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Death may occur when opiates are combined with other depressants such as benzodiazepines, barbiturates, gabapentinoids, thienodiazepines, alcohol or other GABAergic substances.[1]

It is strongly discouraged to combine these substances, particularly in common to heavy doses.

Common substances that affect the u-opioid receptor: morphine, codeine, diacetylmorphine (Heroin), naloxone (Narcan), methadone, tramadol.
Poppy pod scored to release opium latex
Dried pods for preparation of tea or solvent extraction of alkaloids

An opioid is any psychoactive chemical that resembles morphine or other opiates in its pharmacological effects. Opioids work by binding to opioid receptors, which are found principally in the central and peripheral nervous system and the gastrointestinal tract.[citation needed] The receptors in these organ systems mediate both the beneficial effects and the side effects of opioids.

Although the term opiate is often used as a synonym for opioid, the term opiate is properly limited to the natural alkaloids found in the resin of the opium poppy (Papaver somniferum), while opioid refers to both opiates and synthetic substances, as well as to opioid peptides.[citation needed]

Opioid dependence can develop with ongoing administration, leading to a withdrawal syndrome with abrupt discontinuation.[citation needed] Opioids are not only well known for their addictive properties, but also for their ability to produce a feeling of euphoria, motivating some to use opioids recreationally.


Opioids are based upon morphine and opium-like structures. They work via their similar chemical structures to the endogenous opioids in the body. Morphine derived opioids, known as morphinans, contain a benzene ring attached to two partially unsaturated cyclohexane rings (phenanthrene) and a 4th nitrogenous ring attached to the core at carbons 9 and 13. There are several classes of opioids which differ greatly in structure from each other. For example, fentanyl and its analogues are structurally unique from morphinans and tramadol derivaties.


Metabolic pathway of codeine and morphine courtesy of Pharmgkb.org

Opioids are known to mimic endogenous endorphins. Endorphins are responsible for analgesia (reducing pain), causing sleepiness, and feelings of pleasure. They can be released in response to pain, strenuous exercise, orgasm, or excitement.[citation needed] This mimicking of natural endorphins results in the drug's euphoric, analgesic (pain relief) and anxiolytic (anti-anxiety) effects.

Receptor types

Opioids act on the three main classes of opioid receptor in the nervous system, μ, κ, δ (mu, kappa, and delta). Each opioid is measured by its agonistic or antagonistic effects towards the receptors, with the responses to the different receptor sub-types (e.g., μ1 and μ2) providing even more effects. Opioid receptors are found mainly within the brain, but also within the spinal cord and digestive tract.[citation needed]

Delta (δ)

The delta receptor is responsible for the analgesia, antidepressant and convulsant effects as well as physical dependence.

Kappa (κ)

The kappa receptor is responsible for the analgesia, anticonvulsant, dissociative and deliriant effects as well as dysphoria, neuroprotection and sedation.

Mu (μ)

The mu receptor is responsible for analgesia, physical dependence, respiratory depression, euphoria, and possible vasodilation.


The nociceptin receptor is responsible for anxiety, depression, appetite and development of tolerance to μ agonists.[citation needed]

Zetta (ζ)

The zetta opioid receptor, also known as opioid growth factor receptor (OGFr) is responsible for tissue growth, neural development, and is further implicated in the development in some cancers. The endogenous ligand for OGFr is met-enkephalin, which is also a powerful endogenous delta opioid receptor agonist.

Subjective effects

The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. The listed effects should be taken with a grain of salt and will rarely (if ever) occur all at once, but heavier doses will increase the chances and are more likely to induce a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include injury or death.

Physical effects

Cognitive effects

Visual effects

Pharmacological classes

Naturally occuring


Toxicity and harm potential


This toxicity and harm potential section is a stub.

As such, it may contain incomplete or even dangerously wrong information. You can help by expanding upon or correcting it.
We also recommend that you practice diligent independent research and the most thorough harm reduction practices when using this substance.

When used in safe dosages, in terms of physical and neurological toxicity most opiods are markedly safe with the long-term effects generally consisting of constipation.[citation needed] The negative aspects associated with opioids do not stem from physiological toxicity but psychological addiction and dependence.[citation needed]

It is strongly recommended that one use harm reduction practices when using this class of substances.

Tolerance and addiction potential

Due to the highly euphoric nature of these substances, the recreational use and abuse of opioids has an extremely high rate of addiction and dependence. This is combined with a tolerance which builds up quickly, necessitates that the user take increasingly high dosages in order to get the same effects.

The risk of fatal opioid overdoses rise sharply after a period of cessation and relapse, largely because of reduced tolerance.[2] To account for this lack of tolerance, it is safer to only dose a fraction of one's usual dosage if relapsing. It has also been found that the environment one is in can play a role in opioid tolerance. In one scientific study, rats with the same history of heroin administration were significantly more likely to die after receiving their dose in an environment not associated with the drug in contrast to a familiar environment.[3]

See also

External links


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This article does not cite enough references.

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  1. Risks of Combining Depressants (Tripsit) | https://tripsit.me/combining-depressants/
  2. Why Heroin Relapse Often Ends In Death - Lauren F Friedman (Business Insider) | http://www.businessinsider.com.au/philip-seymour-hoffman-overdose-2014-2
  3. Siegel, S., Hinson, R., Krank, M., & McCully, J. (1982). Heroin “overdose” death: contribution of drug-associated environmental cues. Science, 216(4544), 436–437. https://doi.org/10.1126/science.7200260