Bitter taste receptor gene polymorphisms are an important factor in the development of nicotine dependence in African Americans
- 1Department of Psychiatry and Neurobehavioral Sciences, University of Virginia, Charlottesville, Virginia, USA
- 2ACT Center for Tobacco Treatment, Education and Research, Department of Otolaryngology and Communicative Sciences, University of Mississippi Medical Center, Jackson, Mississippi, USA
- 3Department of Public Health Sciences, University of Virginia, Charlottesville, Virginia, USA
- Professor M D Li, Department of Psychiatry and Neurobehavioral Sciences, University of Virginia, 1670 Discovery Drive, Suite 110, Charlottesville VA 22911, USA; Ming_Li{at}virginia.edu
- Received 17 January 2008
- Revised 28 February 2008
- Accepted 23 April 2008
- Published Online First 4 June 2008
Abstract
Context: Bitter sensitivity varies among individuals and ethnic groups partly due to polymorphisms in taste receptor genes (TAS2Rs). Although previous psychophysical studies suggest that taste status plays a role in nicotine dependence (ND), genetic evidence is lacking.
Objectives: To determine whether single nucleotide polymorphisms (SNPs) in TAS2R16 and TAS2R38 are associated with ND and if the effects differ by sex and ethnicity.
Design, setting, and participants: 2037 individuals from 602 nuclear families of African American (AA) or European American (EA) origin were recruited from the US mid-south states during 1999–2004.
Main outcome measures: ND was assessed by three measures: indexed Smoking Quantity (SQ), Heaviness of Smoking Index (HSI), and the Fagerström Test for Nicotine Dependence (FTND). Peripheral blood samples were obtained for DNA extraction and genotyping.
Results: The TAS2R38 taster haplotype PAV was inversely associated (p = 0.0165), and the non-taster haplotype AVI was positively associated (p = 0.0120), with SQ in AA smokers. The non-taster haplotype was positively associated with all ND measures in AA female smokers (p = 0.01~0.003). No significant associations were observed in the EA sample.
Conclusions: TAS2R38 polymorphisms are an important factor in determining ND in AAs. Heightened oral sensitivity confers protection against ND. Conversely, decreased sensitivity represents a risk factor for ND, especially in AA females. Together, our findings suggest that taster status plays a role in governing the development of ND and may represent a way to identify individuals at risk for developing ND, particularly in AA smokers.
Footnotes
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Funding: This work was supported by NIH grant R01-DA12844 to MDL.
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Competing interests: None.
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Patient consent: Obtained.
