Monoamine oxidase inhibitors (MAO) are biological substances that, by reducing the rate of chemical reactions of the enzyme monoamine oxidase, prevent the destruction of various monoamines (this group includes serotonin, norepinephrine, dopamine, phenylethylamine, tryptamine and octamine). This increases the concentration of the active element between two neurons or between a neuron and an effector molecule (a particle that binds to proteins to increase biological activity).
IN medical purposes MAOIs are used as antidepressants and sometimes to treat Parkinson's disease and narcolepsy attacks - pathological condition nervous system, which causes drowsiness and a sudden “attack” of sleep.
Based on their pharmacological properties, MAOIs are divided into:
So, let's take a brief look at each group and learn about the active ingredients, properties and trade names.
Table 1
| № | Active ingredient | Brief description | Trade name |
| 1. | Iproniazid | Has a pronounced hepatotoxic effect. In this regard, it is used and prescribed very rarely. Can be used for no more than 2 weeks. | "Iprazide" |
| 2. | Nialamid | The chemical structure is similar to iproniazid, but has a more gentle toxic effect. Improves general condition and helps recover from depression. Appearance therapeutic effect observed after 1-2 weeks. | "Nialamide" |
| 3. | Isocarboxazid | Activates certain natural components in the brain to maintain mental balance. | "Marplan" |
| 4. | Phenelzine | Prescribed to reduce depressive syndrome. Reduces restlessness and anxiety. | "Nardil" |
| 5. | Tranylcypromine | Recommended during treatment mental illness, which develop against the background depressive states. Has a stimulating effect. Can be metabolized to amphetamine. | "Parnat" |
Table 2
| № | Active ingredient | Brief description | Trade name |
| 1. | Moclobemide | Prescribed for depression and social phobia. Blocks the destruction of norepinephrine and serotonin. | "Aurorix" |
| 2. | Pyrazidol | Shows therapeutic effects in patients with apathetic attacks and depressive disorders. It is also prescribed for agitation – strong emotional arousal, which is manifested by feelings of anxiety and fear. The drug is widely used in psychiatric practice. | "Pirlindol" |
| 3. | Bethol | Indications: depressive syndrome, anxiety and delusional disorders, hallucinations. For alcoholism: asthenosubdepressive syndrome. | "Befol" |
| 4. | Incazan | Pharmacological properties are similar to pyrazidol. Activates norepinephrine and serotonin in the central nervous system. Widely used in mental disorders: schizophrenia, manic-depressive psychosis, sudden mood swings, and also to improve blood circulation in the brain. When treating alcoholism, the drug is recommended to be taken during the period of remission. | "Metralindole" |
| 5. | Beta-carboline derivatives | β-Carboline base is main structure for many alkaloids that are isolated from plant components. Medicines containing this substance can be used in the fight against alcoholism and depression. Derivatives are also used in antiviral, antibacterial and antitumor therapy. In addition, active compounds help combat rheumatoid arthritis, osteoarthritis, bronchial asthma. | "Garman", "Garmin" |
Table 3
| № | Active ingredient | Brief description | Trade name |
| 1. | Selegilin | Pharmacological group: antiparkinsonian drug. Selegin is involved in dopamine metabolism (inhibits). Thus, there is an increase in the neurotransmitter in various departments brain. The time it takes for the enzyme to recover is 2 weeks. | "Yumex", "Stillin" |
| 2. | Rasagiline | Antiparkinsonian drug. Recommended for the treatment of true Parkinson's disease, as well as in the presence of symptoms that indicate this pathology. The product has an effect due to the accumulation of special natural compounds in the brain. The drug is taken according to the schedule; sudden withdrawal or sharp increase in dose can lead to serious consequences. | "Azilect" |
| 3. | Pargilin | Antidepressant, recommended for mental and nervous disorders. When combined with the drug Methyclothiazide, it may lower blood pressure. | "Pargilin" |
Surely each of us has been exposed. Thanks to drastic life changes, human body as if it develops “mental immunity”, thereby increasing its regenerative abilities. Thus, before using psychotropic drugs (monoamine oxidase inhibitors), you should find out whether they are really necessary to survive depression or stress.
According to their pharmacological properties, monoamine oxidase inhibitors are divided into reversible and irreversible, selective and non-selective.
Selective MAOIs inhibit primarily one type of MAO, while non-selective MAOIs inhibit both types.
Irreversible MAOIs interact with monoamine oxidase, forming chemical bonds with it. The enzyme then becomes unable to perform its functions and is metabolized, and instead the body synthesizes a new one, which usually takes about two weeks.
Reversible MAOIs bind to the active site of the enzyme and form a relatively stable complex with it. This complex gradually dissociates, releasing the MAOI, which then enters the blood and is excreted from the body, leaving the enzyme intact.
Strictly speaking, it is not entirely correct to classify tranylcypramine into this group, since it is a reversible inhibitor, however, it may take up to 30 days to dissociate its complex with the enzyme and completely remove it from the body. In addition, it exhibits some selectivity towards MAO-A.
There is no need to follow a diet when taking reversible MAOIs.
MAOIs, by blocking the destruction of monoamines by monoamine oxidase, increase the content of one or more mediator monoamines (norepinephrine, serotonin, dopamine, phenylethylamine, etc.) in the synaptic cleft and enhance monoaminergic (monoamine-mediated) transmission nerve impulses(neurotransmission). For this reason, for medical purposes, these substances are used mainly as antidepressants. MAO-Bs are also used in the treatment of parkinsonism and narcolepsy.
The combination of monoamine oxidase inhibitors with substances that affect monoamine metabolism can lead to an unpredictable increase in their effect and be life-threatening.
List of drugs to avoid:
A significant danger when using MAOIs is the consumption of foods containing various monoamines and their metabolic precursors. Primarily tyramine and its metabolic precursor amino acid tyrosine, as well as tryptophan. Tyramine, like amphetamine psychostimulants, causes the release of catecholamines from nerve endings. Taking it together with MAOIs is fraught with hypertensive crisis. Tryptophan is used by the body to produce serotonin, and eating foods containing large amounts of it can lead to serotonin syndrome.
Foods to avoid:
Products to be treated with caution:
Irreversible, non-selective MAOIs require avoidance of the above-mentioned substances and products during use and for two weeks after use. In the case of reversible MAOIs, dietary restrictions are usually less stringent and apply to the time the substance remains in the body (no more than a day). You should also refrain from using drugs and surfactants listed in the list together with reversible MAOIs until they are completely eliminated.
Most tryptamines are good substrates for MAO-A. DMT and 5-MeO-DMT, when taken orally, are metabolized by it in the gastrointestinal tract and liver, without having time to enter the blood, so they are inactive when taken orally. 4-Hydroxy-DMT (psilocin) is less susceptible to degradation by MAO because its hydroxyl group at the 4th position makes it difficult to bind to the active site of the enzyme, making it orally active. Alkyl substituents on the amino group that are larger than methyl (ethyl, propyl, cyclopropyl, isopropyl, allyl, etc.) also hinder the metabolism of tryptamines with such substituents through MAO, therefore all such tryptamines are active when taken orally. Alpha-methyl in the molecules of tryptamines such as AMT and 5-MeO-AMT significantly impedes their metabolism by MAO, and turns them, de facto, from substrates into weak inhibitors of this enzyme.
Inhibition of peripheral MAO-A - in the gastrointestinal tract and liver by strong MAOIs allows tryptamines such as DMT and 5-MeO-DMT to be orally active, as well as enhance and prolong the effects of other tryptamines such as psilocin and DET. On the other side, long-term use MAOIs as antidepressants significantly reduce the effects of psychedelics. This occurs, obviously, due to changes in the monoaminergic systems of the brain caused by increased levels of monoamines. The nature of this phenomenon currently remains unclear, and is not explained by a simple loss of sensitivity of the serotonin receptors with which psychedelics interact.
Thus, taking MAOIs with tryptamines or immediately before using tryptamines prolongs, and in some cases enhances, the effects of the latter, and also makes it possible to use tryptamines such as DMT orally. This is the basis of the principle of action of ayahuasca, and similar mixtures, including the so-called pharmacohoasca, in which pure DMT is used instead of plant components, and both traditional Banisteriopsis Caapi and Peganum Harmala seeds, or their extracts, can be used as MAOIs. or even moclobemide (Aurorix). At the same time, taking an irreversible MAOI a few days before taking a psychedelic will weaken its effect. The same thing will happen with long-term use of both irreversible and reversible MAOIs before taking a psychedelic.
Taking 5-MeO-DMT with an MAOI is not safe. Many people note strong and unpleasant side effects of this combination, including serotonin syndrome. In addition, such an experience is psychologically extremely difficult for many people, and can pose serious risks to mental health.
Tryptamines that significantly increase monoamine levels in the synaptic cleft, such as AMT, 5-MeO-AMT and AET, can be lethal when combined with MAOIs. There is some concern about the safety of using MAOIs with tryptamines such as DPT.
The metabolism of LSD is currently not well understood, but MAO does not appear to be involved in any way. However, according to some participants, when used in conjunction with harmala, its effects are enhanced and prolonged. The same applies to other ergolines.
MAO plays a minor role, or even practically does not participate in the metabolism of phenylethylamine psychedelics. Therefore, taking MAOIs together with them is devoid of practical meaning. Although, according to some users, both harmala and moclobemide enhance the effect of some PEAs, such as 2C-B. In most cases, taking MAOIs with phenylethylamine psychedelics does not pose any serious health risks. However, the use of MAOIs with sulfur-containing phenylethylamines such as 2C-T-7 and Aleph-7 should be avoided due to their controversial and poorly studied effects on brain monoamine levels and high toxicity. Combinations of MAOIs with TMA-6 and TMA-2 may also be unsafe.
| Antidepressants ( N06A) | |
|---|---|
| Non-selective monoamine reuptake inhibitors |
Desipramine * Imipramine Clomipramine Opipramol * Trimipramine * Lofepramine * Dibenzepine * Amitriptyline Nortriptyline * Protriptyline Doxepin * Iprindol Melitracene Butriptyline * Dosuleptin Amoxapine Dimethacrine Amineptine Maprotiline Quinupramine |
| Selective serotonin reuptake inhibitors |
Zimeldine Fluoxetine Citalopram Paroxetine Sertraline Alaproclat Fluvoxamine Etoperidone Escitalopram Trazodone |
| Non-selective monoamine oxidase inhibitors |
Isocarboxazid Nialamide Phenelzine Tranylcypromine Iproniazid * Iprocloside |
| Monoamine oxidase type A inhibitors | Moclobemide Toloxatone Pyrazidol |
| Other antidepressants | Oxytriptan Tryptophan Mianserin |
Depression is not just “I have today Bad mood" It's dangerous and serious condition, which is associated with an imbalance of certain chemical compounds in the brain. MAO inhibitors are used to normalize this imbalance, as well as to treat Parkinson's disease. We offer a list of such drugs and their brief characteristics.
These drugs are intended to treat severe depression, in which other medications do not give the desired result. They provide a long-lasting pharmacological effect, which lasts from 1 to 2 weeks after the end of therapy, but have many contraindications and can provoke quite serious adverse reactions. Therefore, their use can be considered a last resort. Such medications are prescribed by a psychiatrist or neurologist.
Such drugs are used extremely rarely today, since they do not combine well with other drugs, are toxic (very harmful to the liver), and are very diverse side effects. In addition, their use requires the patient to follow a certain diet: cheese, coffee, wine, beer, cream, and smoked meats must be excluded from the diet. They are prescribed to eliminate neurotic, involutional, cyclomatic depression and treat chronic alcohol dependence.
The list of irreversible MAO inhibitors with non-selective action is quite wide. Here's what they include:
Important! Although these drugs are sold without a prescription, they are not the first choice in the treatment of depression. Such drugs can cause clinical deterioration, fatal side effects, and increase the risk of suicide. Thus, they should only be taken with the doctor's permission.
With the help of drugs included in this group, only one pathology is treated - Parkinson's disease. Since they are highly specialized, the list of these MAO inhibitors is not too long. Here are the trade names of such drugs under which they are sold in the pharmacy chain:
Important! All of these drugs should not be combined with serotonic drugs, including fluoxetine.
Such drugs belong to the second generation of MAO inhibitors. They help alleviate the condition of those who suffer from asthenic, melancholic syndrome and asthenodynamic disorders. They have several advantages over their predecessors: their use is not accompanied by dangerous side effects, the patient will not have to adhere to dietary restrictions.
This group of MAO inhibitors is the most extensive. The list of medications includes, in particular:
Important! All MAO inhibitors are prohibited for pregnant and lactating women.
Hi all! Today you will learn a terrible spell in medicine! It is so strong that it can kill a person, so this information is more of an educational nature. She is interesting and beautiful, like some kind of bizarre poisonous snake. We will not describe how to apply this knowledge in real life, they are dangerous and should only be used by the best specialists in the field of biology.
Agree, sometimes you want to read something unusual, in the “” style, with the goal of “finding out” and, perhaps, telling your friends. You can check it out, after graduation there will be something to talk about, or at least think about. Even the title of the topic: “MAO inhibitors” sounds pretty good.
Activators and inhibitors are the 2 main directions in the regulation of biological processes. Activators and inhibitors are often compounds, and in biology there are no 100% activating or inhibitory substances. While we gain a big advantage in one thing, we lose in another.
To make it easier to understand, remember your feelings from the games. When you “win”, processes associated with , and serotonin are activated, but, for example, GABA is suppressed. Feeling of pleasure and happiness, and suppression of calm and prudence. 
So, when we activate something, we suppress something and vice versa. It's a balance.
Inhibitors are suppressors/destroyers.
Before clarifying this term, it is important to recall the basics of synaptic transmission of neurotransmitters, when one neuron releases transmitters into the synaptic cleft, into the space from where they are absorbed by the 2nd neuron. While the transmitters are in neither the first nor the second neuron, in the middle, the smart body selects their excess with the help of the enzyme monoamine oxidase.
This word just sounds scary, let's break it down into parts: “mono” means one, “amine” implies an amine group, 1 nitrogen atom, 2 hydrogen. Oxidase comes from the word “oxide” - oxygen, redox reactions.
So it turns out that monoamine oxidase, that is, MAO, is a substance that oxidizes and destroys monoamines. And monoamines are neurotransmitters. 
- monoamine oxidase, which destroys transmitters such as dopamine, norepinephrine and serotonin from the synaptic cleft and sends the excess back to the first neuron, for re-accumulation in vesicles and “shooting” into the space to the second neuron. Creates a circulation so that our lazy body does not have to re-create neurotransmitters from amino acids.
Imagine how you fill a mug with water, and the water begins to overflow and flow down the walls. In our body, “extra water” does not spread, but returns back to the container from where you poured the water into the mug. In this context, “water” refers to neurotransmitters.
MAO-A is found in the outer membrane of mitochondria in cells.
MAO-B– monoamine oxidase, also located in mitochondria and destroys dopamine and other less significant, significant mediators. For reference, more than a hundred different neurotransmitters are already known.
Monoamine oxidase inhibition refers to the process whereby the suppressors of monoamines are “inhibited.” As we remember from mathematics, minus by minus is a plus. Thus, similar processes occur in cells. By inhibiting monoamine oxidase, we destroy something that was meant to destroy something else. 
Monoamine oxidase inhibitors- these are strong substances that can change a person beyond recognition, in particular, his behavior. The stronger these inhibitors, these substances, the stronger the changes. A situation may arise when drinking coffee, or, even worse, taking nootropics, will cause such rapid expression and the production of mediators that the effect of strong psychostimulant drugs will be obtained. Well, we understand how a person’s behavior changes under drugs.
Inhibitors are also divided into more or less “strong”; it is not a binary system where inhibition either occurs or not. It's more of a scale where 0 is no inhibition, and 100 is a conditional 100%. A fatal outcome is possible for a person when taking “strong” substances that act on neurotransmitters and “strong” MAO inhibitors. 
In science, they are usually classified into reversible and irreversible, selective and non-selective.
Selective act on a specific monoamine oxidase A or B. By blocking the destruction of certain substances in our brain. Non-selective ones block both types.
Irreversible practically destroy MAO, forcing the body to launch a new creation of the enzyme, which takes about 2 weeks. Reversible can be said to bind MAO for a certain time.
Now such a terrible term as an irreversible non-selective monoamine oxidase inhibitor is becoming more or less clear to you. But non-selective ones are now almost never used.
Regarding application, then many antidepressants have selective reversible MAOIs. They act on serotonin and dopamine, temporarily increasing their levels in the synaptic cleft. Application areas of irreversible are many diseases that are long-term or chronic, e.g. chronic alcoholism, Parkinson's disease.
Dangerous, they are also strong, google “list of MAO inhibitors” and you will get a bunch of drug names. We will consider those MAOIs whose effect is not so pronounced: Rhodiola Rosea, Yohimbine, Green tea, Nutmeg, Tobacco, Tyramine.
Crime may be genetically based. There are statistically significant correlations between crime rates and MAO activity (http://www.ncbi.nlm.nih.gov/pubmed/7792602). A special case of this correlation is Brunner's syndrome. 
This syndrome was first noted in the 90s. in one American family, where 14 men had the MAO-A mutation. This mutation caused their bodies to produce more dopamine, norepinephrine and serotonin. In effect, this meant partial inhibition of monoamine oxidase throughout life. These people had below average IQs and were prone to aggressive and impulsive behavior. Moreover, it has been proven that children with weak MAO activity are more prone to antisocial behavior in adulthood (Frazzetto G, Di Lorenzo G, Carola V).
Hence the assumption that genetics, MAO mutations, are involved in low IQ and aggressive, criminal behavior.
Has a connection with increased activity MAO. It was found that in depression, MAO activity is increased by 34% on average (PMID 17088501).
When taking antidepressants based on MAOIs, and, in general, when taking MAOIs, special attention is paid to the selection proper nutrition. If in ordinary life While eating fish, meat, and dairy products is considered beneficial, while taking an MAOI course, all of this can cause side effects. These foods are rich in beneficial amino acids, from which mediators are synthesized, so if you eat a lot of fish, you will get a lot of tryptophan. And from it serotonin will be produced, there will be a lot of serotonin (after all, it is not destroyed by MAO). A person will get serotonin syndrome: nausea, dizziness, etc. That’s why they say that consuming medicinal MAOIs and nootropics that pump, for example, dopamine, will result in hyperstimulation with all that it implies. 
MAOIs interact mainly with catecholamines and serotonin; they do not inhibit, say, . It has its own “MAO”, called acetylcholine transferase.
— Monoamine oxidase is a substance that can determine not only our behavior and lifestyle, but also our character type.
— The body benefits from normal, average values of MAO activity. If it is higher than normal, you will be prone to depression; if it is lower, you will have lower IQ and hot temper.
—MAO inhibitors increase levels of norepinephrine, dopamine and serotonin. Examples: yohimbine, rhodiola, green tea.
Well, I hope you liked the information! See you soon!
Monoamine oxidase inhibitors (MAOIs) are chemicals, which inhibit the activity of monoamine oxidase enzymes. They have long been used as drugs to treat depression. These substances are especially effective in treating atypical depression. These drugs are also used to treat Parkinson's disease and some other diseases. Because of potentially dangerous dietary and drug interactions, monoamine oxidase inhibitors have historically been used as a last resort, used only when other antidepressants (eg, selective serotonin reuptake inhibitors and tricyclic antidepressants) have failed. New MAO research shows that much of the concern about dangerous dietary side effects stems from misconceptions and misinformation, and that despite the proven effectiveness of drugs in this class, they are not used often enough in medicine. New research also questions the validity of perceived severity food reactions, information about which is taken from data based on outdated research.
In the past, MAO inhibitors were prescribed to patients resistant to tricyclic antidepressants. Newer MAO inhibitors, such as selegiline (usually used to treat Parkinson's disease) and the reversible MAO inhibitor moclobemide, represent more safe alternative These drugs are still sometimes used as first line of treatment. However, these substances do not always act as effectively as their predecessors. MAOIs have been found effective in the treatment of panic disorder with agoraphobia, social phobia, atypical depression or mixed anxiety and depression, bulimia and post-traumatic stress disorder, and borderline personality disorder. There is evidence of the effectiveness of MAOIs in the treatment of obsessive-compulsive disorder (OCD), trichotillomania, body dysmorphic disorder, and avoidant personality disorder, but these data are from uncontrolled clinical sources. MAOIs may also be used in the treatment of Parkinson's disease, acting in particular on MAO-B (thus affecting dopaminergic neurons), as well as providing an alternative for migraine prevention. Inhibition of MAO-A and MAO-B is used to treat depression and anxiety. MAO inhibitors are especially often prescribed to outpatients with “neurotic depression” complicated panic disorder or hysterical dysphoria, which involves repeated episodes of depressed mood in response to feelings of rejection.
MAOIs work by inhibiting monoamine oxidase activity, preventing the breakdown of monoamine neurotransmitters, thereby increasing their availability. There are two isoforms of monoamine oxidase, MAO-A and MAO-B. MAO-A predominantly deaminates serotonin, melatonin, epinephrine and norepinephrine. MAO-B preferentially deaminates phenylethylamine and residual amines. Dopamine is deaminated equally by both types of isoforms.
First-generation MAOIs irreversibly inhibit monoamine oxidase. When they react with monoamine oxidase, they permanently deactivate it, and the enzyme cannot function until it is replaced in the body with a new one, which can take about two weeks. Some newer MAO inhibitors, the most notable of which is moclobemide, are reversible, meaning they can be dissociated from the enzyme to facilitate normal catabolism of the substrate. The level of inhibition is thus controlled by the concentration of the substrate and the MAOI. Harmaline, found in the plants harmala vulgaris, ayahuasca, spirit vine and red stratum, is reversible MAO-A inhibitor(OIMA).
In addition to reversibility, MAO inhibitors vary in MAO receptor selectivity. Some MAO inhibitors can inhibit MAO-A and MAO-B equally, while other MAO inhibitors have been developed for specific purposes. Inhibition of MAO-A reduces the breakdown primarily of serotonin, norepinephrine and dopamine; Selective inhibition of MAO-A allows metabolism via MAO-B. Taking drugs that affect serotonin when taken with another drug that increases serotonin levels can result in a potentially fatal interaction called serotonin syndrome. When taking MAOIs with irreversible and non-selective inhibitors (for example, older generation MAOIs), as a result of interaction with tyramine in the diet, the development of hypertensive crisis. Tyramine is destroyed by action of MAO-A and MAO-B, so inhibition of this action may lead to its excessive accumulation, so the patient should carefully monitor his tyramine intake. MAO-B inhibition primarily reduces the breakdown of dopamine and phenylethylamine, so there are no dietary restrictions associated with this. MAO-B will also metabolize since the only differences between dopamine, phenylethylamine and tyramine are the two phenylhydroxyl groups on carbons 3 and 4. 4-OH does not sterically hinder MAO-B on tyramine. Two MAO-B drugs, selegiline and rasagiline, have been approved by the FDA without dietary restrictions except for high-dose treatment, in which case they lose their selectivity.
When administered orally, MAO inhibitors inhibit the catabolism of dietary amines. When consuming foods containing tyramine (the so-called “cheese effect”), a person may experience a hypertensive crisis. Hyperserotonemia may develop when consuming foods containing tryptophan. The amount of substance required to produce a response varies greatly among individuals and depends on the degree of inhibition, which in turn depends on dose and selectivity. The exact mechanism by which tyramine causes the hypertensive response is not well understood, but it is thought that tyramine displaces norepinephrine from the vesicles in which it is stored. This can cause a cascade of effects in which excess quantities norepinephrine can lead to the development of a hypertensive crisis. Another theory suggests that a hypertensive crisis causes the proliferation and accumulation of catecholamines. It is tyrosine, and not tyramine, that is the precursor of catecholamines. Tyramine is a breakdown product. In the intestine and during fermentation, the amino acid tyrosine is decarboxylated into tyramine. Under normal circumstances, tyramine is deaminated in the liver to inactive metabolites, but when hepatic MAO (primarily MAO-A) is suppressed, the "first pass" of tyramine is blocked, which can lead to increased circulating levels of tyramine. Increased amounts of tyramine compete with for transport across the blood-brain barrier (with the help of aromatic amino acids), where it can penetrate adrenergic nerve endings. After penetration into the cytoplasmic space, tyramine is transported by the vesicular monoamine transporter into synaptic vesicles, thereby displacing norepinephrine. The massive movement of norepinephrine from its vesicular storage into the intercellular space can accelerate the development of a hypertensive crisis. Untreated hypertensive crises can cause stroke or cardiac arrhythmia. Both types of intestinal MAO inhibition can lead to the development of hyperthermia, nausea and psychosis when consuming substances high in . Foods and drinks with potentially high levels of tyramine include: liver and fermented substances such as alcoholic drinks and aged cheeses. found in foods such as beans. These dietary restrictions are not necessary for individuals taking selective inhibitors MAO-B in normal or low doses. Of particular note is the fact that some meat extracts and yeast extracts (Bovril, Marmite, Vegemite) contain extremely high level, and they should also not be consumed while taking such medications.
nothing was known, and over the next four decades fewer than 100 people died from hypertensive crisis. Presumably due to the sudden onset and violent nature of the reaction, MAOIs gained a reputation for being so dangerous that for a time they were completely discontinued in America. However, it is now believed that when MAOIs are used under the supervision of a qualified psychiatrist, this class of drugs is a viable alternative even for long-term use. The most significant risk associated with the use of MAO inhibitors is the potential for interaction with medicines, both over-the-counter and prescription-only drugs, illicit drugs or medications, and some supplements (such as St. John's wort). It is very important that the doctor monitors such combinations in order to avoid possible adverse reactions. For this reason, many users have an MAOI card, which gives all the emergency information medical care about drugs that the patient should avoid (for example, the dose of adrenaline in this case should be reduced by 75%, and the duration of exposure should be increased). The risk of MAOI drugs interacting with other drugs or certain products is especially dangerous because patients taking such drugs often take the attitude that they "don't care if they live or not." MAO inhibitors should not be combined with other psychoactive substances (antidepressants, painkillers, stimulants and illicit substances) except under expert advice. Certain combinations may cause death, including combination with SSRIs, TCAs, MDMA, meperidine, tramadol and dextromethorphan. Drugs that affect epinephrine, norepinephrine or dopamine should be administered in much lower doses due to potentiation and long-lasting effects. Nicotine, a common substance in tobacco addiction, has a “relatively weak” addictive potential when used alone. When administered concomitantly with MAOIs, the addictive potential increases dramatically, resulting in an allergenic musculoskeletal response in rats, which is a measure of the addictive potential of a substance. This may result in difficulty quitting smoking, since tobacco contains natural compounds in addition to nicotine.
Antidepressants, including MAO inhibitors, have addictive properties, the most notable result of which is withdrawal syndrome which can be severe, especially if the MAOI is stopped suddenly or too quickly. However, the dependence potential of MAO inhibitors or antidepressants in general is not as significant as that of benzodiazepines. To minimize or prevent withdrawal symptoms, the dose may be gradually reduced over several weeks, months, or years. MAO inhibitors, like any other antidepressants, cannot change the course of the disease, so it is possible that when stopping treatment, the patient may return to the state he had before starting treatment. This circumstance significantly complicates switching a patient from an MAOI to an SSRI, since after taking one drug and before starting another, it is necessary complete cleansing body systems. With a gradual dose reduction, the patient will face the fact that for several weeks he will have to deal with depression without pharmacological support during the drug-free interval. This may be preferable to the risk of developing interaction effects between the two drugs, but often this trial is not easy for the patient.
MAO inhibitors are known to have numerous drug interactions, including the following types substances: 1. Substances that are metabolized by monoamine oxidase, as they can increase their effect several times. 2. Substances that increase the activity of serotonin, norepinephrine or dopamine, since excess of any of these neurochemicals can lead to serious acute consequences, including the development of serotonin syndrome, hypertensive crisis and psychosis, respectively. Such substances include: - Phenethylamines: 2C-B, mescaline, phenethylamines, etc. - Amphetamines: amphetamine, MDMA, dextroamphetamine, methamphetamine, DOM, etc. - Tryptamines: DMT, psilocin/psilocybin (“magic mushrooms”), etc. - Lysergamides: ergolines/LSA, LSD (“acid”), etc. - Serotonin, norepinephrine and/or dopamine reuptake inhibitors: - Serotonin reuptake inhibitors (SSRIs): citalopram, dapoxetine, escitalopram, fluvoxamine, paroxetine, . - Serotonin-norepinephrine reuptake inhibitors: desvenlafaxine, duloxetine, milnacipran, . - Norepinephrine-dopamine reuptake inhibitors: amineptine, bupropion, methylphenidate, nomifensine. - Norepinephrine reuptake inhibitors: atomoxetine, mazindol, reboxetine. - Tricyclic antidepressants (TCAs): butriptyline, clomipramine, dozulepine, doxepin, imipramine, lofepramine, nortriptyline, protriptyline, trimipramine. - Tetracyclic antidepressants: amoxapine, maprotiline. - Phenylpiperidine opioid derivatives: meperidine/pethidine, tramadol, methadone, dextropropoxyphene, propoxyphene. - Others: brompheniramine, chlorpheniramine, cocaine, cyclobenzaprine, dextromethorphan (DXM), ketamine, MDPV, nefazodone, phencyclidine (PCP), pheniramine, sibutramine, trazodone. - Substances that release serotonin, norepinephrine and/or dopamine: 4-methylaminorex (4-MAR), amphetamine, benzphetamine, cathine, cathinone, diethylcathinone, levmethamphetamine, lisdexamfetamine, MDMA (“ecstasy”), methamphetamine, pemoline, phendimetrazine, phenethylamine ( PEA), phentermine, propylhexedrine, pseudoephedrine, phenylephrine, . - Precursors of serotonin, norepinephrine and/or dopamine: 5-HTP, L-phenylalanine, L-tyrosine. - Anesthetics used in surgery and dentistry, local and general action, in particular those containing adrenaline. Doesn't exist in dentistry universal practice regarding the use of MAO inhibitors such as phenelzine, it is therefore important to inform all physicians, especially dentists, about the potential effect of MAO inhibitors in local anesthesia. In preparation for dental procedures It is advisable to stop taking phenelzine, however, because it takes two weeks to stop taking it, this option is not always desirable or practical. Dentists using local anesthesia, it is recommended to use a non-epinephrine based anesthetic such as 3% carbocaine. Special attention During the procedure, you should pay attention to your blood pressure. The anesthetic level should be regularly and correctly replenished, since non-epinephrine anesthetics begin to act later and wear off more quickly. Patients taking phenelzine should notify their psychiatrists before undergoing any dental treatment. - Some other supplements: Hypericum perforatum (St. John's wort), inositol, Rhodiola rosea, S-adenosyl-L-methionine (SAME), . - Other monoamine oxidase inhibitors.
The heyday of MAOI popularity occurred for the most part from 1957 to 1970. The initial popularity of “classical” non-selective irreversible MAO inhibitors has waned due to the presence of dangerous interactions of these drugs with sympathomimetic drugs and products containing tyramine, which can lead to the development of a hypertensive crisis. As a result, physician use of previous generation MAOIs has decreased. When scientists discovered that there were two different MAO enzymes (MAO-A and MAO-B), they developed MAO-B selective compounds (such as selegiline, which is used to treat Parkinson's disease) to reduce side effects and serious drug interactions. . Further improvement has occurred with the development of compounds (moclobemide and toloxatone) that are not only selective, but also cause reversible MAO-A inhibition and have a reduced rate of dietary and drug interactions. Irreversible MAO inhibitors were the first open antidepressants, but their popularity has declined with the advent of safe antidepressants; This new class of antidepressants has fewer side effects, especially the dangerous irreversible interaction of MAOIs with tyramine-containing foods, sometimes called “cheese syndrome,” which leads to severe hypertension. However, reversible MAO inhibitors do not have these adverse hypertensive consequences. Moclobemide was the first reversible MAO-A inhibitor introduced into widespread clinical practice. Its features as a reversible inhibitor give it a number of advantages over previous generation irreversible MAO inhibitors. On February 28, 2006, the US FDA approved a transdermal form of the MAOI selegiline, called Emsam, for the treatment of depression.
In the episode "The Late Shaft" of the detective TV drama Castle, Bobby Mann was taking MAO inhibitors. His killer used this fact to cause a negative interaction with the drug, which led to Bobby's death, which appeared to be a simple heart attack. In the episode "Cut" of Law & Order, a surgeon puts a patient on painkillers that interact with the MAO inhibitors she is taking, leading to her death. The pilot episode of Law & Order was based on true events. Journalist Sidney Zion questioned the sudden death of his daughter Libby Zion in a Manhattan emergency room on October 4, 1984. The cause of death was listed as "mysterious infection." The father convinced the authorities to open a criminal case. This was done after it was discovered that his daughter had taken certain medications before her death, including Demerol, which reacted with the drug Nardil, which the victim was taking. The district attorney filed a murder charge against the doctor who approved the use of drugs on Libby. This incident led to many reforms in medical education and restrictions on the number of working hours for health care workers. In the end, it turned out that the main cause of death was drug abuse.
