Evidence map›Paper›PMID 39327304›Full record

ArticleEuropean archives of psychiatry and clinical neuroscience2025

Unveiling causal relationships between addiction phenotypes and inflammatory cytokines: insights from bidirectional mendelian randomization and bibliometric analysis.

Shirui Cao, Longtao Yang, Xuemei Wang, Wenhan Yang, Fei Tang, Shixiong Tang, Jun Liu

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Article in European archives of psychiatry and clinical neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Shirui Cao *Department of Radiology, The Second Xiangya Hospital of Central South University, Changsha, China.
Longtao Yang *Department of Radiology, The Second Xiangya Hospital of Central South University, Changsha, China.
Xuemei Wang *Department of Laboratory Medicine, The Second Xiangya Hospital, Central South University, Changsha, China.
Wenhan YangDepartment of Radiology, The Second Xiangya Hospital of Central South University, Changsha, China.
Fei TangDepartment of Radiology, The Second Xiangya Hospital of Central South University, Changsha, China.
Shixiong TangDepartment of Radiology, The Second Xiangya Hospital of Central South University, Changsha, China.
Jun LiuDepartment of Radiology, The Second Xiangya Hospital of Central South University, Changsha, China. junliu123@csu.edu.cn.ORCID http://orcid.org/0000-0002-7851-6782

Funding

Clinical Research Center For Medical Imaging In Hunan Province in China 2020SK4001Fundamental Research Funds for Central Universities of the Central South University 1053320230244Innovative Province Special Construction Foundation of Hunan Province 2019SK2131National Natural Science Foundation of China U22A20303the Science and Technology Innovation Program of Hunan Province 2021RC4016
6 · The paper itself

Abstract

Observational studies have suggested associations between multiple inflammatory factors and tobacco and alcohol use, but establishing causation is challenging in epidemiological investigations. We employed genetic association data about the circulating levels of 41 cytokines obtained from the genome-wide association study (GWAS), which contained 8293 Finnish participants. Genetic data on 5 substance use phenotypes were obtained from the GWAS dataset containing 1.2 million European subjects. Then, we conducted a bidirectional mendelian randomization (MR) study. The forward results indicated that smoking cessation was positively correlated with hepatocyte growth factor (HGF), interleukin-10 (IL-10), and stem cell factor (SCF); cigarettes per day was a risk factor associated with high expression in stromal cell-derived factor 1α (SDF-1 A), interferon-γ (IFN-G), IL-4, and granulocyte colony-stimulating factor (G-CSF); drinks per week and smoking initiation were risk factors respectively correlated with reduced HGF and IL-2RA levels. During inverse MR analysis, the findings revealed that both IL-16 and IL-18 increased the risk of cigarettes per day; macrophage inflammatory protein-1β (MIP-1B) and tumor necrosis factor-β (TNF-B) inhibited and promoted smoking cessation, respectively; macrophage colony-stimulating factor (M-CSF) elevated the risk of drinks per week, while interferon inducible protein 10 (IP-10) had a contrary role; IL-7 and M-CSF respectively prolonged and shortened age of initiation of regular smoking. This study provides genetic proof supporting a causal relationship between various inflammatory factors and addiction phenotypes. Further comprehensive investigations are required to uncover underlying biological mechanisms. In addition, bibliometric studies have shown that oxidative stress is one of the most important orientations in alcohol and tobacco addiction research, where an in-depth investigation of its pro-inflammatory mechanisms would facilitate the development of potential therapeutic biological targets and drugs.

Indexed as

Behavior, AddictiveBibliometricsCytokinesInflammationMendelian Randomization AnalysisSubstance-Related DisordersFinlandGenome-Wide Association StudyHumansPhenotypeCytokinesAlcohol use disorderCausal relationshipInflammatory cytokinesMendelian randomizationTobacco use disorder

Identifiers

PMID39327304

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.