Twin and family studies have demonstrated strong familial inheritance patterns for SUDs (Prom-Wormley, Ebejer, Dick, & Bowers, 2017). Heritability (h2) estimates across SUDs vary, but broadly suggest that genetic influences account for approximately 50% of the risk. The best-known indicator of genetic risk is having a parent with a substance use disorder, but the transmission of risk from parent to child isn’t purely genetic. Another of our recent papers found that resident children of parents who have substance use disorders and related behavioral challenges will engage in similar behaviors more than the genetics of the child would predict. The parents not only pass on their genes but create a riskier environment for the kids.
How do genetics interact with environmental factors in addiction development?
Overall, the scientific outlook emphasizes a complex interplay between multiple genes alcoholism symptoms and environmental factors that shape addiction vulnerability. There is no way to predict what perfect combination of genetic and environmental factors will lead to addiction. However, choosing to seek treatment and overcome addiction is possible for everyone, regardless of what contributed to developing a substance use disorder. Certain mental health conditions like bipolar disorder, depression, attention deficit hyperactivity disorder (ADHD), and schizophrenia make people more likely to develop substance use disorders, sometimes due to self-medicating their symptoms with drugs or alcohol. Scientists can identify genes that influence how people react to and process certain drugs of abuse like opioids, stimulants, and alcohol. One person can take an antihistamine like Benadryl and experience extreme drowsiness; another may get a boost of energy from the same dose.
Careers at NIMH
Anyone can struggle with addiction, which means that regardless of DNA, anyone can also overcome addiction with proper care and treatment. The results of Dickson’s research are likely to reveal new therapeutic or preventative treatments for drug addiction and uncover a means of identifying people susceptible to addiction. Knowing who’s at risk for addiction would allow for more precisely targeted prevention strategies. While there’s much more to know about these addiction genes, so far, there’s a connection.
Further studies probing this relationship will be needed to fully disentangle the nuance of the shared and unique genetic etiology across the spectrum of alcohol consumption levels (e.g. normative consumption, binge drinking) and AUD. Another potential direction is the integration of human genetic data with findings from animal models of addiction endophenotypes (Reynolds et al., 2020). The coding variants in these genes provide a protective effect for AUD by producing aversive effects when drinking alcohol, often resulting in lower levels of consumption and AUD risk (Edenberg & Mcclintick, 2018). Additional studies have examined subdomains of alcohol consumption, suggesting potential etiological differences between alcohol consumption frequency and alcohol consumption quantity (Mallard et al., 2020; Marees et al., 2020b). That said, people with the highest levels of risk were four times more likely to develop a substance use disorder than people with the lowest levels of risk, so we can already help people understand their risk level and optimize their health choices. It has been estimated that 50%-70% of an individual’s risk for cannabis use disorder is due to genetic factors, although environmental factors also play a role.
Genetic Factors
Use these free digital, outreach materials in your community and on social media to spread the word about mental health. Use these free education and outreach materials in your community and on social media to spread the word about mental health and related topics. NAChRs are widely distributed in the brain, and their subunit composition is cell and region specific. The α4β2 and α3β4 subtypes also can contain the α5 subunit, which is believed to increase the rate of channel desensitization and calcium permeability.
This biological foundation helps explain individual differences in addiction risk and highlights targets for personalized treatment strategies. Addiction is a multifactorial disorder, so environmental and other influences play a significant role. Still, it appears some genes can contribute to the risk of developing a substance use disorder (SUD). Genetics researchers have leveraged new CUD genomics data to complete a genetically-informed analysis with unprecedented power, which showed causal relationships between CUD and with risk for developing SUDs in April 2024.
- One means to reduce phenotypic heterogeneity is to classify more genetically or neurobiological homogeneous phenotypes or use ENDOPHENOTYPES as an intermediate phenotype between an addicted phenotype and the biological processes responsible for the manifestation of that disorder.
- Genetic discoveries help in tailored therapies by identifying specific genes and pathways involved in substance use disorders, which leads to targeted treatments.
- These hormones trigger various alterations throughout the body that induce epigenetic changes.
- White Oak Recovery Center is committed to transforming the lives of people struggling with substance use and mental health disorders with researched, fact-based content.
- Cross-trait genetic correlations, genomicSEM (Grotzinger et al., 2019), interesting patterns of pleiotropy have emerged (Abdellaoui, Smit, Van Den Brink, Denys, & Verweij, 2021; Hatoum et al., 2021; Jang et al., 2020).
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- Evidence from family, adoption, and twin studies converges on the relevance of genetic factors in the development of addictions including SUDs and gambling.7–13 Weighted mean heritabilities for addictions computed from several studies of large cohorts of twins are shown in Fig.
- Genetics contributes significantly to vulnerability to this disorder, but identification of susceptibility genes has been slow.
- Understanding these genetic influences enables the development of targeted prevention strategies and personalized treatments.
All information and content on this website are for informational and educational purposes only. Our content is https://ecosober.com/blog/is-addiction-genetic-hereditary-addiction-factors/ not a substitute for professional medical advice, diagnosis, or treatment. It should not be used in place of the advice of a physician or other qualified healthcare providers. Studies have shown that people with underdeveloped amygdalas, the part of the brain that controls emotions, behavior, and motivation, are more likely to be affected by drugs and alcohol.
Genome-Wide Association Studies (GWAS)
Peer pressure, social norms, and cultural attitudes toward substance use can shape an individual’s behavior and increase the risk of addiction. One gene therapy being tested in mice generates antibodies that trap methamphetamine, preventing it from reaching the brain. In another, mice transplanted with genetically modified skin cells make an enzyme that degrades cocaine. Each new addiction-related gene discovered is a potential “drug target.” Researchers can focus on the gene product (protein) and develop a drug to modify its activity.
These epigenetic marks can affect health and even the expression of the traits passed to children. For example, when a person uses https://helpingtreefoundation.org.in/index.php/2020/11/19/substance-abuse-information-and-resources/ cocaine, it can mark the DNA, increasing the production of proteins common in addiction. Increased levels of these altered proteins correspond with drug-seeking behaviors in animals. Addiction is not solely determined by genetics or environment alone; rather, it results from complex interactions between the two. Genetic predispositions can influence how vulnerable an individual is to environmental stressors such as childhood trauma, peer pressure, or exposure to drugs.
If a SNP appears more often in people with a disease than those without, it is thought to either directly affect susceptibility to that disease or be a marker for another variation that does. Family studies that include identical twins, fraternal twins, adoptees, and siblings suggest that as much as half of a person’s risk of becoming addicted to nicotine, alcohol, or other drugs depends on his or her genetic makeup. Finding the biological basis for this risk is an important avenue of research for scientists trying to solve the problem of drug addiction. The identification of specific genes and functional loci moderating vulnerability has been challenging because of the genetic complexity of addictive disorders. This complexity derives from multiple sources including incomplete penetrance, phenocopies, variable expressivity, gene–environment interactions, genetic heterogeneity, polygenicity, and epistasis.
ND also can be assessed by diagnostic criteria based on the DSM-IV.86 However, these symptoms are ultimately aggregated into a dichotomous classification as “dependent” or “not dependent,” which limits its usefulness for research into the causes of addiction. Given that a diagnosis of dependence can be assigned by meeting various combinations of criteria, the diagnosis is conceptually heterogeneous. To expand the breadth of the diagnosis criteria and thereby improve the self-reported assessment of ND, new scales such as the Wisconsin Inventory of Smoking Dependence Motives91 and the Nicotine Dependence Syndrome Scale92 were developed.