Most prescribed antidepressant

Pluses

+ There is practically no effect on the work of the heart.

+ Does not cause sedation.

+ Effective for patients with motor retardation and excessive daytime sleepiness.

Cons

- May cause weight loss.

— Hypoglycemia is possible in diabetes mellitus.

- Contraindicated in severe renal impairment.

7. Fluvoxamine

Another SSRI drug. Fluvoxamine is similar to Prozac Fluoxetine but is fast acting and may cost cheaper. The effect is in a more active slowing down of the reuptake of serotonin by neurons. It is indicated for depression of various origins, as well as obsessive-compulsive disorders. The average daily dose is 100 mg.

Pros

+ Lower price than traditional Prozac.

+ Faster action than him.

+ Relatively minor side effects (diarrhea, dry mouth, drowsiness).

Cons

- Contraindicated in diabetes.

- Pregnant women - with caution, lactation - prohibited.

- Causes nausea in some patients.

8. Sertraline

One of the widely used and universal drugs of the SSRI group. They treat almost any depressive condition, panic disorder, social phobia. However, in severe clinical cases, sertraline may not be effective enough. The standard dose is 50 mg/day.

Pros

+ No cardiotoxicity.

+ The patient's psychomotor activity does not change.

+ Does not increase body weight.

+ Combines well with other groups of antidepressants.

Cons

— In the first 2 weeks there may be problems with sleep, diarrhea.

- Side effects of a sexual nature.

- Contraindicated in pregnant women.

9. Escitalopram

The drug is classified as an SSRI. Its difference is in its effectiveness in depression, which is accompanied by involuntary movements (tic, tremor, chewing, smacking). Escitalopram is prescribed to patients with panic, anxiety, phobias, obsessive thoughts or actions. The daily dose is 20 mg.

Pluses

+ Effective in tardive dyskinesia.

+ One of the most powerful SSRIs.

+ More pronounced thymoleptic effect (improvement of mood) compared to many antidepressants of the same group.

Cons

- In some patients, anxiety increases within 2 weeks after starting treatment.

— Gastrointestinal disorders, insomnia, agitation are possible.

— Use during pregnancy only in extreme cases, incompatible with feeding.

10. Venlafaxine

Belongs to the SNRI group. In addition to blocking the reuptake of serotonin, venlafaxine has a similar effect on another neurotransmitter, norepinephrine. The medicine is prescribed for depressive conditions of various origins, social phobias, anxiety, panic. Usually take 150 mg per day.

Pros

+ Better tolerated by patients than most tricyclics.

+ More pronounced effect than classic SSRIs.

+ Fewer contraindications.

Cons

- Traditional side effects of most antidepressants: nausea, drowsiness, dry mouth, diarrhea or constipation.

- May increase eye pressure.

- The most severe withdrawal syndrome among antidepressant drugs.

This list is not to be used as a recommendation. In any case, consult your doctor before purchasing. Be healthy!

Venlafaxine (Velaxin) - the most effective antidepressant?

partners Keywords / keywords: Antidepressants, Depression, Demonstrative medicine, Personal experience, Neurons, Recommendations, Effectiveness, Velaxin, Neuropsychiatry

Summary

Evidence-based medicine has failed to provide conclusive evidence that antidepressants differ in their effectiveness in treating depression. Therefore, scientists base their judgments on the effectiveness of drugs on "personal experience." There is another way to determine the most effective antidepressant. To do this, it is necessary to compare data on the activity of neurons in depression and the ability of antidepressants to act on these neurons. This comparison suggests that the most effective antidepressants are amitriptyline, imipramine, and venlafaxine (in high daily doses). But only venlafaxine is used in our country in therapeutic doses. Therefore, venlafaxine is the most effective antidepressant.

Persistent attempts by pharmaceutical companies to prove with the help of evidence-based medicine that their antidepressant is the most effective in the treatment of depression have so far been unsuccessful. This is agreed not only by individual critics of such studies, but also by large teams of scientists who make recommendations for the pharmacotherapy of depressive disorders. In any case, they proceed from the fact that evidence-based medicine data indicate a comparable activity of antidepressants in the treatment of depression (1, 2, 3). Therefore, to determine the most effective drugs, scientists resort to the “personal experience” accumulated in the treatment of patients (4), which is always subjective. This method of determining the most effective antidepressants is vulnerable to criticism. An alternative to "personal experience" is a comparison of the mechanisms of formation of depression (pathogenesis) and the therapeutic properties of drugs.

It is known that the symptoms of depression are accompanied by a decrease in the activity of different neurons: norepinephrine (↓H), dopamine (↓D), serotonin (↓C), and melatonin (↓M) neurons (Table 1).

Table 1. Decreased activity of neurons in various symptoms of depression (5, 6, 7).

Neuronal activity	Symptoms of depression	"Traditional" names for depressions
↓ND	Deterioration of mood - weakening of positive emotions: melancholy, depression, apathy, decreased interest and pleasure in activities usually associated with positive emotions, gloomy and pessimistic vision of the future	Sad, apathetic, anhedonic
↓CH	Deterioration of mood - increased negative emotions: sadness, spleen, irritation, low self-esteem and feelings of self-doubt, ideas of guilt and self-abasement, anxiety, fear, nervousness	Aching, self-torturing, anxious, dysphoric
↓SND	Deterioration of mood - weakening of positive and strengthening of negative emotions: melancholy and anxiety, anxiety and apathy	Sad-anxious, anxious-apathetic
↓N	Psychomotor retardation: loss of energy and increased fatigue, difficulty in concentrating and holding attention, slowing down of information processes, retardation of movements	Asthenic, adynamic
↓SND	Somatic: pain and other discomforts in the body, loss of appetite and weight loss	Somatized, hypochondriacal
↓SNM	Somatic: pathology of circadian rhythms (sleep disturbances, early awakening, peak of feeling unwell in the morning or in the first half of the day).	-

The main of these symptoms, reflecting deterioration (decrease) in mood (3, 6), are associated with a deterioration in the functioning of norepinephrine and dopamine (↓ND), norepinephrine and serotonin (↓SN), as well as serotonin, norepinephrine and dopamine neurons (↓SND). Accordingly, all depressions can be divided into three classes. The first of these includes ↓ND-depressions. They proceed with the weakening of positive emotions. The second option covers ↓CH-depressions. They are characterized by an increase in negative emotions. Finally, the third one includes ↓SDI-depressions. They are accompanied by both a weakening of positive and an increase in negative emotions. In all three of these variants of depression, phenomena of psychomotor retardation (↓H-symptoms) and / or somatic symptoms (↓SDI or ↓SNM) can be observed. From the presented data, it follows that for the successful treatment of any depression, it is necessary to increase the activity, first of all, of norepinephrine, dopamine and serotonin neurons (↑SND). Accordingly, this is how the most effective antidepressants should act. In other words, they must be ↑SDI drugs.

To increase the activity of serotonin, norepinephrine and dopamine neurons, antidepressants have only three mechanisms. They can be neurotransmitter reuptake inhibitors (RIIs), regulatory receptor-influencing agents (RIARs), or monoamine oxidase type A reversible inhibitors (RIMAO-A) (Table 2).

Table 2. Antidepressants known in Russia, their effect on neurons and the "formula" of the mechanism of action (4, 5, 6, 8).

*- white color - the drug does not affect neurons, dark gray - a pronounced increase in activity, light gray - a moderate increase in activity,

**- in high doses

However, the vast majority of antidepressants used in Russia are classified as IOPs (Table 2). It is this pharmacological property that determines the ability to activate neurons in 66.7% of drugs related to tricyclic (TCA) and tetracyclic (TCA) antidepressants, as well as selective serotonin reuptake inhibitors (SSRIs) and selective serotonin and noradrenaline reuptake inhibitors (SNRIs) . Three more drugs (14.3%) combine the properties of IOP and SVR. Trazodone (a serotonin modulating antidepressant - CMA), milnacipran (SNRI) and vortioxetine (a multimodal antidepressant - MMA) have this mixed mechanism of action.

A similar situation is observed throughout the world. Most antidepressants are PIOs. For example, in the US, these include 8 of the 10 most commonly prescribed drugs (duloxetine, dezvenlafaxine, citalopram, setralin, fluoxetine, escitalopram, paroxetine, venlafaxine) (9). Another one - vilazodone - combines the property of the IOP with a different mechanism of action. In some countries (for example, the USA), the reputation of the PHI is so high that they try not to register antidepressants that do not have such a mechanism of action at all (10).

IOPs are not only allowed to enter the medical services market on a priority basis, but they are also considered a kind of “standard”. After all, their mechanism of action leaves neurotransmitters (serotonin, norepinephrine or dopamine) where they usually realize their effects - “between” neurons in the so-called. "intersynaptic gap" (5). As a result, serotonin, norepinephrine or dopamine act on nerve cells for a longer time, and neurons are activated more than usual. It is also important that this mechanism of action is completely reversible, since it does not contribute to the creation of new neurotransmitters (their synthesis) and does not inhibit their decay (metabolism). And this is very important for the safety of treatment.

But not all antidepressants are strong IODs (4, 5). For some drugs, this mechanism of action is much less pronounced (Table 2). Thus, pipofesin (TcA), which is indicated only for mild to moderate depression (11), most likely moderately activates serotonin, norepinephrine, and dopamine neurons. Trazodone (CmA) and vortioxetine (MmA) are the IOS of serotonin (Table 2). But this mechanism of action is less pronounced in them compared to SSRIs (4, 12).

Antidepressants can only be strong PIDs on serotonin (SSRIs: sertraline, paroxetine, citalopram, escitalopram, fluoxetine, fluvoxamine, TcA: clomipramine), norepinephrine (NcA: maprotiline; SNRI: milnacipran), or both of these neurotransmitters (TcA: amitriptyline, imipramine; SNRIs: venlafaxine and duloxetine) (4, 5, 13, 14). With regard to dopamine, all modern drugs are only weak IODs (TcA: amitriptyline, imipramine, clomipramine, pipofezin; SNRI: venlafaxine in high daily doses), or they do not affect the metabolism of this neurotransmitter at all (4, 5, 6, 13, 14) . In addition, in some IODs, the ability to affect different nerve cells depends on the dose (7).

Thus, venlafaxine (SNRI), especially at low daily doses (75-150 mg), is more of an IOD of serotonin and affects serotonin neurons. At the same time, it has an active metabolite dezvenlafaxine. This substance abroad is itself an antidepressant, and its properties differ from venlafaxine. Dezvenlafaxine is a potent IRI of serotonin and norepinephrine, and at high doses is a weak IRI of dopamine. The amount of dezvenlafaxine is considered to be half of the prescribed daily dose of venlafaxine. With an increase in the dosage of the latter, the concentration in the blood of its active metabolite also increases. Accordingly, venlafaxine, administered at a dose of 150–225 mg/day, is converted by dezvenlafaxine to the IOD of serotonin and norepinephrine. As a result, it effectively activates serotonin and norepinephrine neurons (Table 2). If the daily dose is further increased, then venlafaxine (together with dezvenlafaxine) will acquire the properties of the IOP of dopamine. Then the drug will activate not only serotonin and norepinephrine neurons, but also dopamine neurons, although much weaker (Table 2).

Turning now to SVR (mianserin - HcA, mirtazapine - norepinephrine and selective serotonin antidepressant - NaSSA, agomelatine - melatonergic antidepressant), let's point out the reason why they lose at least strong IOPs in the effectiveness of their effect on neurons (Table 2). ). With the help of PP, it is not the excitation of nerve cells, but rather the “fine tuning” of their “tone” (5, 8, 15). Therefore, "pure" SVRs are quite rare among antidepressants.

On the other hand, there are many IOPs in which the effect on the RR is an additional mechanism of action. But due to its relative weakness, it is not even mentioned in the drug instructions (16, 17, 18). For example, milnacipran (SNRI) refers to the IOD of serotonin and norepinephrine (16). This property gives the antidepressant the ability to effectively activate norepinephrine neurons and, to a lesser extent, serotonin neurons (6). At the same time, milnacipran, due to its effect on RR, contributes to a moderate increase in the “tone” of dopamine nerve cells (19). However, this property is not mentioned in the drug instructions. And only in some IOPs, the effect on RR is still mentioned in the guidelines for the medical use of antidepressants. This feature is characteristic of trazodone (CmA) and vortioxetine (MmA) (5, 8, 20). Both antidepressants are IOS serotonin. This property allows them to moderately activate serotonin neurons (Table 2). And due to the effect on the RR, they slightly increase the "tone" of norepinephrine and dopamine nerve cells.

Finally, two more drugs (OIMAO-A: pirlindol and moclobemide) to activate neurons inhibit (inhibit) the work of an enzyme - monoamine oxidase, which destroys neurotransmitters (serotonin, norepinephrine, dopamine) (5, 20, 21, 22, 23), as inside neurons, and outside them - in the intersynaptic gap. It would seem that this mechanism of action should be very strong, because as a result, the amount of serotonin, norepinephrine and dopamine increases both inside the neuron and outside it. However, this effect is typical, first of all, for the so-called. irreversible inhibitors of monoamine oxidase, which form stable chemical bonds with this enzyme (24). After that, it can no longer perform its functions and breaks down, and instead the body is forced to synthesize a new enzyme, which usually takes about two weeks. As a result, irreversible monoamine oxidase inhibitors are indeed highly active antidepressants. However, due to the high efficiency of the mechanism of action, they are poorly tolerated, they can even be toxic, and their use in our country has practically ceased.

A different picture is observed in the case of pirlindol and moclobemide (20, 22). The effect of these drugs on the enzyme is reversible (RIMAO). The fact is that their relationship with the enzyme is only relatively stable. Its gradual disappearance leads to the release of monoamine oxidase, while the enzyme itself remains intact (24). In addition, pirlindol and moclobemide selectively inhibit the activity of only one of the types of monoamine oxide - "A" (OIMAO-A), while the other type "B" continues to work almost with the same strength. All these features significantly reduce the effectiveness of RIMAO-A, which is why the considered mechanism of action is much less common than IOP (Table 2). At the same time, these features make RIMAO-A more tolerable drugs that weakly activate serotonin, norepinephrine, and dopamine neurons.

The presented features of the mechanisms of action of antidepressants can be represented as a letter formula consisting of the first letters of the name of the neuron on which it acts (↑s, ↑n, ↑n, ↑m). Moreover, in the case of pronounced activation of the nerve cell, you can use an uppercase letter (↑С, ↑Н, ↑Д, ↑М), and with a weak one - a lowercase letter (↑s, ↑n, ↑d, ↑m). It turns out an individual "formula" of the mechanism of action of an antidepressant (hereinafter simply "formula"), which reflects its pharmacological activity much more accurately than the name of the group.

Such "formulas" testify to the existence of "triple" action drugs. These include:

• ↑SND-antidepressants (active effect on serotonin and norepinephrine neurons and weaker effect on dopamine neurons):
  • amitriptyline (TcA),
  • imipramine (TCA)
  • venlafaxine (SNRI) in high daily doses
• ↑ SND-antidepressants (active effect on serotonin neurons and weaker effect on noradrenaline and dopamine neurons):
  • clomipramine (TCA)
• ↑SND-antidepressants (active effect on norepinephrine neurons and weaker effect on serotonin and dopamine neurons):
  • milnacipran (SNRI)
• ↑SND-antidepressants (weak effect on serotonin, norepinephrine and dopamine neurons):
  • pipofezin (TCA),
  • pirlindol (OIMAO-A),
  • moclobemide (OIMAO-A),
  • trazodone (CmA),
  • vortioxetine (Mma)
• ↑ndm-antidepressants (weak effect on norepinephrine, dopamine and melatonin neurons):
  • agomelatine (MeA)

There are drugs "double" action. These include:

• ↑CH-antidepressants (active effect on serotonin and norepinephrine neurons):
  • duloxetine (SNRI)
  • venlafaxine (SNRI) at average daily doses
• ↑CH-antidepressants (active effect on serotonin neurons and weak on norepinephrine)
  • maprotiline (ncA)
• ↑sn-antidepressants (weak effect on serotonin and norepinephrine neurons)
  • mianserin (NZA),
  • mirtazapine (HaSSA)

Finally, single-acting drugs include:

• ↑C-antidepressants (active effect on serotonin neurons):
  • sertraline (SSRI),
  • paroxetine (SSRI),
  • citalopram (SSRI),
  • escitalopram (SSRI),
  • fluoxetine (SSRI),
  • fluvoxamine (SSRI).

The presented data make it easy to determine that the most effective antidepressants will be "triple" action, whose formula contains the largest number of capital letters. These are ↑SNd-antidepressants that actively affect serotonin and norepinephrine neurons and, to a lesser extent, dopamine neurons: amitriptyline (TcA), imipramine (TcA), venlafaxine (SNRI) in high daily doses. This set of pharmacological properties allows them to influence all three variants of depression (↓ND with a decrease in positive emotions; ↓SN with an increase in negative emotions; ↓SDI-depression with a decrease in positive and an increase in negative emotions), which may be accompanied by phenomena of psychomotor retardation (↓ H-symptoms) and/or somatic symptoms (↓SNM or ↓SNM).

The presented very short list of the most effective antidepressants correlates well with the "personal experience" of foreign experts who create recommendations. It has already been mentioned above that TcA and SNRIs are recognized as the most powerful drugs there (4). Some recommendations have more precise instructions. It reports that, along with TcA, only one SNRI, venlafaxine, is the most effective (3). But experts always stipulate that they cannot provide any objective evidence of their point of view. One can only regret that they did not want to turn to the features of the formation of symptoms of depression and the mechanism of action of antidepressants. If we take into account the relationship between them, then the "personal experience" of experts becomes quite understandable and even "public".

This analysis puts venlafaxine in an exceptional position, especially in our country. It is well known that in Russia TcA (amitriptyline and imipramine) are prescribed very sparingly in low doses, which are usually less than therapeutic doses (25, 26). This is due to the pronounced side effects inherent in amitriptyline and imipramine. Meanwhile, any drug, including TcA, when administered at doses that do not reach the therapeutic range, loses its effectiveness. As a result, in our country, only venlafaxine can claim to be the most effective antidepressant. And this drug is widely used in our country in the form of Velaksin (Egis). He was recommended by leading scientific organizations carrying out cutting-edge research in the field of psychiatry. Among them are the Federal State Budgetary Institutions “State Scientific Center for Social and Forensic Psychiatry named after V.P. Serbsky" and "Moscow Research Institute of Psychiatry" of the Ministry of Health of Russia, St. Petersburg Research Institute. V.M. Bekhterev (27, 28). Long-acting capsules (Velaxin retard) are also well known (29), which have been shown to significantly reduce the side effect of the drug, such as nausea (30). In addition, the study of Velaksin was successfully carried out not only in psychiatry, but also in neurology (31). It remains to recommend that this antidepressant be used as widely as possible in the treatment of depression.

M.Yu Drobizhev's video on the same topic can be viewed at the link: https://youtu.be/C4J_SaQb1uw

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M.Yu. Drobizhev, Doctor of Medical Sciences, Head of the Educational Department of the Training Center of the Association of Medical and Pharmaceutical Universities of Russia

Contact information – [email protected]

E.Yu. Antokhin, Candidate of Medical Sciences, Associate Professor, Head of the Department of Clinical Psychology and Psychotherapy, Orenburg State Medical University, Ministry of Health of Russia.

R.I. Palaeva – Assistant of the Department of Clinical Psychology and Psychotherapy of FSBEI HE “Orenburg State Medical University” of the Ministry of Health of Russia.