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Journal of Addiction Research & Therapy
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  • Editorial   
  • J Addict Res Ther, Vol 16(5)

Uncovering Genetic Biomarkers in Substance Use Disorders: Toward Precision Medicine in Addiction Therapy

Murali Krishnan Nambirajan*
Independent Public Health Consultant and Epidemiologist, Chennai, India
*Corresponding Author: Murali Krishnan Nambirajan, Independent Public Health Consultant and Epidemiologist, Chennai, India, Email: muralikrishnan1232@gmail.com

Received: 01-May-2025 / Manuscript No. jart-25-165893 / Editor assigned: 05-May-2025 / PreQC No. jart-25-165893 (PQ) / Reviewed: 15-May-2025 / QC No. jart-25-165893 / Revised: 23-May-2025 / Manuscript No. jart-25-165893 (R) / Published Date: 30-May-2025

Keywords

Genetic biomarkers; Substance use disorders; Precision medicine; Addiction genetics; Genomic profiling; Personalized treatment; Pharmacogenomics; Gene-environment interaction; Risk prediction; Molecular psychiatry

Introduction

Substance Use Disorders (SUDs) represent a major public health crisis, characterized by chronic relapse, comorbid psychiatric conditions, and a high burden on healthcare systems. Despite the availability of behavioral and pharmacological treatments, current therapeutic approaches are often generalized and fail to address the heterogeneity among individuals with addiction [1-5].

This gap in personalized care has fueled interest in identifying genetic biomarkers—molecular indicators that can predict susceptibility, treatment response, and relapse risk in SUDs. The integration of genomics into addiction research offers a powerful avenue to transform clinical practice through precision medicine, wherein therapies are tailored to an individual’s genetic makeup. Advances in genome-wide association studies (GWAS), epigenetics, and next-generation sequencing have revealed promising genetic variants and biological pathways implicated in addiction. These discoveries, if translated effectively, have the potential to revolutionize screening, diagnosis, and individualized treatment strategies in addiction therapy [6-10].

Discussion

The foundation of using genetic biomarkers in addiction therapy lies in understanding how heritable factors influence vulnerability to substance use and addiction-related behaviors. Twin, family, and adoption studies have long demonstrated that genetics accounts for 40–60% of the variance in susceptibility to SUDs. GWAS have identified risk alleles across various substances, including alcohol, opioids, nicotine, and stimulants. For example, polymorphisms in the OPRM1 gene, encoding the mu-opioid receptor, are associated with altered responses to opioid use and treatment with medications such as naltrexone. Similarly, variations in the CHRNA5-A3-B4 gene cluster have been linked to nicotine dependence, and ALDH2 and ADH1B variants are well-established in alcohol metabolism and risk.

These genetic markers do not act in isolation; they interact with environmental exposures such as stress, trauma, and peer influence, shaping the developmental trajectory of addiction. Identifying gene-environment interactions (GxE) is critical for developing risk models that accurately reflect real-world complexity. For instance, individuals with certain FKBP5 variants may exhibit heightened addiction vulnerability only when exposed to early life adversity, highlighting the importance of epigenetics and stress reactivity.

Genetic biomarkers are also being explored for their potential in treatment stratification. In pharmacogenomics, variations in drug metabolism genes such as CYP2D6, CYP3A4, and CYP2C19 affect how patients process medications used in addiction treatment. These differences influence the efficacy and side-effect profiles of drugs like methadone, buprenorphine, and disulfiram. By incorporating genetic screening into clinical decision-making, clinicians can optimize medication choices and dosing strategies, improving outcomes and minimizing adverse effects.

Conclusion

The identification and application of genetic biomarkers in substance use disorders represent a transformative step toward precision medicine in addiction therapy. By uncovering the molecular underpinnings of addiction vulnerability, treatment response, and relapse risk, genomic research offers the tools to move beyond one-size-fits-all approaches. While challenges remain in terms of data integration, diversity, ethics, and clinical implementation, the promise of genetically informed addiction care is undeniable. With continued investment in research, interdisciplinary collaboration, and a commitment to ethical practice, genetic biomarkers can drive the development of more effective, personalized, and sustainable interventions for individuals affected by addiction. This paradigm shift has the potential not only to improve clinical outcomes but also to reduce stigma and promote recovery through science-based, individualized care.

References

  1. Rockhill C, Kodish I, DiBattisto C, Macias M, Varley C, et al. (2010) Anxiety disorders in children and adolescents. Curr Probl Pediatr Adolesc Health Care 40: 66-99.

    Indexed at, Google Scholar, Crossref

  2. Bhatia MS, Goyal A (2018) Anxiety disorders in children and adolescents: Need for early detection. J Postgrad Med 64: 75-76.

    Indexed at, Google Scholar, Crossref

  3. Wang R, Wu Z, Huang C, Hashimoto K, Yang L, et al. (2022) Deleterious effects of nervous system in the offspring following maternal SARS-CoV-2 infection during the COVID-19 pandemic. Translational Psychiatry 12: 232.

    Google Scholar, Crossref

  4. Meyer JS and Quenzer LF (2005) Psychopharmacology; drugs, the brain and behaviour. Sinauer Associates, Sunderland, Massachusetts. 11: 248-272.

    Google Scholar

  5. Narita M, Funada M, Suzuki T (2001) Regulations of opioid dependence by receptor types. Pharmacology and therapeutics 89:1-15.

    Indexed at, Google Scholar, Crossref

  6. Kling MA, Carso RE, Borj R (2000) Opioid receptor imaging with positron emission tomography and [(18)F]cyclotoxy in long-term methadone-treated former heroin addicts. J Pharmacol Exp Ther 295: 1070-1076.

    Indexed at, Google Scholar

  7. Robinson TE, Berrigde KC (2001) Incentive sensitization and addiction. Addiction 96: 103-114.

    Indexed at, Google Scholar, Crossref

  8. Bruton L, Lazo L, Parker K (2005) Goodman & Gilman’s; The pharmacological basis of therapeutics. New York, McGraw-Hill 590, USA.

    Google Scholar, Crossref

  9. Behar M, Bagnulo R, Coffin PO (2018) Acceptability and Feasibility of Naloxone prescribing in primary health care settings: A systematic Review. Prev Med 114: 79-88.

    Indexed at, Google Scholar, Crossref

  10. Lewanowitch T, Miller JH, Irvin R (2006) Reversal of morphine, methadone and heroin induced affects in mice by naloxone methiodite. Life Sciences 78: 682-688.

    Indexed at, Google Scholar, Crossref

Citation: Murali KN (2025) Uncovering Genetic Biomarkers in Substance Use Disorders: Toward Precision Medicine in Addiction Therapy. J Addict Res Ther 16: 781.

Copyright: © 2025 Murali KN. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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