ArticleAddictive behaviors2018
The role of nicotinic receptor genes (CHRN) in the pathways of prenatal tobacco exposure on smoking behavior among young adult light smokers.
Article in Addictive behaviors, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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4 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.
- Pooled it
- Sex- and Genotype-Dependent Nicotine-Induced Behaviors in Adolescent Rats with a Human Polymorphism (rs2304297) in the 3'-UTR of theInternational journal of molecular sciences · 2022Article
- Estimating causal and time-varying effects of maternal smoking on youth smoking.Addictive behaviors · 2021Article
- Cholinergic receptor nicotinic beta 3 subunit polymorphisms and smoking in male Chinese patients with schizophrenia.EC psychology and psychiatry · 2021Article
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Authors and funding
8 authors at 6 institutions in 1 country.
Funding
Abstract
backgroundPrenatal tobacco exposure (PTE) is associated with more frequent smoking among young, light smokers. Little is known about how nicotinic acetylcholine receptor (CHRN) genes may contribute to this relationship.
methodsData were drawn from a longitudinal cohort of young light smokers of European ancestry (N = 511). Three single nucleotide polymorphisms (SNPs) among offspring, rs16969968 and rs6495308 in CHRNA5A3B4 and rs2304297 in CHRNB3A6, were analyzed with respect to whether they 1) predict PTE status; 2) confound the previously-reported effects of PTE on future smoking; 3) have effects on youth smoking frequency that are mediated through PTE; and 4) have effects that are moderated by PTE.
resultsrs2304297 and rs6495308 were associated with increased likelihood and severity of PTE, respectively. In a path analysis, rs16969968 directly predicted more frequent smoking in young adulthood (B = 1.50, p = .044); this association was independent of, and not mediated by, PTE. The risk of rs16969968 (IRR = 1.07, p = .015) and the protective effect of rs2304297 (IRR = 0.84, p < .001) on smoking frequency were not moderated by PTE. PTE moderated the effect of rs6495308, such that these alleles were protective against later smoking frequency only among non-exposed youth (IRR = 0.85, p < .001).
conclusionsThe association between offspring CHRNB3A6 and PTE is a novel finding. The risk of rs16969968 on youth smoking is independent and unrelated to that of PTE among young, light smokers. PTE moderates the protective effect of rs6495308 on youth smoking frequency. However, PTE's pathway to youth smoking behavior was not explained by these genetic factors, leaving its mechanism(s) of action unclear.
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