Disinhibition is medically recognized as an orientation towards immediate gratification, leading to impulsive behavior driven by current thoughts, feelings, and external stimuli, without regard for past learning or consideration of future consequences. [1] [2] [3] This is usually manifested through recklessness, poor risk assessment, and a disregard for social conventions.

At its lower levels of intensity, disinhibition can allow one to overcome emotional apprehension and suppressed social skills in a manner that is moderated and controllable for the average person. This can often prove useful for those who suffer from social anxiety or a general lack of self-confidence.

However, at its higher levels of intensity, the disinhibited individual may be completely unable to maintain any semblance of self-restraint, at the expense of politeness, sensitivity, or social appropriateness. This lack of constraint can be negative, neutral, or positive depending on the individual and their current environment.

Disinhibition is often accompanied by other coinciding effects such as amnesia and anxiety suppression in a manner which can further decrease the person's observance of and regard for social norms. It is most commonly induced under the influence of moderate dosages of GABAergic depressants, such as alcohol [4] , benzodiazepines [5] , phenibut, and GHB. However, it may also occur under the influence of certain stimulants [6] , entactogens [7] , and dissociatives [8] .

This effect seems to be mentioned within the following trip reports:

I Am a Big Gushing Fool

on 04/2016 - nervewing
  • 5-APDB 100 mg Oral in gel cap


  1. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.), 820. Arlington, VA: American Psychiatric Publishing. | https://doi.org/10.1176/appi.books.9780890425596.GlossaryofTechnicalTerms
  2. Zamboni, G., Huey, E. D., Krueger, F., Nichelli, P. F., & Grafman, J. (2008). Apathy and disinhibition in frontotemporal dementia Insights into their neural correlates. Neurology, 71(10), 736-742. | https://dx.doi.org/10.1212%2F01.wnl.0000324920.96835.95
  3. Källmén, H., & Gustafson, R. (1998). Alcohol and disinhibition. European Addiction Research, 4(4), 150-162. | https://doi.org/10.1159/000018948
  4. Topper, S. M., Aguilar, S. C., Topper, V. Y., Elbel, E., & Pierce-Shimomura, J. T. (2014). Alcohol disinhibition of behaviors in C. elegans. PLoS One, 9(3), e92965. | https://doi.org/10.1371/journal.pone.0092965
  5. Paton, C. (2002). Benzodiazepines and disinhibition: a review. Psychiatric Bulletin, 26(12), 460-462. | https://doi.org/10.1192/pb.26.12.460
  6. Fillmore, M. T., Rush, C. R., & Marczinski, C. A. (2003). Effects of d-amphetamine on behavioral control in stimulant abusers: the role of prepotent response tendencies. Drug and alcohol dependence, 71(2), 143-152. | https://doi.org/10.1016/S0376-8716(03)00089-9
  7. Ando, R. D., Benko, A., Ferrington, L., Kirilly, E., Kelly, P. A., & Bagdy, G. (2006). Partial lesion of the serotonergic system by a single dose of MDMA results in behavioural disinhibition and enhances acute MDMA-induced social behaviour on the social interaction test. Neuropharmacology, 50(7), 884-896. | https://doi.org/10.1016/j.neuropharm.2005.12.010
  8. Lissek, S., & Güntürkün, O. (2003). Dissociation of extinction and behavioral disinhibition: the role of NMDA receptors in the pigeon associative forebrain during extinction. Journal of Neuroscience, 23(22), 8119-8124. | https://doi.org/10.1523/JNEUROSCI.23-22-08119.2003




The following people contributed to the content of this article: