Self-medication

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.[14][15]

The self-medication hypothesis (SMH) originated in papers by Edward Khantzian, Mack and Schatzberg,[16] David F. Duncan,[17] and a response to Khantzian by Duncan.[18] The SMH initially focused on heroin use, but a follow-up paper added cocaine.[19] The SMH was later expanded to include alcohol,[20] and finally all drugs of addiction.[14][21][5]

According to Khantzian's view of addiction, drug users compensate for deficient ego function[16] by using a drug as an "ego solvent", which acts on parts of the self that are cut off from consciousness by defense mechanisms.[14] According to Khantzian,[19] 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.[17] 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.[17][22]

Khantzian revisited the SMH, suggesting there is more evidence that psychiatric symptoms, rather than personality styles, lie at the heart of drug use disorders.[14] 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.[14] 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.[14]

Meanwhile, Duncan's work focuses on the difference between recreational and problematic drug use.[23] 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.[24] 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.[25] 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.[17]

Some mental illness sufferers attempt to correct their illnesses by using certain drugs. Depression is often self-medicated with alcohol, tobacco, cannabis, or other mind-altering drug use.[26] 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,[27] and may lead to addiction/dependence, among other side effects of long-term use of the drug.

Sufferers of posttraumatic stress disorder have been known to self-medicate, as well as many individuals without this diagnosis who have suffered from (mental) trauma.[28]

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.[14]

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 relief from depressive affect and anxiety.[14][15] 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.[15][21] People with social anxiety disorder commonly use these drugs to overcome their highly set inhibitions.[29]

Psychostimulants, such as cocaine, amphetamines, methylphenidate, caffeine, and nicotine, produce improvements in physical and mental functioning, including increased energy and alertness. Stimulants tend to be most widely used by people suffering from ADHD, which can either be diagnosed or undiagnosed. Because a significant portion of people suffering from ADHD have not been diagnosed they are more prone to using stimulants like caffeine, nicotine or pseudoephedrine to mitigate their symptoms. It's worth noting that the unawareness concerning the effects of illicit substances such as cocaine, methamphetamine or mephedrone can result in self-medication with these drugs by individuals affected with ADHD symptoms. This self medication can effectively prevent them from getting diagnosed with ADHD and receiving treatment with stimulants like methylphenidate and amphetamines.

Stimulants also can be beneficial for individuals who experience depression, to reduce anhedonia[15] and increase self-esteem.,[20] however in some cases depression may occur as a comorbid condition originating from the prolonged presence of negative symptoms of undiagnosed ADHD, which can impair executive functions, resulting in lack of motivation, focus and contentment with one's life, so stimulants may be useful for treating treatment-resistant depression, especially in individuals thought to have ADHD. The SMH also hypothesizes that hyperactive and hypomanic individuals use stimulants to maintain their restlessness and heighten euphoria.[15][19][20] Additionally, stimulants are useful to individuals with social anxiety by helping individuals break through their inhibitions.[15] Some reviews suggest that students use psychostimulants to self medicate for underlying conditions, such as ADHD, depression or anxiety.[5]

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 be used as self-medication for aggression and rage.[19][21] 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.[15]

Modern research into novel antidepressants targeting opioid receptors suggests that endogenous opioid dysregulation may play a role in medical conditions including anxiety disorders, clinical depression, and borderline personality disorder.[30][31][32] BPD is typically characterized by sensitivity to rejection, isolation, and perceived failure, all of which are forms of psychological pain.[33] As research suggests that psychological pain and physiological pain both share the same underlying mechanism, it is likely that under the self-medication hypothesis some or most recreational opioid users are attempting to alleviate psychological pain with opioids in the same way opioids are used to treat physiological pain.[34][35][36][37]

Cannabis is paradoxical in that it simultaneously produces stimulating, sedating and mildly psychedelic properties and both anxiolytic or anxiogenic properties, depending on the individual and circumstances of use. 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.[15]

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.[38][39][40][41][42] 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.[43]

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.[43]

Nicotine addiction seems to worsen mental health problems. Nicotine withdrawal depresses mood, increases anxiety and stress, and disrupts sleep. Although nicotine products temporarily relieve their nicotine withdrawal symptoms, an addiction causes stress and mood to be worse on average, due to mild withdrawal symptoms between hits. Nicotine addicts need the nicotine to temporarily feel normal.[7][44] Nicotine industry marketing has claimed that nicotine is both less harmful and therapeutic for people with mental illness, and is a form of self-medication. This claim has been criticised by independent researchers.[6]

Self medicating is a very common precursor to full addictions and the habitual use of any addictive drug has been demonstrated to greatly increase the risk of addiction to additional substances due to long-term neuronal changes. Addiction to any/every drug of abuse tested so far has been correlated with an enduring reduction in the expression of GLT1 (EAAT2) in the nucleus accumbens and is implicated in the drug-seeking behavior expressed nearly universally across all documented addiction syndromes. This long-term dysregulation of glutamate transmission is associated with an increase in vulnerability to both relapse-events after re-exposure to drug-use triggers as well as an overall increase in the likelihood of developing addiction to other reinforcing drugs. Drugs which help to re-stabilize the glutamate system such as N-acetylcysteine have been proposed for the treatment of addiction to cocaine, nicotine, and alcohol.[45]