What is the difference between zoloft and citalopram

This is in agreement with escitalopram having the highest cumulative probability of being among the four best treatments in terms of acceptability in a recent review: escitalopram Compared with other SSRIs, a higher incidence of adverse effects was indicated for paroxetine treatment, including sedation, constipation, sexual dysfunction, discontinuation syndrome, weight gain, and congenital malformations, in a review of head-to-head studies Marks et al.

A review of tolerability based on data from randomized controlled clinical trials involving about patients with short-term and long-term treatments indicated that paroxetine was associated with significantly higher incidence of adverse events related to sexual dysfunction, as well as more discontinuation symptoms, than escitalopram Baldwin et al.

In general, these findings are consistent with a recent review on the overall profile of paroxetine Gibiino and Serretti, Diarrhea is another common adverse event worth noting for antidepressants. Consistent with this, a recent meta-analysis found that sertraline was indeed associated with a higher incidence of diarrhea than comparator drugs including paroxetine Cipriani et al. The review by Gartlehner et al. Some basic pharmacokinetic and pharmacodynamic properties of escitalopram, paroxetine, and sertraline are compared in Table 2.

In general, the three antidepressants produce good absorption, distribution, and clearance profiles at their therapeutic doses. Paroxetine is approved at clinical dosages of Frequently, treatment with sertraline or paroxetine needs to be titrated by the physician to obtain the optimal dose for the individual patient. The pharmacokinetic and pharmacodynamic properties of escitalopram, paroxetine, and sertraline.

Aspects of drug—drug interactions provide clinically relevant differences between escitalopram, paroxetine, and sertraline Hiemke and Hartter, Thus, escitalopram may be superior to paroxetine and sertraline in this regard. The primary target mediating the therapeutic actions of escitalopram, paroxetine, and sertraline is the SERT, and all three drugs have very high affinity at the SERT Table 3.

Paroxetine has the highest affinity at the SERT, whereas escitalopram has the highest degree of selectivity i. The clinical trial data, in head-to-head comparisons and in meta-analyses and as described in literature reviews, have shown higher efficacy for escitalopram and sertraline treatment of depression than paroxetine, with data also showing that escitalopram is associated with higher efficacy compared with other SSRIs.

The efficacy of escitalopram may at least in part be ascribed to its actions at allosteric sites of the SERT Chen et al.

The SERT has two types of binding site, the orthosteric binding site also referred to as the primary site to which escitalopram and other SSRIs bind, resulting in inhibition of its uptake function, and one or more allosteric sites Chen et al.

Many studies have led to the thorough characterization of the allosteric mechanism of escitalopram Wennogle and Meyerson, ; Plenge and Mellerup, ; Chen et al. In binding experiments with the SERT, the allosteric activity of escitalopram is characterized by its ability to prolong its own dissociation kinetics Chen et al. By binding to both the orthosteric and allosteric binding sites, escitalopram elicits a more complete and sustained inhibition of 5-HT uptake, leading to higher extracellular 5-HT levels in vivo and faster 5-HT 1A autoreceptor desensitization, as reviewed previously Sanchez et al.

Additional elucidation of this mechanism includes in-vitro as well as in-vivo studies demonstrating that specific mutations in the SERT disrupt the allosteric effect of escitalopram, and that R -citalopram, a less active enantiomer of citalopram citalopram is also an antidepressant , inhibits the efficacy of escitalopram Zhong et al.

This makes escitalopram the only SERT-related antidepressant that shows dual allosteric and chiral advantages El Mansari et al. As noted in Table 3 , paroxetine is also allosteric, but its allosteric effect is weaker Chen et al.

In comparison, sertraline and many other antidepressants e. A putative model showing that escitalopram, paroxetine, and sertraline interact with the primary orthosteric and allosteric binding sites at the SERT leading to differential increases in extracellular 5-HT levels. In each diagram, the SERT is shown to be located at serotonergic neurons and to have the primary and allosteric binding sites.

Allosteric site binding enhances their binding to the primary site, resulting in more pronounced increases in extracellular 5-HT levels and potentially signaling through SERT-interacting proteins SIPs Sanchez et al. Drawing is based on previously published diagrams by Zhong et al. It is worth noting that for the SSRIs fluoxetine and paroxetine, enantiomers have also been studied. The different ability of escitalopram, paroxetine, and sertraline in increasing extracellular levels of 5-HT in relation to SERT occupancy in the rat brain has been demonstrated, which indicates that the allosteric property of escitalopram may translate to physiological conditions Brennum et al.

As shown in Fig. At escitalopram, paroxetine, and sertraline doses of 0. These differences do not reflect the in-vitro SERT inhibitory potency rank order Table 3 and potentially support that there is an additional site of action presumably an allosteric site that mediates the more efficacious uptake inhibition by escitalopram, in addition to binding to the orthosteric site of the SERT.

Increase in extracellular levels of 5-HT by escitalopram, paroxetine, and sertraline in relation to SERT occupancy in the rat. The ability of escitalopram, paroxetine, and sertraline to increase 5-HT levels in rat prefrontal cortex via SERT inhibition is shown. Rats in the microdialysis experiments were anesthetized and the drugs were administered by the subcutaneous route. SERT occupancy was measured by in-vivo binding using [ 3 H]citalopram as radioligand.

SERT occupancy relationships for escitalopram, paroxetine, and sertraline. Thus, due to the plateau in SERT occupancy seen for these antidepressants, higher doses are thought to be unable to further increase efficacy, but rather to incur additional side effects, which may contribute to higher discontinuation rates Preskorn, Although it is clear that the primary target of escitalopram, paroxetine, and sertraline is the SERT, the precise cellular and physiological changes following uptake inhibition that mediate their antidepressant actions are poorly understood.

It takes antidepressants, including the SSRIs, 1—2 weeks to produce their therapeutic effect, probably because slower neuroadaptive and neurochemical changes in the brain following the elevation of 5-HT levels are required for the therapeutic effect Blier and de Montigny, ; Zhong et al.

For example, the recovery of raphe 5-HT neuronal firing after the desensitization of 5-HT 1A autoreceptors is thought to reflect the neuroadaptive process underlying the delayed onset of antidepressant action Blier and de Montigny, ; El Mansari et al.

For escitalopram, it takes 2 weeks before 5-HT neuronal firing returns to control levels in rats, but for most SSRIs, it takes at least 3 weeks, suggesting a faster onset of action for escitalopram, possibly due to its action at the allosteric site El Mansari et al.

This is consistent with the indication of escitalopram having a faster clinical onset than other SSRIs Lepola et al. Among other neurochemical changes during antidepressant treatment, the neurotropin brain-derived neurotrophic factor BDNF was recently reviewed Zhong et al.

As a potential biomarker, BDNF shows decreased levels in the blood of depressed patients and this can predict treatment response for escitalopram, paroxetine, and sertraline Yoshimura et al. Thus, neurotropins such as BDNF might hold key insights associated with the neuroadaptive and neurochemical changes during antidepressant treatment, which may help differentiate the actions of SSRIs. Further studies in this area are warranted.

Although it is believed that the therapeutic effects of escitalopram, paroxetine, and sertraline are mediated through their actions at the SERT, some side effects also can be explained by their off-target effects at other transporters and receptors Richelson, , Potencies of this order of magnitude may be potentially meaningful at clinical exposure levels. Thus, commonly reported adverse effects of paroxetine are symptoms of sedation, constipation, and visual disturbance, which could be ascribed to anticholinergic activity Pae and Patkar, Indeed, paroxetine has considerable potency for muscarinic receptors, allowing it to affect these receptors at the blood levels expected during treatment Table 2.

A study in mice, in which the anticholinergic effects of paroxetine were measured using oxotremorine-induced tremor, spontaneous defecation, and passive avoidance performance tests, also supports the notion of paroxetine having anticholinergic activity in vivo Fujishiro et al. It was found that paroxetine induced more anticholinergic effects than fluvoxamine another SSRI , although its effects were lower than those of a tricyclic clomipramine, as expected Fujishiro et al.

In a comparative study of escitalopram and paroxetine, the anticholinergic activity was assessed as blockade of hypothermia induced by the muscarinic agonist oxotremorine Fig. Oxotremorine caused dose-dependent hypothermia, which was prevented by paroxetine but not escitalopram Fig. The role of dopamine reuptake inhibition DAT activity was also measured as stimulation of spontaneous locomotor activity Fig. Sertraline produced a significant increase in the spontaneous locomotor activity compared with vehicle controls at doses close to those that produce 5-HT reuptake inhibition, that is, the minimal effective dose of 2.

In line with these behavioral observations, Kitaichi et al. It is difficult to predict the functional net effect of this combined SERT and DAT inhibition, as there is a high degree of functional connectivity between the monoaminergic neurotransmitter systems, but sertraline may potentially differ from an SSRI that is devoid of DAT inhibition.

Thus, in the dorsal raphe nucleus, activation of dopaminergic D 2 receptors increases whereas activation of serotonergic 5-HT 1A receptors decreases the activity of 5-HT neurons. In-vivo measurements of the effects of escitalopram, paroxetine, and sertraline on muscarinic cholinergic and DAT activities in mice. The anticholinergic and DAT-inhibiting effects of escitalopram, paroxetine, and sertraline are shown in oxotremorine-induced hypothermia a and spontaneous locomotor activity b, c in mice.

The test was conducted at room temperature and started at 11 a. Drug or vehicle was injected subcutaneously 30 min before oxotremorine. The rectal temperature was measured before drug and oxotremorine administration and after 30 min. The test was conducted in cages equipped with infrared light sources and photocells and the number of light beam interruptions was used as measure of locomotor activity.

The mice were placed individually in the test cages and were habituated for 30 min before administration of drug. NE reuptake inhibition was assessed as antagonism of tetrabenazine-induced ptosis in mice, and paroxetine showed NE reuptake-inhibiting activity at doses close to those that produced 5-HT reuptake inhibition Sanchez, Tetrabenazine is a monoamine-depleting agent producing immobility and ptosis. The latter effect is mediated by alpha adrenoceptors and has been shown to be reversed by compounds with NE reuptake inhibitory activities Arnt et al.

For example, escitalopram was found to be associated with significantly lower duration of sick leave compared with duloxetine during treatment Wade et al.

Direct comparison analyses in clinical trials do not indicate a risk of EPS for escitalopram or sertraline Baldwin et al.

The exact mechanism for development of EPS is not fully understood, although it is generally accepted that dysfunction in dopaminergic transmission of the nigrostriatal pathway plays a key role Glazer, ; Tuppurainen et al. Reduced DA transmission in the form of DA receptor blockade by antipsychotic treatment in schizophrenia is frequently manifested by the side effects of EPS and hyperprolactinemia, since dopamine exerts a potent and tonic inhibition of prolactin secretion under normal conditions Kane, However, a more recent review of spontaneous reports suggested that paroxetine, but not sertraline or escitalopram, was associated with a higher risk of hyperprolactinemia Trenque et al.

An earlier analysis with the identification of 61 spontaneous reports concluded that SSRI use seems to be only moderately associated with EPS compared with other antidepressants, and suggests that patients with an already compromised dopaminergic function may be more susceptible Schillevoort et al.

Escitalopram, paroxetine, and sertraline have well-established efficacy and tolerability profiles based on decades of clinical use as some of the most widely prescribed antidepressants.

Although these antidepressants belong to the same general class SSRIs and all have demonstrated therapeutic efficacy, differences exist with respect to efficacy and tolerability, as shown by head-to-head comparisons and meta-analyses. There are studies demonstrating the superiority of escitalopram compared with paroxetine as well as a combined group of various SSRIs including paroxetine and sertraline.

Although sertraline has moderate drug—drug interaction issues, its DAT inhibitory properties may result in a different pharmacodynamic profile. Therefore, when compared with paroxetine and sertraline, escitalopram as an ASRI different from classical SSRIs consistently shows advantages in efficacy and tolerability profiles, and nonclinical data have offered possible mechanisms through which escitalopram could be more efficacious based on its interaction with orthosteric and allosteric binding sites at the SERT.

Connie Sanchez and Elin H. Reines are full-time employees of H. Stuart A. It is important you adhere to the dosage limits set by your prescriber. Serotonin syndrome has been reported with all SSRIs. This is a condition related to abnormally high levels of serotonin, and can result in the patient feeling agitated, dizzy, and having an increased heart rate.

This can be brought on by the use of two serotonergic drugs together. Celexa is a prescription antidepressant medication.

It belongs to a class of medications known as selective serotonin reuptake inhibitors. It is prescribed to treat major depressive disorder , and it works by increasing available serotonin in the neuron synapse. Celexa is available in 10 mg, 20 mg, and 40 mg strengths. Zoloft is a prescription antidepressant medication used in the treatment of major depressive disorder as well as other anxiety and psychiatric disorders.

Zoloft is in a class of drugs known as selective serotonin reuptake inhibitors SSRIs. Zoloft is available as oral tablets in 25 mg, 50 mg, and mg strengths, as well as an oral liquid concentrate. Celexa and Zoloft are both antidepressants in the same class, but they are not the same drug. They have different active ingredients, and while both are approved in the treatment of depression , each carries some unique indications for use in other mental health conditions as well.

Celexa and Zoloft have both been shown to be valuable, efficacious, and tolerable treatments for depression. However, Celexa shows an earlier onset of symptom relief which may be a significant factor in drug choice. Celexa and Zoloft are pregnancy category C, meaning there have not been adequate human studies to determine efficacy.

The use of SSRIs must be weighed against the potential harm to the fetus while also considering the well-being of the mother. Skip to main content Search for a topic or drug. Celexa vs. By Kristi C. Torres, Pharm. Updated on Sep. Top Reads in Drug vs. Toujeo vs Lantus: Main Differences and S Dulera vs Advair: Main Differences and S Suboxone vs Methadone: Main Differences Looking for a prescription?

Search now! Type your drug name. Premature ejaculation. Separation anxiety disorder. Almotriptan Eletriptan Oxitriptan. Dexmethylphenidate Methylphenidate. Alosetron Ondansetron Ramosetron. Aspirin Ibuprofen Naproxen Diclofenac. Report Abusive Comment Thank you for helping us to improve our forums.

Is this comment offensive? Please tell us why. Restricted Content You must have JavaScript enabled to enjoy a limited number of articles over the next days. Please click here to continue without javascript..

Psychiatric Medicine in Primary Care Shop Now: Search Products.