University research suggests individuals with greater sensitivity to bitter tastes are less likely to develop a dependence on nicotine than those with a lower sensitivity to such tastes.
“If a person is a [sensitive] taster, then that person is less likely to become a smoker,” said lead investigator Ming Li, professor of psychiatry and neurobehavioral sciences. “In other words, [being a] taster is kind of protective and [being a] non-taster is kind of like a risk factor.”
Li explained that the research project consisted of two components, the first of which was published in the Journal of Medical Genetics and the second of which was published in the American Journal of Human Genetics. The first component of the research focused on genetic analysis of DNA samples taken from more than 2,200 human subjects over a period of nearly 10 years, Li said. The individuals taking part in the study were classified as tasters, non-tasters or intermediate, Li said. If a person was classified as a non-taster, he or she was more likely to become a smoker.
The second component of the research introduced a mathematically based methodology that provided a novel method of detecting gene-gene interaction for other human genetic researchers, Li said, and was used to analyze genetic data on two taste receptor genes, known as TAS2R16 and TAS2R38. The researchers found that these two genes interact with each other in the development of smoking dependence. This component of the research extended the finding of the first report, and together the research offers a “complete story,” Li said.
Jamie Mangold, a former research assistant in Li’s lab who was primarily involved in the first component of the study, commented that the development of the research between the two publications focused on the role of the taste receptor genes.
There was evidence in earlier research, Mangold said, indicating that people who are more sensitive to bitter substances are less likely to be smokers and drinkers. Mangold said she looked through the literature and thought that taste could be a major factor.
“With publication of the first paper, we kind of decided that the TAS2R16 gene was not a primary player … but after the second paper we realized that the TAS2R16 gene may also be important through its interaction with TAS2R38,” Mangold said.
Li explained that older methodologies could only handle either binary traits, such as whether a person did or did not have a disease, or continuous traits, such as height. Moreover, Li said, these methods could not account for all the variables that may affect an individual’s characteristics, such as age, gender and ethnicity.
“With our method, you can correct [the algorithm] for all [factors] that you think may affect this disease,” Li said.
Xiang-Yang Lou, assistant professor of psychiatry and neurobehavioral sciences and first author of the second paper, said his portion of the study showed a relatively small, but still noticeable, relation between the two interacting genes and nicotine dependency. Lou explained that this is likely because smoking is a complex, multivariable behavior; however, he emphasized that the findings in his report were noteworthy because they had a low level of statistical error for the relatively small quantities with which they dealt.
“This new method is better than [the previously] existing method and able to detect even a relatively small difference,” Lou said. “Genetic researchers are very interested in finding these kinds of interactions these days.”
While the two components of the project were largely independent efforts within the research group, Lou noted, the second paper referred to data that had been examined in the first.
In contrast to the size and longevity of the sample for the first project, Lou said he used data from more than 600 families in a simulation of the algorithm to validate the new method and data from about 400 families in the final nicotine dependence study.
Ultimately, Mangold explained, the new findings may prove valuable for future medical use.
“This in particular would be a useful way to screen out for those who would be more susceptible,” Mangold said. “So early on before smoking behavior begins, if one is screened for this genotype, we may actually be able to predict who may become dependent and then actually target more preventive programs toward them.”
Source: Prateek Vasireddy, Cavalier Daily