Institutional members access full text with Ovid®

Share this article on:

Genetic and Environmental Variation in Taste: Associations With Sweet Intensity, Preference, and Intake

Duffy, Valerie B. PhD, RD; Peterson, Julie M. MS, RD; Dinehart, Mary E. RD; Bartoshuk, Linda M. PhD

Professional Network

Taste and oral sensations from foods and beverages drive food selection. The present study explored whether markers of variation in taste were associated with variability in sweet sensation, sweet preference, and intake of added sugar. Following the pioneering work of Fischer and colleagues from the 1960s, variation in taste was described using the bitterness of 6-n-propylthiouracil (PROP) and that of quinine hydrochloride (QHCl). These markers represent variation in taste, resulting from genetic and environmental influences. In 38 females and 44 males, those who tasted PROP as least bitter but QHCl as most bitter reported the greatest preference for and intake of added sugars (reported frequency of consuming high added sugar foods or percent energy from added sugar). Individuals who were discordant in the PROP versus QHCl bitterness showed most variance in sweet preference and intake. These findings suggest that genetic and environmental variation in taste influences dietary behaviors toward sweet foods. Dietetics practitioners can apply this information by assessing dietary preferences and assisting individuals who prefer sweet foods and beverages to incorporate them into healthful and enjoyable diets.

ORAL SENSATIONS from foods and beverages play a primary role in what is preferred and ultimately eaten.1 Sensory inputs from true taste (sweet, sour, salty, bitter), oral somatosensation (touch, temperature, pain), and retronasal olfaction (olfactory perception through the oral cavity) form oral sensation. For example, strawberry ice cream has a sweet taste, creamy texture (oral somatosensation), and strawberry flavor (retronasal olfaction). Preference ratings of this food are formed to each component (the ice cream is too sweet) and to the composite oral sensation (I really like this ice cream).

Liking for sweet taste is observed in newborn infants2 and is affected by early exposure, maternal, and genetic influences.3 Given the number of factors that influence sweet preference and intake in adults, do markers of variation in taste explain some of the variability in sweet preference and intake in adults? This is relevant to dietetics; energy from added sugars can average from nearly 16%4 to over 20%5 according to nationwide monitoring, and high intakes of added sugars compromise dietary quality6 especially for those wishing to reduce energy intake. Dietetics professionals can assist consumers in incorporating sweet tasting foods into diets that are enjoyable, healthful, and meet individual needs.7

Fox accidentally discovered genetic variation in the bitterness of phenylthiocarbamide (PTC).8 Early family studies suggested that individuals who could not taste PTC (nontasters) carried 2 recessive alleles, while those who taste PTC as bitter (tasters) carried either 1 or both dominant alleles (eg,9,10); about 25% of the US population are nontasters. Examination of a variety of compounds showed that a particular chemical group (C―S[double bond]N) was responsible for the bitters; 6-n-propylthiouracil (PROP) proved to be a better compound to study because it lacked the sulfurous odor of PTC. Early studies focused on variations in the frequency of tasters by sex and race (reviewed by), Bartoshuk et al11 as well as association between tasting and disease. Fischer was the first to focus on the possibility that this variation might be related to food preferences as well.12 He compared the characteristic bimodal threshold distribution for PROP with the normal distributions produced by stimuli representing the 4 taste qualities (NaCl, sucrose, quinine, and hydrochloric acid), with particular emphasis on the quinine thresholds.13 Fischer believed that his quinine measure reflected a general ability to taste; combining this general measure with the specific ability to taste PTC/PROP compounds produced a group of “acute tasters” who had more food dislikes, tended to avoid smoking,14 and were thinner.15

Current research has added to our understanding of the possible links between oral sensation and dietary behaviors. Modern psychophysical tools allow us to scale perceived intensities, which are likely to be more closely associated with oral sensations experienced during eating and thus to nutrition outcomes than are measures of threshold.16 Measuring perceived PROP bitterness permitted the separation of PROP tasters into medium and supertasters (eg, reference 11). Medium and supertasters of PROP have similar thresholds; however, the suprathreshold bitterness of PROP is more intense for supertasters. Supertasters perceive all tastants (salt, sweet, sour, bitter) as more intense than do nontasters (see reference 17 for a review); anatomical studies show that supertasters have more fungiform papillae (the structures that house taste buds on the anterior tongue).11,18,19 Because fungiform papillae are innervated by pain and touch fibers,20 supertasters also perceive more intense oral irritation (eg, chilis17–21) and oral touch (eg, creamy/oily sensations from fats).19,22,24 The identification of the PROP gene25 showed that supertasters do not necessarily carry 2 dominant alleles, as was once suspected. Rather, supertasters carry 1 or both of the dominant genes but must also have a high density of fungiform papillae (Duffy, Reed, and Bartoshuk, unpublished data, 2003). Thus, additional genes controlling density play important roles in all of the associations between PROP tasting and dietary behaviors.

Studies of taste pathology add to the importance that Fisher attributed to the bitterness of quinine as reflective of general taste function. Exposure to a variety of factors can change bitter taste across the lifespan (eg, sex hormones, pathology). With regard to pathology, the chorda typami nerve (branch of cranial nerve VII) has been most studied.26–30 The chorda tympani is vulnerable to damage by pathogens and head trauma as it travels from the tongue through the middle ear to the central nervous system. Damage to (or anesthesia of) the chorda tympani nerve can actually increase taste sensations (particularly bitter) from other taste nerves (glossopharyngeal branch of cranial nerve IX and cranial nerve X) 26–30 and oral somatosensory sensations from the trigeminal nerve (cranial nerve V).31,32 However, damage to (or anesthesia of) the chorda tympani nerve can blunt retronasal olfactory sensations from cranial nerve I.33,34

An anecdote from the 1800s from Brillat-Savarin's book The Physiology of Taste describes enhanced taste and oral somatosensory sensations from chorda tympani nerve damage. A prisoner who had his tongue cut off for punishment reported being able to taste fairly well but sour or bitter things caused him unbearable pain.35 In 1965, Bull33 described oral sensory changes in individuals who underwent unilateral chorda tympani damage during middle-ear surgery. Approximately 2 of 3 complained of alterations in “taste,” including inability to differentiate between coffee and tea, and the perception that foods, such as bread and chocolate, were doughy and greasy, respectively. These complaints represent changes in true taste, oral somatosensation, and retronasal olfaction.

Fischer studied acute tasters who were concordant for tasting PROP and quinine. We now have a greater understanding of how genetic and environmental influences can alter taste and thus produce oral sensory responses that show discordance between PROP and quinine. One could be born a genetic nontaster but, through pathology, lose chorda tympani function with a compensatory increase of oral sensations (particulary bitterness) from the other cranial nerves. Conversely, one could be born a genetic supertaster and suffer more extensive damage to taste and thus experience reduced taste.

Variation in sweet preference and dietary behaviors has been shown to associate with perceived bitterness of PROP. As sucrose concentration increases, some individuals (ie, “likers”) report increasing preference while others (ie, “dislikers”) report decreasing preference.36 Looy and Weingarten37 found that PROP tasters were almost always sweet dislikers, while PROP nontasters were almost always sweet likers. In support of this, we38 showed that those who tasted PROP as most bitter (assessed through magnitude matching) had the lowest preference for sweet foods, an effect that was seen only in women. A pilot study on dental caries also suggests PROP effects on intake of sweet foods. Children who were PROP nontasters were most likely to have dental caries,39 a condition associated with exposure to dietary sugars.40

School of Allied Health, University of Connecticut, Storrs, Conn (Dr Duffy and Ms Peterson and Dinehart); and the Department of Surgery, Section of Otolaryngology, Yale University School of Medicine, New Haven, Conn (Dr Bartoshuk).

Corresponding author: Valerie B. Duffy, PhD, RD, School of Allied Health, University of Connecticut, Storrs, CT 06269-2101 (e-mail:

This study was funded by grants from the NRICGP/USDA (2002-00788 and 9603745), NIH DC00283, and USDA/Food Stamp Education through the Connecticut Department of Public Health. The authors thank Audrey K. Chapo, MS, RD, for helpful comments on the manuscript.

© 2003 Lippincott Williams & Wilkins, Inc.