|Addiction and dependence glossary|
Psychological dependence is a state that involves emotional–motivational withdrawal symptoms, e.g. anxiety and anhedonia, upon cessation of drug use or certain behaviours. It develops through frequent exposure to a psychoactive substance or behaviour, though behavioural dependence is less talked about. The specific mechanism involves a neuronal counter-adaption, which could be mediated through changes in neurotransmittor activity or altered receptor expression. Withdrawal symptoms can be attenuated by environmental enrichment and physical activity. Psychological dependence is not to be confused with physical dependence, which induces physical withdrawal symptoms upon discontinuation of use. However they are not mutually exclusive.
Symptoms of psychological dependence include:
Psychological dependence is caused by consistent and frequent exposure to a drug or behavioural activity. It is often associated with effects of drug use, but it can also be caused by behaviourial activity e.g. pornography.
The mechanism that generates dependence involves a neuronal counter-adaption, which is localized to areas of the brain responsible for a drug's positive reinforcement. This adaption occurs as a change in neurotransmitter activity or in receptor expression.
Change in neurotransmittor activity
Studies have shown that in rats experiencing ethanol withdrawal, stimulant withdrawal or opioid withdrawal, the nucleus accumbens shows lower levels of serotonin and dopamine than controls. These decreases are associated with depression and anxiety.
In anatomically distinct areas of the rat brain, withdrawal is linked to lower levels of GABA and neuropeptide Y as well as higher levels of dynorphin, corticotropin-releasing factor, and norepinephrine; these fluctuations can contribute to psychological dependence.
Altered receptor expression
Changes in receptor expression have also been linked to various symptoms of drug withdrawal. For example, in a study of rats undergoing nicotine withdrawal there has been observed a down regulation of α6β2*n-icotinic acetylcholine receptors in the mesostriatal dopaminergic pathways.
Methods for reducing dependence
A study examined how rats experienced morphine withdrawal in different surroundings. The rats was either placed in an standard environment (SE) or in an enriched environment (EE). The study concluded that EE reduced depression and anxiety withdrawal symptoms.
Another study tested whether swimming exercises affected the intensity of perceivable psychological symptoms in rodents during morphine withdrawal. It concluded that the anxious and depressive states of the withdrawal were reduced in rats from the exercise group.
Distinction between psychological and physical dependence
|Physical dependence||Psychological dependence|
The major differences between psychological dependence and physical dependence are the symptoms they cause. While symptoms of psychological dependence relate to emotional and motivational impairment, physical dependence entails somatic symptoms e.g. increased heart rate, sweating, tremor. The type of dependence experienced after chronic use varies between different substances (see table 1).
Although psychological dependence and physical dependence are distinct entities, they should not be characterized as mutually exclusive. Empirical studies have shown that cravings, which are traditionally associated with psychological dependence, involve a physiological element.
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Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type [nucleus accumbens] neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.41. ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.
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Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home. Depending on the level of severity, this disorder is classified as mild, moderate, or severe.
Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug. In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder.
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