Sweetness is abasic taste most commonly perceived when eating foods rich in sugars. Sweet tastes are generally regarded as pleasurable. In addition to sugars likesucrose, many otherchemical compounds are sweet, includingaldehydes,ketones, andsugar alcohols. Some are sweet at very low concentrations, allowing their use as non-caloricsugar substitutes. Suchnon-sugar sweeteners includesaccharin,aspartame,sucralose andstevia. Other compounds, such asmiraculin, may alter perception of sweetness itself.
The perceived intensity of sugars and high-potency sweeteners, such asaspartame andneohesperidin dihydrochalcone, are heritable, with gene effect accounting for approximately 30% of the variation.[1]
Thechemosensory basis for detecting sweetness, which varies between both individuals and species, has only begun to be understood since the late 20th century. One theoretical model of sweetness is themultipoint attachment theory, which involves multiple binding sites between a sweetness receptor and a sweet substance.
Newborn human infants also demonstrate preferences for high sugar concentrations and prefer solutions that are sweeter thanlactose, the sugar found in breast milk.[2][3] Sweetness appears to have the highesttaste recognition threshold, being detectable at around 1 part in 200 of sucrose in solution. By comparison,bitterness appears to have the lowest detection threshold, at about 1 part in 2 million for quinine in solution.[4]
Studies indicate that responsiveness to sugars and sweetness has very ancient evolutionary beginnings, being manifest aschemotaxis even inmotile bacteria such asE. coli.[5]
In the natural settings that human primate ancestors evolved in, sweetness intensity should indicateenergy density, while bitterness tends to indicatetoxicity.[6][7][8] The high sweetness detection threshold and low bitterness detection threshold would have predisposed our primate ancestors to seek out sweet-tasting (and energy-dense) foods and avoid bitter-tasting foods. Even amongst leaf-eating primates, there is a tendency to prefer immature leaves, which tend to be higher in protein and lower in fibre and poisons than mature leaves.[9] The "sweet tooth" thus has an ancient heritage, and while food processing has changed consumption patterns,[10][11] human physiology remains largely unchanged.[12] Biologically, a variant infibroblast growth factor 21 increases craving for sweet foods.
A great diversity ofchemical compounds, such asaldehydes andketones, are sweet. Among common biological substances, all of the simple carbohydrates are sweet to at least some degree.Sucrose (table sugar) is the prototypical example of a sweet substance. Sucrose in solution has a sweetness perception rating of 1, and other substances are rated relative to this.[13] For example, another sugar,fructose, is somewhat sweeter, being rated at 1.7 times the sweetness of sucrose.[13] Someamino acids are mildly sweet: of theproteinogenic amino acids,L-alanine,glycine,L-proline andL-serine are the sweetest.[14] Some other amino acids, such asL-valine, are perceived as both sweet and bitter.[14] Additionally, many D-enantiomers of proteinogenic amino acids have a sweet taste, even when their L- enantiomer lacks any sweet taste, such as in the case of D-asparagine versus L-asparagine.[15]
The sweetness of 5% solution of glycine in water compares to a solution of 5.6% glucose or 2.6% fructose.[16]
A number of plant species produceglycosides that are sweet at concentrations much lower than common sugars. The most well-known example isglycyrrhizin, the sweet component oflicorice root, which is about 30 times sweeter than sucrose. Another commercially important example isstevioside, from theSouth American shrubStevia rebaudiana. It is roughly 250 times sweeter than sucrose. Another class of potent natural sweeteners are the sweet proteins such asthaumatin, found in theWest Africankatemfe fruit. Hen egglysozyme, anantibiotic protein found inchicken eggs, is also sweet.
| Name | Type of compound | Sweetness |
|---|---|---|
| Lactose | Disaccharide | 0.16 |
| Maltose | Disaccharide | 0.33 – 0.45 |
| Trehalose (α,α-trehalose) | Disaccharide | max. 0.45[23] |
| Isomaltulose | Disaccharide | 0.40 - 0.50[24] |
| L-serine | Amino acid | 0.53 – 0.55 |
| L-proline | Amino acid | 0.37 – 0.76 |
| Sorbitol | Polyalcohol | 0.6 |
| Galactose | Monosaccharide | 0.65 |
| Glucose | Monosaccharide | 0.74 – 0.8 |
| Glycine | Amino acid | 0.6 – 0.89 |
| L-alanine | Amino acid | 0.77 – 1.10 |
| Sucrose | Disaccharide | 1.00 (reference) |
| Xylitol | sugar alcohol | 1.02[25] |
| Fructose | Monosaccharide | 1.17 – 1.75 |
| Sodium cyclamate | Sulfonate | 26 |
| Steviol glycoside | Glycoside | 40 – 300 |
| Aspartame | Dipeptidemethylester | 180 – 250 |
| Acesulfame potassium | Oxathiazinone dioxide | 200 |
| Sodium saccharin | Sulfonyl | 300 – 675 |
| Sucralose | Modified disaccharide | 600 |
| Monellin | Protein | 800 to 2000 |
| Thaumatin | Protein | 2000 |
| Neotame | Aspartame analog | 8000 |
| Sucrooctate | Guanidine | 162,000 (estimated) |
| Bernardame | Guanidine | 188,000 (estimated) |
| Sucrononic acid | Guanidine | 200,000 (estimated) |
| Carrelame | Guanidine | 200,000 (estimated) |
| Lugduname | Guanidine | 230,000 (estimated) |
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. 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.[20] Some values, such as those for maltose and glucose, vary little. Others, such as aspartame and sodium saccharin, have much larger variation.
Even someinorganic compounds are sweet, includingberyllium chloride andlead(II) acetate. The latter may have contributed tolead poisoning among theancient Roman aristocracy: the Roman delicacysapa was prepared by boiling souredwine (containingacetic acid) in lead pots.[26]
Hundreds of synthetic organic compounds are known to be sweet, but only a few of these are legally permitted[where?] as food additives. For example,chloroform,nitrobenzene, andethylene glycol are sweet, but also toxic.Saccharin,cyclamate,aspartame,acesulfame potassium,sucralose,alitame, andneotame are commonly used.[citation needed]
A few substances alter the way sweet taste is perceived. One class of these inhibits the perception of sweet tastes, whether from sugars or from highly potent sweeteners. Commercially, the most important of these islactisole,[27] a compound produced byDomino Sugar. It is used in some jellies and other fruit preserves to bring out their fruit flavors by suppressing their otherwise strong sweetness.
Two natural products have been documented to have similar sweetness-inhibiting properties:gymnemic acid, extracted from the leaves of theIndian vineGymnema sylvestre andziziphin, from the leaves of the Chinesejujube (Ziziphus jujuba).[28] Gymnemic acid has been widely promoted withinherbal medicine as a treatment for sugar cravings and diabetes.
On the other hand, two plant proteins,miraculin[29] andcurculin,[30] cause sour foods to taste sweet. Once the tongue has been exposed to either of these proteins, sourness is perceived as sweetness for up to an hour afterwards. While curculin has some innate sweet taste of its own, miraculin is by itself quite tasteless.
Experiments with laboratory mice showed in 2001 that mice possessing different versions of thegene T1R3 prefer sweet foods to different extents. The sweetness receptor in mammals turned out to be a complex of two related proteins,T1R3 andT1R2 (also called TAS1R2 + TAS1R3), that form aG-protein coupled receptor.[31][32] The cryo-electron microscopy (cryo-EM) structure of the human sweet receptor was solved by scientists atColumbia University in 2025.[32]
Human studies have shown that sweet taste receptors are not only found in the tongue, but also in the lining of the gastrointestinal tract as well as the nasal epithelium, pancreatic islet cells, sperm and testes.[33] It is proposed that the presence of sweet taste receptors in the GI tract controls the feeling of hunger and satiety.
The threshold of sweet taste perception correlates with the time of day, probably due to oscillatingleptin levels in blood that may impact the overall sweetness of food. This may be an evolutionary relict of diurnal animals like humans.[34]
Sweetness perception may differ between species significantly. For example, even among primates sweetness is quite variable.New World monkeys do not findaspartame sweet, whileOld World monkeys andapes (including most humans) all do.[35]Felids like domestic cats cannot perceive sweetness at all.[36] The ability to taste sweetness may be lost in carnivores who do not eat sweet foods like fruits, includingbottlenose dolphins,sea lions,spotted hyenas andfossas.
To depolarize the cell, and ultimately generate a response, the body uses different cells in the taste bud that each express a receptor for the perception of sweet, sour, salty, bitter orumami. Downstream of thetaste receptor, the taste cells for sweet, bitter and umami share the same intracellular signalling pathway.[37] Incoming sweet molecules bind to their receptors, which causes a conformational change in the molecule. This change activates the G-protein, gustducin, which in turn activatesphospholipase C to generate inositol trisphosphate (IP3), this subsequently opens the IP3-receptor and induces calcium release from the endoplasmic reticulum. This increase in intracellular calcium activates theTRPM5 channel and induces cellulardepolarization.[38][39] TheATP release channelCALHM1 gets activated by the depolarization and releases ATP neurotransmitter which activates the afferentneurons innervating the taste bud.[40][41]
Thecolor of food can affect sweetness perception. Adding more red color to a drink increases its perceived sweetness. In a study darker colored solutions were rated 2–10% higher than lighter ones despite having 1% less sucrose concentration.[42] The effect of color is believed to be due to cognitive expectations.[43] Some odors smell sweet and memory confuses whether sweetness was tasted or smelled.[44]
The development oforganic chemistry in the 19th century introduced many new chemical compounds and the means to determine theirmolecular structures. Early organic chemists tasted many of their products, either intentionally (as a means of characterization) or accidentally (due to poor laboratory hygiene). One of the first attempts to draw systematic correlations between molecules' structures and their tastes was made by a German chemist, Georg Cohn, in 1914. He hypothesized that to evoke a certain taste, a molecule must contain some structural motif (called asapophore) that produces that taste. With regard to sweetness, he noted that molecules containing multiplehydroxyl groups and those containingchlorine atoms are often sweet, and that among a series of structurally similar compounds, those with smallermolecular weights were often sweeter than the larger compounds.
In 1919, Oertly and Myers proposed a more elaborate theory based on a then-current theory of color in synthetic dyes. They hypothesized that to be sweet, a compound must contain one each of two classes of structural motif, aglucophore and anauxogluc. Based on those compounds known to be sweet at the time, they proposed a list of six candidate glucophores and nine auxoglucs.
From these beginnings in the early 20th century, the theory of sweetness enjoyed little further academic attention until 1963, whenRobert Shallenberger andTerry Acree proposed the AH-B theory of sweetness. Simply put, they proposed that to be sweet, a compound must contain ahydrogen bonddonor (AH) and aLewis base (B) separated by about 0.3nanometres. According to this theory, the AH-B unit of a sweetener binds with a corresponding AH-B unit on the biological sweetness receptor to produce the sensation of sweetness.
The B-X theory was proposed byLemont Kier in 1972.[45] While previous researchers had noted that among some groups of compounds, there seemed to be a correlation betweenhydrophobicity and sweetness. This theory formalized these observations by proposing that to be sweet, a compound must have a third binding site (labeled X) that could interact with a hydrophobic site on the sweetness receptor viaLondon dispersion forces. Later researchers have statistically analyzed the distances between the presumed AH, B, and X sites in several families of sweet substances to estimate the distances between these interaction sites on the sweetness receptor.
The most elaborate theory of sweetness to date is the multipoint attachment theory (MPA) proposed byJean-Marie Tinti andClaude Nofre in 1991. This theory involves a total of eight interaction sites between a sweetener and the sweetness receptor, although not all sweeteners interact with all eight sites.[46] This model has successfully directed efforts aimed at finding highly potent sweeteners, including the most potent family of sweeteners known to date, theguanidine sweeteners. The most potent of these,lugduname, is about 225,000 times sweeter than sucrose.
Despite some recorded instances oftaboos existing prohibiting sugar consumption, no culture is understood to have held taboos against sweet foods generally.[47]
