptoms from returning.
- The maintenance phase. Some people may need to continue their medication for longer and complete a maintenance phase. The goal is to protect at-risk people from recurring depressive symptoms.
Doctors will usually recommend a maintenance phase for people with recurrent MDD or chronic depression.
If a person does not have a satisfactory response to medication, the doctor may try increasing the dosage. However, a higher dosage may cause more side effects, so doctors need to evaluate the risks and benefits of increasing it.
Another strategy to increase the effectiveness of the therapy is to add another medicine. A doctor may advise a person to combine Prozac or Zoloft with certain other antidepressants and other types of medication to improve their symptoms.
The doctor will determine which combinations are the most appropriate for each person while keeping in mind the possibility of drug interactions.
Doctors may also adjust medication dosages and regimens for people who are combining medication therapy and psychotherapy.
As Prozac and Zoloft are both SSRIs, people may experience similar side effects with these drugs.
Zoloft is more likely than Prozac to cause gastrointestinal tract side effects, such as nausea and diarrhea. Men taking Zoloft may also report more sexual dysfunction side effects, such as failure to ejaculate, than those using Prozac.
The following table lists the most common side effects of Prozac and Zoloft, which occur in at least 5% of people.
|decreased appetite||no data available||7%|
|anorexia||10%||no data available|
|anxiety||12%||no data available|
|agitation||no data available||8%|
|nervousness||13%||no data available|
|headache||21%||no data available|
|weakness/lack of energy||11%||no data available|
|flu-like symptoms||5%||no data available|
|decreased sex drive||no data available||6%|
|failure to ejaculate||no data available||8%|
When people are ready to come off their antidepressant medications, they should do so gradually. Stopping Prozac, Zoloft, or any other antidepressant abruptly can cause discontinuation symptoms.
Discontinuation symptoms may include:
- dysphoria, or general unease and dissatisfaction
- electric shock sensations
- emotional lability, or rapid and exaggerated changes in mood
Several short-term studies have shown that children, adolescents, and young adults under 24 years old have an increased risk of suicidal thoughts and behaviors when taking any antidepressants.
Doctors will monitor people taking Prozac, Zoloft, or any other antidepressant for worsening of depressive symptoms, suicidal thoughts, and unusual behaviors.
People with glaucoma and a history of seizures should use Prozac, Zoloft, and other SSRIs with caution because the drugs can make these conditions worse.
- If you know someone at immediate risk of self-harm, suicide, or hurting another person:
- Call 911 or the local emergency number.
- Stay with the person until professional help arrives.
- Remove any weapons, medications, or other potentially harmful objects.
- Listen to the person without judgment.
- If you or someone you know is having thoughts of suicide, a prevention hotline can help. The National Suicide Prevention Lifeline is available 24 hours a day at 1-800-273-8255.
SSRIs, including Prozac and Zoloft, have similar drug interactions.
Serotonin syndrome is a potentially life-threatening interaction that occurs as a result of combining drugs that increase serotonin in the body.
Doctors should avoid prescribing Prozac, Zoloft, and other SSRIs alongside the following drugs:
- tricyclic antidepressants (TCAs)
- St. John’s wort
- monoamine oxidase inhibitors (MAOIs)
Some of the signs and symptoms of serotonin syndrome include:
- a high body temperature
- increased heart rate
- muscle rigidity
- overactive reflexes
- abnormal muscle contractions
- dilated pupils
- abnormal eye movements
- dry mucous membranes
- flushed skin
- increased bowel sounds
People cannot take MAOIs, another type of antidepressant, with Prozac, Zoloft, or any other SSRIs because the risk of developing serotonin syndrome is very high.
Anyone taking an MAOI must stop taking it at least 2 weeks before starting SSRI treatment.
Doctors have reported QT prolongation in people taking Prozac and Zoloft. QT prolongation is a potentially fatal heart rhythm dysfunction.
This heart condition is more common in people who take other drugs that can prolong the QT interval on an electrocardiograph. These include certain antipsychotics, antibiotics, and anti-arrhythmic medications.
Some people can experience abnormal bleeding when combining Prozac, Zoloft, and other SSRIs with drugs that can increase bleeding, such as:
|Capsule (30 capsules)||10 mg: $3.00
20 mg: $3.00
40 mg: $3.00
|10 mg: $461.85
20 mg: $474.70
40 mg: $947.40
|no information available||no information available|
|Tablet (30 tablets)||10 mg: $4.00
20 mg: $26.76
60 mg: $96.35
|no information available||25 mg: $3.99
50 mg: $7.17
100 mg: $6.52
|25 mg: $313.61
50 mg: $313.61
100 mg: $313.61
|Liquid oral solution (1 bottle)||120 ml: $12.81||no information available||60 ml: $25.10||60 ml: $216.18|
Can you take Prozac and Zoloft together?
People should not take Prozac and Zoloft together. These drugs are in the same drug class and have the same actions. Taking both drugs will not improve symptoms but can cause additional side effects.
When people are not feeling the intended effects of either Prozac or Zoloft, the doctor may increase the dosage or alter the treatment regimen by adding another antidepressant or antipsychotic drug that has different actions on the brain.
Prozac and Zoloft are part of the same family of antidepressants, and both raise the levels of serotonin in the brain. Both drugs have FDA approval for the treatment of MDD, and they also have other approved and nonapproved uses.
The safe warnings relating to taking Prozac or Zoloft are similar, as are many of the side effects, although these can vary from person to person. Zoloft may be harsher on the stomach, while Prozac is more likely to cause headaches.
Both drugs are generally effective and safe, but people taking Prozac or Zoloft should follow up with their doctor to discuss their symptoms and side effects to ensure that they are taking the most effective dosage.
If treatment is successful, the doctor will slowly reduce the dosage if possible to eventually stop the medication. People should not abruptly stop taking Prozac or Zoloft.
Depression is characterized by persistent low mood and feelings of hopelessness, and it is one of the most common mental disorders in the United States. In 2014, there were an estimated 15.7 million U.S. adults who experienced at least one major depressive episode, representing around 6.7 percent of the country’s adults.
Treatments for depression generally include talking therapies in conjunction with medication. The class of drugs most commonly prescribed is selective serotonin reuptake inhibitors (SSRIs), and these include brands such as Prozac and Zoloft.
SSRIs can help some people with depression, but they are not perfect; not everyone responds well to them, and side effects including nausea, insomnia, agitation, and erectile dysfunction can be unpleasant.
Also, SSRIs can take some time to kick in; although some people might feel some benefit within hours or even minutes, most people do not feel the full antidepressant effect until they have been taking the drugs for weeks or even months.
How do SSRIs work?
In the brain, messages are sent between neurons by releasing neurotransmitters into a gap between the cells, or the synapse. Serotonin is one such neurotransmitter. It is released from the first neuron and binds to receptors on the second neuron.
Normally, once serotonin has been released into the synapse and relayed its message, the majority is reabsorbed into the first nerve cell for reuse at a later date. SSRIs prevent serotonin from being reabsorbed. In this way, they ensure that serotonin hangs around in the synapse for a longer time, exerting more of an effect.
Although SSRIs have been known to medical science since the 1950s, their exact mechanism is not understood. This is because there are at least 1,000 types of neuron that can be influenced by a surge in serotonin, and some of these neurons may be excited, while others might be inhibited.
The mixed response is because there are 14 subtypes of serotonin receptor throughout the body and any single nerve could have a cocktail of receptor types. Teasing out which receptor subtype is playing the most significant role has proven challenging.
The role of the dentate gyrus
A group of scientists from Rockefeller University in New York City, NY, recently set out to take a closer look at the action of SSRIs on a particular type of nerve cell. The team was headed up by Lucian Medrihan and Yotam Sagi, both research associates in the Laboratory of Molecular and Cellular Neuroscience, and Paul Greengard, Nobel laureate.
Their findings were recently published in the journal Neuron.
“Many different types of synapses throughout the brain use serotonin as their neurotransmitter. An issue of major importance has been to identify where in the myriad of neurons the antidepressants initiate their pharmacological action.”
The team concentrated on a group of cells in the dentate gyrus (DG). According to the authors, they chose the DG because previous work has established that “SSRI treatment promotes a variety of synaptic, cellular, and network adaptations in the DG.”
Specifically, the team investigated cholecystokinin (CCK)-expressing neurons within the DG. These neurons were of interest because they are heavily influenced by neurotransmitter systems that are associated with mood disorders, such as depression.
Finding the right receptor
Using a technique called translating ribosome affinity purification, the team were able to identify the serotonin receptors on CCK cells. Sage explains, “We were able to show that one type of receptor, called 5-HT2A, is important for SSRIs’ long-term effect, while the other, 5-HT1B, mediates the initiation of their effect.
The next step in the study involved efforts to mimic SSRIs’ effects by manipulating CCK neurons in mice. They used chemogenetics to switch nerve cells on or off and implanted tiny electrodes inside the mouse brains.
The findings were clear. When the CCK neurons were inhibited, the pathways important for the mediation of SSRI responses lit up. In other words, the scientists had recreated a Prozac-like effect without using the drug.
To back up these findings, the team used behavioral experiments in a pool and observed swimming patterns. Again, silencing the CCK neurons created behavior that was similar to that displayed by the mice that had been given SSRIs: they swam for longer with increased vigor.
According to the researchers, understanding the importance of the DG and the specific cells important for treating depression will help to design faster-acting, more effective antidepressants with fewer side effects.
The work was carried out using techniques that would have been impossible just 5 years ago, and the studies that follow are likely to improve our understanding even further.
A study is challenging the relationship between depression and an imbalance of serotonin levels in the brain, and brings into doubt how depression has been treated in the U.S. over the past 20 years.
Researchers at the John D. Dingell VA Medical Center and Wayne State University School of Medicine in Detroit have bred mice who cannot produce serotonin in their brains, which should theoretically make them chronically depressed. But researchers instead found that the mice showed no signs of depression, but instead acted aggressively and exhibited compulsive personality traits.
This study backs recent research indicating that selective serotonin reuptake inhibitors, or SSRIs, may not be effective in lifting people out of depression. These commonly used antidepressants such as Prozac, Paxil, Celexa, Zoloft, and Lexapro, are taken by some 10% of the U.S. population and nearly 25% of women between 40 and 60 years of age. More than 350 million people suffer from depression, according to the World Health Organization, and it is the leading cause of disability across the globe.
The study was published in the journal ACS Chemical Neuroscience. Donald Kuhn, the lead author of the study, set out to find what role, if any, serotonin played in depression. To do this, Kuhn and his associates bred mice who lacked the ability to produce serotonin in their brains, and ran a battery of behavioral tests on them. In addition to being compulsive and extremely aggressive, the mice who could not produce serotonin showed no signs of depression-like symptoms. The researchers also found, to their surprise, that under stressful conditions, the serotonin-deficient mice behaved normally.
A subset of the mice who couldn’t produce serotonin were given antidepressant medications and they responded in a similar manner to the drugs as did normal mice. Altogether, the study found that serotonin is not a major player in depression, and science should look elsewhere to identify other factors that might be involved. These results could greatly reshape depression research, the authors say, and shift the focus of the search for depression treatments.
The study joins others in directly challenging the notion that depression is related to lower levels of serotonin in the brain. One study has shown that some two-thirds of those who take SSRIs remain depressed, while another study has even found them clinically insignificant.
Critics of common antidepressants claim they’re not much better than a placebo, yet may still have unwanted side effects.
SSRIs started to become widely used in the 1980s. Their introduction was heralded by the psychiatric community as a new era where safer drugs that directly targeted the causes of depression would become the standard. While SSRIs aren’t more effective than the older antidepressants, such as tricyclics and monoamine oxidase inhibitors, they are less toxic.
An earlier study by the National Institute of Mental Health found that two out of three patients with depression don’t fully recover using modern antidepressants.
These results “are important because previously it was unclear just how effective (or ineffective) antidepressant medications are in patients seeking treatment in real-world settings,” said James Murrough, a research fellow at the Mount Sinai School of Medicine Mood and Anxiety Disorders Program.
The concept that depression is a result of low brain serotonin levels and, therefore, that selective serotonin reuptake inhibitors (SSRIs) are an effective treatment for the disorder is a myth, says a UK psychiatrist.
Moreover, David Healy, MD, professor of psychiatry, Hergest Unit, Bangor, Wales, United Kingdom, believes that SSRIs were a treatment looking for a condition and that doctors and patients were co-opted into the myth by clever marketing, resulting in better treatments being sidelined.
“This history raises a question about the weight doctors and others put on biological and epidemiological plausibility. Does a plausible (but mythical) account of biology and treatment let everyone put aside clinical trial data that show no evidence of lives saved or restored function?,” Dr Healy asks.
“In other areas of life the products we use, from computers to microwaves, improve year on year, but this is not the case for medicines, where this year’s treatments may achieve blockbuster sales despite being less effective and less safe than yesterday’s models,” he adds.
The editorial was published online April 21 in the BMJ.
Doctors, Patients Co-opted
Outlining the history of SSRIs, Dr Healy says that in the 1960s, the notion that serotonin levels are lower in persons with depression was rejected, and SSRIs were shown to be less effective than tricyclic antidepressants. The SSRIs were then marketed as tranquilizers, for which they were equally unsuccessful.
Continue —> Low Serotonin, Depression Link a Myth?.
[ARTICLE] A Combined Therapeutic Approach in Stroke Rehabilitation: A Review on Non-Invasive Brain Stimulation plus Pharmacotherapy -Full Text PDF
Stroke is a leading cause of disability in the United States. Available treatments for stroke have only a modest effect on motor rehabilitation and about 50-60% of stroke patients remain with some degree of motor impairment after standard treatment.
Non-invasive brain stimulation (NIBS) techniques have been proposed as adjuvant treatments to physical therapy for motor recovery after stroke. High frequency rTMS and anodal tDCS can be delivered over the affected motor cortex in order to increase cortical excitability and induce brain plasticity with the intention to enhance motor learning and achieve functional goals in stroke patients. Similarly, low frequency rTMS and cathodal tDCS can be delivered to the unaffected motor cortex to reduce interhemispheric inhibition and hinder maladaptive plasticity.
The use of several drugs such as amphetamines, selective serotonin reuptake inhibitors (SSRIs), levodopa and cholinergic agents have been also proposed to enhance the motor function. Given that both NIBS and pharmacotherapy might provide some treatment effect independently for motor rehabilitation in stroke and with the rationale that they could work in a synergistic fashion, we believe that a combined therapy- NIBS plus pharmacotherapy- can lead to better outcomes than one or the other alone. In this paper we review the literature that support the potential use of a combined approach in stroke recovery and present the studies that have already investigated this idea
…Some studies have found that women who use common antidepressants early in pregnancy face a raised risk of miscarriage, but new research suggests the link might be better explained by the depression, rather than the drugs that treat it…