An Exploration of Taste–Emotion Mappings from the Perspective of Food Design Practitioners

This paper explores taste-emotion mappings and how they may inform the design of user experience in HCI. We report interviews with 7 food industry professionals and discuss the findings against laboratory-based psychology studies. While the sweet-positive affect and bitter-negative affect mappings were confirmed, those for sour, salty and umami tastes were challenged. Our outcomes highlight a more nuanced understanding of taste-emotion mappings, the influence of taste intensity and the importance of narrative and temporality when designing taste experience in naturalistic settings

The perception of quinine taste intensity is associated with common genetic variants in a bitter receptor cluster on chromosome 12

The perceived taste intensities of quinine HCl, caffeine, sucrose octaacetate (SOA) and propylthiouracil (PROP) solutions were examined in 1457 twins and their siblings. Previous heritability modeling of these bitter stimuli indicated a common genetic factor for quinine, caffeine and SOA (22–28%), as well as separate specific genetic factors for PROP (72%) and quinine (15%). To identify the genes involved, we performed a genome-wide association study with the same sample as the modeling analysis, genotyped for approximately 610 000 single-nucleotide polymorphisms (SNPs). For caffeine and SOA, no SNP association reached a genome-wide statistical criterion. For PROP, the peak association was within TAS2R38 (rs713598, A49P, P = 1.6 × 10−104), which accounted for 45.9% of the trait variance. For quinine, the peak association was centered in a region that contains bitter receptor as well as salivary protein genes and explained 5.8% of the trait variance (TAS2R19, rs10772420, R299C, P = 1.8 × 10−15). We confirmed this association in a replication sample of twins of similar ancestry (P = 0.00001). The specific genetic factor for the perceived intensity of PROP was identified as the gene previously implicated in this trait (TAS2R38). For quinine, one or more bitter receptor or salivary proline-rich protein genes on chromosome 12 have alleles which affect its perception but tight linkage among very similar genes precludes the identification of a single causal genetic variant

Factors Associated with Revision Surgery after Internal Fixation of Hip Fractures

Background: Femoral neck fractures are associated with high rates of revision surgery after management with internal fixation. Using data from the Fixation using Alternative Implants for the Treatment of Hip fractures (FAITH) trial evaluating methods of internal fixation in patients with femoral neck fractures, we investigated associations between baseline and surgical factors and the need for revision surgery to promote healing, relieve pain, treat infection or improve function over 24 months postsurgery. Additionally, we investigated factors associated with (1) hardware removal and (2) implant exchange from cancellous screws (CS) or sliding hip screw (SHS) to total hip arthroplasty, hemiarthroplasty, or another internal fixation device. Methods: We identified 15 potential factors a priori that may be associated with revision surgery, 7 with hardware removal, and 14 with implant exchange. We used multivariable Cox proportional hazards analyses in our investigation. Results: Factors associated with increased risk of revision surgery included: female sex, [hazard ratio (HR) 1.79, 95% confidence interval (CI) 1.25-2.50; P = 0.001], higher body mass index (fo

Suppression of Bitterness Using Sodium Salts

Bitterness is an ongoing taste problem for both the pharmaceutical and food industries. This paper reports on how salts (NaCl, NaAcetate, NaGluconate, LiCl, KCl) and bitter compounds (urea, quinine-HCö, caffeine, amiloride-HCö, magnesium sulfate, KCl) interact to influence bitter perception. Sodium salts differentially suppress bitterness of these compounds; for example urea bitterness was suppressed by over 70% by sodium salts, while MgSO4 bitterness was not reduced. This study indicated that lithium ions had the same bitter suppressing ability as sodium ions, however the potassium cation had no bitter suppression ability. Changing the anion attached to the sodium did not affect bitter suppression, however, as the anion increased in size, perceived saltiness decreased. This indicates that sodium's mode of action is at the peripheral taste level, rather than a cognitive affect.A second experiment revealed that suppressing bitterness with a sodium salt in a bitter/sweet mixture causes an increase in sweetness. This suggests adding salt to a food matrix will not only increase salt perception, but also potentiate flavor by differential suppression of undesirable tastes such as bitter, while increasing more desirable tastes such as sweet

The Molecular Basis of Individual Differences in Phenylthiocarbamide and Propylthiouracil Bitterness Perception

AbstractIndividual differences in perception are ubiquitous within the chemical senses: taste, smell, and chemical somesthesis [1–4]. A hypothesis of this fact states that polymorphisms in human sensory receptor genes could alter perception by coding for functionally distinct receptor types [1, 5–8]. We have previously reported evidence that sequence variants in a presumptive bitter receptor gene (hTAS2R38) correlate with differences in bitterness recognition of phenylthiocarbamide (PTC) [9–11]. Here, we map individual psychogenomic pathways for bitter taste by testing people with a variety of psychophysical tasks and linking their individual perceptions of the compounds PTC and propylthiouracil (PROP) to the in vitro responses of their TAS2R38 receptor variants. Functional expression studies demonstrate that five different haplotypes from the hTAS2R38 gene code for operatively distinct receptors. The responses of the three haplotypes we also tested in vivo correlate strongly with individuals' psychophysical bitter sensitivities to a family of compounds. These data provide a direct molecular link between heritable variability in bitter taste perception to functional variations of a single G protein coupled receptor that responds to compounds such as PTC and PROP that contain the N-C=S moiety. The molecular mechanisms of perceived bitterness variability have therapeutic implications, such as helping patients to consume beneficial bitter-tasting compounds—for example, pharmaceuticals and selected phytochemicals