Statistics on Smell and Taste

On this page:

• Smell
  • Statistics
  • Summary Report
  • Books and Articles
  • More Information
• Taste
  • Statistics
  • Summary Report
  • Books and Articles
  • More Information

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Smell: Statistics

Source: Compiled from fact sheets produced by the National Institute on Deafness and Other Communication Disorders (NIDCD).

• One to 2 percent of the North American population below the age of 65 years experience smell loss to a significant degree.

  According to estimates based on reported research, 1 to 2 percent of the North American population below the age of 65 experience smell loss to a significant degree. Smell loss is much greater in older populations, with nearly half of individuals 65 to 80 years old seemingly experiencing smell loss and nearly three-quarters of those over the age of 80 experiencing such loss.

  Note: These are the best estimates available from studies using actual smell tests. Surveys asking about smell ability without the administration of tests are likely to underestimate smell loss, since many individuals are not aware of their dysfunction unless it is marked. This phenomenon has been noted not only in "normal" populations, but also in individuals diagnosed with disorders associated with smell disorders such as Alzheimer's disease and idiopathic Parkinson's disease.

• More than 200,000 people visit a physician each year for help with smell disorders or related problems.

• Women at all ages are generally more accurate than men in identifying odors, although smoking can adversely affect that ability in both men and women.

• Smell cells (along with taste cells) are the only sensory cells that are regularly replaced throughout a person's life span.

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Smell: Summary Report

Credits

The vast majority of patients presenting to physicians with chemosensory (smell and taste) disturbances, including "taste disturbances," exhibit olfactory dysfunction. As with the case of the taste system, the olfactory system plays a significant role in eating, as most food and beverage flavors are, in fact, dependent upon this system. Such common "tastes" as chocolate, coffee, strawberry, apple, peach, pizza, steak sauce, and chicken actually reflect olfactory-mediated sensations that require the integrity of CN I. Molecules are released and propelled upwards towards the olfactory receptors via the nasal pharynx during mastication and deglutition (Burdach & Doty, 1987).

The olfactory receptors, unlike the receptors of most sensory systems, are directly exposed to the outside environment, save their protection by a thin layer of mucus, making them relatively susceptible to damage from such exogenous agents as viruses, bacteria, pollutants, and airborne toxins. Moreover, since the axons of the olfactory receptor cells extend through the foramina of the cribriform plate to synapse within the olfactory bulb of the central nervous system (CNS), they are extremely vulnerable to shearing and tearing from movement of the brain relative to the cranium. This occurs, for example, in accelerative/decelerative head trauma injuries, even in the absence of fractures, contusions or other objective evidence of trauma (Doty et al., 1997b). The direct route of the olfactory receptor cells from the nasal cavity to the brain makes the olfactory receptors a major conduit for the movement of environmental agents into the brain, in effect bypassing elements of the blood brain barrier. Among agents known to use this route as a means of entrance into the CNS are such viruses as polio virus (e.g., Bodian & Howe, 1940), rabies virus (e.g., Dean et al., 1963), Herpes simplex virus (e.g., Dinn, 1980), and human immunodeficiency virus (e.g., Brody et al., 1991).

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In light of the olfactory anatomy, it is perhaps not surprising the most common causes of permanent smell loss are (a) upper respiratory infections, such as the common cold, (b) head trauma or rapid head acceleration or deceleration, and (c) rhinosinusitis. Although the data are limited, these three causes account for the majority of patients who present to physicians with chemosensory disturbance (Duncan & Seiden, 1995). The percent of patients presenting to specialized centers with these etiologies vary slightly from institution to institution, depending upon their referral bases or referral criteria. In general, about a quarter of patients in such populations have smell loss secondary to URI's, about 20% secondary to head trauma, and 15% secondary to rhinosinusitis (Deems et al., 1991). Other less common causes of smell loss include chronic alcoholism (Shear et al., 1992), epilepsy Kohler et al., 2001), Kallmann's syndrome (Hudson et al., 1994), Korsakoff's psychosis (Mair et al., , pseudohypoparathyroidism (Doty et al., 1997a) and a number of common neurological disorders, including multiple sclerosis (Doty et al., 1997b, 1999), schizophrenia (Moberg et al., 1999), Huntington's disease (Blysma et al., 1998; Moberg & Doty, 1997), Alzheimer's disease (Doty et al., 1987; Murphy et al., 1999), and idiopathic Parkinsonism (Doty et al., 1988). In the case of multiple sclerosis, the smell dysfunction is directly related to the number of plaques within the subtemporal and orbitofrontal cortices, waxing and waning in relation to plaque activity (Doty et al., 1997, 1999). In the case of AD and PD, smell loss appears to be the first clinical sign of the disorder, occurring long before the cardinal signs of the syndromes. In the case of PD, smell loss is unrelated to anti-parkinson medication use and is more common (~ 90%) than tremor (~85%) (Doty et al., 1992). Smell testing can aid in differential diagnosis, since some neurological diseases, often misdiagnosed as Alzheimer's disease or idiopathic Parkinson's disease, are unaccompanied by meaningful olfactory loss (e.g., major affective disorder (McCaffrey et al., 2000), progressive supranuclear palsy (Doty et al., 1993), essential tremor (Busenbark et al., 1992) and MPTP-induced parkinsonism (Doty et al., 1992).

It is important to note that smell testing of patients at risk for AD may be the best predictor of who later will be clinically diagnosed with AD (Murphy et al., 1988). For example, in an epidemiological study of 1,604 non-demented community-dwelling senior citizens 65 years of age or older, scores on a 12-item odor identification test were a better predictor than scores on a global neuropsychological test of cognitive decline over a subsequent 2-year time period (Graves et al., 1999). Persons who were anosmic and possessed at least one APOE-4 allele had 4.9 times the risk of having cognitive decline than normosmic persons not possessing this allele (i.e., an odds ratio of 4.9). This is in contrast to the 1.23 times greater risk for cognitive decline in normosmic individuals possessing at least one such APOE allele. When the data were stratified by sex, women who were anosmic and possessed at least one APOE-4 allele had an odds ratio of 9.71, compared to an odds ratio of 1.90 for women who were normosmic and possessed at least one allele. The corresponding odds ratios for men were 3.18 and 0.67, respectively.

Exposure to a number of toxic agents can induce smell loss. Olfactory loss can occur as a result of exposure to toxins in general air pollution and in workplace settings, where litigation becomes a consideration. In addition to directly damaging the olfactory neuroepithelium, some toxins may produce damage indirectly by inducing upper respiratory inflammatory responses or infections that, in turn, induce such damage. The best scientific documentation of toxic exposure in humans is for acrylates, methacrylates, and cadmium, with the former being typically being reversible after removal from the workplace and the latter inducing, in unregulated settings, longer-lasting or permanent effects. Schwartz et al. (1989) tested the olfactory function of 731 workers at a chemical plant that manufactured acrylates and methacrylates. A nested case-control study designed to assess the cummulative effects of exposure on olfactory function found crude exposure odds ratios (95% confidence intervals) of 2.0 (1.1, 3.8) for all workers and 6.0 (1.7, 21.5) for workers who had never smoked cigarettes. Logistic regression analysis, adjusting for multiple confounders, found exposured odds ratos of 2.8 (1.1, 7.0) and 13.5 (2.1, 87.6) in these same respectives groups and a dose-response relationship between the olfactory and cumulative exposure scores. Decreased odds ratios were associated with increasing duration since last exposure to the chemicals, implying some degree of reversibility. This seems less likely for cadmium, although similarly sophisticated studies have not been performed. Yin-Zeng et al. (1985) reported that 28% of individuals who had worked five years or more in a cadmium-refining plant claimed having anosmia, although quantitative testing was not performed. The average concentration of airborne cadmium was said to be relatively low (between 0.004 and 0.187 mg/m3), but still slightly above the current OSHA permissible exposure limit of 0.005 mg/m3). Rose et al. (1992) found moderate to severe hyposmia, but not anosmia, to n-butanol in 55 workers exposed for an average of 12 years to cadmium fumes, a phenomenon correlated with body burden of cadmium, as measured by urinalysis. Rydzewski et al. (1998) compared the olfactory thresholds of 73 workers involved in the production of cadmium-nickle batteries to that of 43 nonexposed, age- and smoking-matched controls. Anosmia or hyposmia was found in 45.2% of the cadmium-nickel exposed group, compared to only 4.6% of the controls.

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Smell: Books and Articles

• Doty, R.L., Shaman, P., Applebaum, S.L., Giberson, R., Sikorsky, L., Rosenberg, L.: Smell identification ability: Changes with age. Science 226:1441–1443, 1984.
• Doty, R.L., Gregor, T. Monroe, C.: Quantitative assessment of olfactory function in an industrial setting. Journal of Occupational Medicine 28:457–460, 1986.
• Gilbert, A.N., Wysocki, C.J. The smell survey results. National Geographic Magazine 172: 514–525, 1987.
• Hoffman, H.J., Ishii, E.K., Macturk, R.H. Age-related changes in the prevalence of smell/taste problems among the United States adult population. Annals of the New York Academy of Sciences 855: 716–722, 1998.
• Ship, J.A., Weiffenbach, J.M. Age, gender, medical treatment, and medication effects on smell identification. Journal of Gerontology 48: 26–32, 1993.
• References for Editorial Comment:
• Doty, R.L., Reyes, P. & Gregor, T. Presence of both odor identification and detection deficits in Alzheimer's disease. Brain Research Bulletin 18:597–600, 1987.
• Doty, R.L., Deems, D. & Stellar, S. Olfactory dysfunction in Parkinson's disease: A general deficit unrelated to neurologic signs, disease stage, or disease duration. Neurology 38:1237–1244, 1988.
• Nordin, S., Monsch, A.U., Murphy, C. Unawareness of smell loss in normal aging and Alzheimer's disease: discrepancy between self-reported and diagnosed smell sensitivity. Journal of Gerontology 50: 187–192, 1995.

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• Study Citations:
• Barthold, S.W. Olfactory neural pathway in mouse hepatitis virus nasoencephalitis. Acta Neuropathologica 76: 502–506, 1988.
• Bodian, D. & Howe, H.A. An experimental study of the role of neurons in the dissemination of poliomyelitis virus in the nervous system. Brain 63: 135–162, 1940.
• Brody, D., Serby M., Etienne, N. & Kalkstein, D.S. Olfactory identification deficits in HIV infection. American Journal of Psychiatry 148:248–250, 1991.
• Burdach, K. & Doty, R.L. Retronasal flavor perception: Influences of mouth movements, swallowing and spitting. Physiology & Behavior 41:353–356, 1987.
• Busenbark, K.L., Huber, S.I., Greer, G., Pahwa, R. & Koller, W.C. Olfactory function in essential tremor. Neurology 42:1631–1632, 1992.
• Bylsma, F.W., Moberg, P.J., Doty, R.L. & Brandt, J. Odor identification in Huntington's disease patients and asymptomatic gene carriers. Journal of Neuropsychiatry & Clinical Neuroscience 9:598–600, 1997.
• Dean, D., Evans, W. & McClure, R. Pathogenesis of rabies. Bulletin of the World Health Organization. 29: 803–811, 1963.
• Deems, D.A., Doty, R.L., Settle, R.G., Moore-Gillon, V., Shaman, P., Mester, A.F., Kimmelman, C.P. Brightman, V.J. & Snow, J.B., Jr. Smell and taste disorders: A study of 750 patients from the University of Pennsylvania Smell and Taste Center (1981–1986). Archives of Otolaryngology -- Head and Neck Surgery 117:519–528, 1991.
• Dinn, J.J. Transolfactory spread of virus in herpes simplex encephalitis. British Journal of Medicine 281: 1932, 1980.
• *Doty, R.L. Olfaction. Annual Review of Psychology. 52: 423–452, 2001.
• Doty, R.L., Deems, D. & Stellar, S.: Olfactory dysfunction in Parkinson's disease: A general deficit unrelated to neurologic signs, disease stage, or disease duration. Neurology 38:1237–1244, 1988.
• Doty, R.L., Fernandez, A.D., Levine, M.A., Moses, A. & McKeown, D.A. Olfactory dysfunction in type I pseudohypoparathyroidism: dissociation from Gs alpha protein deficiency. Journal of Clinical Endocrinology & Metabolism 82: 247–250, 1997a.
• Doty, R.L., Golbe, L.I., McKeown, D.A., Stern, M.B., Lehrach, C.M. & Crawford, D. Olfactory testing differentiates between progressive supranuclear palsy and idiopathic Parkinson's disease. Neurology, 43: 962–965, 1993.
• *Doty, R.L. & Hastings, L.M. Neurotoxic exposure and olfactory impairment. In M.L. Bleeker (Ed.), Clinics in Occupational and Environmental Medicine (Neurotoxicology), 2001 1: 547–575.

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• Doty, R.L., Li, C., Mannon, L. & Yousem, D.G. Olfactory dysfunction in multiple sclerosis. New England Journal of Medicine 336: 1918–1919, 1997b.
• Doty, R.L., Li, C., Mannon, J. & Yousem, D.M. Olfactory dysfunction in multiple sclerosis: Relation to longitudinal changes in plaque numbers in central olfactory structures. Neurology 53: 880–882, 1999.
• *Doty, R.L. & Mishra, A. Influences of nasal obstruction, rhinitis, and rhinosinusitis on the ability to smell. Laryngoscope 111: 409–423, 2001.
• Doty, R.L., Reyes, P. & Gregor, T.: Presence of both odor identification and detection deficits in Alzheimer's disease. Brain Research Bulletin 18:597–600, 1987.
• Doty, R.L., Singh, A., Tetrude, J. & Langston, J.W. Lack of olfactory dysfunction in MPTP-induced parkinsonism. Annals of Neurology, 32:97–100, 1992.
• Doty, R.L., Stern, M.B., Pfeiffer, C., Gollomop, S.M. & Hurtig, H.I. Bilateral olfactory dysfunction in early stage treated and untreated idiopathic Parkinson's disease. Journal of Neurology, Neurosurgery and Psychiatry, 55:138–142, 1992.
• Doty, R.L., Yousem, D.M., Pham, L.T., Kreshak, A.A. & Lee, W.W. Olfactory dysfunction in patients with head trauma. Archives of Neurology 54: 1131–1140, 1997c.
• Duncan, H.J. & Seiden, A.M. Long-term follow-up of olfactory loss secondary to head trauma and upper respiratory tract infection. Archives of Otolaryngology -- Head & Neck Surgery. 121: 1183–1187, 1995.
• Graves, A.B., Bowen, J.E., Rajaram, L., McCormick, W.C., McCurry, S.M., Schellenberg, G.D. & Larson, E.B. Impaired olfaction as a marker for cognitive decline: interaction with apolipoprotein E epsilon4 status. Neurology 53:1480–1487, 1999.
• Hudson, R., Laska, M., Berger, T., Heye, B., Schopohl, J. & Danek, A. Olfactory function in patients with hypogonadotropic hypogonadism: an all-or-none phenomenon? Chemical Senses 19: 57–69, 1994.

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• Kohler, C.G., Moberg, P.J., Gur, R.E., O'Connor, M.J., Sperling, M.R. & Doty, R.L. Olfactory dysfunction in schizophrenia and temporal lobe epilepsy. Neuropsychiatry, Neuropsychology, & Behavioral Neurology 14 :83–88, 2001.
• McCaffrey, R.J., Duff, K. & Solomon, G.S. Olfactory dysfunction discriminates probable Alzheimer's dementia from major depression: a cross-validation and extension. Journal of Neuropsychiatry and Clinical Neuroscience. 12: 29–33, 2000
• *Mesholam, R.I., Moberg, P.J., Mahr, R.N., Gur, R.E. & Doty, R.L. Olfaction and dementia: A meta-analytic review of olfactory functioning in Alzheimer's and Parkinson's Disease. Archives of Neurology 55: 84–90, 1998.
• *Moberg, P.J., Agrin, R., Gur, R.E., Gur, R.C., Turetsky, B.I. & Doty, R.L. Olfactory dysfunction in schizophrenia: A qualitative and quantitative review. Neuropsychopharmacology 21: 325–340, 1999.
• Moberg, P.J. & Doty, R.L. Olfactory function in Huntington's disease patients and at-risk offspring. International Journal of Neuroscience 89: 133–139, 1997.
• *Murphy, C. Loss of olfactory function in dementing disease. Physiology & Behavior 66:177–182, 1999.
• Murphy, C., Bacon, A.W., Bondi, M.W. & Salmon, D.P. Apolipoprotein E status is associated with odor identification deficits in nondemented older persons. Annals of the New York Academy of Sciences 855:744–750, 1998.
• Rose, C.S., Heywood, P.G. & Costanzo, R.M. Olfactory impairment after chronic occupational cadmium exposure. Journal of Occupational Medicine 34:600–605, 1992.
• Rydzewski, B., Sulkowski, W. & Miarzynaska, M. Olfactory disorders induced by cadmium exposure: A clinical study. International Journal of Occupational Medicine and Environmental Health. 11: 235–245, 1998.
• *Schiffman, S.S. & Nagle, H.T. Effect of environmental pollutants on taste and smell. Otolaryngology—Head & Neck Surgery 106: 693–700, 1992.
• Schwartz, B., Doty, R.L., Frye, R.E., Monroe, C. & Barker, S. Olfactory function in chemical workers exposed to acrylate and methacrylate vapors. American Journal of Public Health 79: 613–618, 1989.
• Shear, P.K., Butters, N., Jernigan, T.L., DiTraglia, G.M., Irwin, M., Schuckit, M.A. & Cermak, L.S. Olfactory loss in alcoholics: correlations with cortical and subcortical MRI indices. Alcohol 9 :247–255, 1992.

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Smell: More Information

For more items on these and other topics in human communication and its disorders, do your own search. Some search strategies give you more information than you are looking for and others are too narrow. You will want to adapt the strategy for your particular needs, but to get you started, go to the NLM PubMed and paste in the search topic you have chosen. Be sure to notice how many entries the search will provide, before trying to print them. These searches have been limited by years, but you may want to broaden them.

Alzheimer's Disease—alzheimer's disease[mh] & (ep[sh] OR incidence[mh] OR prevalence[mh])& ( communications disorders [mh] OR deafness[mh] OR "hearing impairment" OR "hearing disorders"[mh] OR "sensation disorders"[mh])—limits Publication Date from 1997, English ; alzheimer's disease[mh] & (ep[sh] OR incidence[mh] OR prevalence[mh])& ( communications disorders [mh] OR deafness[mh] OR "hearing impairment" OR "hearing disorders"[mh] OR "sensation disorders"[mh])—limits Publication Date from 1992, English, Reviews

Taste—"taste"[MESH] AND (epidemiology[mh] OR incidence[mh] OR prevalence[mh] OR "occupational exposure"[mh] OR "environmental exposure"[mh]) Limits: Publication Date from 1997, English; "taste"[MESH] AND (epidemiology[mh] OR incidence[mh] OR prevalence[mh] OR "occupational exposure"[mh] OR "environmental exposure"[mh]) Limits: Publication Date from 1992, English, Review

Tongue—"tongue"[MESH] AND (epidemiology[mh] OR incidence[mh] OR prevalence[mh] OR "occupational exposure"[mh] OR "environmental exposure"[mh]) Limits: Publication Date from 1997, English, Human; "tongue"[MESH] AND (epidemiology[mh] OR incidence[mh] OR prevalence[mh] OR "occupational exposure"[mh] OR "environmental exposure"[mh]) Limits: Publication Date from 1992, English, Review, Human

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Taste: Statistics

Source: Compiled from fact sheets produced by the National Institute on Deafness and Other Communication Disorders (NIDCD).

• Approximately 25 percent of Americans are nontasters, 50 percent are medium tasters, and 25 percent are "supertasters."

• More than 200,000 people visit a physician for chemosensory problems such as taste disorders each year. Many more taste disorders go unreported.

• Some people are surprised to learn that flavors are recognized mainly through the sense of smell. If you hold your nose while eating chocolate, for example, you will have trouble identifying the chocolate flavor—even though you can distinguish the food's sweetness or bitterness. That is because the distinguishing characteristic of chocolate (what differentiates it from caramel, for example) is sensed largely by its odor.

• Taste cells (along with smell cells) are the only sensory cells that are regularly replaced throughout a person's life span. Taste cells usually last about 10 days.

Taste: Summary Report

Credits

Taste buds, located mainly on the lingual surface, palate, and oropharynx, are primarily responsible for mediating sweet, sour, bitter, salty, and metallic sensations. The physiologic role of the taste system is multifold and includes (a) triggering ingestive and digestive reflex systems that alter the secretion of oral, gastric, pancreatic, and intestinal juices (Schiffman, 1997; Giduck et al., 1987), (b) reinforcing the ingestive process by enhancing the feelings of pleasure and satiety (Warwick et al., 1993), and (c) enabling the determination of the quality of sampled foodstuffs and distinguishing nutrients (which usually taste "good", e.g., sweet) from potential toxins (which usually taste "bad", e.g., bitter)(McLaughlin and Margolskee, 1994). Although rarely appreciated, taste dysfunction can alter food choices and patterns of consumption, producing weight loss, malnutrition, and in some cases impaired immunity and even death. Apparent increased sensitivity and aversion to bitter-tasting substances on the part of the pregnant mother during the first trimester presumably reflects the need to detect and avoid bitter tasting poisons and teratogens during this critical phase of fetal development (Duffy et al., 1998). Similarly, increased preferences for salty and bitter tasting substances during the remainder of pregnancy likely encourages the eating of a varied diet and the ingestion of much needed electrolytes to expand fluid volume. In someone who is hypertensive or diabetic, taste loss can lead to a dangerous tendency to over-compensate for the loss by adding additional salt or sugar to the food.

Whole mouth taste dysfunction is rare, largely because of the redundant innervation of the taste buds (some buds are innervated by CN VII, some by CN IX, and some by CN X). Nonetheless, such function decreases with aging to some degree, can be influenced by central tumors and lesions (e.g., ischemic infarcts secondary to stroke), and is altered adversely by a number of medications. Regional taste deficits, which are much more common, often go undetected, reflecting, in part, the aforementioned redundant neural innervation. Regional deficits can be quite marked. For example, in one study none of 12 elderly persons detected NaCl presented to small regions of the tongue, unlike 12 younger individuals who exhibited no problems with such detection (Matsuda & Doty, 1995). Importantly, taste sensitivity, as measured by detection thresholds, is directly related to the number of taste papillae and taste buds stimulated, implying that some taste disorders are conceivably accounted for by changes in the peripheral lingual anatomy (Doty et al., 2001; Miller et al., 2002).

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The most debilitating taste disorders are those in which a persistent, often chronic, bad taste is present, such as a bitter or salty taste. The causes of such dysgeusias are poorly understood, although they usually appear later in life. In additional to dental and oral health considerations (e.g., the presence of dissimilar metals in oral appliances, purulent discharge from infected teeth or gums), viruses, physical damage to one or more taste nerves, and various medicines are a cause of some dysgeusias. Among offending medicines are lipid reducing agents, antibiotics, and antihypertensive, anxiolytic, and antidepressant drugs. Fortunately, most dysgeusias spontaneously resolve over time (Deems et al., 1996).

Formal determinations of the prevalence of taste dysfunction in the general population are not available, although a large literature exists on differential sensitivity to bitter tasting agents, such as phenothiocarbamide (PTC) and 6-n-propylthiouracil (PROP). Variations in sensitivity seem to vary among genetically disparate populations, although the methods of determining such differential sensitivity are varied. Based upon suprathreshold scaling, some investigators have divided individuals into nontasters, medium tasters, and supertasters. In the case of PROP, Bartoshuk et al. (1998) estimate that approximately 25% of Americans are nontasters, 50%, medium tasters, and 25%, supertasters. Such tasting ability correlates with the number of fungiform papillae, as well as sensitivity to some other agents (e.g., NaCl, sucrose), begging the question as to whether sensitivity to PROP is a simple reflection of the number of taste buds. However, the relationship between such a classification scheme and clinical pathology, if any, has not been elucidated. Interestingly, PTC sensitivity is reportedly higher in some patient populations (e.g., tuberculosis), suggesting a linkage with susceptibility to some diseases (Freire-Maia & Quelce-Salgado, 1997).

Taste problems are much less prevalent than olfactory ones. In patients presenting to taste and smell centers with chemosensory dysfunction, the vast majority exhibit no taste demonstrable dysfunction at all (Deems et al., 1991; Goodspeed et al., 1986), even though most exhibit bilateral deficits in olfactory functioning. However, most such studies have employed whole-mouth taste tests.

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Taste: Books and Articles

• Bartoshuk, L.M., Duffy, V.B., Lucchina, L.A., Prutkin, J., and Fast, K. PROP (6-n-propylthiouracil) supertasters and the saltiness of NaCl. Annals of the New York Academy of Sciences. 855:793–796, 1998.
• Deems, D.A., Doty, R.L., Settle, R.G., Moore-Gillon, V., Shaman, P., Mester, A.F., Kimmelman, C.P. Brightman, V.J. & Snow, J.B., Jr. Smell and taste disorders: A study of 750 patients from the University of Pennsylvania Smell and Taste Center (1981–1986). Archives of Otolaryngology -- Head and Neck Surgery 117:519–528, 1991.
• Deems, D.A., Yen, D.M., Kreshak, A. & Doty, R.L. Spontaneous resolution of dysgeusia. Archives of Otolaryngology -- Head and Neck Surgery 122: 961–963, 1996.
• Doty, R.L., Bagla, R., Morgenson, M. & Mirza, N. NaCl thresholds: Relationship to anterior tongue locus, area of stimulation, and number of fungiform papillae. Physiology & Behavior 72: 373–378, 2001.
• Duffy, V.B., Bartoshuk, L.M., Striegel-Moore, R. and Rodin, J. Taste changes across pregnancy. Annals of the New York Academy of Sciences 855:805–809, 1998.
• Freire-Maia, A. & Quelce-Salgado, A. Taste sensitivity to P.T.C. in samples from three Brazilian populations. Annals of Human Genetics 24:-102, 1997.
• Giduck, S.A., Threatte, R.M. & Kare, M.R. Cephalic reflexes: their role in digestion and possible roles in absorption and metabolism. Journal of Nutrition 117:1191–1196, 1987.
• Goodspeed, R.B., Gent, J.F. & Catalanotto, F.A. Chemosensory dysfunction: clinical evaluation results from a taste and smell clinic. Postgraduate Medicine 81–251–260, 1987.
• Matsuda, T. & Doty, R.L. Age-related taste sensitivity to NaCl: Relationship to tongue locus and stimulation area. Chemical Senses 20: 283–290, 1995.
• *McLaughlin, S. & Margolskee, R.F. The sense of taste. American Scientist 82:538–545, 1994
• Miller, S.L., Mirza, N. & Doty, R.L. Electrogustometric thresholds: Relationship to anterior tongue locus, area of stimulation, and number of fungiform papillae. Physiology & Behavior 75: 753–757, 2002.
• *Schiffman, S.S. Taste and smell losses in normal aging and disease. Journal of the American Medical Association 278:1357–1362, 1997
• *Schiffman, S.S. & Gatlin, C.A. Clinical physiology of taste and smell. Annual Review of Nutrition 13: 405–436, 1993.
• Warwick, Z.S., Hall, W.G., Pappas, T.N. & Schiffman, S.S. Taste and smell sensations enhance the satiating effect of both a high-carbohydrate and a high-fat meal in humans. Physiology & Behavior 53:553–563, 1993

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Taste: More Information

For more items on these and other topics in human communication and its disorders, do your own search. Some search strategies give you more information than you are looking for and others are too narrow. You will want to adapt the strategy for your particular needs, but to get you started, go to the NLM PubMed and paste in the search topic you have chosen. Be sure to notice how many entries the search will provide, before trying to print them. These searches have been limited by years, but you may want to broaden them.

Alzheimer's Disease—alzheimer's disease[mh] & (ep[sh] OR incidence[mh] OR prevalence[mh])& ( communications disorders [mh] OR deafness[mh] OR "hearing impairment" OR "hearing disorders"[mh] OR "sensation disorders"[mh])—limits Publication Date from 1997, English ; alzheimer's disease[mh] & (ep[sh] OR incidence[mh] OR prevalence[mh])& ( communications disorders [mh] OR deafness[mh] OR "hearing impairment" OR "hearing disorders"[mh] OR "sensation disorders"[mh])—limits Publication Date from 1992, English, Reviews

Taste—"taste"[MESH] AND (epidemiology[mh] OR incidence[mh] OR prevalence[mh] OR "occupational exposure"[mh] OR "environmental exposure"[mh]) Limits: Publication Date from 1997, English; "taste"[MESH] AND (epidemiology[mh] OR incidence[mh] OR prevalence[mh] OR "occupational exposure"[mh] OR "environmental exposure"[mh]) Limits: Publication Date from 1992, English, Review

Tongue—"tongue"[MESH] AND (epidemiology[mh] OR incidence[mh] OR prevalence[mh] OR "occupational exposure"[mh] OR "environmental exposure"[mh]) Limits: Publication Date from 1997, English, Human; "tongue"[MESH] AND (epidemiology[mh] OR incidence[mh] OR prevalence[mh] OR "occupational exposure"[mh] OR "environmental exposure"[mh]) Limits: Publication Date from 1992, English, Review, Human

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