The Neurobiological Development of Addiction


Developing Addiction

AddictionDrugs of abuse often cause changes in the brain that oftentimes increases the risk of developing an addiction; however, not every individual who uses a substance becomes addicted to it.[1] In fact, exposure to a substance that leads to addiction also depends upon the antecedent properties of the brain.1 For instance, research states that there is a shared biological vulnerability that underlies substance dependencies.1 These vulnerabilities are referred to as “the addictive process” which involves three interrelated sets of functions: motivation-reward, affect regulation, and behavioral inhibition.1 The article “The Neurobiological Development of Addiction: An Overview” by Aviel Goodman, M.D. focuses on the factors that apply to addictive disorders.1

here According to Goodman, researchers state that predisposition to an addictive disorder stems from the interaction of multiple genes.[2] However, while a large number of genes contributes to an individual’s risk of substance addiction, not one gene is solely responsible for the complete genetic influence.[3] In fact, most of the genetic responsibility regarding developing a substance use disorder is shared among multiple substances.[4] However, genetic variants associated with the development of an addictive disorder can be categorized according to their involvement in motivation-reward, affect regulation, or behavioral inhibition.1

Motivation-Reward: Increasing Likelihood of Addiction

see url Regarding motivation-reward, they homozygous 11 genotype of the dopamine D1 receptor is associated with the following: alcohol abuse, cigarette smoking, illicit drug use, gambling, compulsive shopping, and compulsive eating.[5] Also, the Taq A1 allele of the D2 receptor is associated with alcoholism, cigarette smoking, illicit drug use, gambling, and exaggerated reward value of food, as well as the decreased responsiveness of the reward system to certain rewarding stimuli and heightened responsiveness to events that increase dopamine in the reward system.[6] This promotes the development of an addictive disorder, as motivation is intensified and behaviors are then repeated to increase the dopamine in the reward system.1

quirky dating bios Regarding affect regulation, the gene that encodes for the serotonin transporter protein has a variant site that is characterized by two alleles: one short and one long. The short allele is associated with alcoholism, heroin addiction, cigarette smoking, pathological gambling, bulimia, and binge eating.[7] It is also been found to be associated with affective instability, anxiety-related personality traits, and heightened sensitivity to mild stressors.7 Another allele of the gene, the A allele, is associated with alcoholism, methamphetamine abuse, heroin abuse, cigarette smoking, and all eating disorders.[8]

http://clgsecurities.com/?hixorisima=stuttgarter-nachrichten-bekanntschaften&16c=99 Dopamine D4 and D5 receptors are involved with behavioral inhibition and attention processing.1 In fact, the long allele of a polymorphism in the D4 receptor gene is associated with impulsive personality traits, a risk factor for adolescent alcohol and drug abuse, heroin use, opiate addiction, pathological gambling, binge eating, and food cravings.[9]

Addiction: Beginning at Birth?

http://beerbourbonbacon.com/?niokis=100-free-asian-online-dating&aaf=45 According to Goodman, a considerable portion of brain development occurs after birth, during the first two years of life, and it is highly responsive to the environment.1 Research states that exposure to adverse environments during infancy may create an over-reactive stress response system that leads to impairments in motivation-reward, affect regulation, and behavioral inhibition, causing an addictive disorder.1 For example, children who spend their first two years of life in an institutionalized setting where sufficient caregiving is unavailable are at an increased risk for impairments in affect regulation and behavioral inhibition, leading to an addictive disorder later on.1 When sufficient caregiving is unavailable, children are likely to develop anxiety or depression, have decreased social interaction, and have increased impulsive behavior.[10]

broker opzioni digitali piu popolare Research also states that adverse childhood experiences are associated with the development of addictive disorders.1 One study by Schuck and Widom found that childhood victimization plays a role in the development of addictive disorders.[11] In fact, child abuse can sensitize the stress response system, rendering individuals abused during childhood as vulnerable to stress and stress-related disorders.1 These disorders also increase dendritic atrophy, accelerate neuronal degeneration, and subvert neuronal regeneration in the hippocampus and hippocampal and prefrontal cortex.[12] Adult survivors of child abuse have been found to have changes in their hippocampal structure and function.[13] Stress-induced processes lead to impulsive behavior and addictive disorders.1

www solo opzionibinarie com [1] Goodman, A. (2009, August 28). The Neurological Development of Addiction: An Overview. Psychiatric Times. Retrieved from http://www.psychiatrictimes.com/addiction/content/article/10168/1444777.

[2] Kendler KS. “A gene for…”: the nature of gene action in psychiatric disorders. Am J Psychiatry. 2005;162:1243-1252.

[3] Uhl GR, Liu QR, Naiman D. Substance abuse vulnerability loci: converging genome scanning data. Trends Genet. 2002;18:420-425.

[4] Vanyukov MM, Tarter RE, Kirisci L, et al. Liability to substance use disorders, 1: common mechanisms and manifestations. Neurosci Biobehav Rev. 2003;27: 507-515.

[5] Comings DE, Gade R, Wu S, et al. Studies of the potential role of the dopamine D1 receptor gene in addictive behaviors. Mol Psychiatry. 1997;2:44-56.

[6] Kirsch P, Reuter M, Mier D, et al. Imaging gene-substance interactions: the effect of the DRD2 TaqIA polymorphism and the dopamine agonist bromocriptine on the brain activation during the anticipation of reward. Neurosci Lett. 2006;405:196-201.

[7] Kirsch P, Reuter M, Mier D, et al. Imaging gene-substance interactions: the effect of the DRD2 TaqIA polymorphism and the dopamine agonist bromocriptine on the brain activation during the anticipation of reward. Neurosci Lett. 2006;405:196-201.

[8] Gratacòs M, González JR, Mercader JP, et al. Brain-derived neurotrophic factor Val66Met and psychiatric disorders: met?-analysis of case-control studies confirm association to substance-related disorders, eating disorders, and schizophrenia. Biol Psychiatry. 2007;61:911-922.

[9] Lusher J, Ebersole L, Ball D. Dopamine D4 receptor gene and severity of dependence. Addict Biol. 2000;5:471-474.

[10] Pryce CR, Feldon J. Long-term neurobehavioural impact of the postnatal environment in rats: manipulations, effects and mediating mechanisms. Neurosci Biobehav Rev. 2003;27:57-71.

[11] Schuck AM, Widom CS. Childhood victimization and alcohol symptoms in females: causal inferences and hypothesized mediators. Child Abuse Negl. 2001;25:1069-1092.

[12] Uno H, Tarara R, Else JG, et al. Hippocampal damage associated with prolonged and fatal stress in primates. J Neurosci. 1989;9:1705-1711.

[13] de Geus EJ, van’t Ent D, Wolfensberger SP, et al. Intrapair differences in hippocampal volume in monozygotic twins discordant for the risk for anxiety and depression. Biol Psychiatry. 2007;61:1062-1071. Addiction.

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