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WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.
DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.
Mirtazapine (trade name Remeron, among others) is an antidepressant substance of the piperazinoazepine class. At high doses, it has been reported to act as an atypical psychedelic and sedative. It is classified as a noradrenergic and specific serotonergic antidepressant (NaSSA).[2]
Mirtazapine was developed in the Netherlands and introduced in the United States in 1996.[3] Its patent expired in 2004 and generic versions have been widely available since.[4] It is used primarily in the treatment of major depressive disorder and other mood disorders.[5][6] It has also been prescribed off-label for the treatment of
generalized anxiety disorder,[7] social anxiety disorder,[8][9] obsessive-compulsive disorder,[8][10] panic disorder,[8][11] post-traumatic stress disorder,[8] low appetite,[12][13][14] insomnia,[15][16] nausea/vomiting,[17][18][19]
itching,[20][21] and headaches and migraines.[18][22][23]
Higher doses of mirtazapine (that exceed the recommended prescription dose) are reported to produce an unusual mixture of psychedelic and sedative effects. Subjective effects include sedation and mild-moderate versions of open and closed-eye visuals, conceptual thinking, and euphoria.
Mirtazapines has potential paradoxical effects concerning it's sedative effects. Anecdotal reports and studies suggest it's Sedation decreases as the dose increases. (7.5mg is more sedating than 15mg.) One theory suggests it has minor Stimulant effects that overpowers it's sedative effects. [citation needed]
The toxicity and health risks of recreational mirtazapine use is not known. It is highly advised to use harm reduction practices if using this substance.
Mirtazapine is a synthetic tetrahedral molecule of the piperazino-azepine and phenethylamine group of compounds. It is comprised of a fusion of pyridine, benzene, azepine, and piperazine rings. It is a tetracyclic antidepressant, named so because of their four-ring structure. Mirtazapine is the 6-aza analog of mianserin, which is pharmacologically similar in function.
Mirtazapine enhances central adrenergic and serotonergic transmission, possibly by acting as an antagonist at central presynaptic alpha 2 adrenergic inhibitory autoreceptors and heteroreceptors. This agent is a potent antagonist of 5-hydroxytryptamine type 2 (5-HT2), 5-HT3, and histamine 1 (H1) receptors, and a moderate antagonist of peripheral alpha 1 adrenergic and muscarinic receptors.[24]
Pharmacology
Mirtazapine inhibits presynaptic serotonin (5-HT)-2 and alpha-2 adrenergic auto- and hetero-receptors, thereby increasing serotonergic and noradrenergic neurotransmission. The increased amount of 5-HT released interacts with postsynaptic 5-HT1 receptors, which may be relevant to the antidepressant effects of the drug. The affinity of mirtazapine for central alpha-2 adrenoreceptors is 10 times higher than for peripheral receptors, resulting in fewer peripheral effects related to increased blood pressure. Mirtazapine is an antagonist at postsynaptic 5-HT2A, 5-HT2C, and 5-HT3 receptors. The blockade of these receptors may result in a lower incidence of certain adverse effects (e.g., anxiety, insomnia, nausea) than occurs with antidepressants that do not antagonize these receptors. Mirtazapine significantly antagonizes histamine H1 receptors at low doses, and this activity is associated with sedation and appetite stimulation. Higher doses have a greater effect on norepinephrine release relative to antihistamine effects, which may offset the sedative potential and appetite stimulation observed at low doses. Mirtazapine has muscarinic antagonist properties, which may be associated with xerostomia, constipation, and other anticholinergic effects. Orthostatic hypotension is the result of the peripheral alpha-1 adrenergic antagonism of the drug. Mirtazapine does not have clinically significant receptor affinity for dopamine, 5-HT1A, or 5-HT1B, and has no effects on the central reuptake of either norepinephrine or serotonin.:[25][26]
While mirtazapine has some affinity for the 5-HT2A receptor, it acts as an antagonist[7] thus it is unlikely that this mechanism is responsible for its psychedelic and deliriant effects.
Additionally, Mirtazapine has also been observed to indirectly agonize the following GCPR in humans:
Mirtazapine has also been found to modulate the κ3 opioid receptor, supporting the claim that mirtazapine causes pain relief[33] and adds to the sedative and hallucinogenic effects of mirtazapine[34][35]. This even may explain mirtazapine's withdrawal/discontinuation effects as well as its promotion of diuresis and a possible increase in food intake (usually resulting in weight gain).
It should be noted that although some of these effects are observed in those who take mirtazapine recreationally (or one off dosing) most neurophysiological effects are observed in those with on-going use (15, 30 and 45 mg daily prescribed for depression, etc) due to a maintained level of mirtazapine in the body.
The oral bioavailability of mirtazapine is about 50%. It is found mostly bound to plasma proteins, about 85%. It is metabolized primarily in the liver by demethylation and hydroxylation via cytochrome P450 enzymes, CYP1A2, CYP2D6, CYP3A4.[7] One of its major metabolites is desmethylmirtazapine. The overall elimination half-life is 20–40 hours. It is conjugated in the kidney for excretion in the urine, where 75% of the drug is excreted,[36] and about 15% is eliminated in feces.[37]
Subjective effects
Although mirtazapine exhibits almost exclusively psychedelic effects, the hallucinations that accompany it do have distinctively deliriant-like effects. For example, they are often delirious in their believability and rarely comprised of condensed visual geometry. Instead they tend to be solid and extremely realistic in appearance.
The mental processes, thought patterns and general head space experienced during a high dose mirtazapine experience is one that is typically described to be completely devoid of insight. In contrast to many other substances with hallucinogenic properties, it produces no introspection, personal problem solving or creativity enhancing effects; for this reason it is generally reported that mirtazapine holds no therapeutic potential when used as a hallucinogen.
Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWikicontributors. As a result, they should be viewed with a healthy degree of skepticism.
It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.
Physical effects
Sedation - In terms of energy level alterations, mirtazapine is extremely sedating and often results in an overwhelmingly lethargic state. This causes users to suddenly feel as if they are extremely sleep deprived and have not slept for days, forcing them to sit down and generally feel as if they are constantly on the verge of passing out instead of engaging in physical activities. This sense of sleep deprivation increases proportional to dosage and eventually becomes powerful enough to force a person into complete unconsciousness. It is a state which often leaves people feeling extremely lethargic and tired the following day.
Spontaneous bodily sensations - The "body high" of mirtazapine can be described as a pleasurable, warm, soft and all-encompassing tingling sensation. This maintains a consistent presence that steadily rises with the onset and hits its limit once the peak has been reached and is not capable of becoming anything but mildly euphoric even at high dosages. This is accompanied by strange but mild throbbing or aching sensations.
Tactile hallucination - Unique tactile hallucinations are commonly felt within this substance. These can be described as bizarrely structured vibrations and pulsations that spontaneously manifest themselves across the skin at various locations and propagate outwards for a short distance from its center.
Motor control loss - If physical activities such as walking are forcibly engaged in, a distinct but not completely incapacitating loss of motor control is noticed as well as the consistent feeling that you are walking on top of a trampoline and not a normal solid floor.
Appetite enhancement - The above components are also accompanied by an intense appetite enhancement that is identical in strength to “the munchies” experienced with cannabis.[38]
Bronchodilation - This can cause swallowing to be extremely difficult and uncomfortable, as with some other anticholinergics such as diphenhydramine. As with diphenhydramine, it is most prominent during the onset phase of the experience and often fades away as the peak sets in.
Cognitive euphoria or Cognitive dysphoria - Some reports of recreational mirtazapine use describe mild euphoria, while others either produce a neutral state of mind or dysphoria due to the pronounced side effects.
In terms of complexity, the visual geometry found within high dose mirtazapine trips can be said to be completely on par with that of LSD or psilocin. It can be comprehensively described as intricate in complexity, abstract in style, structured in organization, equally organic and synthetic in style, dimly lit in lighting, monotone is scheme, glossy in shading, equal in sharp and soft edges, large in size, fast in speed, smooth in motion, equal in rounded and angular corners, non-immersive in depth and consistent in intensity.
At higher dosages, Level 8A and Level 8B are not present simply because the sedating effects are too overwhelming to allow people to remain conscious at such a high level. Many users report an almost menacing feeling, following a sinister and ominous style with a colour scheme that generally consists of greys and blues.
Internal hallucination (autonomous entities; settings, sceneries, and landscapes; perspective hallucinations and scenarios and plots) - The internal hallucinations which mirtazapine induces are generally only present as spontaneous breakthroughs at higher dosages as one is falling asleep. This effect's variations are delirious in believability, interactive in style, new experiences in content, autonomous in controllability and solid in appearance. The most common way in which they manifest themselves are through hypnagogic scenarios which the user may experience as they are drifting off to sleep. These are short and fleeting but frequent and completely believable and convincing as they happen. In terms of the theme they often take the form of bizarre and extremely nonsensical plots. These can also be observed in hypnopompic states (when one is waking from sleep).
Mirtazapine is not known to cause brain damage, and has extremely low toxicity relative to dose. Similar to other psychedelic drugs, there are relatively few physical side effects associated with mirtazapine exposure. Various studies have shown that in reasonable doses in a careful context, it presents no negative cognitive, psychiatric or toxic physical consequences of any sort.
Dependence and abuse potential
Mirtazapine is not habit-forming when used as a hallucinogen and the desire to use it can actually decrease with use. It is most often self-regulating.
Tolerance to the effects of mirtazapine are built almost immediately after ingestion. After that, it takes about 3 days for the tolerance to be reduced to half and 7 days to be back at baseline (in the absence of further consumption).
Overdose
Mirtazapine is considered to be relatively safe in the event of an overdose,[39] although it is considered slightly more toxic in overdose than most of the SSRIs (except citalopram).[40] Unlike the TCAs, mirtazapine showed no significant cardiovascular adverse effects at 7 to 22 times the maximum recommended dose.[41] Case reports of overdose with as much as 30 to 50 times the standard dose described the drug as relatively nontoxic, compared to TCAs.[42][43]
Twelve reported fatalities have been attributed to mirtazapine overdose.[44][45] The fatal toxicity index (deaths per million prescriptions) for mirtazapine is 3.1 (95% CI: 0.1 to 17.2). This is similar to that observed with SSRIs.[46]
As such, it may contain incomplete or wrong information. You can help by expanding it.
Mirtazapine is legally approved for medical purposes worldwide. However, it is illegal to sell and possess in most countries without a prescription.
Switzerland: Mirtazapine is listed as a "Abgabekategorie B" pharmaceutical, which generally requires a prescription.[citation needed]
Turkey: Mirtazapine is classed as anti-depressant so it is prescription only drug[citation needed] but the law is often unenforced.
United Kingdom: Mirtazapine is a licensed prescription-only medicine (POM) in the United Kingdom.[47] It is not a criminal offence to possess this medicine without a valid prescription. This medicine can legally be obtained with a valid prescription or through legal import of the medicine for personal use as outlined in Section 13 of the Medicines Act 1968.[48]
↑Roland A. Carlstedt (14 December 2009). Handbook of Integrative Clinical Psychology, Psychiatry, and Behavioral Medicine: Perspectives, Practices, and Research. Springer Publishing Company. p. 290. ISBN978-0-8261-1094-7. Retrieved 23 April 2012.
↑ "REMERON (mirtazapine) tablet, film coated [Organon Pharmaceuticals USA]". DailyMed. Organon Pharmaceuticals USA. October 2012. Retrieved 24 October 2013.
↑Schatzberg, A. F., Cole, J. O., DeBattista, C. (2010). Manual of clinical psychopharmacology. 3 (7th ed ed.). American Psychiatric Pub. ISBN9781585623778.CS1 maint: Extra text (link)
↑Gorman, J. M. (1999). "Mirtazapine: clinical overview". The Journal of Clinical Psychiatry. 60 Suppl 17: 9–13; discussion 46–48. ISSN0160-6689.
↑Carpenter, L., Leon, Z., Yasmin, S., Price, L. (1 June 1999). "Clinical Experience with Mirtazapine in the Treatment of Panic Disorder". Annals of Clinical Psychiatry. 11 (2): 81–86. doi:10.3109/10401239909147053. ISSN1040-1237.
↑Tajti, J., Almási, J. (June 2006). "[Effects of mirtazapine in patients with chronic tension-type headache. Literature review]". Neuropsychopharmacologia Hungarica: A Magyar Pszichofarmakologiai Egyesulet Lapja = Official Journal of the Hungarian Association of Psychopharmacology. 8 (2): 67–72. ISSN1419-8711.
↑Boer, T. de (1996). "The pharmacologic profile of mirtazapine". The Journal of Clinical Psychiatry. 57 Suppl 4: 19–25. ISSN0160-6689.
↑ 28.028.1Goodman, L. S., Brunton, L. L., Chabner, B., Knollmann, B. C., eds. (2011). Goodman & Gilman’s pharmacological basis of therapeutics (12th ed ed.). McGraw-Hill. ISBN9780071624428.CS1 maint: Extra text (link)
↑Kennis, L. E., Bischoff, F. P., Mertens, C. J., Love, C. J., Van den Keybus, F. A., Pieters, S., Braeken, M., Megens, A. A., Leysen, J. E. (3 January 2000). "New 2-substituted 1,2,3,4-tetrahydrobenzofuro[3,2-c]pyridine having highly active and potent central alpha 2-antagonistic activity as potential antidepressants". Bioorganic & Medicinal Chemistry Letters. 10 (1): 71–74. doi:10.1016/s0960-894x(99)00591-0. ISSN0960-894X.
↑Dapoigny, M., Abitbol, J. L., Fraitag, B. (October 1995). "Efficacy of peripheral kappa agonist fedotozine versus placebo in treatment of irritable bowel syndrome. A multicenter dose-response study". Digestive Diseases and Sciences. 40 (10): 2244–2249. doi:10.1007/BF02209014. ISSN0163-2116.
↑Pande, A. C., Pyke, R. E., Greiner, M., Wideman, G. L., Benjamin, R., Pierce, M. W. (October 1996). "Analgesic efficacy of enadoline versus placebo or morphine in postsurgical pain". Clinical Neuropharmacology. 19 (5): 451–456. doi:10.1097/00002826-199619050-00009. ISSN0362-5664.
↑Rimoy, G. H., Wright, D. M., Bhaskar, N. K., Rubin, P. C. (1994). "The cardiovascular and central nervous system effects in the human of U-62066E. A selective opioid receptor agonist". European Journal of Clinical Pharmacology. 46 (3): 203–207. doi:10.1007/BF00192549. ISSN0031-6970.
↑Al-Majed, A., Bakheit, A. H., Alharbi, R. M., Abdel Aziz, H. A. (2018). "Mirtazapine". Profiles of Drug Substances, Excipients, and Related Methodology. 43: 209–254. doi:10.1016/bs.podrm.2018.01.002. ISSN1871-5125.
↑Schatzberg, A. F., Nemeroff, C. B., eds. (2009). The American Psychiatric Publishing textbook of psychopharmacology (4th ed ed.). American Psychiatric Pub. ISBN9781585623099.CS1 maint: Extra text (link)
↑Taylor, D., Paton, C., Kapur, S., eds. (2012). The Maudsley prescribing guidelines in psychiatry (11. ed ed.). Wiley. ISBN9780470979488.CS1 maint: Extra text (link)
↑Nikolaou P, Dona A, Papoutsis I, Spiliopoulou C, Maravelias C. "Death Due to Mirtazapine Overdose". in "Abstracts of the XXIX International Congress of the European Association of Poison Centres and Clinical Toxicologists, May 12–15, 2009, Stockholm, Sweden". Clinical Toxicology. 47 (5): 436–510. 2009. doi:10.1080/15563650902952273.
↑Baselt, RC (2008). Disposition of Toxic Drugs and Chemicals in Man (8th ed.). Foster City, CA: Biomedical Publications. pp. 1045–7. ISBN978-0-9626523-7-0.
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