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Excerpt from Chapter 1: Let Us Play with Our Senses
Flavor Unworthy of the Name
We are discovering the subtleties of olfaction, but we lack the words to describe gustatory perceptions. Using the word flavor is an error ... in taste.
Gastronomy is also the art of speaking about the taste of dishes. Unfortunately, we lack the words, and the use of English is obscuring the French vocabulary. Goût, saveur, arôme, even flaveur... . What do these French terms signify? Researchers at INRA (L’Institut National de la Recherche Agronomique) in Jouy-en-Josas are providing the keys for understanding olfaction; their advances, as well as neurophysiology, show that the word flaveur, from the English flavor, has no place in French.
Peppery, Sweet, Salty: Your Sacred Balms
Taste is a sensation ... a gustatory one; the sensation one experiences when one eats has many components. Let us bring some food toward the mouth. First, our eyes show us its form and color; visual sensations are an integral part of taste. The most recent proof is the experiment carried out by the Bordeaux Institute of Enology (see “An Enological Slant” below), in which tasters described the taste of a white wine, colored red, with the words used for red wines, because the sight of red gave them the taste of red wine in the mouth. (The added colorants did not change the taste of wine tested blind.)
Tactile sensations play a part as well, but our culture and the widespread use of packaging has made us forget that touch, apart from in the mouth, is a component of taste. If our fingers discover small crystals on fruit jellies made from beets and sugar, and then sprinkled with crystallized sugar, we will experience it as blueberry or black currant fruit jellies.
Then we bring the food toward the mouth and we perceive its odor, which results from evaporation of food molecules. The more volatile these odorant molecules are, the greater number of receptor cells they stimulate in the nose.
Here physiologists have made progress by discovering the intermediaries between odorant molecules and receptor cells in the nose: the OBP (for odorant-binding proteins, that is, proteins that bind odorant molecules). First identified in insects, these proteins that bind to odorant molecules before leading them to the olfactory receptors have been discovered in the human organism. In 2000, E. Lacazette and his team found human genes analogous to the insect genes that code these proteins. At the INRA Center in Jouy-en-Josas, Loïc Briand and his colleagues demonstrated that these proteins are expressed in the nasal mucous. In vitro, synthetic proteins, copied from a human OBP, bound to numerous odorant molecules from the class of aldehydes and fatty acids.
Let us return to the question of vocabulary. The nose, which captures odorant molecules, perceives odors. Those odorant molecules are sometimes called “aromas,” confusing them with the sensation they engender; that is clearly a mistake, because a sensation is not a molecule. Moreover, preparations composed of odorant molecules judiciously blended are improperly called aromas.
Among the molecules evaporating in this way, certain ones do not stimulate the olfactory receptors but rather the receptors linked to a fascicule of nerve fibers with three branches, called the trigeminal nerve. That is the case with the menthol molecule, present in mint, which has an odor and which also communicates the sensation of coolness; to the olfactory sensation is added a so-called trigeminal sensation.
Now the food enters the mouth. Some of its molecules pass into the saliva and are then bound to molecules, called receptors, on the surface of special cells in the oral cavity. These molecules, called “sapid,” give the sensation of “tastes.” The cells that bear the receptors of sapid molecules are grouped together into papillae (the little rounded zones that we can see on the tongue). These are commonly called “taste buds” in English. But since we call the perception of taste “gustation,” what should we call the perception of tastes? I propose “sapiction.”
Warmed and broken down by mastication, the food also lets odorant molecules evaporate in the mouth; those molecules then rise along the back of the mouth toward the nose, through the retronasal fossae. This is still a matter of olfaction. In the mouth other food molecules act in different ways; some molecules stimulate the temperature sensors, others “excite.” Cells or sensors detect mechanical characteristics; thus we perceive hard, soft, greasy, wet, and so on.
An Orchestra of Sensations
The whole of all these sensations, sapictive (tastes), olfactive (odors), physical, thermal, trigeminal ... is the taste. Perceived by physiology, it is interpreted by the brain, which attaches qualities to it according to individual or social experiences (memories, emotions, training, etc.).
And what about flavor in all of this? Some food science specialists have proposed that the term brings together tastes and odor, but why combine these two sensations, since flavor is inaccessible? We cannot measure the sum of tastes and odor (at best, we can see it with the recent OBP findings, and we can begin to appreciate odors experimentally), and we can never perceive it, since our taste inextricably mixes tastes, odors, and other sensations. Flavor, neither perceptible nor measurable, is analogous to the angels that theology counts on the head of a pin.
Actually, the introduction of the word flaveur into French seems to result from a confusion with the English “flavor.” Thus, according to the British Standards Institute: “Flavor: the combination of taste and smell ... influenced by sensations of pain, heat, and cold, and by tactile sensations.” Thus the French word flaveur seems to be a faulty translation of the English word “flavor,” which translates into the French word goût—taste.
Let us stamp out that vile flaveur—we do have taste, after all!
Physiologists have identified a receptor for molecules that, like menthol, give the impression of coolness. They will be able to synthesize “cooler” molecules.
Why are drinks with mint refreshing, even when they are served hot? At the University of San Francisco, D. McKemy, W. Neuhausser, and D. Julius have identified the ADN that codes a neuronic receptor upon which the menthol molecule acts, the molecule that is responsible for the refreshing effect of mint. Then these neurophysiologists identified the receptors activated by cold and they again found the one for menthol. An important discovery!
How do we detect hot or cold? When a hot or cold stimulus, a liquid that we are drinking, for example, passes a certain temperature threshold, specialized neurons in the mouth emit chemical signals that convey the sensorial information to the spinal cord and the brain. That is how the somatosensory system detects changes in skin or mucous membrane temperature.
A few years ago, neurophysiologists identified the vanilloid receptor VR1, present on the surface of tongue neurons and activated by capsaicin, the principal molecule in hot pepper, which we recognize by its “burning” taste. They then demonstrated that VR1 receptors were responsible for the perception of heat through the neurons at a moderate temperature threshold; then they observed that another receptor, VRL-1, that is analogous to the first but that does not react to capsaicin, is activated by temperatures above 52°C. These two receptors belong to a family of ducts called ionic ducts, through which ions—and thus information—pass in transit from the exterior to the interior of the neurons. D. McKemy and his colleagues then questioned whether other molecules of the same type participated in the perception of—not heat this time but—cold, with the idea that cold receptors were perhaps the same as those for the coolness of menthol.
This inquiry is more than academic. For decades, chemists have been modifying the menthol molecule to obtain molecules giving the sensation of coolness without the taste of mint. Unfortunately, these new molecules are difficult to synthesize and the sensory results not always convincing. Thus there was incentive for studying the receptors of the cooling action of menthol to better determine the nature of molecules that stimulate that receptor.
We have known for half a century that menthol and analogous molecules act upon the trigeminal nerve, the three branches of which irrigate the nose, mouth, and face. At the same time, physiologists have identified in mammals the small group of trigeminal fibers that discharge at between 15 and 30°C and transmit the sensation of cold to the brain, as well as the fibers that react at temperatures below 15°C. Other studies have shown that cold (about 20°C) prompts influxes of calcium ions in those neurons sensitive to cold. Thus physiologists suspected that the sensation of cold resulted from the opening of the calcium ducts. D. McKemy and his colleagues adopted the method used for discovering the vanilloid receptor and tested the reactions of neurons isolated from rats, to cold, menthol, and its analogues.
Having isolated neurons that react to menthol and to cold, the neurophysiologists recovered the segments of ADN used by the neurons for making the various proteins (the receptors are proteins) of these neurons. Then they introduced those ADN segments into cells derived from embryo kidneys. Finally, using a fluorescence microscope, they examined the modifications in the calcium ion currents in the cells after exposure to menthol. Our researchers thus identified the genetic sequence that codes the menthol receptor: a protein called CMR1 that belongs to the same family as the vanilloid receptor for spicy and for hot.
The question was posed once again: Do cooling molecules and cold act upon the same receptors? To elucidate this point, the specialists first used genetically modified cells to test reactions to eucalyptol, menthol, camphor, cyclohexanol, and icilin (about two hundred times more powerful than menthol), and they observed that menthol, eucaplyptol, and icilin act upon this type of receptor. Then they tested reactions to the cold in frog oocytes that had been transfected by the receptor. When they reduced the temperature from 35°C to about 5°C, a significant current of calcium ions was released. In other words, the same receptor is responsible for the reaction to mentholated coolness and to cold. Finally, D. McKemy and his colleagues have shown that the receptor is an ionic duct stimulator expressed in the small neurons of the trigeminal ganglia. Their original hypothesis was confirmed, all the more so when they observed that dogs tremble with cold when menthol is injected into their blood. The discovery of a strong chemical resemblance between the CMR1 receptor and a protein identified in the epithelium of the prostate explains this phenomenon. The article in Nature in which the three neurophysiologists present their work includes this note under the authors’ names: “The three authors contributed equally to the published work.” The scientific community understands from this note that the authors are aware of the importance of their discovery and that they anticipate the consequences of their work. Knowing the molecular structure of the receptor, chemists will be able to synthesize molecules capable of binding more specifically to that receptor than menthol or even icilin does, opening a considerable market, as the lovers of mint chewing gum know.
Tastes and Receptors
The discovery of a gustatory receptor for amino acids puts compounds that amplify tastes on the right track.
Molecular biology can identify the receptors of aromatic and sapid molecules; to a molecular question, a molecular response. Also, month after month, discoveries in the physiology of gustation follow one upon another. Cold receptors were discovered to be the same as those for menthol; C. Zuker, at the Howard Hughes Institute, and N. Ryba, at the Odontology Institute of Bethesda, then identified a protein that constitutes a gustatory receptor of amino acids.
Gourmandism is based on perceptions that are agreeable because they are vital to survival. The organism recognizes molecules it needs and toxic molecules that it must avoid. Sugar, which provides energy, is perceived as agreeable; alkaloids, often toxic, have an unpleasant bitterness (bitter tastes are only appreciated through cultivation; think of beer, which children do not like).
In addition to the tastes recognized by language, like sweet, salty, and sour, many others exist. For example, the taste umami has been recognized for a decade as the taste of kombu algae (kelp) broth, a taste owed to alanine and glutamic acid. Besides those two, other amino acids (the constituent molecules in proteins) are also reputed to have tastes, but their descriptions vary according to the individual.
It is not easy to determine the tastes of foods, because they cannot be separated from the odor, the appearance, the texture, the hotness, the cold... . To “approximate” the taste of amino acids, we can place on the tongue a mature, slightly salty cheese at room temperature, while using a small pump to blow a current of air into the nose (to eliminate the odor).
C. Zuker and N. Ryba identified the constituent proteins for the receptors of various sweet and bitter molecules in gustatory cells. They published in Nature their studies on the receptor named T1R1+3, which, among mammals, is activated by amino acids. Formed by two already known gustatory receptors (T1R1 and T1R3), the complex T1R1+3 detects the L amino acids, those which we need to live, but not the D amino acids, symmetrical to the L amino acids in reverse, their mirror image, and not used by the organism.
Before their work, type T1R and T2R receptors had been identified. Gustatory cells equipped with T2R-type receptors detect bitter molecules; those that have T1R1 and T1R3 proteins detect sweet molecules.
Amino Acids Revealed
Physiologists first studied the receptors in the T1R family, which recognizes amino acids such as monoglutamate, gamma-aminobutyric acid (or GABA), and arginine. The receptors in the T1R family are of many types and form various gustatory receptors. For example, we have seen that T1R2 and T1R3 are sometimes expressed together (they thus form a receptor of sweet), as are T1R1 and T1R3; only T1R3 has been observed in isolation in gustatory cells.
Using embryo kidney cells, through gene insertion, physiologists have caused various receptors to be expressed in various combinations, beginning with cells that simultaneously express T1R2 and T1R3. The reaction of receptors was detected by the movements of calcium ions (made evident using fluorescent markers) between the interior and the exterior of the cells. No L amino acid activated these genetically modified cells, whereas several D amino acids (which have a taste described as sweet by humans and are also pleasing to mice) unleashed notable cell activity. Then the researchers tested cells expressing either T1R1 receptors or T1R3 receptors; they did not react to the L amino acids either. On the other hand, the simultaneous expression of two T1R1 and T1R3 receptors prompted an intense reaction with the L amino acids, while the D amino acids provoked no reaction.
Having thus observed a detection of amino acids, the physiologists pursued the investigation by testing other molecules that engender a sensation analogous to umami, like inosine monophosphate (IMP). In rats this molecule provokes a gustatory activation detected by electrical registerings of gustatory nerves. In the experiments with renal cells possessing receptors T1R1+3, the reaction with L amino acids was considerably increased by IMP, which is thus a true “taste enhancer” (alone, IMP prompts no reaction). On the market, this molecule would meet with great success among gourmands!
Is the T1R1+3 receptor a umami receptor? Its reactions with many amino acids, as well as with sodium monoglutamate (MSG), seems to indicate that it is, but is it a principal or secondary receptor? The discovery leaves many questions open. For example, this receptor reacts with most L amino acids, even though all amino acids do not have the same taste. Some are equally pleasing to mice and humans, while others are neutral. Some are perceived as bitter by human tasters and rejected by the mice. Worse still, only a few amino acids have a taste analogous to umami.
With the help of cells that express the receptor, we will be able to study various molecules in order to understand what foods offer the umami-type taste. Sensorial tests have revealed that this taste is provided by cheese, meat, milk, tomatoes, asparagus, and certain seafood, but we will now be able to discover new molecules to replace “taste enhancers” like MSG or the inositides, now widely (excessively?) used by the food industry.
The Bitter Tooth
Teeth are indispensable to a good perception of the sweet, salty, and bitter tastes of foods. A single perception is lacking... .
Common sense is no guarantee of sound reasoning. On the pretext that we smell food twice when we eat (once when the food reaches the nose before entering the mouth; once when the odorant molecules released by mastication rise toward the nose through the retronasal fossae), it was decided that olfaction was the principal sense for taste. Moreover, the frequent loss of smell caused by colds made us believe that smell was everything and the perception of taste hardly anything.
Neurophysiological discoveries in the last decades are undermining this dogma. Why has it not been observed that the nonperception of tastes, exactly like the nonperception of odor, completely eliminates the sensation of taste? The experience of burning one’s mouth on food that is too hot is sadly familiar ... and demonstrative. And so? Sensorial neurophysiology shows that taste is a synthetic sensation composed of information of many different kinds: visual, olfactive, “sapictive” (the perception of tastes), trigeminal (hot, cool), mechanical... . And the loss of a single kind of information from the synthetic sensation is disastrous for taste recognition (which is the “goal” of the gustatory system that, shaped by evolution, aims to ensure the recognition of food).
“A single person lacking, and it is all unpeopled,” lamented Lamartine. All the perceptions are necessary to be able to obtain the taste of a food. Does this idea hold for the consistency of a food as well? Annick Faurion at the Jouy-en-Josas INRA and his colleagues at the universities of Paris and Tours researched the influence, if any, of dental treatments on taste.
Dental treatments, especially the extraction of teeth, are frequent. In a prospective study, D. M. Shafer and his colleagues at the Odontology School in Phoenix analyzed taste deficits among half the patients who had had their third molars removed. These deficits resulted from damage to gustatory nerve fibers. Similarly, it was observed that dental surgery can diminish gustatory sensations for as long as six months, as a result of compression, stretching, or edema in the lingual nerve.
In order to learn if dental treatments cause a loss of gustatory sensitivity, A. Faurion and his colleagues considered 387 healthy, nonsmoking subjects, under no medical treatments; their mouths were x-rayed if necessary. The subjects were divided into groups according to the number of dental extractions or treatments of the dental canal, and their sensitivity to tastes was determined using an electrogustrometric technique. This consisted of stimulating little zones on the tongue with the help of a small electrode. Under the effect of the current, ions contained in the saliva were put in contact with papilla receptors, and the threshold of sensitivity was the smallest amount of current giving rise to the perception of taste. Nine zones of the tongue were tested: the tip; the anterior edges where the density of so-called fungiform papillae is maximal; the dorsal part, left and right, where the density of those papillae is minimal; the edges of the tongue; and the posterior part, both sides. For each determination of threshold, the electrode was placed on the tongue and, after a time of adaptation to the parasitic mechanical stimulation, a current was applied for one second. The subjects had only to say that they perceived a sensation. (The subjects did not know if a current was applied or not.)
The results are unequivocal: The greater number of unafferent teeth (or teeth without nerves), the higher the threshold of gustatory sensitivity (that is, sensitivity is diminished). It is not a question of age; no matter what their age, subjects having more than seven “dead” teeth have thresholds of perception higher than those of other subjects. Inversely, according to age group, no statistical difference was observed for subjects having fewer dead teeth. Moreover, an association was observed between the localization of deficits in taste perception and the position of extracted or treated teeth. The highest thresholds for anterior sites, unrelated to an anterior injury, showed that the neurophysiological convergence of somatosensory dental paths and sapictive paths could be responsible for the lessening of sapictive sensitivity.
Thus, the loss of taste in older individuals does not seem to result from a disappearance of taste buds, as is often believed, but rather from tooth loss and poor perception of the consistency of foods. To remain creatures of taste, let us keep our teeth!
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