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===Sweetness===
===Sweetness===

[[File:Signal Transaction of the Sweet Taste.svg|thumb|The diagram above depicts the signal transduction pathway of the sweet taste. Object A is a taste bud, object B is one taste cell of the taste bud, and object C is the neuron attached to the taste cell. I. Part I shows the reception of a molecule. 1. Sugar, the first messenger, binds to a protein receptor on the cell membrane. II. Part II shows the transduction of the relay molecules. 2. G Protein-coupled receptors, second messengers, are activated. 3. G Proteins activate adenylate cyclase, an enzyme, which increases the cAMP concentration. Depolarization occurs. 4. The energy, from step 3, is given to activate the K+, potassium, protein channels.III. Part III shows the response of the taste cell. 5. Ca+, calcium, protein channels is activated.6. The increased Ca+ concentration activates neurotransmitter vesicles. 7. The neuron connected to the taste bud is stimulated by the neurotransmitters.]]

{{Main|Sweetness}}
{{Main|Sweetness}}
{{See also|Miraculin|Curculin}}
{{See also|Miraculin|Curculin}}

Revision as of 13:15, 2 June 2015

Template:Two other uses

Taste bud

Taste, gustatory perception, or gustation[1] is the sensory impression of food or other substances on the tongue and is one of the five traditional senses.

Taste is the sensation produced when a substance in the mouth reacts chemically with taste receptor cells located on taste buds. Taste, along with smell (olfaction) and trigeminal nerve stimulation (registering texture, pain, and temperature), determines flavors of food or other substances. Humans have taste receptors on taste buds (gustatory calyculi) and other areas including the upper surface of the tongue and the epiglottis.[2][3]

The tongue is covered with thousands of small bumps called papillae, which are visible to the naked eye. Within each papilla are hundreds of taste buds.[4] The exception to this is the filiform papillae that do not contain taste buds. There are between 2000 and 5000[5] taste buds that are located on the back and front of the tongue. Others are located on the roof, sides and back of the mouth, and in the throat. Each taste bud contains 50 to 100 taste receptor cells.

The sensation of taste can be categorized into five basic tastes: sweetness, sourness, saltiness, bitterness, and umami. Taste buds are able to differentiate among different tastes through detecting interaction with different molecules or ions. Sweet, umami, and bitter tastes are triggered by the binding of molecules to G protein-coupled receptors on the cell membranes of taste buds. Saltiness and sourness are perceived when alkali metal or hydrogen ions enter taste buds, respectively.[6]

The basic tastes contribute only partially to the sensation and flavor of food in the mouth — other factors include smell,[2] detected by the olfactory epithelium of the nose;[7] texture,[8] detected through a variety of mechanoreceptors, muscle nerves, etc.;[9] temperature, detected by thermoreceptors; and "coolness" (such as of menthol) and "hotness" (pungency), through chemesthesis.

As taste senses both harmful and beneficial things, all basic tastes are classified as either aversive or appetitive, depending upon the effect the things they sense have on our bodies.[10] Sweetness helps to identify energy-rich foods, while bitterness serves as a warning sign of poisons.[11]

Taste perception fades with age: On average, people lose half their taste receptors by the time they turn 20.[4] Not all animals can sense all tastes.[12]

Introduction

History

In the West, Aristotle postulated in c. 350 BCE[13] that the two most basic tastes were sweet and bitter.[14] He was one of the first to develop a list of basic tastes.[15]

Ayurveda, an ancient Indian healing science, has its own tradition of basic tastes, comprising sweet, salty, sour, pungent, bitter & astringent.[16]

Similarly, the Ancient Chinese regarded spiciness as a basic taste.

Recent discoveries

The receptors for the basic tastes of bitter, sweet and umami have been identified. They are G protein-coupled receptors.[17] The cells that detect sourness have been identified as a subpopulation that express the protein PKD2L1. The responses are mediated by an influx of protons into the cells but the receptor for sour is still unknown. The receptor for amiloride-sensitive attractive salty taste in mice has been shown to be a sodium channel.[18] There is some evidence for a sixth taste that senses fatty substances.[19]

In 2010, researchers found bitter taste receptors in lung tissue, which cause airways to relax when a bitter substance is encountered. They believe this mechanism is evolutionarily adaptive because it helps clear lung infections, but could also be exploited to treat asthma and chronic obstructive pulmonary disease.[20]

Innervation

Taste is brought to the brainstem by 3 different cranial nerves:[citation needed]

Basic tastes

For a long period, it was commonly accepted[who?] that there is a finite and small number of "basic tastes" of which all seemingly complex tastes are ultimately composed. Just as with primary colors, the "basic" quality of those sensations derives chiefly from the nature of human perception, in this case the different sorts of tastes the human tongue can identify. As of the early twentieth century, physiologists and psychologists believed there were four basic tastes: sweetness, sourness, saltiness, and bitterness. At that time umami was not proposed as a fifth taste[21] but now a large number of authorities recognize it as the fifth taste.[citation needed] In Asian countries within the sphere of mainly Chinese and Indian cultural influence, pungency (piquancy or hotness) had traditionally been considered a sixth basic taste.[citation needed]

Sweetness

The diagram above depicts the signal transduction pathway of the sweet taste. Object A is a taste bud, object B is one taste cell of the taste bud, and object C is the neuron attached to the taste cell. I. Part I shows the reception of a molecule. 1. Sugar, the first messenger, binds to a protein receptor on the cell membrane. II. Part II shows the transduction of the relay molecules. 2. G Protein-coupled receptors, second messengers, are activated. 3. G Proteins activate adenylate cyclase, an enzyme, which increases the cAMP concentration. Depolarization occurs. 4. The energy, from step 3, is given to activate the K+, potassium, protein channels.III. Part III shows the response of the taste cell. 5. Ca+, calcium, protein channels is activated.6. The increased Ca+ concentration activates neurotransmitter vesicles. 7. The neuron connected to the taste bud is stimulated by the neurotransmitters.
Main article: Sweetness
See also: Miraculin and Curculin

Sweetness, usually regarded as a pleasurable sensation, is produced by the presence of sugars and a few other substances. Sweetness is often connected to aldehydes and ketones, which contain a carbonyl group. Sweetness is detected by a variety of G protein coupled receptors coupled to the G protein gustducin found on the taste buds. At least two different variants of the "sweetness receptors" must be activated for the brain to register sweetness. Compounds the brain senses as sweet are thus compounds that can bind with varying bond strength to two different sweetness receptors. These receptors are T1R2+3 (heterodimer) and T1R3 (homodimer), which account for all sweet sensing in humans and animals.[22] Taste detection thresholds for sweet substances are rated relative to sucrose, which has an index of 1.[23][24] The average human detection threshold for sucrose is 10 millimoles per liter. For lactose it is 30 millimoles per liter, with a sweetness index of 0.3,[23] and 5-Nitro-2-propoxyaniline 0.002 millimoles per liter.

Sourness

"Sour" redirects here. For other uses, see Sour (disambiguation).
Look up sour in Wiktionary, the free dictionary.

The diagram depicts the signal transduction pathway of the sour or salty taste. Object A is a taste bud, object B is a taste receptor cell within object A, and object C is the neuron attached to object B. I. Part I is the reception of hydrogen ions or sodium ions. 1. If the taste is sour, H+ ions, from an acidic substances, pass through their specific ion channel. Some can go through the Na+ channels. If the taste is salty Na+, sodium, molecules pass through the Na+ channels. Depolarization takes place II. Part II is the transduction pathway of the relay molecules.2. Cation, such as K+, channels are opened. III. Part III is the response of the cell. 3. An influx of Ca+ ions is activated.4. The Ca+ activates neurotransmitters. 5. A signal is sent to the neuron attached to the taste bud.

Sourness is the taste that detects acidity. The sourness of substances is rated relative to dilute hydrochloric acid, which has a sourness index of 1. By comparison, tartaric acid has a sourness index of 0.7, citric acid an index of 0.46, and carbonic acid an index of 0.06.[23][24]

Sour taste is detected by a small subset of cells that are distributed across all taste buds in the tongue. Sour taste cells can be identified by expression of the protein PKD2L1,[25] although this gene is not required for sour responses. There is evidence that the protons that are abundant in sour substances can directly enter the sour taste cells. This transfer of positive charge into the cell can itself trigger an electrical response. It has also been proposed that weak acids such as acetic acid, which are not fully dissociated at physiological pH values, can penetrate taste cells and thereby elicit an electrical response. According to this mechanism, intracellular hydrogen ions inhibit potassium channels, which normally function to hyperpolarize the cell. By a combination of direct intake of hydrogen ions (which itself depolarizes the cell) and the inhibition of the hyperpolarizing channel, sourness causes the taste cell to fire action potentials and release neurotransmitter. The mechanism by which animals detect sour is still not completely understood.

The most common food group that contains naturally sour foods is fruit, such as lemon, grape, orange, tamarind, and sometimes melon. Wine also usually has a sour tinge to its flavor, and if not kept correctly, milk can spoil and develop a sour taste. Children in the US and UK show a greater enjoyment of sour flavors than adults,[26] and sour candy is popular in North America[27] including Cry Babies, Warheads, Lemon drops, Shock Tarts and sour versions of Skittles and Starburst. Many of these candies contain citric acid.

Saltiness

"Saltiness" redirects here. For the saltiness in the water, see Salinity.

Saltiness is a taste produced primarily by the presence of sodium ions. Other ions of the alkali metals group also taste salty, but the further from sodium, the less salty the sensation is. The size of lithium and potassium ions most closely resemble those of sodium, and thus the saltiness is most similar. In contrast, rubidium and cesium ions are far larger, so their salty taste differs accordingly.[citation needed] The saltiness of substances is rated relative to sodium chloride (NaCl), which has an index of 1.[23][24] Potassium, as potassium chloride (KCl), is the principal ingredient in salt substitutes and has a saltiness index of 0.6.[23][24]

Other monovalent cations, e.g. ammonium, NH4+, and divalent cations of the alkali earth metal group of the periodic table, e.g. calcium, Ca2+, ions generally elicit a bitter rather than a salty taste even though they, too, can pass directly through ion channels in the tongue, generating an action potential.

Bitterness

The diagram depicted above shows the signal transduction pathway of the bitter taste. Bitter taste has many different receptors and signal transduction pathways. Bitter indicates poison to animals. It is most similar to sweet. Object A is a taste bud, object B is one taste cell, and object C is a neuron attached to object B. I. Part I is the reception of a molecule.1. A bitter substance such as quinine, is consumed and binds to G Protein-coupled receptors.II. Part II is the transduction pathway 2. Gustducin, a G protein second messenger, is activated. 3. Phosphodiesterase, an enzyme, is then activated. 4. Cyclic nucleotide, cNMP, is used, lowering the concentration 5. Channels such as the K+, potassium, channels, close.III. Part III is the response of the taste cell. 6. This leads to increased levels of Ca+. 7. The neurotransmitters are activated. 8. The signal is sent to the neuron.

Bitterness is the most sensitive of the tastes, and many perceive it as unpleasant, sharp, or disagreeable, but it is sometimes desirable and intentionally added via various bittering agents. Common bitter foods and beverages include coffee, unsweetened cocoa, South American mate, bitter gourd, olives, citrus peel, many plants in the Brassicaceae family, dandelion greens, wild chicory, and escarole. The ethanol in alcoholic beverages tastes bitter,[28] as do the additional bitter ingredients found in some alcoholic beverages including hops in beer and orange in bitters. Quinine is also known for its bitter taste and is found in tonic water.

Main article: Bitter taste evolution

Bitterness is of interest to those who study evolution, as well as various health researchers[23][29] since a large number of natural bitter compounds are known to be toxic. The ability to detect bitter-tasting, toxic compounds at low thresholds is considered to provide an important protective function.[23][29][30] Plant leaves often contain toxic compounds, yet even amongst leaf-eating primates, there is a tendency to prefer immature leaves, which tend to be higher in protein and lower in fiber and poisons than mature leaves.[31] Amongst humans, various food processing techniques are used worldwide to detoxify otherwise inedible foods and make them palatable.[32] Furthermore, the use of fire, changes in diet, and avoidance of toxins has led to neutral evolution in human bitter sensitivity. This has allowed several loss of function mutations that has led to a reduced sensory capacity towards bitterness in humans when compared to other species.[33]

The threshold for stimulation of bitter taste by quinine averages a concentration of 8 μM (8 micromolar).[23] The taste thresholds of other bitter substances are rated relative to quinine, which is thus given a reference index of 1.[23][24] For example, Brucine has an index of 11, is thus perceived as intensely more bitter than quinine, and is detected at a much lower solution threshold.[23] The most bitter substance known is the synthetic chemical denatonium, which has an index of 1,000.[24] It is used as an aversive agent (a bitterant) that is added to toxic substances to prevent accidental ingestion. This was discovered in 1958 during research on lignocaine, a local anesthetic, by MacFarlan Smith of Gorgie, Edinburgh, Scotland.[citation needed]

Research has shown that TAS2Rs (taste receptors, type 2, also known as T2Rs) such as TAS2R38 coupled to the G protein gustducin are responsible for the human ability to taste bitter substances.[34] They are identified not only by their ability to taste for certain "bitter" ligands, but also by the morphology of the receptor itself (surface bound, monomeric).[35] The TAS2R family in humans is thought to comprise about 25 different taste receptors, some of which can recognize a wide variety of bitter-tasting compounds.[36] Over 550 bitter-tasting compounds have been identified, of which about 100 have been assigned to one or more specific receptors.[37] Recently it is speculated that the selective constraints on the TAS2R family have been weakened due to the relatively high rate of mutation and pseudogenization.[38] Researchers use two synthetic substances, phenylthiocarbamide (PTC) and 6-n-propylthiouracil (PROP) to study the genetics of bitter perception. These two substances taste bitter to some people, but are virtually tasteless to others. Among the tasters, some are so-called "supertasters" to whom PTC and PROP are extremely bitter. The variation in sensitivity is determined by two common alleles at the TAS2R38 locus.[39] This genetic variation in the ability to taste a substance has been a source of great interest to those who study genetics.

Umami

Main article: Umami

Umami is an appetitive taste[10] and is described as a savory[40][41] or meaty[41][42] taste. It can be tasted in cheese[43] and soy sauce,[44] and while also found in many other fermented and aged foods, this taste is also present in tomatoes, grains, and beans.[43] Monosodium glutamate (MSG), developed as a food additive in 1908 by Kikunae Ikeda,[45] produces a strong umami taste.[44] See TAS1R1 and TAS1R3 pages for a further explanation of the amino-acid taste receptor. A loanword from Japanese meaning "good flavor" or "good taste",[46] umami (旨味) is considered fundamental to many Eastern cuisines[47] and was first described in 1908,[48] although it was only recently recognized in the West as a basic taste.[44][49]

Some umami taste buds respond specifically to glutamate in the same way that "sweet" ones respond to sugar. Glutamate binds to a variant of G protein coupled glutamate receptors.[50][51]

Measuring relative tastes

Measuring the degree to which a substance presents one basic taste can be achieved in a subjective way by comparing its taste to a reference substance.

Sweetness is subjectively measured by comparing the threshold values, or level at which the presence of a dilute substance can be detected by a human taster, of different sweet substances.[52] Substances are usually measured relative to sucrose,[53] which is usually given an arbitrary index of 1[54][55] or 100.[56] Fructose is about 1.4 times sweeter than sucrose; glucose, a sugar found in honey and vegetables, is about three-quarters as sweet; and lactose, a milk sugar, is one-half as sweet.[b][52]

The sourness of a substance can be rated by comparing it to very dilute hydrochloric acid (HCl).[57]

Relative saltiness can be rated by comparison to a dilute salt solution.[58]

Quinine, a bitter medicinal found in tonic water, can be used to subjectively rate the bitterness of a substance.[59] Units of dilute quinine hydrochloride (1 g in 2000 mL of water) can be used to measure the threshold bitterness concentration, the level at which the presence of a dilute bitter substance can be detected by a human taster, of other compounds.[59] More formal chemical analysis, while possible, is difficult.[59]

Functional structure

Main article: Gustatory system
Sweetness

Sweetness is produced by the presence of sugars, some proteins, and a few other substances.[citation needed] It is often connected to aldehydes and ketones, which contain a carbonyl group.[citation needed]Sweetness is detected by a variety of G protein-coupled receptors coupled to a G protein that acts as an intermediary in the communication between taste bud and brain, gustducin.[60] These receptors are T1R2+3 (heterodimer) and T1R3 (homodimer), which account for sweet sensing in humans and other animals.[61]

Sourness

Sourness is acidity,[62][63] and, like salt, it is a taste sensed using ion channels.[64] Hydrogen ion channels detect the concentration of hydronium ions that are formed from acids and water.[citation needed] In addition, the taste receptor PKD2L1 has been found to be involved in tasting sour.[65]

Saltiness

Saltiness is a taste produced best by the presence of cations (such as Na+
, K+
 or Li+
)[64] and, like sour, it is tasted using ion channels.[64]

Other monovalent cations, e.g., ammonium, NH+
4, and divalent cations of the alkali earth metal group of the periodic table, e.g., calcium, Ca2+
, ions, in general, elicit a bitter rather than a salty taste even though they, too, can pass directly through ion channels in the tongue.[citation needed]

Bitterness

Research has shown that TAS2Rs (taste receptors, type 2, also known as T2Rs) such as TAS2R38 are responsible for the human ability to taste bitter substances.[66] They are identified not only by their ability to taste certain bitter ligands, but also by the morphology of the receptor itself (surface bound, monomeric).[67]

Umami

The amino acid glutamic acid is responsible for umami,[68][69] but some nucleotides (inosinic acid[47][70] and guanylic acid[68]) can act as complements, enhancing the taste.[47][70]

Glutamic acid binds to a variant of the G protein-coupled receptor, producing an umami taste.[50][51]

Further sensations

The tongue can also feel other sensations not generally included in the basic tastes. These are largely detected by the somatosensory system.

Pungency (also spiciness or hotness)

Main articles: Pungency and Scoville scale

Substances such as ethanol and capsaicin cause a burning sensation by inducing a trigeminal nerve reaction together with normal taste reception. The sensation of heat is caused by the food's activating nerves that express TRPV1 and TRPA1 receptors. Two main plant-derived compounds that provide this sensation are capsaicin from chili peppers and piperine from black pepper. The piquant ("hot" or "spicy") sensation provided by chili peppers, black pepper, and other spices like ginger and horseradish plays an important role in a diverse range of cuisines across the world—especially in equatorial and sub-tropical climates, such as Ethiopian, Peruvian, Hungarian, Indian, Korean, Indonesian, Lao, Malaysian, Mexican, New Mexican, Singaporean Southwest Chinese (including Szechuan cuisine), Vietnamese, and Thai cuisines.

This particular sensation, called chemesthesis, is not a taste in the technical sense, because the sensation does not arise from taste buds, and a different set of nerve fibers carry it to the brain. Foods like chili peppers activate nerve fibers directly; the sensation interpreted as "hot" results from the stimulation of somatosensory (pain/temperature) fibers on the tongue. Many parts of the body with exposed membranes but no taste sensors (such as the nasal cavity, under the fingernails, surface of the eye or a wound) produce a similar sensation of heat when exposed to hotness agents. Asian countries within the sphere of, mainly, Chinese, Indian, and Japanese cultural influence, traditionally consider pungency a sixth basic taste.

Coolness

Some substances activate cold trigeminal receptors even when not at low temperatures. This "fresh" or "minty" sensation can be tasted in spearmint, menthol, ethanol, and camphor. Caused by activation of the same mechanism that signals cold, TRPM8 ion channels on nerve cells, unlike the actual change in temperature described for sugar substitutes, this coolness is only a perceived phenomenon.

Numbness

Both Chinese and Batak Toba cooking include the idea of 麻 (má or mati rasa), a tingling numbness caused by spices such as Sichuan pepper. The cuisines of Sichuan province in China and of the Indonesia province North Sumatra often combine this with chili pepper to produce a 麻辣 málà, "numbing-and-hot", or "mati rasa" flavor.[71] These sensations although not taste fall into a category of Chemesthesis.

Astringency

Some foods, such as unripe fruits, contain tannins or calcium oxalate that cause an astringent or puckering sensation of the mucous membrane of the mouth. Examples include tea, red wine, rhubarb, and unripe persimmons and bananas.

Less exact terms for the astringent sensation are "dry", "rough", "harsh" (especially for wine), "tart" (normally referring to sourness), "rubbery", "hard" or "styptic".[72]

When referring to wine, dry is the opposite of sweet, and does not refer to astringency. Wines that contain tannins and so cause an astringent sensation are not necessarily classified as "dry," and "dry" wines are not necessarily astringent.

In the Indian Ayurvedic tradition, one of the six tastes is astringency (kasaaya).[73]

Metallicness

A metallic taste may be caused by food and drink, certain medicines or amalgam dental fillings. It is generally considered an off flavor when present in food and drink. A metallic taste may be caused by galvanic reactions in the mouth. In the case where it is caused by dental work, the dissimilar metals used may produce a measurable current.[74] Some artificial sweeteners are perceived to have a metallic taste, which is detected by the TRPV1 receptors.[75] Blood is considered by many people to have a metallic taste.[76][77] A metallic taste in the mouth is also a symptom of various medical conditions, in which case it may be classified under the symptoms dysgeusia or parageusia, referring to distortions of the sense of taste,[78] and can be caused by various kinds of medication, including saquinavir[78] and zonisamide,[79] and occupational hazards, such as working with pesticides.[80]

Calcium

The distinctive taste of chalk has been identified as the calcium component of that substance.[81] In 2008, geneticists discovered a CaSR calcium receptor on the tongues of mice. The CaSR receptor is commonly found in the gastrointestinal tract, kidneys, and brain. Along with the "sweet" T1R3 receptor, the CaSR receptor can detect calcium as a taste. Whether closely related genes in mice and humans means the phenomenon exists in humans as well is unknown.[82][83]

Fattiness

Recent research reveals a potential taste receptor called the CD36 receptor.[84][85][86] CD36 was targeted as a possible lipid taste receptor because it binds to fat molecules (more specifically, long-chain fatty acids),[87] and it has been localized to taste bud cells (specifically, the circumvallate and foliate papillae).[88] There is a debate over whether we can truly taste fats, and supporters of our ability to taste free fatty acids (FFAs) have based the argument on a few main points: there is an evolutionary advantage to oral fat detection; a potential fat receptor has been located on taste bud cells; fatty acids evoke specific responses that activate gustatory neurons, similar to other currently accepted tastes; and, there is a physiological response to the presence of oral fat.[89] Although CD36 has been studied primarily in mice, research examining human subjects' ability to taste fats found that those with high levels of CD36 expression were more sensitive to tasting fat than were those with low levels of CD36 expression;[90] this study points to a clear association between CD36 receptor quantity and the ability to taste fat.

Other possible fat taste receptors have been identified. G protein-coupled receptors GPR120 and GPR40 have been linked to fat taste, because their absence resulted in reduced preference to two types of fatty acid (linoleic acid and oleic acid), as well as decreased neuronal response to oral fatty acids.[91]

Monovalent cation channel TRPM5 has been implicated in fattiness taste as well,[92] but it is thought to be involved primarily in downstream processing of the taste rather than primary reception, as it is with other tastes such as bitter, sweet, and umami.[89]

Heartiness (kokumi)

Some Japanese researchers refer to the kokumi of foods. This sensation has also been described as mouthfulness,[93]: 290  and appears to be related to a number of γ-L-glutamyl peptides, which activate a calcium-sensing receptor which is also sensitive to glutathione.[93]

Temperature

Temperature can be an essential element of the taste experience. Food and drink that—in a given culture—is traditionally served hot is often considered distasteful if cold, and vice versa. For example, alcoholic beverages, with a few exceptions, are usually thought best when served cold, but soups—again, with exceptions—are usually only eaten hot. A cultural example is soda. In North America it is almost always preferred cold, regardless of season. In South America soda is almost exclusively consumed lukewarm in winter[citation needed], though not in Brazil, where it is only consumed cold.

Other concepts

Supertasters

Main article: Supertaster

A supertaster is a person whose sense of taste is significantly more sensitive than average. The cause of this heightened response is likely, at least in part, due to an increased number of fungiform papillae.[94] Studies have shown that supertasters require less fat and sugar in their food to get the same satisfying effects. However, contrary to what one might think, these people actually tend to consume more salt than the average person. This is due to their heightened sense of the taste of bitterness, and the presence of salt drowns out the taste of bitterness. (This also explains why supertasters prefer salted cheddar cheese over non-salted.)[95]

Aftertaste

Main article: Aftertaste

Aftertastes arise after food has been swallowed. An aftertaste can differ from the food it follows. Medicines and tablets may also have a lingering aftertaste, as they can contain certain artificial flavor compounds, such as aspartame (artificial sweetener).

Acquired taste

Main article: Acquired taste

An acquired taste often refers to an appreciation for a food or beverage that is unlikely to be enjoyed by a person who has not had substantial exposure to it, usually because of some unfamiliar aspect of the food or beverage, including a strong or strange odor, taste, or appearance.

Disease

Patients with Addison's disease, pituitary insufficiency, or cystic fibrosis sometimes have a hyper-sensitivity to the four primary tastes.[96]

Disorders of taste

See also

Notes

Footnotes

a. ^ It has been known for some time that these categories may not be comprehensive. In Guyton's 1976 edition of Textbook of Medical Physiology, he wrote:

On the basis of physiologic studies, there are generally believed to be at least four primary sensations of taste: sour, salty, sweet, and bitter. Yet we know that a person can perceive literally hundreds of different tastes. These are all supposed to be combinations of the four primary sensations...However, there might be other less conspicuous classes or subclasses of primary sensations",[97]

b. ^ Some variation in values is not uncommon between various studies. Such variations may arise from a range of methodological variables, from sampling to analysis and interpretation. In fact there is a "plethora of methods"[98] Indeed, the taste index of 1, assigned to reference substances such as sucrose (for sweetness), hydrochloric acid (for sourness), quinine (for bitterness), and sodium chloride (for saltiness), is itself arbitrary for practical purposes.[57]

Some values, such as those for maltose and glucose, vary little. Others, such as aspartame and sodium saccharin, have much larger variation. Regardless of variation, the perceived intensity of substances relative to each reference substance remains consistent for taste ranking purposes. The indices table for McLaughlin & Margolskee (1994) for example,[23][99] is essentially the same as that of Svrivastava & Rastogi (2003),[100] Guyton & Hall (2006),[57] and Joesten et al. (2007).[54] The rankings are all the same, with any differences, where they exist, being in the values assigned from the studies from which they derive.

As for the assignment of 1 or 100 to the index substances, this makes no difference to the rankings themselves, only to whether the values are displayed as whole numbers or decimal points. Glucose remains about three-quarters as sweet as sucrose whether displayed as 75 or 0.75.

Citations

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General

Reference #30 (Wooding et al.) is helpful, but it is incorrect. The discovery that variants in the TAS2R38 gene underlie the ability to taste PTC and PROP was reported a year earlier in: Kim, U.-K., Jorgenson, E., Coon, H., Leppert, M., Risch, N., and D. Drayna. Positional Cloning of the human quantitative trait locus underlying taste sensitivity to phenylthiocarbamide. Science 299:1221-1225 (2003). I was the senior and communicating author on both of these papers.

Dennis Drayna, PhD NIDCD/National Institutes of Health

Further reading

External links

Look up sour in Wiktionary, the free dictionary.
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