Search results
Results From The WOW.Com Content Network
The hijack model of substance addiction explains that drugs that elicit positive emotion mediate incentive motivation in the nucleus accumbens of the brain. Put another way, addictive substances act on ancient and evolutionarily conserved neural mechanisms associated with positive emotions that evolved to mediate incentive behavior.
Models of addiction risk that have been proposed in psychology literature include an affect dysregulation model of positive and negative psychological affects, the reinforcement sensitivity theory model of impulsiveness and behavioral inhibition, and an impulsivity model of reward sensitization and impulsiveness. [1] [5] [6]
The common biomolecular mechanisms underlying addiction – CREB and ΔFosB – were reviewed by Eric J. Nestler in a 2013 review. [3] Genetics and mental disorders may precipitate the severity of a drug addiction. It is estimated that 50% of healthy individuals developing an addiction can trace the cause to genetic factors. [4]
Addiction affects the brain circuits of reward and motivation, learning and memory, and the inhibitory control over behavior. [24] There are different schools of thought regarding the terms dependence and addiction when referring to drugs and behaviors. One adopted belief is that "drug dependence" equals "addiction."
Substance dependence, also known as drug dependence, is a biopsychological situation whereby an individual's functionality is dependent on the necessitated re-consumption of a psychoactive substance because of an adaptive state that has developed within the individual from psychoactive substance consumption that results in the experience of withdrawal and that necessitates the re-consumption ...
Many neurobiological theories of addiction place repeated or continued use of the drug in the path of addiction development. For example, researchers have theorized that addiction is the result of the shift from goal-directed actions to habits and ultimately, to compulsive drug-seeking and taking. [18] [19]
Under the model of alcoholism, alcohol use disorder is viewed as chronic problem for which abstinence is required. [4] A brain disease model of addiction, based on the extent of neuroadaptation and impaired control, is main position advanced for proposing a disease model of alcohol use disorder. [5]
Edward Khantzian was a professor of psychiatry at Harvard Medical School. [1] Beginning in the 1970s, [2] he developed a progressively more coherent and empirically-grounded self-medication hypothesis of drug abuse, [3] [4] which states that individuals use drugs in an attempt to self-medicate states of distress and suffering.