Still, it appears some genes can contribute to the risk of developing a substance use disorder (SUD). During adolescence, for example, environmental factors like family and peer influence may play a more dominant role in the initiation of substance use. As a person ages, their genetic predispositions may become more prominent in the transition from casual use to a substance use disorder. Research confirms a substantial genetic component to the risk of developing an addiction. These studies indicate that genetic factors can account for 40% to 60% of a person’s vulnerability to addiction.
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In this introduction we use the term addiction rather than the term “dependence” as described in DSM IV to avoid confusion with physical dependence, which is neurobiologically and clinically distinct from addiction. We refer to addiction as the phenotype characterized by the compulsive administration of the drug and the loss of control over its intake despite its adverse consequences to the individual. Note that, while relevant, we have not included a paper on the role of genes in brain development; readers interested in this topic are referred to various published reviews in the literature (Toga and Thompson 2005; Hariri 2009; Jedema et al. 2010; Mochida and Walsh 2004).
Nicotine use disorder
Future research must attempt to fully understand the genetic impact behind alcohol dependency in order to discover genetically tailored treatment for alcoholism. Alcohol addiction is a global burden; therefore, it has been immensely studied throughout the decades. Repeated administration of ethanol is the cause of neurological alteration within the circuits that control motivational processes. This leads is addiction genetic to affecting how arousal, reward, and stress are encoded in the brain, creating a vicious cycle. Additionally, chronic use of alcohol induces a change in the aforementioned neurotransmitters leading to sensitization and tolerance.
The Scientific Understanding of Addiction’s Genetic Basis
For example, during substance intake, 5-HT levels increase which is correlated with a boost https://www.seniorsafehomes.org/find-sober-living-houses-near-you-4/ in mood while in withdrawal syndrome there is hypoactivity of the serotonin system which may contribute to dysphoria (26-29). Mounting evidence places the dopaminergic-mesolimbic system as the leading system in the development of addiction, due to its role in encoding motivation and reward (21). Research conducted on mice has emphasized the influence of epigenetic alterations on resilient phenotypes. Thus, in contrast to susceptible mice, resilient ones did not have alterations in the expression of the G9a histone methyltransferase enzyme in their nucleus accumbens when experiencing chronic stress (18). In individuals who are vulnerable to addiction, repetitive exposure to the agent induces long-lasting neuroadaptative changes that further promote drug-seeking behaviors and ultimately lead to persistent and uncontrolled patterns of use that constitute addiction.
- Inhalants define a class of substances based on the route of administration (inhalatory or breathing in volatile chemical vapors).
- Thus, thegenes and SNPs found through GWAS have had little overlap with previous findingsbased on candidate genes/pathways and linkage analyses.
- Once acquainted with alcohol, the nucleus accumbens willincrease dopamine activity in the anticipation of the substancereinforcing repeated consumption.
- These studies indicate that genetic factors can account for 40% to 60% of a person’s vulnerability to addiction.
Next, we discuss the limited number of candidate genes which have shown consistent replication, and the implications of emerging genomewide association findings for the genetic architecture of addictions. Approximately 50% of the variability in opioid dependence is due to additive genetic effects 33, with around 38% of the variability accounted for by genetic risk factors unique to opioid use 34. Several GWAS with modest sample sizes (the largest comprising 10,544 cases) have reported genome-wide significant loci 35,36,37,38,39, however none were replicated using an independent sample. A GWAS of 82,707 European American individuals identified a coding variant in the OPRM1 (opioid receptor mu 1) gene, which was later replicated in 2 independent cohorts 40 and further strengthened in a larger multi-trait GWAS of opioid addiction 41. A subsequent meta-analysis of seven cohorts identified three genome-wide significant lead SNPs in a European ancestry meta-analysis, including variants in the FURIN and OPRM1 genes 42. Furthermore, a multi-trait analysis of GWAS (MTAG) combining OUD with AUD and CUD revealed 18 independent genome-wide significant loci, suggesting common (i.e., shared) genetic factors contribute to the development of multiple substance use disorders 42.
- There is a considerable need for computational approaches to generate and interpret results from genetic studies for addiction.
- NAChRs are widely distributed in the brain, and their subunit composition is cell and region specific.
- Without addressing these root causes, people may continue seeking emotional turmoil as a way to process or avoid dealing with painful memories.
- Parsing the exact mechanisms through which genes affect externalizing behavior will require closer collaborations between the fields of behavior genetics and cognitive neuroscience and may provide targets for future intervention efforts.
For example, studies on family history show that individuals with relatives who have substance use disorders are two to four times more likely to develop similar problems. Large-scale genetic analyses further reinforce that inherited genetic traits contribute substantially to addiction vulnerability. For example, specific genes like ALDH2 amphetamine addiction treatment and ADH1B are involved in breaking down alcohol. Differences in these genes can influence a person’s tolerance to alcohol and the severity of their withdrawal symptoms, both of which can contribute to the development of a substance use disorder.
Onegenome-wide association study on cocaine addiction identified anSNP which maps to an intron of the FAM53B gene. This gene isbelieved to be linked with axonal extension during development andcell proliferation (89). Secondarily, alcoholism affects the expression ofGABAA genes resulting in substance tolerance (27,32).Other genes identified that are involved in the metabolism ofalcohol are ADH1B and ALDH2, including GABRA2,CHRM2, KCNJ6 and AUTS2. Additionally, they control motor activity,intestinal tract motility and peristalsis, the hypothalamicneuroendocrine axis and limbic system regulation of emotionalbehavioral, modulating euphoric responses and opposing stress(31-33).These effects glorify opioids in substance users. Endorphins impact addiction via two routes, either bystimulating the mesolimbic dopamine system also independently, byan increase in endorphins in the extracellular space in the nucleusaccumbens (34). Addiction is a multifactorial process and it isdifficult to understand why some individuals are more susceptibleto developing addictive behavior than others.
A review of tobacco abuse and its epidemiological consequences
A family history of addiction can significantly increase the risk of developing a substance use disorder. Children with parents who struggle with addiction are more likely to face similar challenges as they grow older. Environmental factors, such as early exposure to substance abuse and behavioral modeling, also contribute to the risk.
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