Home » Misc » Can you drink on effexor

Can you drink on effexor


Effexor and Alcohol: What You Need To Know

Effexor is a brand name for a prescription medication called venlafaxine.

Venlafaxine is a type of antidepressant called a serotonin-norepinephrine reuptake inhibitor, or SNRI.

SNRIs work by rebalancing chemicals in your brain called neurotransmitters.

By doing so, the medication can improve your mood, sleep, appetite, and energy levels, among other things.

It is used to treat many psychiatric conditions including depression, anxiety, and panic disorders.

It is also sometimes used to treat ADHD and obsessive compulsive disorder.

Effexor, like many antidepressants, doesn’t interact well with specific medications and other substances.

One of those substances is alcohol: Both Effexor and alcohol can impair mental and motor skills and may exacerbate each other’s effects.

In this article, I’ll discuss how Effexor works, why doctors remain cautious about mixing the medication with alcohol, and what kinds of side effects you might experience while taking your prescription drug.  

Feeling Down?

Take our free assessment and learn about your options.

Get Started

What is Effexor?

Effexor is a brand name version of venlafaxine, a type of antidepressant called a serotonin-norepinephrine inhibitor, or SNRI.

It’s used to treat anxiety and depression, among other psychiatric conditions.

Effexor is available in two forms, an immediate-release tablet that comes in five dosage strengths (25 mg, 37.5 mg, 50 mg, 75 mg, and 100 mg), and an extended-release tablet called Effexor XR that comes in three dosage strengths (7.5 mg, 75 mg, and 150 mg).

The generic version of Effexor is called venlafaxine.

The generic and brand name versions contain the same active ingredient and are equally effective.

The generic is usually more affordable.

The recommended starting dose of Effexor is 75 mg for most patients.

However, your doctor or mental health provider may suggest another amount based on your personal medical history and the severity of your symptoms.

Effexor uses 

Doctors use Effexor to help patients manage behavioral health, mood disorders, chronic pain, and other health conditions.

The Food and Drug Administration has approved it for the treatment of major depressive disorder (MDD), generalized anxiety disorder (GAD), social anxiety disorder (social phobia), and panic disorder (panic attacks). 

When appropriate, healthcare providers will prescribe venlafaxine off-label to treat other conditions like attention deficit hyperactivity disorder (ADHD), obsessive-compulsive disorder (OCD), premenstrual dysphoric disorder (PMDD), and post-traumatic stress disorder (PTSD).

On occasion, they may also recommend it for some people who suffer from chronic pain conditions like diabetic neuropathy, migraines, cataplexy, narcolepsy, and hot flashes.  

How Effexor works

Effexor works by rebalancing and regulating the chemicals in your brain to improve your mood, increase your appetite, reduce sleep challenges and help you experience a higher quality of life.

Under normal circumstances, your brain uses neurotransmitters called serotonin, dopamine, and norepinephrine as a way to communicate with itself and other areas of the body.

Once these chemicals have carried their message, they’re usually reabsorbed by the brain, a process called “reuptake.”

When you take an antidepressant medication like Effexor, it blocks your brain from reabsorbing the neurotransmitters serotonin and norepinephrine, increasing the amount circulating in your body.

Though researchers are still working to understand the roots of depression and anxiety, clinical studies suggest a connection between the availability of neurotransmitters in the brain and symptoms of depression, anxiety, and other mental and physical ailments.

So when reuptake is blocked, the increased availability of these chemicals can improve mood and decrease symptoms of anxiety and depression.

Effexor begins to work as soon as it enters the body, but most patients don’t notice substantial changes to their appetite or sleep patterns until they have taken their medication for 1-2 weeks.

Within 4-6 weeks, most people report improved depression symptoms and more energy, among other effects.

Effexor and Alcohol

Alcohol affects the central nervous system, depressing brain function, and calming neurotransmitter activity.

As a result, it can counteract the potential benefits of Effexor and can make it more difficult for the drug to work properly.

Even a small amount of alcohol use can significantly increase feelings of anxiety and depression, even if it seems to help those symptoms temporarily. It can also increase the risk of adverse side effects.

Risk of overdose

In 2006, the Food and Drug Administration, along with Wyeth Pharmaceuticals, the manufacturer of Effexor, issued a letter warning healthcare professionals of overdoses among some patients taking Effexor. 

They found that those who had overdosed had consumed alcohol or other drugs in addition to Effexor.

Symptoms of overdose listed in the letter included rapid heart rate, loss of consciousness, seizure, vomiting, dizziness, and death.

If you or a loved one is experiencing severe symptoms or is experiencing suicidal thoughts, call 9-1-1 or go to your nearest emergency room for immediate medical attention. You can also get free 24/7 support from a suicide and crisis expert by calling or texting 988. If you’d prefer to chat online, you can chat with a suicide and crisis expert by visiting the Lifeline Chat.

Potential severe side effects

Like other medications, Effexor comes with a risk of side effects, some more uncomfortable than others.

Alcohol consumption while taking Effexor increases the chances of experiencing severe side effects and can make symptoms worse. 

The following symptoms are a few you might experience while mixing alcohol use and Effexor:

  • Decreased motor function and coordination 
  • Memory loss
  • Reduced attention span
  • Difficulty thinking 
  • Dizziness or vertigo
  • Delayed reactions
  • Diminished inhibition 
  • Anxiety, nervousness, or agitation 
  • Blackouts 
  • Poor decision-making
  • Falls 

Because the effects of alcohol and Effexor include significantly reduced mental and motor skills, the Food and Drug Administration says patients who mix even occasional alcohol use with their prescription drug should not drive or operate heavy machinery while under the influence.  

Alcohol and depression

Substance abuse is closely correlated with depression.

Many patients who are not receiving adequate mental health care may turn to alcohol and other substances to manage their symptoms and feel better, if only temporarily. 

Because alcohol is a depressant, it slows the neurotransmitter activity inside the brain.

As a result, people who drink may feel a slight lift when they first drink, but ultimately alcohol intake only worsens depressive symptoms.

Studies have shown that people with substance abuse disorders often have more severe, prolonged episodes of depression and anxiety—and those who are depressed have worse alcohol abuse problems, too.

Alcohol abuse is also closely associated with increased thoughts of suicide.

Common Effexor Side Effects

Effexor is not for everyone.

Like most medications, it comes with a risk of side effects for certain patients.

Most of the time, side effects are mild and tolerable.  

The most common side effects of Effexor include: 

  • Decreased appetite
  • Constipation
  • Diarrhea 
  • Dry mouth 
  • Excessive sweating
  • Headache
  • Increased blood pressure 
  • Increased fatigue
  • Insomnia
  • Nervousness, agitation, or restlessness
  • Sexual dysfunction
  • Stomach upset or nausea

In rare cases, Effexor can cause more severe side effects.

Call your doctor if you begin to suffer from any of the following symptoms while taking Effexor:

  • Blurred vision
  • Changes in your taste or salivation
  • Decreased blood pressure
  • Eye pain or swelling around the eye
  • Increased urination or difficulty urinating
  • Irregular menstrual cycles
  • Irregular or increased heartbeat
  • Mental confusion or difficulty concentrating
  • Muscle weakness
  • Teeth grinding

Effexor can increase irritability, hostility, and suicidal thoughts, particularly among teenagers and young adults.

If you or someone you know has thoughts of harming themselves or others, call 9-1-1 or go to your nearest hospital for immediate medical attention. You can also get free 24/7 support from a suicide and crisis expert by calling or texting 988. If you’d prefer to chat online, you can chat with a suicide and crisis expert by visiting the Lifeline Chat.

Effexor can cause symptoms if you stop it too suddenly without lowering your dose slowly. If you would like to stop taking Effexor, talk to your provider about a plan to wean off the medication to prevent uncomfortable side effects.

When Can I Start Drinking if I’m No Longer Taking Effexor?

When you decide to stop taking Effexor, your healthcare provider will work with you to figure out how long you will need to taper off the medication safely without putting you at increased risk for developing discontinuation syndrome, also called withdrawal.

They will also be able to advise you on the best time for you to begin drinking alcohol or taking other medications that might interfere with Effexor before it’s left your system.

Effexor is generally out of your system within 12-24 hours, but can continue to have some effects for up to three weeks.

Feeling Down?

Take our free assessment and learn about your options.

Get Started

When to See a Doctor for Depression

Feeling temporarily sad, blue, or out of sorts is a normal part of life.

But if you don’t feel like yourself for a period of more than two weeks, it may be time to consider talking to a doctor about your experience. 

Common symptoms of depression include: 

  • Experiencing weight gain or weight loss 
  • Feeling drained, lethargic, or without energy 
  • Feeling sad, hopeless, worthless, guilty, or empty
  • Feeling unable to experience or anticipate happiness or pleasure
  • Feeling uncharacteristically irritable or angry
  • Feeling uninterested in activities you once enjoyed
  • Having difficulty sleeping (insomnia) or sleeping too much 
  • Having trouble concentrating, thinking, or making decisions
  • Increased nervousness, restlessness, anxiety, or agitation
  • Physical aches and pains
  • Slowed movement or speech

If you are concerned that you might be experiencing depression, talking to your doctor is the best way to get evaluated, get treated, and get your quality of life back on track.

How K Health Can Help

Think you might need a prescription for Effexor (Venlafaxine)?

K Health has clinicians standing by 24/7 to evaluate your symptoms and determine if Effexor is right for you.

Get started with our free assessment, which will tell you in minutes if treatment could be a good fit. If yes, we’ll connect you right to a clinician who can prescribe medication and have it shipped right to your door.

Frequently Asked Questions

What happens if you drink on Effexor?

Alcohol can increase symptoms of anxiety and depression and may increase your risk of a dangerous Effexor overdose. Doctors recommend not drinking while taking Effexor or other antidepressants.

Can you drink alcohol when taking venlafaxine?

Alcohol can counteract the potential benefits of venlafaxine and can make it more difficult for the drug to work properly. It can also increase the risk of adverse side effects. For those reasons, doctors suggest patients abstain from alcohol use while taking venlafaxine (Effexor).

What will happen if I mix antidepressants with alcohol?

Antidepressants and alcohol can negatively interact with one another, reducing the efficacy of the prescription medication and increasing the risk of adverse side effects. Doctors recommend that you do not drink while taking antidepressants.

K Health articles are all written and reviewed by MDs, PhDs, NPs, or PharmDs and are for informational purposes only. This information does not constitute and should not be relied on for professional medical advice. Always talk to your doctor about the risks and benefits of any treatment.

K Health has strict sourcing guidelines and relies on peer-reviewed studies, academic research institutions, and medical associations. We avoid using tertiary references.

  • The Effects of Venlafaxine and Cognitive Behavioral Therapy Alone and Combined in the treatment of Co-Morbid Alcohol Use-Anxiety Disorders. (2013).
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3981550/

  • Label for Effexor XR. (2017).
    https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/020699s107lbl. pdf

  • Venlafaxine (Effexor). (2020).
    https://www.nami.org/About-Mental-Illness/Treatments/Mental-Health-Medications/Types-of-Medication/Venlafaxine-(Effexor)

  • Alcohol’s Damaging Effects on the Brain. (2004).
    https://pubs.niaaa.nih.gov/publications/aa63/aa63.htm

  • Selective Serotonin Reuptake Inhibitors (SSRIs) Information. (2014).
    https://www.fda.gov/drugs/information-drug-class/selective-serotonin-reuptake-inhibitors-ssris-information

  • Dietary patterns and depression risk: A meta-analysis. (2017).
    https://www.sciencedirect.com/science/article/abs/pii/S0165178117301981

  • The Benefits of Exercise for the Clinically Depressed. (2004).
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC474733/

  • Comparing Talk Therapy and Other Depression Treatments With Antidepressant Medicines. (2016).
    https://www.ncbi.nlm.nih.gov/books/NBK396564/

  • Effexor XR. (n.d.).
    https://www.accessdata.fda.gov/drugsatfda_docs/label/2005/020699s054,057lbl.pdf

  • Suicidal Behavior and Alcohol Abuse. (2010).
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2872355/

  • Tests of Causal Links Between Alcohol Abuse or Dependence and Major Depression. (2009).
    https://jamanetwork.com/journals/jamapsychiatry/article-abstract/483005

  • Alcohol Use Disorder and Depressive Disorders. (2019).
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6799954/

  • The neuroscience of depressive disorders: A brief review of the past and some considerations about the future. (2018).
    https://journals.sagepub.com/doi/full/10.1177/2398212818799269

  • Venlafaxine. (2022).
    https://clincalc.com/DrugStats/Drugs/Venlafaxine

Effexor and Alcohol: The Dangers of Mixing Drugs

The risks of mixing drugs and alcohol are dangerous, especially if there is a possible interaction between the drug and the alcohol. Interactions can negatively affect your body, especially your liver, circulation, and brain. Your social life and family life can also be hurt by addiction.  

Yet many people still mix alcohol and drugs regardless of the detrimental effects on their bodies and mental health. Effexor is a common anti-depressant and anti-anxiety medication that, when mixed with alcohol, can actually worsen the symptoms of depression and further deteriorate a person’s mental well-being.

There are various reasons not to mix Effexor and alcohol, one of them being that it can become extremely addictive very quickly, getting the user hooked on the mix, which can further damage the user’s body, mind, and lifestyle. 

The effects of this toxic combination can quickly become a dangerous combination that can create both short-term and lasting side effects that can affect all aspects of your life, including your mental health and your physical health. 

This addiction can derail lives, so it is important to understand this situation’s aspects. Please read on to understand more about the mixture of Effexor and alcohol, how to tell if you have an addiction, and the best ways to fight this addiction.

Are There Any Risks to Mixing Effexor and Alcohol?

Yes, there are many risks to mixing Effexor and alcohol in your body. The combination of these two substances can have adverse effects that can reverse the effect of Effexor on anxiety and depression, cause physical harm, and even mental health issues.

Many people with depression can turn to alcohol as a coping mechanism to help them through their depression, which is not recommended. Alcohol is a depressant, meaning that it represses the brain. Alcohol use for a long time has been connected to worsened depression and anxiety symptoms, so mixing it with an anti-depressant and anti-anxiety drug like Effexor can adversely affect your treatment plan.

Effexor is also known to have side effects that replicate the effect that alcohol has, so a combination of the two substances can increase the feeling of being under the influence.

Some signs that Effexor and alcohol are mixing and affecting your body are confusion, dizziness, slowed reflexes or reaction time, blackouts, memory loss, anxiety or nervous spells, physical coordination problems, and showing signs of being far more intoxicated for what you drank.

The biggest risk of mixing Effexor and alcohol is internal bleeding. This is because Effexor, like many other drugs in its family, can cause bleeding issues because it slows the amount of time it takes for platelets to form clots and stop bleeding. Alcohol has a blood-thinning effect, so when the two come together, a user can be at extremely high risk for the following blood problems:

  • Bruising easily
  • Blacking out
  • Worsen depression symptom
  • Bleeding problems
  • Bleeding inside the brain
  • Bleeding in the stomach
  • Nosebleeds

The mental health aspect of mixing Effexor and alcohol should not be overlooked either. People with depression or anxiety taking Effexor to treat their symptoms can experience worsened symptoms or panic attacks while mixing Effexor and alcohol. In addition, you may feel emptiness, paranoia, moodiness, irritability, a decrease in your appetite, and sadness. 

The alcohol can reverse the effect of Effexor, causing the treatment from the drug to be rendered ineffective altogether. The amount of alcohol needed to counteract Effexor varies from person to person because of many factors, including dosage, alcohol type, body weight, and when the drugs were taken.

Is It More Than an Accident? Signs That an Addiction May Be at Hand When Mixing Drugs Like Effexor and Alcohol

Due to the various risks associated with drinking alcohol and taking Effexor, it is best to avoid drinking alcohol while taking Effexor. It can quickly become a harmful addiction because the heightened effects of intoxication can become addicting to someone who is depressed or anxious.

Becoming addicted to any substance that alters your mental and physical state can quickly become an issue in your life that can affect various sectors of your world. 

An addiction to mixing Effexor and alcohol may not be apparent at first. However, you may begin to see a pattern forming in your drinking behavior, your sober behavior, and the reasons you are taking your medication. 

When people are addicted to mixing Effexor and alcohol, they will often drink every day to get to the altered state that the combination of substances can give them. The altered, intoxicated state of the two substances together is much stronger than just drinking without the drug, so users can quickly create a mental addiction to the two together.  

An addiction can also be spotted if the patient using Effexor only takes their dose of Effexor to drink and experience a more intense intoxication. People who are depressed and anxious have a higher tendency to form addictions to substances because they can numb the pain that they are feeling emotionally for some time, even if it is only for a little while before it gets worse. 

Those with a history of addiction should not mix Effexor with alcohol because it is highly likely that they can easily become addicted to drinking unhealthy amounts of alcohol, particularly while they are on their medication.

If you find yourself only taking your Effexor so that you can experience further intoxication when you drink, you may have an addiction to Effexor and alcohol. Other signs include feeling symptoms of withdrawal if you do not drink every day, blacking out or experiencing memory loss when you are drinking, feeling like alcohol is controlling your life, drinking alone, drinking during the morning or daytime, drinking to fall asleep, or drinking an unhealthy amount of alcohol daily.

If you are experiencing any of these signs, you may have an addiction to mixing alcohol and Effexor. While this may be scary to realize, it is a step in the right direction to healing and fixing your body. There are many ways that you can combat this addiction, and we are happy to provide you with several helpful ways below. 

How To Get Help If Addicted To Mixing Drugs Like Effexor And Alcohol

If you find yourself addicted to mixing drugs with alcohol, including Effexor and alcohol, you can get help to eliminate this addiction. The first and most important step is to get yourself a strong support system that is trustworthy and knows you well, inside and out. 

Gathering some family members, a partner, longtime best friend, siblings, or other trusted members of your inner circle and explaining that you are struggling with an addiction may be very daunting. However, this is one of the most important steps in recovery.

People who have strong support systems are more likely to achieve recovery and stay in recovery than those who try to face their addiction independently. Make sure that the people you pick to support you are with you 100% and will help you avoid your triggers. 

Another tip is to avoid situations where you can drink while on your medication. For example, do not go to a bar or buy alcohol if you know that you have taken your Effexor. This is difficult because it can cause you to miss out on social events or test your willpower which is fragile when you are addicted to a substance. 

Rely on your support system to help you avoid these situations and keep yourself occupied to avoid buying alcohol and drinking because you are bored, sad, or anxious. Find lifestyle habits like meditation, yoga, running, or creative outlets that allow you to express and rid yourself of boredom or intense emotions without the use of alcohol. 

Lifestyle changes can help you feel fresh and ready to begin a new chapter of your life, so do not be afraid to try some new healthy habits. Begin going to the gym, try fixing your sleep schedule, get outside, and go for walks, hikes, or runs! There are plenty of ways to get out your emotions and energy without drinking on Effexor. Plus, all of these can help your depression or anxiety as well!

Lastly, the best way to combat addiction is to go to rehab. Rehab is often considered a scary place where you can be stripped of all your freedoms, but rehab is not like that. The purpose of rehab is to help you become yourself again, rid of weights like an addiction that prevents you from living your best life. 

Relying on professionals and therapists to help you get to the roots and causes of your addictions is an extremely good way to combat addiction. You deserve care and help, so please, reach out to us to get in touch with our professionals waiting to help you get your life back. The team at our addiction treatment facility in Orange County is standing by to help.

Sources:

Ocean Recovery has strict sourcing guidelines and relies on peer-reviewed studies, academic research institutions, and medical associations for our references. We avoid using tertiary references as our sources. You can learn more about how we source our references by reading our editorial policy.

  1. Ghio L, Puppo S, Presta A. Venlafaxine and risk of upper gastrointestinal bleeding in elderly depression. Curr Drug Saf. 2012;7(5):389-390. doi:10.2174/157488612805076589
  2. The University of Michigan. The Effects of Combining Alcohol with Other Drugs | University Health Service. Accessed July 29, 2022. https://uhs.umich.edu/combine

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. nine0005

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. nine0005

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: longing, depression, apathy, decreased interest and pleasure in activities usually associated with positive emotions, gloomy and pessimistic vision of the future Sad, apathetic, anhedonic
↓SN nine0007 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 Dreary-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 nine0007 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. nine0005

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. Known antidepressants in Russia, their effect on neurons and the "formula" of the mechanism of action (4, 5, 6, 8).

nine0025 SWRR nine0025 ↑SNd
INN Group names Years of appearance Growth of neuronal activity* and its mechanism "Formula" of the drug
↑С ↑N ↑D ↑M
Imipramine TcA 50s IOZ IOZ IOZ ↑SNd
Amitriptyline 60s IOZ nine0007 IOZ IOZ ↑SNd
Clomipramine 60s IOZ IOZ IOZ ↑Snd
Pipofezin 70s IOZ IOZ IOZ ↑snd
Trazodone SMA 70s IOZ SWRR SWRR ↑snd
Maprotilin Chca 70s IOZ IOZ ↑cN
Mianserin 70s SWRR ↑sn
Pirlindol OIMAO-A 70s OIMAO-A OIMAO-A OIMAO-A ↑snd
Moclobemide 80s OIMAO-A OIMAO-A OIMAO-A ↑snd
Fluoxetine SSRI 70s IOZ nine0028 ↑С
Paroxetine 70s IOZ ↑С
Citalopram 70s IOZ nine0028 ↑С
Fluvoxamine 70s IOZ ↑С
Sertraline 80s IOS ↑С
Escitalopram 2000s IOZ ↑С
Venlafaxine SNRI 80s IOZ IOZ ↑CH
Venlafaxine** 80s IOZ IOZ IOZ
Duloxetine 80s IOZ IOZ ↑CH
Milnacipran 80s IOZ IOZ SWRR ↑snd
Mirtazapine NaSSA 80s SWRR SWRR ↑sn
Agomelatine MeA 2000s SWRR SWRR SWRR ↑ndm
Vortioxetine mma 2010s IOZ SWRR SWRR ↑snd

*- 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. nine0005

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). nine0005

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. nine0005

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). nine0005

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). nine0005

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 RR, it is not the excitation of nerve cells that is carried out, but rather the “fine tuning” of their “tone” (5, 8, 15). Therefore, "pure" SVRs are quite rare among antidepressants. nine0005

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 disintegrates, 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. nine0005

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. nine0005

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 a capital 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. nine0005

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): nine0696
  • 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) in 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 (ChsA),
      • 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). nine0005

    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". nine0005

    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

    References.

    1. depression. The treatment and management of depression in adults (updated edition). National Clinical Practice Guideline 90. https://www.nice.org.uk/guidance/cg90/evidence/full-guidance-243833293
    2. Won E, Park SC, Han KM, Sung SH, Lee HY, Paik JW, Jeon HJ, Lee MS, Shim SH, Ko YH, Lee KJ, Han C, Ham BJ, Choi J, Hwang TY, Oh KS, Hahn SW , Park YC, Lee MS J Evidence-based, pharmacological treatment guideline for depression in Korea, revised edition. Korean Med Sci. 2014 Apr;29(4):468-84. doi: 10.3346/jkms.2014.29.4.468.
    3. Bauer M., Pfennig A., Severus E., Weibrau P.S., J. Angst, Müller H.-J. Clinical guidelines of the World Federation of Societies of Biological Psychiatry for the biological therapy of unipolar depressive disorders. Part 1: Acute and ongoing treatment of unipolar depressive disorders as of 2013. Modern therapy of mental disorders 2015;4:33-39.
    4. Antidepressant therapy and other treatments for depressive disorders. Report of the CINP Working Group based on a review of the evidence. Ed. V.N. Krasnov. M., 2008. - 215 S.
    5. Stahl S.M. Stahl's essential psychopharmacology: neuroscientific basis and practical application. — 3nd ed. Cambridge University Press, 2008. - 1117P.
    6. Drobizhev M. Yu., Fedotova A. V., Kikta S. V., Antokhin E. Yu. Between depression and fibromyalgia: the fate of an antidepressant. Journal of Neurology and Psychiatry. S.S. Korsakov. 2016;116(4): 114-120. DOI:10.17116/jnevro201611641114-120.
    7. Drobizhev M.Yu., Kikta S.V., Fedotova A.V., Serdyuk O.V. Just depression. Questions and answers. LLC "Marketing Machine" M., 2013. 100C.). nine0700
    8. Shagiakhmetov F.Sh., Anokhin P.K., Shamakina I.Yu. Vortioxetine: mechanisms of multimodality and clinical efficacy. Social and Clinical Psychiatry 2016;26(4): 84-96
    9. Hrenchir T. 10 Most-Prescribed Antidepressant Medications. http://www.newsmax.com/Health/Health-Wire/most-prescribed-antidepressant-medications/2015/09/02/id/673123/
    10. Pae CU Agomelatine: a new option for treatment of depression? Expert Opin Pharmacother. 2014 Mar;15(4):443-7. doi:10.1517/14656566.2014.877889.).
    11. Azafen MB - official instructions for use. https://medi.ru/instrukciya/azafen-mb_9646/
    12. Sanchez C, Asin KE, Artigas F. Vortioxetine, a novel antidepressant with multimodal activity: review of preclinical and clinical data. Pharmacol Ther. Jan 2015;145:43-57. Doi:10.1016/j.pharmthera.2014.07.001
    13. Sharma H, Santra S, Dutta A. Triple reuptake inhibitors as potential next-generation antidepressants: a new hope? Future Medical Chem. 2015;7(17):2385-406. Doi: 10.4155/fmc.15.134. nine0700
    14. Stahl SM, Grady MM, Moret C, Briley M. SNRIs: their pharmacology, clinical efficacy, and tolerability in comparison with other classes of antidepressants. CNS Spectr. 2005;10:732-747.
    15. Valdoxan - official instructions for use. https://medi.ru/instrukciya/valdoksan_5084/.
    16. Ixel - official instructions for use. https://medi.ru/instrukciya/iksel_11711/
    17. Prozac - official instructions for use. https://medi.ru/instrukciya/prozak_10337/
    18. Saroten - official instructions for use. https://medi.ru/instrukciya/saroten_11880/
    19. Kohno T, Kimura M, Sasaki M, Obata H, Amaya F, Saito S. Milnacipran inhibits glutamatergic N-methyl-D-aspartate receptor activity in spinal dorsal horn neurons. Mol Pain. 2012 Jun 19;8:45.
    20. Brintellix (Brintellix). https://www.rlsnet.ru/tn_index_id_87791.htm4
    21. Mashkovsky M.D., Andreeva N.I., Polezhaeva A.I. Pharmacology of antidepressants - M., Medicine, 1983. -240С.
    22. Pyrazidol - official instructions for use. https://medi.ru/instrukciya/pirazidol_10633/
    23. Aurorix https://www.rlsnet.ru/tn_index_id_419.htm
    24. Bykov Yu. V., Bekker R. A., Reznikov M. K. Resistant depressions. Practical guide. - Kyiv: Medkniga, 2013. - 400 p. - ISBN 978-966-1597-14-2.
    25. Serdyuk O.V., Ovchinnikov A.A., Kutuzova N.A., Drobizhev M.Yu., Retyunsky K.Yu. The practice of using antidepressants in psychiatry (CIRKADIAN-I program). Doctor. 2010:2; 2-5.15. nine0700
    26. Drobizhev M.Yu., Ovchinnikov A.A. Kikta S.V. Mechanisms of action of antidepressants and pathogenesis of mental disorders. What are the matches? Social and Clinical Psychiatry 2017. 27(3):94-101.
    27. Krasnov VN, Kryukov VV Velaxin® (venlafaxine) in the modern therapy of depression: results of the first Russian multicenter efficacy and safety study. Psychiatry and psychopharmacotherapy. 2007;9(4), http://www.consilium-medicum.com/magazines/special/psychiatry/article/15426
    28. Mosolov S.N., Kostyukova E.G., Gorodnichev A.V., Timofeev I.V., Ladyzhensky M.Ya., Serditov O.V. Clinical efficacy and tolerability of venlafaxine (Velaxin) in the treatment of moderate and severe depression. Modern therapy of mental disorders. 2007;3:58-63.
    29. Avedisova A.S., Zakharova K.V., Kanaeva L.S., Vazagaeva T.I., Aldushin A.A. Psychiatry and psychopharmacotherapy. 2009;11(1):36-40.
    30. Avedisova A.S. Venlafaxine (velaxin): results of international trials of a third-generation antidepressant. Psychiatrist. and a psychopharmacologist. 2006; 11(2):2-7.
    31. Mosolov S.N. Clinical use of modern antidepressants. SPb., 1995.-565C.

    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.

    S. V. Kikta, Candidate of Medical Sciences, Head. Department of the Federal State Budgetary Institution "Polyclinic No. 3" of the Office of the President of the Russian Federation, Moscow

    Depression

    Russian Academy of Medical Sciences
    SCIENTIFIC CENTER FOR MENTAL HEALTH









    DEPRESSION (from hope to certainty).
    (INFORMATION FOR PATIENTS AND THEIR FAMILY MEMBERS)















    MOSCOW
    2008


    Oleichik I.V. - Candidate of Medical Sciences, Leading Researcher of the Department for the Study of Endogenous Mental Disorders and Affective States

    © 2008, Oleichik I.V. nine0897 © 2008, NTsPZ RAMS

    The vast experience accumulated by mankind and reflected in many literary works convincingly shows that sadness (sadness, spleen) has always gone side by side with people, being one of the natural human emotions. None of us is immune from failures, illness, breakups, loss of loved ones, financial collapse. Each person can face something inevitable and inevitable, when it seems that life loses its meaning, and despair becomes boundless. However, normally, sadness, sadness and melancholy, as natural reactions to traumatic events, weaken over time and the person's condition returns to normal without special treatment. The situation is different with depressions, which are mental disorders that differ from natural physiological reactions in greater intensity, special severity of experiences and persistence of manifestations. True depression rarely goes away on its own, requiring persistent, sometimes long-term treatment. nine0897 A depressive state (from the Latin word depressio - suppression, oppression) is a disease that concerns not only an individual specific sick person, but is also a significant burden of modern society, since it is spreading more and more widely in the world, causing enormous damage to the health of the population and the state. economy. And this applies to all countries, regardless of their level of social development. Every year, at least 200 million people in the world fall ill with depression. Perhaps these figures are even higher, since most victims of depression do not seek help because they are not aware of the painfulness of their condition. Scientists have calculated that almost one in five people who have reached adulthood will experience at least one episode of depression during their lifetime. nine0897 In the most general sense, a depressive state is one of the possible forms of a person's response to the impact of stress factors. In some cases, depression can be triggered by external negative influences, for example, mental trauma, excessive educational or work overload, infection or other serious somatic disease, traumatic brain injury, changes in the hormonal background, which is especially important for the female body, regular certain medications, such as hormones, blood pressure medications, alcohol or other drug abuse. In other cases, depressive states develop as a manifestation of such mental illnesses, in which the main influence is heredity or characteristics of the nervous system (cyclothymia, dysthymia, manic-depressive psychosis, schizophrenia, etc.). If, based on the description of depressive symptoms set out later in our brochure, you realize that you have indeed developed a depressive state, do not fall into despair, do not “try to control yourself”, remember that depression is not a manifestation of weakness of will or character, on the contrary, weakening of volitional qualities is one of the main symptoms of depression. Depression is a disease like rheumatism, arthritis or hypertension, it responds well to treatment, resulting in almost always a full recovery. You should not blame yourself for the occurrence of depression, it does not indicate either your fault, or your weakness, or the possible development of a more severe mental pathology. Below we will tell you about the symptoms of depression, which can be extremely diverse. nine0005

    Manifestations of depression

    Manifestations of depression can be very different. Depressive states can be manifested by a violation of almost all aspects of mental life: mood, memory, will, activity, which is expressed in the appearance of sadness, sadness, mental and muscle retardation, lasting at least 2 weeks. Depressed mood during depression can manifest itself as mild sadness, sadness, and boundless despair. Often it is accompanied by a feeling of melancholy, unbearable heaviness in the soul, with excruciating pain behind the sternum, a feeling of hopelessness, deep depression, hopelessness, helplessness, despair and uncertainty. At the same time, the patient is completely immersed in his gloomy experiences, and external events, even the most joyful ones, do not affect him, do not affect his mood, and sometimes even worsen the latter. A constant "companion" of a depressive mood is also anxiety of varying severity: from mild anxiety or tension to violent excitement, riot. Anxiety and bad mood arise at the mere thought of the need to make some kind of decision or change your plans due to suddenly changed circumstances. Anxiety can also manifest itself on the physical (bodily) level in the form of belching, intestinal cramps, loose stools, frequent urination, shortness of breath, palpitations, headaches, increased sweating, etc.
    The picture of depression is complemented by the disappearance of desires, interests, a pessimistic assessment of everything around, ideas of one's own low value and self-blame. Deficiency of vital impulses is manifested in patients with a variety of symptoms - from lethargy, physical weakness to a state of weakness, loss of energy and complete impotence. Where an important decision is required, a choice between different options, human activity is sharply hampered. Depressed people are well aware of this: they complain that insignificant everyday tasks, small issues that used to be solved almost automatically, take on the significance of complex, painful, insoluble problems. At the same time, a person feels that he began to think, act and speak slowly, notes the suppression of instincts (including food and sexual instincts), the suppression or loss of the instinct of self-preservation and the lack of the ability to enjoy life up to complete indifference to what used to be liked evoked positive emotions. nine0897 People suffering from depression often feel "stupid", "mentally retarded", "feeble-minded". Thinking in depression becomes viscous, painful, requires special efforts, one mental image is hardly forced out by the next. The sick person is oppressed by the feeling of his own intellectual insolvency, professional collapse. Depressed patients can hardly describe their painful experiences to the doctor. Only after getting out of depression, many of them say that the mood at that moment was lowered, thinking was slow, all undertakings (including treatment) seemed in vain, and the years lived were empty and useless. However, at the time of the first visit to the doctor, they could not explain this because of the almost complete absence of thoughts in their heads, “para-lich of thinking”. With depression, there are also often complaints of memory loss, which is why those suffering from it assume that they have "Alzheimer's disease", "schizophrenia", "senile dementia", which is not true. Especially often these complaints are found in depressions that develop in adolescence. nine0897 Typical story
    Aleksey, 18 years old, 1st year student of a technical university, describes his condition during depression in this way:
    “From childhood, I was fond of technology and modeling, I could read special literature for hours, won school and regional olympiads in mathematics and physics. After graduating from school, my dream came true - I brilliantly passed the exams to a prestigious university. Then it seemed to me that the whole world was at my feet, I flew with happiness "as if on wings." In September, I happily began to study. At the beginning, everything worked out well, but after 2 months I began to notice that it was becoming increasingly difficult for me to absorb what I read, I did not remember the simplest text, I could not solve problems that I used to “click like nuts”. Trying to achieve success through many hours of brainstorming or drinking a few cups of coffee led to the fact that I completely stopped thinking about anything. It seemed to me that I was "finally and irreversibly stupid." At night I sobbed, wrapped in a blanket and thought about how best to commit suicide. Luckily, I met a senior in the library and shared my problems with him. My new acquaintance said that he experienced something similar and advised me to contact the psychiatrist of the student clinic. After the examination, I was diagnosed with juvenile depression and sent for treatment to a specialized medical center. After 2 months, I felt completely healthy, returned to my studies and caught up with my classmates. nine0005

    Depression can also be accompanied by real setbacks: for example, a decrease in academic performance, the quality of work, family conflicts, sexual disorders and their consequences for personal relationships. As a rule, the significance of these failures is exaggerated and as a result there is a false sense of the irreparability of what happened, "the collapse of all hopes. "
    Another generally recognized danger of depression is the possibility of suicidal thoughts, which often lead to suicide attempts. The condition of a person suffering from depression can suddenly deteriorate sharply, which happens either without clear external causes, or under the influence of traumatic situations, unpleasant news. It is during these hours, and sometimes even minutes, that a fatal decision is made. Factors that increase the risk of suicide in depression are past suicide attempts, the severity and duration of the depressive state, the presence of anxiety in its structure, prolonged insomnia, loneliness or alienation in the family, alcohol and drug abuse, loss of work and a sharp change in lifestyle, as well as relatives commit suicide. nine0897 Typical story
    Eugene E., 35 years old, leading manager of the company.
    Almost all my life, my career went “on the ascending”, the goals set were clear, clear and achievable. The marriage was extremely harmonious, two beloved children grew up. He devoted almost all the time to the affairs of the company, occasionally, once every 1-2 months, he escaped with his family out of town, to the country. He often lacked sleep, stayed late at work, took home assignments, and was deeply worried about the affairs of the company. Gradually, irritability, fatigue, insomnia, difficulty concentrating appeared, more and more often he suffered a “fiasco” in intimate life. Thoughts appeared that life was lived in vain, that it is a "chain of tragic mistakes" that led to a dead end. He began to believe that the choice of work, friends, family was wrong, for which now "retribution has come." Analyzing the past years for a long time, he found more and more evidence and examples of his "duplicity, hypocrisy, insincerity, etc." I realized that the only way to solve all problems is to voluntarily leave this life. At the same time, he believed that by this act he would free the family from the “burden”, “loser”, “loser”. I decided, having locked myself in the garage, to get poisoned by the exhaust gases of the car. However, by chance, in a semi-conscious state, he was discovered by an employee of a garage cooperative. He explained what happened as an "accident". The thought of leaving life did not leave the patient. I decided to shoot myself with a gas pistol, which I had long ago acquired for self-defense. After a shot in the mouth, in a serious condition, he was taken to the Research Institute. Sklifasovsky, from where he was discharged a week later. The alarmed wife, suspecting something was wrong, decided to consult her husband with a psychiatrist. He was admitted to the clinic. He agreed to this only out of respect for family relations, he himself believed that treatment by psychiatrists was completely useless, because. his situation is hopeless and no medicines will help here, but will only "stupefy" his psyche. However, after two weeks of taking a modern antidepressant, the patient's point of view changed. Everything began to look not so bleak and hopeless, interest in work and life in general returned, I began to feel more cheerful, more energetic, interest in intimate life appeared. He took work to the clinic, called up colleagues. After two months of treatment, he fully returned to his usual life. With bewilderment, he recalled his thoughts about insolvency, the collapse of life, suicide. He took the drug prophylactically for about six months, then, on the recommendation of a doctor, he gradually reduced the dose and stopped taking it. Over the next two years, the condition remained stable, career growth continued, another child was born. nine0005

    Depression is also characterized by sleep disturbances, which occur in approximately 80% of patients. As a rule, these are early awakenings with the inability to fall asleep, lack of a sense of sleep, difficulty falling asleep. These disorders, as well as restless sleep with unpleasant dreams, are often the very first symptoms of incipient depression.
    If the depression is not deep, it is sometimes difficult to recognize it. This is due to the fact that people are ashamed to tell others about their problems, to admit to "weaknesses". Quite often, especially in Russia, depressive states are masked by alcohol abuse (“vodka heals”). In addition, often patients suffering from depression, in order to "shake themselves up", "throw into all serious", engage in casual sex, are fond of gambling or extreme sports, leave to serve on a contract in "hot spots", lead an idle lifestyle with constant attendance at entertainment events. Surrounding people, relatives who do not have psychiatric knowledge, often accuse them of debauchery, drunkenness, riotous lifestyle, parasitism. Meanwhile, this behavior is a kind of “cry for help”, an attempt to fill the spiritual emptiness brought by depression with new acquaintances and impressions. nine0897 Depressive conditions can occur in shallow forms that are easily treatable, but at least a third of depressions are more severe. Such depressions are characterized by:
    - ideas of guilt, sometimes reaching the degree of delirium, i.e. unshakable conviction in their sinfulness, low value (patients consider themselves great sinners, believe that because of them all relatives and Mankind will die, that they are “moral freaks” from birth, supposedly deprived of the foundations of morality and a sense of empathy for other people that they have no place on earth They find in their past numerous "confirmations" of what has been said above, they believe that the doctor and other patients are aware of these transgressions and express contempt and indignation with their facial expressions and gestures, but in the words “they hide, deny the obvious. ” Both the patients themselves and their relatives must remember this in order to prevent the impending threat in time: remove all firearms, piercing and cutting objects, ropes, potent drugs and poisonous close household fluids, close windows or shutters, do not let the patient go anywhere alone.If these ideas become persistent and cannot be dissuaded, it is urgent to seek advice from a psychiatrist. neurological institution or call a psychiatrist at home. nine0897 - mood swings during the day: in typical cases, the patient, waking up, immediately feels longing. Sometimes, even before full awakening, through a dream he experiences a painful premonition of a heavy coming morning. In the evening, the state of health improves somewhat.
    - the patient may experience a feeling of unmotivated hostility towards relatives, friends, constant internal discontent and irritation, which makes him unbearable for the family.
    - in a number of people suffering from depression, constant doubts, fear for the health and well-being of loved ones, obsessive ones, come to the fore. arising against the will, ideas about the misfortunes and troubles of family members. nine0005

    Typical story
    Dmitry Petrovich, 58 years old, teacher.
    “After minor troubles at work, I began to feel incomprehensible anxiety and agitation. Unpleasant thoughts came into my head that I did something wrong at work, because of which I double-checked everything many times and went home later than everyone else. But even at home, the anxiety did not let go: as soon as the daughter or wife lingered for at least half an hour, terrible pictures of traffic accidents or violence were drawn in the imagination. I fell asleep only in the morning, got up broken and felt sleepy all day. I took Valerian, Corvalol, but it practically did not help. At work, they hinted whether I should take a vacation. Friends advised me to consult a neuropathologist, but he did not find his pathology and sent me to a psychiatrist. I was diagnosed with anxiety depression. After a course of outpatient treatment, I completely recovered. ” nine0005

    - in many cases, depression is characterized by unpleasant sensations in the body, disturbances in the activity of internal organs in the absence of objective signs of a true somatic, i.e. non-mental illness. At the same time, many patients constantly report pain, internal discomfort. Some complain of headaches, pains in the stomach, joints, lower back, others - on disorders in the intestines: constipation, indigestion, irritation of the colon, others pay attention to a decrease in sexual desire and potency. In women, menstruation often becomes painful and irregular. Approximately 50% of depressed people at the doctor's office complain of such physical ailments, without mentioning the depressed mood or state of mind underlying the depression. Experiencing chronic pain or other unpleasant sensations in the body, patients may not realize that they are suffering from depression, even with severe melancholy, considering the latter a reaction to painful bodily discomfort. nine0897 - some patients are convinced that they have some rare and difficult to diagnose disease and insist on numerous examinations in general medical institutions. Doctors call this condition masked (hidden) depression, in which a person may experience pain in the head, in the limbs, behind the sternum, in the abdomen and in any other parts of the body, he may be haunted by anxious fears, he may suffer from insomnia or, on the contrary, too much sleep. nine0897 - Patients may experience disturbances in the cardiovascular system, skin itching or lack of appetite. All of these are manifestations of depression.
    - the pathological sensations that patients experience during such depressions are quite real, painful, but they are the result of a special mental state, and not an internal disease. It must be remembered that the frequency of latent depressions exceeds the number of explicit ones many times over.
    - with such depression, patients, as a rule, also have a changed attitude towards food: they can go without food for a long time and not feel hungry, and sitting down at the table, eat only 1-2 spoons - they have neither strength nor desire for more . nine0897 - a sign of depression can serve as a weight loss of more than 5 kg. within a month. In some people, especially women, the appetite for depression, on the contrary, increases, sometimes reaching the level of excruciating hunger, accompanied by severe weakness and pain in the epigastric region. In some cases, food is taken in excess due to an increased craving for sweets or attempts to distract oneself from painful thoughts by frequent eating.
    Thus, we see that depression is a disease with many different manifestations that do not go away on their own, requiring special, sometimes long-term, medical intervention. Therefore, when the symptoms described above appear, it is necessary to seek help from a psychiatrist who will prescribe and monitor antidepressant treatment. nine0005

    TREATMENT OF DEPRESSIVE DISORDERS


    To date, it can be argued that the vast majority of cases of depression respond well to treatment. According to modern views, effective treatment of depression consists of a combination of pharmacotherapy, psychotherapy and, if necessary, other types of treatment. At the same time, the main role in therapy, of course, belongs to antidepressants - drugs specially designed for the treatment of various types of depression. nine0897 The creation of antidepressants is based on the discovery of scientists that depression develops as a result of a violation of the mechanism of biochemical transmission of nerve impulses in the brain regions responsible for mood, behavior, response to stress, sleep and wakefulness, appetite and some other functions. To ensure the coordination of the work of all these functional divisions, the brain sends special "commands" to them in the form of chemical impulses transmitted from the processes of one nerve cell (neuron) to the processes of another. This transmission is carried out with the help of chemical mediators (neurotransmitters), which, after transmitting a signal, partially return to the original neuron. This process is called neurotransmitter reuptake. Thanks to him, the number of mediators in the microscopic space between the processes of neurons (in the so-called synaptic cleft) decreases, which means that the necessary signals are transmitted worse. Numerous studies have shown that mediators of various structures, in particular, norepinephrine and serotonin, are involved in the transmission of signals that ensure the normal functioning of the nervous system. The first of them has a general activating effect, maintains the level of wakefulness of the body and takes part in the formation of adaptive reactions, and the second has the main antidepressant effect, controls impulsive actions, anxiety, aggressiveness, sexual behavior, falling asleep, feeling of pain, therefore serotonin is called sometimes a "good mood" regulator. A decrease in the number of mediators in the synaptic cleft causes symptoms of depression, while an increase, on the contrary, prevents their appearance. The ability of some drugs in one way or another to increase the concentration of mediators in the synaptic cleft allows them to be used as antidepressants. nine0897 Now antidepressants are used in Russia, which can be conditionally divided into 4 generations according to the time of creation.
    The first antidepressants to find wide clinical use were tricyclic drugs: amitriptyline and imipramine. They have a fairly powerful effect on most depressive states by blocking the reuptake of both norepinephrine and serotonin. However, the real clinical effect of these drugs is significantly offset by their undesirable side effects, which drastically reduce the quality of life of patients during treatment. Side effects of tricyclic antidepressants arise due to the nonspecificity of their effect on receptor structures. Acting in addition to the serotonin and norepinephrine system and other neurotransmitters (acetylcholine, histamine, dopamine), these antidepressants cause side effects such as urinary retention, dry mucous membranes, constipation, palpitations, fluctuations in blood pressure, confusion, tremor, sexual dysfunction. functions, weight gain. In such cases, it is necessary to prescribe other drugs to correct side effects or reduce the therapeutic dose of drugs, which naturally affects the effectiveness of the antidepressant action. It has been observed that up to 50% of patients refuse to take tricyclic antidepressants due to severe side effects. For the same reason, physicians are less likely to prescribe these drugs to patients on an outpatient basis. nine0897 The situation was somewhat improved by the introduction into practice of drugs of the second generation - tetracyclic antidepressants, which, along with the ability to block the reuptake of norepinephrine and serotonin, could also affect some other receptors. Being analogues of tricyclic compounds, these drugs have antidepressant activity comparable to them, but unlike their predecessors, they are safer, since they cause unwanted side effects much less often. In addition to the antidepressant, mianserin (lerivon) has a clear sedative, anti-anxiety and hypnotic effect. Maprotiline (Ludiamil) has a mild balanced antidepressant effect. In general, these drugs are able to cure mild to moderate depression, but are ineffective in patients with severe depression. nine0897 To date, antidepressants of the 3rd generation, such as fluoxetine (Prozac), fluvoxamine (Fevarin), paroxetine (Paxil), sertraline (Zoloft), citalopram (Cipralex) and some other drugs that selectively (selectively) affect the serotonin metabolism system, have received widespread recognition today. , preventing its reuptake in the synaptic cleft. Based on the mechanism of action, these antidepressants are combined into a group of selective serotonin reuptake inhibitors. In addition to treating depression, they are used to correct eating disorders, level panic disorders, so-called social phobias, various obsessive-compulsive disorders and chronic pain symptoms. These drugs have gained popularity due to the possibility of a once-daily intake, concomitant anti-anxiety effect, the presence of a psychostimulant component and a small number of side effects. In addition, they have low toxicity and are well tolerated by elderly patients. However, some researchers note their lack of effectiveness in the treatment of severe forms of depressive states, probably associated with selective activity in relation to only one neurotransmitter - serotonin. It should be noted that in recent years, some American scientists have associated the use of these drugs with an increased risk of suicide, which, however, is not proven. nine0897 Considering the high frequency of side effects in some of the above drugs and the insufficient antidepressant activity in others, psychopharmacologists have taken the path of developing more effective antidepressants - IV generation drugs that selectively block the reuptake of both serotonin and noradrenaline, without affecting other mediators. system and with minor side effects. Currently, 3 drugs meet these requirements: milnacipran (Ixel), duloxetine (Cymbalta) and venlafaxine (Effexor). Their antidepressant activity in the treatment of patients with severe and moderate depression has been confirmed in a number of specially conducted studies, which at the same time showed that these drugs are well tolerated. nine0897 It should be noted that antidepressants of plant origin (negrustin, gelarium hypericum, deprim, etc. ) can be effective in mild depressive states, but there are no reliable data guaranteeing their effectiveness. The opinion of a number of doctors that all depression can be treated with herbs or, say, acupuncture, should be recognized as unfounded.
    For extremely severe depressions that do not improve despite the use of the most powerful antidepressants, electroconvulsive therapy (ECT) can be effective, but this situation is extremely rare and requires careful justification by the commission of doctors and the consent of the patient. nine0897 An important additional role in antidepressant therapy, especially with concomitant anxiety, is played by tranquilizers - anti-anxiety drugs, such as Xanax, phenazepam, diazepam, nitrazepam, atarax, etc. Drugs that can, when taken systematically, prevent mood swings in various depressive disorders include so-called mood stabilizers or mood stabilizers - lithium preparations, carbamazepine, valproic acid salts, lamotrigine, topiramate. With their systematic intake in most patients, the clinical manifestations of depression either completely disappear or become rare and mild, requiring no hospitalization and not significantly affecting the ability to work. nine0897 Antipsychotics play a significant role in the treatment of certain forms of depression. These include both traditional drugs - fluanxol, triftazin, eglonil, teralen, neuleptil, sonapax, and atypical antipsychotics that are gaining more and more recognition among doctors: seroquel, solian, zeldox, rispolept, abilify, serdolect and others.
    In drug therapy of depressive conditions, an unconventional, strictly individual approach is used, with the obligatory provision of fruitful cooperation between the patient and the doctor. Otherwise, there may be a violation of medical recommendations regarding doses and regimens for taking medications. The patient's faith in the possibility of recovery, the absence of prejudice against the "harm" caused by psychotropic drugs, the systematic observance of the prescriptions prescribed by the doctor largely contribute to the achievement of therapeutic success. nine0897 Drug treatment of depression takes time. You should not expect a complete cure already in the first days of taking the drug. It must be remembered that all modern antidepressants begin to act on depressive symptoms no earlier than 1-2 weeks after the start of treatment. Cancellation of an antidepressant, as well as its appointment, should be carried out only by a doctor. Cancellation is usually made no earlier than 6 months from the normalization of the mental state. Even after the complete disappearance of all symptoms of depression, do not rush to stop taking the drug yourself, as there is a risk of an exacerbation of the disease. Therefore, doctors recommend continuing to take the antidepressant for a certain period of time. A common mistake is the premature withdrawal of drugs soon after a significant improvement in the condition or due to "forgetfulness". To avoid this, try to include the drug in the list of daily urgent matters - for example, store it in the bathroom and take it after hygiene procedures. When planning a trip, calculate exactly how many tablets you need for the entire period of absence from home.

    Learn more