Self-medication is a term used to describe the use of drugs (including alcohol) or other self-soothing forms of behavior to treat untreated and often undiagnosed mental distress, stress and anxiety, including mental illnesses and/or psychological trauma.
Self-medication is often seen as gaining personal independence from established medicine. 
As different drugs have different effects, they may be used for different reasons. According to the self-medication hypothesis (SMH), the individuals' choice of a particular drug is not accidental or coincidental, but instead, a result of the individuals' psychological condition, as the drug of choice provides relief to the user specific to his or her condition. Specifically, addiction is hypothesized to function as a compensatory means to modulate effects and treat distressful psychological states, whereby individuals choose the drug that will most appropriately manage their specific type of psychiatric distress and help them achieve emotional stability.
The self-medication hypothesis (SMH) originated in papers by Edward Khantzian, Mack and Schatzberg, David F. Duncan, and a response to Khantzian by Duncan. The SMH initially focused on heroin use, but a follow-up paper added cocaine. The SMH was later expanded to include alcohol, and finally all drugs of addiction.
According to Khantzian's view of addiction, drug users compensate for deficient ego function by using a drug as an "ego solvent", which acts on parts of the self that are cut off from consciousness by defense mechanisms. According to Khantzian, drug dependent individuals generally experience more psychiatric distress than non-drug dependent individuals, and the development of drug dependence involves the gradual incorporation of the drug effects and the need to sustain these effects into the defensive structure-building activity of the ego itself. The addict's choice of drug is a result of the interaction between the psychopharmacologic properties of the drug and the affective states from which the addict was seeking relief. The drug's effects substitute for defective or non-existent ego mechanisms of defense. The addict's drug of choice, therefore, is not random.
While Khantzian takes a psychodynamic approach to self-medication, Duncan's model focuses on behavioral factors. Duncan described the nature of positive reinforcement (e.g., the "high feeling", approval from peers), negative reinforcement (e.g. reduction of negative affect) and avoidance of withdrawal symptoms, all of which are seen in those who develop problematic drug use, but are not all found in all recreational drug users. While earlier behavioral formulations of drug dependence using operant conditioning maintained that positive and negative reinforcement were necessary for drug dependence, Duncan maintained that drug dependence was not maintained by positive reinforcement, but rather by negative reinforcement. Duncan applied a public health model to drug dependence, where the agent (the drug of choice) infects the host (the drug user) through a vector (e.g., peers), while the environment supports the disease process, through stressors and lack of support.
Khantzian revisited the SMH, suggesting there is more evidence that psychiatric symptoms, rather than personality styles, lie at the heart of drug use disorders. Khantzian specified that the two crucial aspects of the SMH were that (1) drugs of abuse produce a relief from psychological suffering and (2) the individual's preference for a particular drug is based on its psychopharmacological properties. The individual's drug of choice is determined through experimentation, whereby the interaction of the main effects of the drug, the individual's inner psychological turmoil, and underlying personality traits identify the drug that produces the desired effects.
Meanwhile, Duncan's work focuses on the difference between recreational and problematic drug use. Data obtained in the Epidemiologic Catchment Area Study demonstrated that only 20% of drug users ever experience an episode of drug abuse (Anthony & Helzer, 1991), while data obtained from the National Comorbidity Study demonstrated that only 15% of alcohol users and 15% of illicit drug users ever become dependent. A crucial determinant of whether a drug user develops drug abuse is the presence or absence of negative reinforcement, which is experienced by problematic users, but not by recreational users. According to Duncan, drug dependence is an avoidance behavior, where an individual finds a drug that produces a temporary escape from a problem, and taking the drug is reinforced as an operant behavior.
Some mental illness sufferers attempt to correct their illnesses by use of certain drugs. Depression is often self medicated with alcohol, tobacco, cannabis, or other mind-altering drug use. While this may provide immediate relief of some symptoms such as anxiety, it may evoke and/or exacerbate some symptoms of several kinds of mental illnesses that are already latently present, and may lead to addiction/dependence, among other side effects of long-term use of the drug.
Due to the different effects of the different classes of drugs, the SMH postulates that the appeal of a specific class of drugs differs from person to person. In fact, some drugs may be aversive for individuals for whom the effects could worsen affective deficits.
Alcohol and sedative/hypnotic drugs, such as barbiturates and benzodiazepines, are central nervous system (CNS) depressants that lower inhibitions via anxiolysis. Depressants produce feelings of relaxation and sedation, while relieving feelings of depression and anxiety. Though they are generally ineffective antidepressants, as most are short-acting, the rapid onset of alcohol and sedative/hypnotics softens rigid defenses and, in low to moderate doses, provides the illusion of relief from depressive affect and anxiety. As alcohol also lowers inhibitions, alcohol is also hypothesized to be used by those who normally constrain emotions by attenuating intense emotions in high or obliterating doses, which allows them to express feelings of affection, aggression, and closeness.
Psychostimulants, such as crack/cocaine, amphetamines, caffeine, and nicotine, produce improvements in physical and mental functioning, including increased energy and feelings of euphoria. Stimulants tend to be used by individuals who experience depression, to reduce anhedonia and increase self-esteem. The SMH also hypothesizes that hyperactive and hypomanic individuals use stimulants to maintain their restlessness and heighten euphoria. Additionally, stimulants are useful to individuals with social anxiety by helping individuals break through their inhibitions.
Opiates, such as heroin and morphine, function as an analgesic by binding to opioid receptors in the brain and gastrointestinal tract. This binding reduces the perception of and reaction to pain, while also increasing pain tolerance. Opiates are hypothesized to self-medicate aggression and rage. Opiates are effective anxiolytics, mood-stabilizers, and anti-depressants, however, people tend to self-medicate anxiety and depression with depressants and stimulants respectively, though this is by no means an absolute analysis.
Cannabis is a euphoriant that is considered to have both stimulating and sedating properties. Depressant properties are more obvious in occasional users, and stimulating properties are more common in chronic users. Khantzian noted that research had not sufficiently addressed a theoretical mechanism for cannabis, and therefore did not include it in the SMH.
Self medicating excessively for prolonged periods of time with benzodiazepines or alcohol often makes the symptoms of anxiety or depression worse. This is believed to occur as a result of the changes in brain chemistry from long-term use. Of those who seek help from mental health services for conditions including anxiety disorders such as panic disorder or social phobia, approximately half have alcohol or benzodiazepine dependence issues.
Sometimes anxiety precedes alcohol or benzodiazepine dependence but the alcohol or benzodiazepine dependence acts to keep the anxiety disorders going, often progressively making them worse. However, some people addicted to alcohol or benzodiazepines, when it is explained to them that they have a choice between ongoing poor mental health or quitting and recovering from their symptoms, decide on quitting alcohol or benzodiazepines or both. It has been noted that every individual has an individual sensitivity level to alcohol or sedative hypnotic drugs, and what one person can tolerate without ill health, may cause another to suffer very ill health, and even moderate drinking can cause rebound anxiety syndrome and sleep disorders. A person suffering the toxic effects of alcohol will not benefit from other therapies or medications, as these do not address the root cause of the symptoms.
- Benefits and risks of self medication
- Khantzian, E.J. (1997). The self-medication hypothesis of drug use disorders: A reconsideration and recent applications. Harvard Review of Psychiatry, 4, 231-244.
- Khantzian, E.J. (2003). The self-medication hypothesis revisited: The dually diagnosed patient. Primary Psychiatry, 10, 47-48, 53-54.
- Khantzian, E.J., Mack, J.F., & Schatzberg, A.F. (1974). Heroin use as an attempt to cope: Clinical observations. American Journal of Psychiatry, 131, 160-164.
- Duncan, D.F. (1974a). Reinforcement of drug abuse: Implications for prevention. Clinical Toxicology Bulletin, 4, 69-75.
- Duncan, D.F. (1974b). Letter: Drug abuse as a coping mechanism. American Journal of Psychiatry, 131, 174.
- Khantzian, E.J. (1985). The self-medication hypothesis of addictive disorders: Focus on heroin and cocaine dependence. American Journal of Psychiatry, 142, 1259-1264.
- Khantzian, E.J., Halliday, K.S., & McAuliffe, W.E. (1990). Addiction and the vulnerable self: Modified dynamic group therapy for drug abusers. New York: Guilford Press.
- Khantzian, E.J. (1999). Treating addiction as a human process. Northvale, NJ: Jason Aronson.
- Duncan, D.F. (1975). The acquisition, maintenance and treatment of polydrug dependence: A public health model. Journal of Psychedelic Drugs, 7, 209-213. http://www.duncan-associates.com/PUBLICHEALTHMODEL.htm
- Duncan, D.F., & Gold, R.S. (1983). Cultivating drug use: A strategy for the 80s. Bulletin of the Society of Psychologists in Addictive Behaviors, 2, 143-147. http://www.addictioninfo.org/articles/263/1/Cultivating-Drug-Use/Page1.html
- Anthony, J., Warner, L., & Kessler, R. (1994). Comparative epidemiology of dependence on tobacco, alcohol, controlled substances and inhalants: Basic findings from the National Comorbidity Study. Experimental and Clinical Psychopharmacology, 2, 244-268.
- Nicholson, T., Duncan, D.F., & White, J.B. (2002). Is recreational drug use normal? Journal of Drug Use, 7, 116-123. http://www.duncan-associates.com/Is-Recreational-Drug-Use-Normal.pdf
- Self-Medication With Alcohol and Drugs by Persons With Severe Mental Illness
- Mental Illness: The Challenge Of Dual Diagnosis
- Post Traumatic Stress Disorder
- Professor C Heather Ashton (1987). "Benzodiazepine Withdrawal: Outcome in 50 Patients". British Journal of Addiction 82: 655–671. http://www.benzo.org.uk/ashbzoc.htm.
- Michelini S; Cassano GB, Frare F, Perugi G (July 1996). "Long-term use of benzodiazepines: tolerance, dependence and clinical problems in anxiety and mood disorders". Pharmacopsychiatry 29 (4): 127–34. doi:10.1055/s-2007-979558. PMID 8858711.
- Wetterling T; Junghanns K (Dec 2000). "Psychopathology of alcoholics during withdrawal and early abstinence". Eur Psychiatry 15 (8): 483–8. doi:10.1016/S0924-9338(00)00519-8. PMID 11175926.
- Cowley DS (Jan 1, 1992). "Alcohol abuse, substance abuse, and panic disorder". Am J Med 92 (1A): 41S–8S. doi:10.1016/0002-9343(92)90136-Y. PMID 1346485.
- Cosci F; Schruers KR, Abrams K, Griez EJ (Jun 2007). "Alcohol use disorders and panic disorder: a review of the evidence of a direct relationship". J Clin Psychiatry 68 (6): 874–80. doi:10.4088/JCP.v68n0608. PMID 17592911.
- Cohen SI (February 1995). "Alcohol and benzodiazepines generate anxiety, panic and phobias" (PDF). J R Soc Med 88 (2): 73–7. PMC 1295099. PMID 7769598. http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1295099&blobtype=pdf.