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Anxiety is medically recognized as the experience of negative feelings of apprehension, worry, and general unease.[1][2] These feelings can range from subtle and ignorable to intense and overwhelming enough to trigger panic attacks or feelings of impending doom. Anxiety is often accompanied by nervous behaviour such as stimulation, restlessness, difficulty concentrating, irritability, and muscular tension.[3] Psychoactive substance-induced anxiety can be caused as an inescapable effect of the drug itself, by a lack of experience with the substance or its intensity, as an intensification of a pre-existing state of mind, or by the experience of negative hallucinations. The focus of anticipated danger can be internally or externally derived.

Anxiety is often accompanied by other coinciding effects such as depression and irritability. It is most commonly induced under the influence of moderate dosages of hallucinogenic compounds, such as cannabinoids,[4] psychedelics,[5] dissociatives, and deliriants.[6] However, it can also occur during the withdrawal symptoms of GABAergic depressants[7] and during stimulant comedowns.[8]

If you have anxiety, you may want to read the anxiety suppression effect. Additionally, if the anxiety is significantly impacting well-being for a prolonged time period, it is highly recommended to seek out therapeutic medical attention and/or a support group.


Fear is not anxiety.[2][3][9][10][11][12] Fear is the response to an immediate threat, whereas anxiety is a set of behaviours attempting to mitigate a perceived future threat. Anxiety disorders are an atypical learning of maladaptive behaviours. While there is substantial evidence indicating anxiety disorders involve genetics and early environmental factors, the practice of anxious thoughts and behavioural patterns also further strengthens their associated neural pathways. Ironically, attempting to avoid anxiety-causing behavioural cues protects the anxiety-causing neural pathways from being extinguished.

Fear and anxiety are defensive neural networks involving many functionally distinct hubs.[10][11][12][13] While there is a substantial overlap between fear and anxiety in these defensive networks, they do differ. Typically the amygdala and bed nucleus of the stria terminalis are the focal points for fear and anxiety respectively, but there are significant problems assigning these as the main center. These hubs generate signals to modify the appropriate defensive neural pathways, but they are not centers for eliciting subjective experience. The body's defensive responses appear before the conscious awareness of feeling threatened, when there is no conscious awareness of feeling threatened, and for survival cues such as hunger. Automatic defensive responses are not by necessity conscious feelings, meaning there are different neural pathways involved for anxiety to be a subjective experience.

Due to the sheer breadth of brain systems involved, the influence of intestinal bacteria,[14] and any potential communicative malfunctioning between any these systems, it's not useful to describe anxiety's underlying neuroanatomy outside of a clinician's context. However, there are specific observable tendencies in anxious individuals:[11]

  • Inflated estimates of threat cost and probability
  • Increased threat attention and hypervigilance
  • Impaired recognition of safety cues
  • Behavioural and cognitive avoidance
  • Heightened reactivity to threat uncertainty

Anxiety disorders are the most common class of mental disorder; one third of the population is affected by an anxiety disorder during their lifetime.[15] It's consistently found that the prevalence in women is twice as high as in men. Patients may suffer from their disorder for years to decades, but it does not mean that it is permanent. There is a high overlap among slightly differing classifications of anxiety disorders, and between anxiety disorders with other mental disorders. It is important to remember that the presence of anxiety is a normal defense mechanism. Anxiety becomes an anxiety disorder when it significantly impacts functional well-being for prolonged periods of time.

Psychoactive substances

Compounds within our psychoactive substance index which may cause this effect include:

... further results

Experience reports

Anecdotal reports which describe this effect within our experience index include:

See also

External links


  1. "Glossary of Technical Terms". Diagnostic and statistical manual of mental disorders (5th ed.): 189–190. 2013. doi:10.1176/appi.books.9780890425596.GlossaryofTechnicalTerms. 
  2. 2.0 2.1 "Anxiety or fear-related disorders". International statistical classification of diseases and related health problems (11th ed.). 2022. Retrieved 20 May 2022. 
  3. 3.0 3.1 "Anxiety Disorders". Diagnostic and statistical manual of mental disorders (5th ed.): 818. 2013. doi:10.1176/appi.books.9780890425596.dsm05. 
  4. Crippa, José Alexandre; Zuardi, Antonio Waldo; Martín-Santos, Rocio; Bhattacharyya, Sagnik; Atakan, Zerrin; McGuire, Philip; Fusar-Poli, Paolo (2009). "Cannabis and anxiety: a critical review of the evidence". Human Psychopharmacology: Clinical and Experimental. 24 (7): 515–523. doi:10.1002/hup.1048. ISSN 0885-6222. 
  5. Wolbach, A. B.; Miner, E. J.; Isbell, Harris (1962). "Comparison of psilocin with psilocybin, mescaline and LSD-25". Psychopharmacologia. 3 (3): 219–223. doi:10.1007/BF00412109. ISSN 0033-3158. 
  6. Datura effects (Erowid) |
  7. "Rebound anxiety in anxious patients after abrupt withdrawal of benzodiazepine treatment". American Journal of Psychiatry. 141 (7): 848–852. 1984. doi:10.1176/ajp.141.7.848. ISSN 0002-953X. 
  8. Williamson, S (1997). "Adverse effects of stimulant drugs in a community sample of drug users". Drug and Alcohol Dependence. 44 (2-3): 87–94. doi:10.1016/S0376-8716(96)01324-5. ISSN 0376-8716. 
  9. Barkus, Christopher; McHugh, Stephen B.; Sprengel, Rolf; Seeburg, Peter H.; Rawlins, J. Nicholas P.; Bannerman, David M. (2010). "Hippocampal NMDA receptors and anxiety: At the interface between cognition and emotion". European Journal of Pharmacology. 626 (1): 49–56. doi:10.1016/j.ejphar.2009.10.014. ISSN 0014-2999. 
  10. 10.0 10.1 Tovote, P., Fadok, J. P., Lüthi, A. (June 2015). "Neuronal circuits for fear and anxiety". Nature Reviews Neuroscience. 16 (6): 317–331. doi:10.1038/nrn3945. Retrieved 21 May 2022. 
  11. 11.0 11.1 11.2 Grupe, D. W., Nitschke, J. B. (July 2013). "Uncertainty and anticipation in anxiety: an integrated neurobiological and psychological perspective". Nature Reviews Neuroscience. 14 (7): 488–501. doi:10.1038/nrn3524. Retrieved 21 May 2022. 
  12. 12.0 12.1 LeDoux, J. E., Pine, D. S. (November 2016). "Using Neuroscience to Help Understand Fear and Anxiety: A Two-System Framework". American Journal of Psychiatry. 173 (11): 1083–1093. doi:10.1176/appi.ajp.2016.16030353. Retrieved 29 May 2022. 
  13. Stahl, S. M. (2013). Stahl’s essential psychopharmacology: neuroscientific basis and practical application (4th ed ed.). Cambridge University Press. ISBN 9781107025981. 
  14. Foster, J. A., McVey Neufeld, K.-A. (May 2013). "Gut–brain axis: how the microbiome influences anxiety and depression". Trends in Neurosciences. 36 (5): 305–312. doi:10.1016/j.tins.2013.01.005. ISSN 0166-2236. Retrieved 29 May 2022. 
  15. Bandelow, B., Michaelis, S. (30 September 2015). "Epidemiology of anxiety disorders in the 21st century". Dialogues in Clinical Neuroscience. 17 (3): 327–335. doi:10.31887/DCNS.2015.17.3/bbandelow. ISSN 1958-5969. Retrieved 30 May 2022.