Test strips impregnated with phenylthiocarbamide (PTC) have been used to identify genetic differences based on whether a bitter taste is perceived. To determine whether smokers who perceive PTC as bitter tasting ("tasters") would differ from those who describe it as tasteless ("non-tasters") on smoking-related variables, we studied 464 current smokers (70% female, 79% White; mean age 30.5+/-9 years) recruited to participate in laboratory experiments and clinical trials. Of these, 217 (47%) reported the PTC strips as tasteless and 154 (33%) as tasting bitter. The remaining 93 (20%) described the taste as salty, sweet, or other and were excluded from further analyses. Comparing tasters with non-tasters, we found significant differences in mean (S.D.) total years smoked (14.5 [9.2] for non-tasters, vs. 12.6 [8.4] for tasters, p<.05), Fagerstrom Tolerance Questionnaire scores (6.4 [2.1] vs. 5.8 [2.1], p<.01), and scores on the Positive Reinforcement scale of the Michigan-Nicotine Reinforcement Questionnaire (8.1 [2.9] vs. 6.8 [3.1], p<.05). Results suggest that among smokers, ability to taste PTC may confer some protection from development of nicotine dependence and positive reinforcement from smoking.
"Among the non-critical adverse effects of smoking, bitter taste impairment is particularly important in the field of public health
[8-11], not only because it affects the quality of life of smokers but also because it may promote the continuation of smoking which will eventually cause critical adverse effects in both smokers and their relatives. However, despite the importance of this as a potential mechanism for the continuation of smoking
[12-14], to the best of our knowledge no study has investigated the biological mechanism of this bitter taste disability. "
[Show abstract][Hide abstract] ABSTRACT: Background
Despite the fact that smokers have deficit in detecting taste, particularly bitter taste, no study has investigated its biological correlate.
In this context, we compared the expression of the bitter taste receptor gene, taste 2 receptor (TAS2R) in the tongues of smokers and non-smokers. Tissue samples were collected from the lateral portion of the tongues of 22 smokers and 22 age- and gender-matched healthy volunteers (19 males and three females) with no history of smoking. Reverse transcriptase-polymerase chain reaction was used to examine the expression of TAS2R in the two groups, and the effect of aging on TAS2R expression was also assessed.
TAS2R expression was significantly lower among smokers than non-smokers (t = 6.525, P < .0001, 11.36 ± 6.0 vs. 2.09 ± 2.8, mean ± SD, non-smokers vs. smokers). Further, a positive correlation between age and expression of TAS2R was observed in non-smokers (r = .642, P = .001), but not smokers (r = .124, P = .584). This correlation difference was significant (Z = 1.96, P = .0496).
Smokers showed a significantly lower expression of the bitter taste receptor gene than non-smokers, which is potentially caused by their inability to acquire such receptors with age because of cigarette smoking, in contrast to non-smokers.
"Third, the differences in taste detection thresholds were not due to smoking per se but may be a characteristic of individuals who are susceptible to become smokers. For example, it has been suggested that sensitivity to bitter compounds such as PTC and PROP may protect against cigarette smoking (Enoch et al., 2001; Kaplan et al., 1964; Snedecor et al., 2006). However, we found that the women who smoked were as likely to be sensitive to PROP as were women who never smoked, a finding which is consistent with a recent study in which 567 individuals were genotyped for polymorphisms that affect taste sensitivity to PROP and PTC (Cannon et al., 2005). "
[Show abstract][Hide abstract] ABSTRACT: Despite popular beliefs that smoking affects the sensitivity and liking of sweet-tasting foods and beverages, few psychophysical studies have examined this phenomenon and none have taken into account the individual's family history of alcoholism (FH+), a predictor of heightened sweet preferences.
A within- and between-subjects study was conducted to determine the effect of both cigarette smoking and an acute exposure to nicotine on sweet taste sensitivity and preferences in women. Two groups were studied on 2 days separated by 1 week: women who were current smokers (n = 27, 18 were FH+) and those who never smoked in their lifetime (n = 22, 9 were FH+). Current smokers smoked nicotine-containing cigarettes during 1 test session and nicotine-free cigarettes during the other. The procedures were identical during both test sessions for the group of never smokers, with the exception that they did not smoke. Two-alternative staircase methods and forced-choice tracking procedures were used to assess sucrose thresholds and preferences, respectively, during both test session. Standardized questionnaires were administered to assess food cravings as well as smoking and alcohol usage and dependence. The Family Interview for Genetic Studies was used to detect alcoholism according to the DSM III criteria for family members up to second-degree relatives.
Acute exposure to nicotine did not affect sucrose detection thresholds or preferences, but smokers had significantly higher sucrose detection thresholds than never smokers. The greater the smoking dose in pack-years, the lower the sucrose sensitivity. Regardless of smoking status, women who were FH+ preferred significantly higher sucrose concentrations and craved sweets more often than women who were not.
Both smoking and having a family history of alcoholism had differential effects on sweet taste. Smoking was associated with decreased sweet taste sensitivity whereas having a family history of alcoholism was associated with heightened sweet preferences. These findings suggests that future research on the effects of smoking on food habits and cravings should take into account family history of alcoholism given its association with sweet liking and the increased likelihood to develop a tobacco disorder.
Alcoholism Clinical and Experimental Research 12/2007; 31(11):1891-9. DOI:10.1111/j.1530-0277.2007.00519.x · 3.21 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Important advances in our understanding of how taste, smell and somatosensation contribute to oral sensation are reviewed and the nutritional and health implications associated with variation in oral sensation are discussed.
Oral sensation is a central integration of taste (salty, sweet, sour, bitter, umami), retronasal olfaction (i.e. smelling through the mouth), and somatosensation (touch, temperature, pain) by the orbitofrontal cortex. There is normal variation in oral sensation across individuals, ranging from those living in a neon orosensory world to those living in a pastel world. Historically, study of this variation revolved around genetically mediated bitterness of phenylthiocarbamide or propylthiouracil, but now it encompasses additional phenotypes (e.g. fungiform papillae number, bitterness of quinine) and emerging receptor genotypes. Aging and exposure to pathogens interact with genetics to further influence oral sensation. Orosensory variation is associated with differences in preference for high-fat foods, sweets, vegetables, and alcoholic beverages. Emerging data suggest this variation influences intake of these foods/beverages and thus diet-related chronic diseases (cardiovascular diseases, certain cancers, obesity).
Oral sensation varies with genetics and gene-environment interactions. As this variation explains some of the differences in what we like/dislike to eat, attempts to reduce disease risk through diet should consider food/beverage preference to promote health and food enjoyment.
Current Opinion in Gastroenterology 04/2007; 23(2):171-7. DOI:10.1097/MOG.0b013e3280147d50 · 4.29 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.